Chronic intermittent hypoxia
and incremental cycling exercise independently depress muscle in vitro maximal
Na+-K+-ATPase activity in well-trained athletes.
Aughey RJ, Gore CJ, Hahn AG, Garnham AP, Clark SA, Petersen AC,
Roberts AD, McKenna MJ.
School of Human Movement, Recreation and Performance (FO22) Victoria University
of Technology, P.O. Box 14428, MCMC, Melbourne, Victoria 8001, Australia.
Athletes commonly attempt to enhance performance by training in normoxia but
sleeping in hypoxia [live high and train low (LHTL)]. However, chronic hypoxia
reduces muscle Na(+)-K(+)-ATPase content, whereas
fatiguing contractions reduce Na(+)-K(+)-ATPase activity, which each may impair
performance. We examined whether LHTL and intense exercise would decrease
muscle Na(+)-K(+)-ATPase activity and whether these
effects would be additive and sufficient to impair performance or plasma K(+)
regulation. Thirteen subjects were randomly assigned to two fitness-matched
groups, LHTL (n = 6) or control (Con, n = 7). LHTL slept at simulated moderate
altitude (3,000 m, inspired O(2) fraction = 15.48%)
for 23 nights and lived and trained by day under normoxic conditions in
Publication Types:
· Clinical Trial
· Randomized Controlled Trial
Effects
of hypoxic interval training on cycling performance.
Roels B, Millet GP, Marcoux CJ, Coste O, Bentley DJ, Candau RB.
UPRES EA 3759 Faculty of Sport Sciences, 700 avenue
Pic St Loup, 34090
PURPOSE: The aim of this study was to test the hypothesis that intermittent
hypoxic interval training improves sea level cycling performance more than
equivalent training in hypoxia or normoxia. METHODS: Thirty-three well-trained
cyclists and triathletes (25.9 +/- 2.7 yr, VO(2max) 66.1 +/- 6.1 mL.min(-1).kg(-1))
were divided into three groups: intermittent hypoxic (IHT, N = 11, P(I)O(2)
of 100 mm Hg), intermittent hypoxic interval training (IHIT, N = 11) and normoxia
(Nor, N = 11, P(I)O(2) of 160 mm Hg) and completed a 7-wk training program,
consisting of two high-intensity (100 or 90% relative peak power output) interval
training sessions each week. Each interval training session was performed
in a laboratory on the subject's own bicycle, in normoxic or hypoxic conditions
for the Nor and the IHT group, respectively. The
IHIT group performed warm-up and cool-down plus recovery from each interval
in hypoxic conditions. In contrast to IHT, interval exercise bouts were performed
in normoxic conditions. RESULTS: Mean power output during a 10-min cycle time
trial improved after the first 4 wk of training by 5.2 +/- 3.9, 3.7 +/- 5.9,
and 5.0 +/- 3.4% for IHIT, IHT, and Nor, respectively, without significant
differences between groups. Moreover, mean power output did not show any significant
improvement in the following 3 wk in any group. VO(2max) (L.min(-1)) increased only in IHIT during the training
period (8.7 +/- 9.1%; P < 0.05). No changes in cycling efficiency or in
hematological variables (P > 0.05) were observed. CONCLUSION: Four weeks
of interval training induced an improvement in endurance performance. However,
short-term exposure to hypoxia (approximately 114 min.wk(-1))
did not elicit a greater increase in performance or any hematological modifications.
Chronic intermittent hypoxia
and incremental cycling exercise independently depress muscle in vitro maximal
Na+-K+-ATPase activity in well-trained athletes.
Aughey RJ, Gore CJ, Hahn AG, Garnham AP, Clark SA, Petersen AC,
Roberts AD, McKenna MJ.
School of Human Movement, Recreation and Performance (FO22) Victoria University
of Technology, P.O. Box 14428, MCMC, Melbourne, Victoria 8001, Australia.
Athletes commonly attempt to enhance performance by training in normoxia but
sleeping in hypoxia [live high and train low (LHTL)]. However, chronic hypoxia
reduces muscle Na(+)-K(+)-ATPase content, whereas
fatiguing contractions reduce Na(+)-K(+)-ATPase activity, which each may impair
performance. We examined whether LHTL and intense exercise would decrease
muscle Na(+)-K(+)-ATPase activity and whether these
effects would be additive and sufficient to impair performance or plasma K(+)
regulation. Thirteen subjects were randomly assigned to two fitness-matched
groups, LHTL (n = 6) or control (Con, n = 7). LHTL slept at simulated moderate
altitude (3,000 m, inspired O(2) fraction = 15.48%)
for 23 nights and lived and trained by day under normoxic conditions in
Publication Types:
· Clinical Trial
· Randomized Controlled Trial
| Eur J Appl Physiol. 2005 Mar;93(5-6):701-7. Epub 2004 Nov 25. |
Aggravated
hypoxia during breath-holds after prolonged exercise.
Lindholm P, Gennser M.
Section of Environmental Physiology, Department of Physiology
and Pharmacology, Karolinska Institutet, Berzelius vag 13, 17177
Hyperventilation prior to breath-hold diving increases the risk of syncope
as a result of hypoxia. Recently, a number of cases of near-drownings in which
the swimmers did not hyperventilate before breath-hold diving have come to
our attention. These individuals had engaged in prolonged exercise prior to
breath-hold diving and it is known that such exercise enhances lipid metabolism
relative to carbohydrate metabolism, resulting in a lower production of CO(2)
per amount of O(2 )consumed. Therefore, our hypothesis was that an exercise-induced
increase in lipid metabolism and the associated reduction in the amount of
CO(2) produced would cause the urge to breathe to
develop at a lower P O(2), thereby increasing the risk of syncope due to hypoxia.
Eight experienced breath-hold divers performed 5 or 6 breath-holds at rest
in the supine position and then 5 or 6 additional breath-holds during intermittent
light ergometer exercise with simultaneous apnoea (dynamic apnoea, DA) on
two different days: control (C) and post prolonged sub-maximal exercise (PPE),
when the breath-holds were performed 30 min after 2 h of sub-maximal exercise.
After C and before the prolonged submaximal exercise subjects were put on
a carbohydrate-free diet for 18 h to start the depletion of glycogen. The
respiratory exchange ratio ( RER) and end-tidal P CO(2), P O(2), and SaO(2) values were
determined and the data were presented as means (SD). The RER prior to breath-holding
under control conditions was 0.83 (0.09), whereas the corresponding value
after exercise was 0.70 (0.05) ( P <0.01). When
the three apnoeas of the longest duration for each subject were analysed,
the average duration of the dynamic apnoeas was 96 (14) s under control conditions
and 96 (17) s following exercise. Both P O(2) and
P CO(2) were higher during the control dynamic apnoeas than after PPE [
Effect of a
repeated series of intermittent hypoxic exposures on ventilatory response
in humans.
Katayama K, Fujita H, Sato K, Ishida K, Iwasaki K, Miyamura M.
The purpose of this study was to elucidate the magnitude
and the time course of ventilatory changes resulting from a repeated series
of hypoxic exposures. Eight healthy males participated in the present study.
The subjects spent 1 h/day in normobaric hypoxia (12% inspired oxygen). Inspired
minute ventilation (V(I)), end-tidal partial pressure
of carbon dioxide (P(ET(CO2))), and arterial oxygen saturation (SaO2) were
measured in a hypoxic tent. These measurements were taken for 10 consecutive
days (series 1), and were taken again after the subjects had been away from
hypoxic exposure for 1 month (series 2). P(ET(CO2))
decreased and SaO2 increased progressively in the hypoxic tent during the
10 days of intermittent hypoxia in series 1. At the onset of series 2 (days
1 to 3), P(ET(CO2)) was significantly lower and SaO2
was significantly higher than those on day 1 during series 1. These results
suggest that humans who have had previous hypoxic exposure adapt sooner to
hypoxic condition due to an increase in the magnitude of hyperventilation
in the first few days of a series of reexposures to hypoxia
Spinal synaptic enhancement with
acute intermittent hypoxia improves respiratory function after chronic cervical
spinal cord injury.
Golder
FJ, Mitchell GS.
Department of Comparative Biosciences,
Respiratory insufficiency is the leading cause of death after high-cervical
spinal cord injuries (SCIs). Although respiratory motor recovery can occur
with time after injury, the magnitude of spontaneous recovery is limited.
We hypothesized that partial respiratory motor recovery after chronic cervical
SCI could be strengthened using a known stimulus for spinal synaptic enhancement,
intermittent hypoxia. Phrenic motor output was recorded before and after intermittent
hypoxia from anesthetized, vagotomized, and pump-ventilated control and C2
spinally hemisected rats at 2, 4, and 8 weeks after injury. Weak spontaneous
phrenic motor recovery was present in all C2-injured rats via crossed spinal
synaptic pathways that convey bulbospinal inspiratory premotor drive to phrenic
motoneurons on the side of injury. Intermittent hypoxia augmented crossed
spinal synaptic pathways [phrenic long-term facilitation; pLTF] for up to
60 min after hypoxia at 8 weeks, but not 2 weeks, after injury. Ketanserin,
a serotonin 2A receptor antagonist, administered before intermittent hypoxia
at 8 weeks after injury prevented pLTF. Serotonergic innervation near phrenic
motoneurons was assessed after injury. The limited magnitude of pLTF at 2
weeks was associated with an injury-induced reduction in serotonin-containing
nerve terminals in the vicinity of phrenic motoneurons ipsilateral to C2 hemisection.
Thereafter, pLTF magnitude progressively increased with the recovery of serotonergic
innervation in the phrenic motor nucleus. Intermittent hypoxia (or pLTF) has
intriguing possibilities as a therapeutic tool, because its greatest efficacy
may be in patients with chronic SCI, a time when most patients have already
achieved maximal spontaneous functional recovery.
Augmented endothelin
vasoconstriction in intermittent hypoxia-induced hypertension.
Allahdadi
KJ, Walker BR, Kanagy NL.
Vascular Physiology Group, Department of Cell Biology and Physiology, University
of New Mexico, Health Sciences Center, Albuquerque, NM 87131, USA.
We reported previously that simulating sleep apnea in rats by exposing them 7 hours per day to intermittent hypoxia/hypercapnia (IH)
elevates plasma endothelin-1 and causes hypertension, which is reversed by
an endothelin-1 antagonist. We hypothesized that in this model of sleep apnea-induced
hypertension, vascular sensitivity to endothelin-1 is increased in combination
with the elevated plasma endothelin-1 to cause the endothelin-1-dependent
hypertension. In small mesenteric arteries with endothelial function disabled
by passing air through the lumen, diameter and vessel wall [Ca2+] were recorded
simultaneously. IH arteries demonstrated increased constrictor sensitivity
to endothelin-1 (percentage max constriction 100+/-0% IH versus 80+/-10% Sham;
P<0.05). This was accompanied by increased calcium sensitivity of IH arteries.
In contrast, constrictor sensitivity and increases in vessel wall [Ca2+] to
KCl and phenylephrine were not different between IH and Sham arteries. We
have shown previously that endothelin-1 constriction in mesenteric arteries
is mediated by endothelin A receptors. In the current study, the selective increase in
endothelin-1 constriction in IH resistance arteries was accompanied by increased
expression of endothelin A receptor expression (densitometry units 271+/-23
IH versus 158+/-25 Sham; P<0.05). Thus, IH hypertension appears to cause
alterations in signaling components unique to endothelin-1 at the receptor
level and in postreceptor signaling that increases calcium sensitivity during
endothelin A activation. Future studies will determine
the specific changes in vascular smooth muscle signaling in IH hypertension
causing this augmented contractile phenotype.
Changes in
ventilatory responses to hypercapnia and hypoxia after intermittent hypoxia
in humans.
Katayama K, Sato K, Matsuo H, Hotta N, Sun Z, Ishida K, Iwasaki K, Miyamura M.
The purpose of this study was to clarify the changes
in hypercapnic and hypoxic ventilatory responses (HCVR and HVR) after intermittent
hypoxia and following the cessation of hypoxic exposure. Twenty-nine males
were assigned to one of four groups, i.e., a hypoxic (EX1-H, n=7) or a control
(EX1-C, n=7) group in Experiment 1, and a hypoxic (EX2-H, n=8) or a control
(EX2-C, n=7) group in Experiment 2. In each experiment, the hypoxic tent system
was utilized for intermittent hypoxia, and the oxygen levels in the tent were
maintained at 12.3+/-0.2%. In Experiment 1, the EX1-H group spent 3 h/day
in the hypoxic tent for 1 week. HCVR and HVR were determined before and after
1 week of intermittent hypoxia, and again 1 and 2 week after the cessation
of hypoxic exposure. In Experiment 2, the subjects in the EX2-H group performed
3 h/day for 2 weeks in intermittent hypoxia. HCVR and HVR tests were carried
out before and after intermittent hypoxia, and were repeated again after 2
weeks of the cessation of hypoxic exposure. The slope of the HCVR in the EX1-H
group did not show a significant increase after 1 week of intermittent hypoxia,
while HCVR in the EX2-H group increased significantly after 2 weeks of intermittent
hypoxia. The HCVR intercept was unchanged following 1 or 2 weeks of intermittent
hypoxia. There was a significant increase in the slope of the HVR after 1
and 2 weeks of intermittent hypoxia. The increased HCVR and HVR returned to
pre-hypoxic levels after 2 weeks of the cessation of hypoxia. These results
suggest that 3 h/day for 2 weeks of intermittent hypoxia leads to an increase
in central hypercapnic ventilatory chemosensitivity, which is not accompanied
by a re-setting of the central chemoreceptors, and that the increased hypercapnic
and hypoxic chemosensitivities are restored within 2 weeks after the cessation
of hypoxia.
Publication Types:
· Clinical Trial
Chronic intermittent hypoxia
increases infarction in the isolated rat heart.
Joyeux-Faure M,
Stanke-Labesque F,
Lefebvre B, Beguin P, Godin-Ribuot D,
Ribuot C, Launois SH, Bessard G, Levy P.
Laboratoire HP2, Hypoxie Physio-Pathologie, Faculte de Pharmacie, Domaine
de la Merci, 38706 La Tronche, France. marie.faure@ujf-grenoble.fr
Coronary heart disease is frequently associated with obstructive sleep apnea
syndrome and treating obstructive sleep apnea appears to significantly improve
the outcome in coronary heart disease. Thus we have developed a rat model
of chronic intermittent hypoxia (IH) to study the influence of this condition
on myocardial ischemia-reperfusion tolerance and on functional vascular reactivity.
Wistar male rats were divided in three experimental groups (n = 12 each) subjected
to chronic IH (IH group), normoxia (N group), or control conditions (control
group). IH consisted of repetitive cycles of 1 min (40 s with inspired O(2)
fraction 5% followed by 20 s normoxia) and was applied for 8 h during daytime,
for 35 days. Normoxic cycles were applied in the same conditions, inspired
O(2) fraction remaining constant at 21%. On day 36,
mean arterial blood pressure (MABP) was measured before isolated hearts were
submitted to an ischemia-reperfusion protocol. The thoracic aorta and left
carotid artery were also excised for functional reactivity studies. MABP was
not significantly different between the three experimental groups. Infarct
sizes (in percent of ventricles) were significantly higher in IH group (46.9
+/- 3.6%) compared with N (26.1 +/- 2.8%) and control (21.7 +/- 2.1%) groups.
Vascular smooth muscle function was similar in aorta and carotid arteries
from all groups. The endothelium-dependent relaxation in response to acetylcholine
was also similar in aorta and carotid arteries from all groups. Chronic IH
increased heart sensitivity to infarction, independently of a significant
increase in MABP, and did not affect vascular reactivity of aorta and carotid
arteries.
Chronic intermittent asphyxia
increases platelet reactivity in rats.
Dunleavy M, Dooley M, Cox D, Bradford A.
Department of
Sleep-disordered breathing is associated with chronic intermittent asphyxia
and with a variety of cardiovascular abnormalities. Cardiovascular morbidity
and mortality are linked to altered platelet function, and platelet function
is affected in sleep-disordered breathing. As there is evidence that chronic
continuous hypoxia may alter platelet number and function, the aim of the
present study was to test the hypothesis that chronic intermittent asphyxia
affects platelet count, activation and aggregation. Rats were treated with
a hypercapnic hypoxic gas mixture (minimum of 6-8% O2, maximum of 10-14% CO2)
for 15 s, twice per minute for 8 h per day for 3 weeks. Blood was analysed
for platelet count, platelet activation (CD62p expression using flow cytometry),
response to low dose ADP, haematocrit, red cell count
and haemoglobin concentration. A platelet function analyser measured the closure
time of an aperture, dependent on platelet aggregation. Compared to controls
(n = 16), chronic intermittent asphyxia (n = 13) reduced body weight and increased
right ventricular weight but had no significant effect on platelet count (control,
880.4 +/- 20.1; treated: 914.1 +/- 35.2 x 10(3) microl(-1); mean +/- S.E.M.),
on the reduction in platelet count in response to ADP (control, reduced to
206.7 +/- 49.0; treated, reduced to 193.8 +/- 35.9 x 10(3) microl(-1)), or
on the percentage of platelets positive for CD62p (control, 5.2 +/- 0.7; treated,
6.0 +/- 0.8%). Chronic intermittent asphyxia significantly (P = 0.037) reduced
the closure time (control, 90.9 +/- 7.7; treated, 77.7 +/- 3.8 s), indicating
greater adhesion and aggregation. There was no significant difference in haematocrit,
red cell count and haemoglobin concentration. In conclusion, chronic intermittent
asphyxia has no effect on platelet count but does increase platelet aggegation
in rats. These data support the idea that chronic intermittent asphyxia alters
platelet function in sleep-disordered breathing.
Inducible nitric oxide synthase
contributes to intermittent hypoxia against ischemia/reperfusion injury.
Ding HL, Zhu HF, Dong JW, Zhu WZ, Yang WW, Yang HT, Zhou ZN.
Physiological Laboratory of Hypoxia,
AIM: To investigate the role of inducible nitric oxide synthase (iNOS)-derived
nitric oxide (NO) in the cardioprotection of intermittent hypoxia (IH) against
ischemia/reperfusion (I/R) injury. METHODS: Langendorff-perfused isolated
rat hearts were used to measure variables of left ventricular function during
baseline perfusion, ischemia, and reperfusion period. Nitrate plus nitrite
(NOx) content in myocardium was measured using a biochemical method. iNOS mRNA and protein expression in rat left ventricles were
detected using reverse transcription polymerase chain reaction (RT-PCR) and
Western blot, respectively. RESULTS: Myocardial function recovered better
in IH rat hearts than in normoxic control hearts. The iNOS-selective inhibitor
aminoguanidine (AG) (100 micromol/L) significantly inhibited the protective
effects of IH, but had no influence on normoxic rat hearts. The baseline content
of NOx in IH hearts was higher than that in normoxic hearts. After 30 min
ischemia, the NOx level in normoxic hearts increased compared to the corresponding
baseline level, whereas there was no significant change in IH hearts. However,
the NOx level in IH hearts was still higher than that of normoxic hearts during
ischemia and reperfusion period. AG 100 micromol/L significantly diminished
the NOx content in IH and normoxic hearts during ischemia and reperfusion
period. The baseline levels of iNOS mRNA and protein in IH hearts were higher
than those of normoxic hearts. Compared to the corresponding baseline level,
iNOS mRNA and protein levels in normoxic rat hearts increased and those in
IH rat hearts decreased after reperfusion. The addition of AG 100 micromol/L
significantly decreased iNOS mRNA and protein expression in IH rat hearts
after I/R. CONCLUSION: IH upregulated the baseline level of iNOS mRNA and
protein expression leading to an increase in NO production, which may play
an important role in the cardiac protection of IH against I/R injury.
| Am J Respir Crit Care Med. 2005 Oct 1;172(7):915-20. Epub 2005 Jun 23. |
Oxidative stress and left ventricular function with chronic
intermittent hypoxia in rats.
Chen L, Einbinder E,
Zhang Q, Hasday J, Balke CW, Scharf SM.
Rationale and Objectives: Obstructive sleep apnea (OSA) is associated with
oxidative stress and myocardial dysfunction. We hypothesized that the chronic
intermittent hypoxia (CIH) component of OSA is sufficient to lead to these
adverse effects.Methods and Results: Rats were exposed to CIH (nadir O(2), 4-5%) for 8 hours/day, 5 days/week, for 5 weeks. Results
were compared with similarly handled controls (HC). Outcomes included blood
pressure (tail cuff plethysmograph), echocardiographic and invasive measures
of left-ventricular (
Effects of
Intermittent Hypoxia on Heart Rate Variability during Rest and Exercise.
Povea C, Schmitt L, Brugniaux J,
Nicolet G, Richalet JP,
Fouillot JP.
Universite Paris 13, Faculte de Medecine,
Povea, Camilo; Laurent Schmitt; Julien Brugniaux; Gerard Nicolet; Jean-Paul
Richalet; and Jean-Pierre Fouillot. Effects of intermittent
hypoxia on heart rate variability during rest and exercise. High Alt.
Med. Biol. 6:215-225, 2005.-Changes in heart rate variability induced by an
intermittent exposure to hypoxia were evaluated in
athletes unacclimatized to altitude. Twenty national elite athletes trained
for 13 days at 1200 m and either lived and slept
at 1200 m (live low, train low, LLTL) or between 2500 and 3000 m (live high,
train low, LHTL). Subjects were investigated at 1200 m prior to and at the
end of the 13-day training camp. Exposure to acute hypoxia (11.5% O(2))
during exercise resulted in a significant decrease in spectral components
of heart rate variability in comparison with exercise in normoxia: total power
(p < 0.001), low-frequency component. LF (p < 0.001),
high-frequency component, HF (p < 0.05). Following acclimatization,
the LHTL group increased its LF component (p < 0.01) and LF/HF ratio during
exercise in hypoxia after the training period. In parallel, exposure to intermittent
hypoxia caused an increased ventilatory response to hypoxia. Acclimatization
modified the correlation between the ventilatory response to hypoxia at rest
and the difference in total power between normoxia and hypoxia (r (2) = 0.65,
p < 0.001). The increase in total power, LF component, and LF/HF ratio
suggests that intermittent hypoxic training increased the response of the
autonomic nervous system mainly through increased sympathetic activity.
Sex Differences
in Blood Pressure Response to Intermittent Hypoxia in Rats.
Hinojosa-Laborde
C, Mifflin SW.
Department of Anesthesiology, University of Texas Health Science Center at
San Antonio, San Antonio, Tex; Department of Pharmacology, University of Texas
Health Science Center at San Antonio, San Antonio, Tex.
Intermittent hypoxia is used to mimic the arterial hypoxemia that occurs during
sleep apnea. The present study examined the blood pressure and heart rate
responses to exposure to intermittent hypoxia in male rats and in female rats
before and after ovariectomy. Rats were instrumented with telemetry transmitters
and blood pressure, heart rate, and activity measured during 7 days of exposure
to intermittent hypoxia (3 minutes of normoxia [21% oxygen] alternating with
3 minutes 10% oxygen between 8 AM and 4 PM, remainder of day at normoxia).
Blood pressure increased in males, females, and ovariectomized females in
response to 7 days of intermittent hypoxia during the hours of exposure to
hypoxia. Blood pressure increased less in intact females (average change in
blood pressure 1.6+/-0.6 mm Hg, n=11) than in females studied after ovariectomy
(5.1+/-1.1 mm Hg, n=6) or males (5.4+/-1.0 mm Hg, n=10). This elevated blood
pressure persisted throughout the remainder of the day when the animals were
not exposed to intermittent hypoxia and remained significantly attenuated
in female rats. Ovariectomy abolished the protection against the elevated
blood pressure response to intermittent hypoxia in females. Heart rate increased
only in males, and only during the period of the day associated with intermittent
hypoxia. Female rats were protected against this tachycardia independent of
the ovarian hormones. These results indicate that females are protected from
the hypertensive and tachycardia effects of intermittent hypoxia.
| Am J Physiol Heart Circ Physiol. 2005 Sep 9; [Epub ahead of print] |
Postnatal intermittent hypoxia
alters baroreflex function in adult rats.
Soukhova-O'hare GK,
Cheng Z, Roberts AA, Gozal D.
Pediatrics,
Chronic perinatal intermittent hypoxia (IH) could have long-term cardiovascular
effects by altering baroreflex function. To examine this hypothesis, we exposed
rats (n=6/group) for postnatal days P1-P30, or prenatal embryonic days E5-
E21, to IH (8% ambient O2 for 90 s following 90 s of 21% of O2, 12 hr/day),
or to normoxia (control). Baroreflex sensitivity (BRS) and cardiac chronotropic
responses were examined in anesthetized animals 3.5 to 5 months later by infusing
phenylephrine (PE) or sodium nitroprusside (NP) (6-12 microg/min, 1-2 min,
i.v.) during normoxia and after 18 min of acute IH (IHA). In controls after
IHA, baroreflex gain was 42% (P<0.05) less than during normoxia. BRS in
the postnatal IH group during normoxia was approximately 50% less than in
control rats and similar to controls after IHA. The heart rate (HR) response
to PE in the IH group was also less than in controls (P<0.05) and was not
changed by IHA. BRS and HR responses in the prenatal IH group were similar
to the normoxic control group. Vagal efferent projections to atrial ganglia
neurons in rats after postnatal IH (n=4) were examined by injecting tracer
into the left nucleus ambiguous. After 35 days of postnatal IH, basket ending
density was reduced by 17% (P<0.001) and vagal axon varicose contacts by
56% (P<0.001) compared to controls. We conclude that reduction of vagal
efferent projections in cardiac ganglia could be a cause of long-term modifications
in baroreflex function.
Intermittent Hypoxia during Development
Induces Long-Term Alterations in Spatial Working Memory, Monoamines, and Dendritic
Branching in Rat Frontal Cortex.
Kheirandish L,
Gozal D, Pequignot JM,
Pequignot J,
Row BW.
Exposure to intermittent hypoxia (IH), such as occurs in sleep-disordered
breathing, is associated with increased apoptosis in vulnerable brain regions
as well as with spatial reference memory deficits in adult and developing
rats. The latter are more susceptible to IH, suggesting that early exposure
to IH may have long-term consequences. Rats were exposed to 14 d of room air
(RA) or IH starting at postnatal d 10. Working memory was then assessed in
the water maze at 4 mo of age using a delayed matching to place task in which
the rats were required to locate a submerged platform hidden in a novel location
on the first trial (T1 or acquisition trial), and then remember that position
after a delay (T2 or test trial). Mean escape latencies and swim distances
were derived and the savings (T1-T2) were used as a measure of working memory.
Male but not female rats exposed to IH showed working memory deficits at both
a 10- and 120-min delay (for both latency and pathlength). Additionally, Sholl
analysis of Golgi-stained neurons revealed decreased dendritic branching in
the frontal cortex, but not the hippocampus, of male rats exposed to IH. Norepinephrine
concentrations, dopamine turnover, and tyrosine hydroxylase activity were
increased similarly in males and females. However, increased dopamine concentrations
were present only in the frontal cortex of female rats. In conclusion, exposure
to IH during a critical developmental period is associated with long-term
alterations in frontal cortical dopaminergic pathways that may underlie gender
differences in neurobehavioral deficits.
Intermittent Hypoxia Induces
Hyperlipidemia in Lean Mice.
Li J, Thorne LN, Punjabi NM, Sun CK, Schwartz AR,
Smith PL, Marino RL, Rodriguez A,
Hubbard WC, O'donnell CP,
Polotsky VY.
Department of Medicine, Divisions of Pulmonary and Critical Care Medicine,
Endocrinology and Metabolism, and Allergy and Clinical Immunology, Johns Hopkins
University, Baltimore, Md; and the Department of Medicine, Division of Pulmonary,
Allergy, and Critical Care Medicine, University of Pittsburgh School of Medicine,
Pennsylvania.
Obstructive sleep apnea, a syndrome leading to recurrent intermittent hypoxia
(IH), has been associated previously with hypercholesterolemia, independent
of underlying obesity. We examined the effects of experimentally induced IH
on serum lipid levels and pathways of lipid metabolism in the absence and
presence of obesity. Lean C57BL/6J mice and leptin-deficient obese C57BL/6J-Lep(ob) mice were exposed to IH for five days to determine
changes in serum lipid profile, liver lipid content, and expression of key
hepatic genes of lipid metabolism. In lean mice, exposure to IH increased
fasting serum levels of total cholesterol, high-density lipoprotein (HDL)
cholesterol, phospholipids (PLs), and triglycerides (TGs), as well as liver
TG content. These changes were not observed in obese mice, which had hyperlipidemia
and fatty liver at baseline. In lean mice, IH increased sterol regulatory
element binding protein 1 (SREBP-1) levels in the liver, increased mRNA and
protein levels of stearoyl-coenzyme A desaturase 1 (SCD-1), an important gene
of TG and PL biosynthesis controlled by SREBP-1, and increased monounsaturated
fatty acid content in serum, which indicated augmented SCD-1 activity. In
addition, in lean mice, IH decreased protein levels of scavenger receptor
B1, regulating uptake of cholesterol esters and HDL by the liver. We conclude
that exposure to IH for five days increases serum cholesterol and PL levels,
upregulates pathways of TG and PL biosynthesis, and inhibits
pathways of cholesterol uptake in the liver in the lean state but does not
exacerbate the pre-existing hyperlipidemia and metabolic disturbances in leptin-deficient
obesity.
| Biol Neonate. 2005 Aug 18;88(4):313-320 [Epub ahead of print] |
Mild Intermittent Hypoxia Does
Not Induce Stress Responses in the Neonatal Rat Brain.
Boss V, Sola A, Wen TC, Decker MJ.
Department of Pharmacology,
We previously demonstrated that intermittent hypoxia evokes persistent changes
in extracellular striatal dopamine, locomotor activity and executive function,
using a rodent model emulating apnea of prematurity in which rat pups are
exposed to 20-second bursts of hypoxic gas mix containing 10% oxygen (60 events/h;
6 h/day) from postnatal days 7 to 11. To determine whether subtle repetitive
hypoxic insults also induce expression of stress-related genes, we employed
real-time RT-PCR to assay gene transcription in neonatal rats subjected to
the same paradigm. In addition, we also measured expression of stress-induced
transcripts in an age-matched cohort following a more severe oxidative stressor:
permanent focal ischemia. Four transcripts were elevated following the ischemic
insult: heat shock protein 70 (Hsp70), CL100, nurr77, and heme oxygenase-1.
In contrast, these transcripts were not regulated in the majority of neonatal
rats exposed to an intermittent hypoxia protocol. Hsp70 was strongly induced,
and CL100 and nurr77 were slightly induced in only 2 of 11 post-hypoxic rats
compared to controls. These data demonstrate that a single ischemic event
elicits expression of specific stress-related genes, whereas 5 days of brief
intermittent hypoxic insults typically do not. Thus, it is unlikely that the
neurochemical and behavioral morbidity observed in juvenile and adult rodents
exposed to intermittent hypoxia during a critical period of brain development
are related to stress-induced changes in gene expression. Copyright (c) 2005
S. Karger AG,
Sleep in athletes undertaking protocols of exposure to
nocturnal simulated altitude at 2650 m.
Kinsman TA, Gore CJ, Hahn AG, Hopkins WG, Hawley JA, McKenna MJ, Clark SA, Aughey RJ, Townsend NE,
Chow CM.
Department of Physiology, Australian Institute of Sport
A popular method to attempt to enhance performance is for athletes to sleep
at natural or simulated moderate altitude (SMA) when training daily near sea
level. Based on our previous observation of periodic breathing in athletes
sleeping at SMA, we hypothesised that athletes' sleep quality would also suffer
with hypoxia. Using two typical protocols of nocturnal SMA (2650 m), we examined
the effect on the sleep physiology of 14 male endurance-trained athletes.
The selected protocols were Consecutive (15 successive exposure nights) and
Intermittent (3x 5 successive exposure nights, interspersed with 2 normoxic
nights) and athletes were randomly assigned to follow either one. We monitored
sleep for two successive nights under baseline conditions (B; normoxia, 600
m) and then at weekly intervals (nights 1, 8 and 15 (N1, N8 and N15, respectively))
of the protocols. Since there was no significant difference in response between
the protocols being followed (based on n=7, for each group) we are unable
to support a preference for either one, although the likelihood of a Type
II error must be acknowledged. For all athletes (n=14), respiratory disturbance
and arousal responses between B and N1, although large in magnitude, were
highly individual and not statistically significant. However, SpO2 decreased
at N1 versus B (p<0.001) and remained lower on N8 (p<0.001) and N15
(p<0.001), not returning to baseline level. Compared to B, arousals were
more frequent on N8 (p=0.02) and N15 (p=0.01). The percent of rapid eye movement
sleep (REM) increased from N1 to N8 (p=0.03) and N15 (p=0.01). Overall, sleeping
at 2650 m causes sleep disturbance in susceptible athletes, yet there was
some improvement in REM sleep over the study duration.
Intimal thickening after arterial
balloon injury is increased by intermittent repetitive hypoxia, but intermittent
repetitive hyperoxia is not protective.
Lau AK, Chaufour X, McLachlan C,
Leichtweis SB,
Celermajer DS,
Sullivan C, Stocker R.
The Heart Research Institute,
Hypoxia increases and hyperoxia decreases experimental atherosclerosis, but
it is unclear if repetitive hypoxic and hyperoxic insults affect intimal thickening
after arterial injury. Rabbits on 2% cholesterol diet for 6 weeks underwent
balloon injury to the abdominal aorta (AA) after week 3, and were then exposed
to normoxia (n=6), or 12h daily of intermittent repetitive hypoxia (n=6) or
hyperoxia (n=6). After week 6, damaged AA and undamaged thoracic aorta (TA)
were assessed for intimal thickening and lipid content. Compared with normoxia,
hypoxia and hyperoxia did not alter the rise in serum cholesterol related
to cholesterol feeding. However, compared to normoxia, hypoxia markedly increased
the intima-to-media ratio in AA (1.18+/-0.09 versus 1.96+/-0.14, P<0.01)
and TA (0.15+/-0.02 versus 0.41+/-0.01, P<0.01) whereas hyperoxia had no
effect on AA disease and increased intimal thickening in TA (0.26+/-0.03,
P<0.01). Hyperoxia promoted positive arterial remodeling in both TA and
AA, resulting in larger luminal size. The cholesterol content in AA was increased
by hypoxia and decreased by hyperoxia, but decreased by both treatments in
TA. Lipophilic antioxidants and the proportion of arterial lipids that was
oxidized were not altered by hypoxia or hyperoxia. These results suggest that
intermittent repetitive hyperoxia is not protective and intermittent repetitive
hypoxia promotes arterial disease in normal and injured arteries independent
of lipid peroxidation
Functional and morphological
changes of the brain in rats exposed to intermittent hypobaric hypoxia after
the repetitive magnesium administration.
Maresova D, Jandova K, Bortelova J,
Trojan S, Trnkova B.
Department of Physiology of the First Faculty of Medicine,
Intermittent hypobaric hypoxia induces functional
and morphological changes of the brain in 25-day-old rats. Administration
of magnesium has partial pro-convulsion effect in hypoxia not exposed rats
and it practically does not influence the excitability of cortical neurones
in rats exposed to intermittent hypoxia. Magnesium administration decreases
the number of NADPH-diaphorase neurones in rats exposed to hypoxia in all
studied areas of the hippocampus and dentate gyrus. In control rats this effect
was only in CA1, CA3 and in the ventral blade of the dentate gyrus. Increased
concentration of magnesium in cells of the hypoxia exposed rats after the
repeated magnesium administration was found.
THE ACUTE AND
CHRONIC CARDIOVASCULAR EFFECTS OF INTERMITTENT HYPOXIA IN C57BL/6J MICE.
Campen MJ, Shimoda LA, O'donnell CP.
Division of Toxicology, Lovelace Respiratory Research Institute,
We investigated the effects of (1) acute hypoxia and (2) five weeks of chronic
intermittent hypoxia (IH) on the systemic and pulmonary circulations of C57BL/6J
mice. Mice were chronically instrumented with either femoral artery or right
ventricular catheters. In response to acute hypoxia (four minutes of 10% O2;
n=6) systemic arterial blood pressure fell (P<0.005) from 107.7 +/- 2.5
to 84.7 +/- 6.5 mmHg while right ventricular pressure increased (P<0.005)
from 11.7 +/- 0.8 to 14.9 +/- 1.3 mmHg. Another cohort of mice was then exposed
to IH for 5 weeks (O2 nadir = 5%, 60 second cycles, 12 h/day), then implanted
with catheters. In response to five weeks of chronic IH, mice (n=8) increased
systemic blood pressure by 7.5 mmHg, left ventricle (LV)+septum weight by
32.2 +/- 7.5 x10 mg/100g b.w. (P<0.015), and right ventricle (RV) weight
by 19.3 +/- 3.2 x10 mg/100g b.w. (P<0.001), resulting in a 14% increase
in the RV/LV+septum weight (P<0.005). We conclude that in C57BL/6J mice,
(1) acute hypoxia causes opposite effects on the pulmonary and systemic circulations
leading to preferential loading of the right heart, and (2) chronic IH in
mice results in mild to moderate systemic and pulmonary hypertension, with
resultant left and right-sided ventricular hypertrophy.
Effects of
intermittent hypoxia on sympathetic activity and blood pressure in humans.
Leuenberger UA,
Brubaker D, Quraishi S, Hogeman CS, Imadojemu VA,
Gray KS.
Division of Cardiology, MC H047, The Pennsylvania State University College
of Medicine, The Milton S. Hershey Medical Center, P.O. Box 850, Hershey,
PA 17033, United States.
Sympathetic nerve activity and arterial pressure are frequently elevated in
patients with obstructive sleep apnea (OSA). The mechanisms responsible for
chronic sympathetic activation and hypertension in OSA are unknown. To determine
whether repetitive apneas raise sympathetic nerve activity and/or arterial
pressure, awake and healthy young subjects performed voluntary end-expiratory
apneas for 20 s per min for 30 min (room air apneas). To accentuate intermittent
hypoxia, in a separate group of subjects, hypoxic gas (inspired O(2)
10%) was added to the inspiratory port for 20 s before each apnea (hypoxic
apneas). Mean arterial pressure (MAP) and muscle sympathetic nerve activity
(MSNA, peroneal microneurography) were determined before and up to 30 min
following the repetitive apneas. Following 30 hypoxic apneas (O(2)
saturation nadir 83.1+/-1.2%), MSNA increased from 17.4+/-2.7 to 23.4+/-2.5
bursts/min and from 164+/-28 to 240+/-35 arbitrary units respectively (P<0.01
for both; n=10) and remained elevated while MAP increased transiently from
80.5+/-3.7 to 83.1+/-3.9 mm Hg (P<0.05; n=11). In contrast, in the subjects
who performed repetitive apneas during room air exposure (O(2)
saturation nadir 95.1+/-0.8%), MAP and MSNA did not change (n=8).
| Respir Physiol Neurobiol. 2005 Jun 23; [Epub ahead of print] |
Functional
assessment of vascular reactivity after chronic intermittent hypoxia in the
rat.
Lefebvre B, Godin-Ribuot D,
Joyeux-Faure M,
Caron F, Bessard G, Levy P, Stanke-Labesque F.
Laboratoire HP2, Hypoxie Physio-Pathologie Respiratoire et Cardiovasculaire,
Faculte de Medecine-Pharmacie, Universite Grenoble I, Inserm Espri EA 3745,
France.
We recently developed a model of chronic intermittent hypoxia (CIH) (FiO(2) 5%, 8h/day, 35 days) in the rat that was associated
with an increased infarction in isolated heart. The aim of the present study
was to characterize its functional consequences on vasoreactivity. Aorta and
carotid artery were studied using organ bath technique while mesenteric vascular
bed was perfused. In the three vascular beds, relaxation to acetylcholine
was similar in CIH and control normoxic (NX) rats. Contractions to noradrenaline
and angiotensin II were similar between CIH and NX rats. In contrast, contraction
to endothelin-1 was increased by 17% (P<0.05) in carotid artery from CIH
rats. Indomethacin pre-treatment reduced by 24% (P<0.001) contraction to
endothelin-1 in carotid artery from CIH rats only. These data suggested that
35-day CIH-exposure induced no change in endothelial function of aorta, carotid
artery and mesenteric bed. In contrast, CIH-exposure induced an increased
contractile response to endothelin-1 in carotid artery, presumably owing to
the release of constrictor cyclooxygenase-derived products.
Effects of
two protocols of intermittent hypoxia on human ventilatory, cardiovascular
and cerebral responses to hypoxia.
Foster GE, McKenzie DC,
Milsom WK, Sheel AW.
School of Human Kinetics,
We determined the ventilatory, cardiovascular and cerebral tissue oxygen response
to two protocols of normobaric, isocapnic, intermittent hypoxia. Subjects
(n = 18, male) were randomly assigned to short-duration intermittent hypoxia
(SDIH, 12% O2 separated by 5 min of normoxia for 1 h) or long-duration intermittent
hypoxia (LDIH, 30 min of 12% O2). Both groups had 10 exposures over a 12 day
period. The hypoxic ventilatory response (HVR) was measured before each daily
intermittent hypoxia exposure on days 1, 3, 5, 8, 10 and 12. The HVR was measured
again 3 and 5 days after the end of intermittent hypoxia. During all procedures,
ventilation, blood pressure, heart rate, arterial oxyhaemoglobin saturation
and cerebral tissue oxygen saturation were measured. The HVR increased throughout
intermittent hypoxia exposure regardless of protocol, and returned to baseline
by day 17 (day 1, 0.84 +/- 0.50; day 12, 1.20 +/- 1.01; day 17, 0.95 +/- 0.58
l min(-1) %S(aO2)(-1); P < 0.01). The change in
systolic blood pressure sensitivity (r = +0.68; P < 0.05) and the change
in diastolic blood pressure sensitivity (r = +0.73; P < 0.05) were related
to the change in HVR, while the change in heart rate sensitivity was not (r
= +0.32; NS). The change in cerebral tissue oxygen saturation sensitivity
to hypoxia was less on day 12, and returned to baseline by day 17 (day 1,
-0.51 +/- 0.13; day 12, -0.64 +/- 0.18; day 17, -0.51 +/- 0.13; P < 0.001).
Acute exposure to SDIH increased mean arterial pressure (+5 mmHg; P < 0.01),
but LDIH did not (P > 0.05). SDIH and LDIH had similar effects on the ventilatory
and cardiovascular response to acute progressive hypoxia and hindered cerebral
oxygenation. Our findings indicate that the vascular processes required to
control blood flow and oxygen supply to cerebral tissue in a healthy human
are hindered following exposure to 12 days of isocapnic intermittent hypoxia.
Hypoxia in head and neck cancer:
how much, how important?
Janssen HL, Haustermans KM,
Balm AJ, Begg AC.
Division of Experimental Therapy, The Netherlands
Cancer Institute, Plesmanlaan 121, 1066 CX
BACKGROUND: Hypoxia develops in tumors because of a less ordered, often chaotic,
and leaky vascular supply compared with that in normal tissues. In preclinical
models, hypoxia has been shown to be associated with treatment resistance
and increased malignant potential. In the clinic, several reports show the
presence and extent of tumor hypoxia as a negative prognostic indicator. This
article reviews the biology and importance of hypoxia in head and neck cancer.
METHODS: A review of literature was carried out and combined with our own
experience on hypoxia measurements using exogenous and endogenous markers.
RESULTS: Hypoxia can increase resistance to radiation and cytotoxic drugs
and lead to malignant progression, affecting all treatment modalities, including
surgery. Hypoxia measurements using electrodes, exogenous bioreductive markers,
or endogenous markers show the presence of hypoxia in most head and neck cancers,
and correlations with outcome, although limited, consistently indicate hypoxia
as an important negative factor. Each hypoxia measurement method has disadvantages,
and no "gold standard" yet exists. Distinctions among chronic, acute,
and intermediate hypoxia need to be made, because their biology and relevance
to treatment resistance differ. Reliable methods for measuring these different
forms in the clinic are still lacking. Several methods to overcome hypoxia
have been tested clinically, with radiosensitizers (nimorazole), hypoxic cytotoxins
(tirapazamine), and carbogen showing some success. New treatments such as
hypoxia-mediated gene therapy await proper clinical testing. CONCLUSIONS: The hypoxia problem
in head and neck cancer needs to be addressed if improvements in current treatments
are to be made. Increased knowledge of the molecular biology of intermediate,
severe, and intermittent hypoxia is needed to assess their relevance and indicate
strategies for overcoming their negative influence.
[Mechanisms of adaptation to
intermittent hypoxic training course in sportsmen of high qualification]
[Article in Ukrainian]
Radziievs'kyi PO.
Boris Grinchenko Kyiv Municipal Pedagogical University.
Normobaric intermittent hypoxic training (IHT) is an effective method for
improvement of the FRS state, increase of the aerobic productivity, as well
as general and special capacity for work in sportsmen of high qualification.
High efficacy of IHT in improving all aspects of sportsmen FRS is a result
of alternating the hypoxic influences and normoxic intervals between them
during which the level of plastic processes remains increased, oxygen tension
in arterial blood and tissues increases to nonnoxic values. After IHT course,
the state of organ respiration improves, the respiration volume, a part of
alveolar ventilation in the minute volume of respiration, oxygen saturation
of arterial blood, hemoglobin content in blood--increase as well as economy
and efficacy of oxygen regimes of organism, general and special (especially
important) physical capacity for work.
The influence
of intermittent altitude exposure to 4100 m on exercise capacity and blood
variables.
Lundby C, Nielsen TK, Dela F, Damsgaard R.
The
This study was performed to investigate the effects
of intermittent hypoxic exposure on blood and exercise parameters. Eight sea
level residents were exposed to 2 h daily stimulus to 4100 m altitude in a
hypobaric chamber for a total of 14 days. Exercise performance was evaluated
at sea level before and after the hypoxic stimulation. Blood samples were
obtained before, during, and at time points up to 14 days after the hypoxic
exposure. No changes were observed in haemoglobin, haematocrit, reticulocytes,
serum transferrin receptors, or EPO levels in the blood. Submaximal cycle
(150 W) ergometer exercise corresponded to a oxygen uptake of 1.9+/-0.1 and
1.9+/-0.1 L min(-1) before and after the intermittent altitude exposure,
respectively. At maximal exercise the workloads attained were 343+/-17 and
354+/-27 W before and after the exposure, with corresponding oxygen uptakes
of 4.0+/-0.2 and 4.2+/-0.2 L min(-1). It is concluded
that intermittent hypoxic exposure to 4100 m altitude for 2 h daily and a
total of 14 days does not affect exercise capacity.
Acute intermittent hypoxia improves
rat myocardium tolerance to ischemia.
Beguin PC, Joyeux-Faure M,
Godin-Ribuot D,
Levy P, Ribuot C.
Laboratoire HP2, Hypoxie Physiopathologie Respiratoire et Cardiovasculaire,
EA3745, ESPRI INSERM, Faculte de Medecine-Pharmacie, Universite Grenoble I,
Domaine de la Merci, 38706 La Tronche Cedex, France.
In this study, we investigated the influence of depth and duration of intermittent
hypoxia (IH) on the infarct size development in isolated rat heart. The role
of nitric oxide synthase (NOS) and ATP-sensitive K+ (K(ATP)) channel was also studied. Wistar male rats were exposed
to IH [repetitive cycles of 1 min, 40 s with inspired oxygen fraction (FI(O2)),
5 or 10%, followed by 20-s normoxia], during 30 min or 4 h. Another group
was exposed to 4 h of continuous hypoxia with 10% FI(O2).
Twenty-four hours later, their hearts were isolated and subjected to a 30-min
no-flow global ischemia-120-min reperfusion sequence. For some hearts, N(omega)-nitro-L-arginine methyl ester (L-NAME) (a nonselective
inhibitor of NOS) or 5-hydroxydecanoic acid (5-HD) (a selective mitochondrial
K(ATP) blocker) was infused before ischemia. Infarct size (in percentage of
ventricles) was significantly reduced by prior IH for 4 h (10% FI(O2)) (21.8 +/- 3.1 vs. 33.5 +/- 2.5% in sham group). This
effect was abolished by L-NAME or 5-HD. Infarct size was not different in
groups subjected to either 30 min of IH or to continuous hypoxia compared
with sham group. In contrast, IH for 4 h (5% FI(O2))
significantly increased infarct size (45.1 +/- 3.6 vs. 33.5 +/- 2.5% in sham
group). Acute IH for 4 h with a minimal FI(O2) of
10% induced a delayed preconditioning against myocardial infarction in the
rat, which was abolished by NOS inhibition and mitochondrial K(ATP) channel
blockade. Depth, duration, and intermittence of hypoxia appeared to be critical
for cardioprotection to occur.
Does intermittent hypoxia increase
erythropoiesis in professional cyclists during a 3-week race?
Villa JG, Lucia A, Marroyo JA, Avila C, Jimenez F, Garcia-Lopez J,
Earnest CP, Cordova A.
Dept. of Physical Education,
In this study we examined the effects of intermittent hypoxia exposure (IHE)
in a group of professional cyclists (n = 6; age 26 +/- 1 yr) competing in
the 2001 Vuelta a Espana. After each daily stage,
treated subjects received four 5-min bouts of normobaric IHE (mean O2 concentration
of 12.6%, simulating a mean altitude of 4,000 m) interspersed with 5-min bouts
of breathing hotel room air (normoxia) until completing a total IHE of 20-min
duration. The primary outcome, compared to a control group of similar characteristics
not receiving IHE (n = 5; age 25 +/- 1 yr), was the % increase in erythropoietin
(Epo) from the beginning to the end of the Vuelta. Statistical analysis showed
that Epo increase tended to be higher (p = 0.052) in the IHE group than in
controls (37.4 +/- 5.8% vs. -4.4 +/- 19.5%, respectively). However IHE had
no effect on reticulocytes or erythrocyte count (p > 0.05).
Cardiovascular alterations by
chronic intermittent hypoxia: importance of carotid body chemoreflexes.
Prabhakar NR,
Peng YJ, Jacono FJ, Kumar GK, Dick TE.
Department of Physiology and Biophysics, School of Medicine,
1. Humans experiencing intermittent hypoxia (IH) owing to recurrent
apnoea syndromes exhibit serious cardiovascular morbidity, including high
blood pressure, increased sympathetic nerve activity, cardiac arrhythmia and
myocardial infarction. Although apnoeas are accompanied by a simultaneous
decrease in arterial O(2) (hypoxia) and an increase
in CO(2) (hypercapnia), studies on experimental animals suggest that hypoxia,
rather than hypercapnia, is the primary stimulus for developing hypertension
and enhanced sympathetic nerve activity. Enhanced hypoxic-sensing ability
of the carotid bodies and the ensuing reflex activation of the sympathetic
nervous system have been suggested to play a critical role in cardiorespiratory
alterations resulting from recurrent apnoeas. 2. The purpose of the present
review is to highlight recent studies demonstrating the effects of IH on carotid
body sensory activity and its consequences on sympathetic activation in a
rodent model of chronic IH. Adult rats exposed to chronic IH (15 s of 5% O(2)
followed by 5 min of 21% O(2), nine episodes per h, 8 h/day for 10 days) exhibited
selective enhancement of carotid body sensory response to hypoxia. In addition,
chronic IH induced a novel form of sensory plasticity in the carotid body,
manifested as sensory long-term facilitation (LTF). Functional changes in
the carotid body occurred in the absence of morphological changes in the chemoreceptor
tissue. 3. Acute hypoxia increased expiratory modulated splanchnic nerve activity
(SNA) and acute IH-induced LTF in SNA. Hypoxia-induced SNA activation was
prevented by bilateral sectioning of the sinus nerves. Rats exposed to chronic
IH exhibited enhanced hypoxia-induced sympathetic activation and augmented
LTF of the SNA. Bilateral sectioning of the sinus nerves abolished these responses,
suggesting chronic IH-induced alterations in carotid body sensitivity contribute
to LTF in SNA and the subsequent cardiovascular alterations.
Intermittent
short-term graded running performance in middle-distance runners in hypobaric
hypoxia.
Ogawa T, Ohba K, Nabekura Y, Nagai J, Hayashi K, Wada H, Nishiyasu T.
Institute of Health and Sports Science,
This study investigated whether in trained middle-distance runners, intermittent
short-term graded running performance is affected by a hypobaric hypoxic environment
(simulated 2,500 m) (H). Seven male middle-distance runners performed an aerobic
performance test and an intermittent short-term graded anaerobic running-performance
test (MART) both in H and in a normobaric normoxic environment (N). VO(2max)
and OBLA were markedly lower (by 18.1% and 8.7%, respectively) in H than in
N. In MART, neither maximal running velocity (V(max))
nor exhaustion-time was different between N and H (454 (7) m min(-1) vs. 451
(6) m min(-1), respectively, and 208.7 (5.2) s vs. 205.7 (4.2) s, respectively).
The blood lactate concentration at sub-maximal running speed (425 m min(-1)) was significantly greater in H than in N (paired t-test:
P<0.05). These results suggest that, in trained middle-distance runners,
intermittent short-term graded running performance is not affected by H, despite
a considerable decrease in aerobic power in H during the aerobic performance
test.
| Comp Biochem Physiol C Toxicol Pharmacol. 2005 Jan;140(1):59-67. |
Adaptations of the antioxidant
system in erythrocytes of trained adult rats: impact of intermittent hypobaric-hypoxia
at two altitudes.
Asha Devi S,
Subramanyam MV,
Vani R, Jeevaratnam K.
Laboratory of Gerontology, Department of Zoology,
We have investigated the effects of daily exposure to intermittent hypobaric-hypoxia
to two simulated altitudes (5700 m and 6300 m) in adult male rats that had
been regularly swim trained in normoxia at sea level prior to exposures. Superoxide
dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px) along
with the oxidative stress (OS) indices, malondialdehyde (MDA) and protein
carbonyl content were measured in erythrocytes and their membranes. Hemoglobin
increased in the trained animals exposed to 5700 m and in untrained rats exposed
to 6300 m. Osmotic fragility in terms of hemolysis increased in altitude exposed
animals. SOD increased in those exposed to 6300 m, while CAT increased in
trained rats exposed to 5700 m and to 6300 m unlike in untrained rats where
CAT increased only at 6300 m. GSH-Px showed varying degrees of elevation in
all animals exposed to both altitudes. Erythrocyte membranes showed significant
elevations in malondialdehyde (MDA) at 6300 m, while elevated protein carbonyls
were noticeable at both altitudes in whole cells and membranes. These results
suggest a positively associated elevation in protein oxidation with altitude
in trained rats. At 5700 m, animals were less stressed, unlike at 6300 m,
as seen from the magnitude of elevations in the OS indices and from the responses
of the antioxidant enzymes.
Hyperbaric oxygen as an
intervention for managing wound hypoxia: its role and usefulness in diabetic
foot wounds.
Strauss MB.
Department of Hyperbaric Medicine, Long Beach Memorial Medical Center, 2801
Atlantic Avenue, PO Box 1428, Long Beach, CA 90801-1428, USA. mstrauss@memorialcare.org
Few topics in diabetic wound management generate as much "heated"
discussion as hyperbaric oxygen (HBO). Hyperbaric oxygen is an intermittent
inhalation therapy in which the patient breathes oxygen at greater than 1
atm of pressure. This requires placement of the patient into a sealed vessel
(chamber) which is capable of withstanding pressurization. This article discusses
the role of HBO as an adjunct to the management of diabetic problem foot wounds
from evidenced-based, approved (by Medicare) indications and cost-effectiveness
perspectives.
| Am J Physiol Regul Integr Comp Physiol. 2005 Jun;288(6):R1571-80. Epub 2005 Jan 27. |
Time-dependent
modulation of carotid body afferent activity during and after intermittent
hypoxia.
Cummings
KJ, Wilson RJ.
Department of Physiology and Biophysics,
The ventilatory response to several minutes of hypoxia consists of various
time-dependent phenomena, some of which occur during hypoxia (e.g., short-term
depression), whereas others appear on return to normoxia (e.g., posthypoxic
frequency decline). Additional phenomena can be elicited by acute, intermittent
hypoxia (e.g., progressive augmentation, long-term facilitation). Current
data suggest that these phenomena originate centrally. We tested the hypothesis
that carotid body afferent activity undergoes time-dependent modulation, consistent
with a direct role in these ventilatory phenomena. Using an in vitro rat carotid
body preparation, we found that 1) afferent activity declined during the first
5 min of severe (40 Torr Po(2)), moderate (60 Torr Po(2)), or mild (80 Torr
Po(2)) hypoxia; 2) after return to normoxia (100 Torr Po(2)) and after several
minutes of moderate or severe hypoxia, afferent activity was transiently reduced
compared with prehypoxic levels; and 3) with successive 5-min bouts of mild,
moderate, or severe hypoxia, afferent activity during bouts increased progressively.
We call these phenomena sensory hypoxic decline, sensory posthypoxic decline,
and sensory progressive augmentation, respectively. These phenomena were stimulus
specific: similar phenomena were not seen with 5-min bouts of normoxic hypercapnia
(100 Torr Po(2) and 50-60 Torr Pco(2)) or hypoxic
hypocapnia (60 Torr
Repeated
measurement of hypoxic ventilatory response as an intermittent hypoxic stimulus.
Koehle MS, Foster GE, McKenzie DC,
Sheel AW.
Department of Family Medicine, Allan McGavin Sport Medicine Centre, University
of British Columbia, Vancouver, BC, Canada V6T 1Z1.
Measurement of hypoxic ventilatory response (HVR) involves an exposure to
hypoxia which, if repeated over several days might act as an intermittent
hypoxic stimulus. The purpose of this study was to measure HVR repeatedly
over 5 days to determine whether it was affected by repeated measurement.
Nine healthy male subjects completed an isocapnic HVR test, on one occasion,
followed 5 days later by one measurement each day for 5 days. Each test lasted
approximately 5-8 min with inspired oxygen concentration declining to as a
low as 5-6%. No systematic trend was observed in HVR over the 5-day period
(p>0.05). There were no significant differences in HVR between any of the
test days. Regression failed to show any trend in HVR over the five sequential
days. The calculated mean coefficient of variation for HVR for each subject
was 27%. There is no evidence that the short exposure to hypoxia as part of
HVR measurement is a co-intervention when measured repeatedly over 5 days
in physiological studies.
Hematologic response to
four weeks of intermittent hypobaric hypoxia in highly trained athletes.
Abellan R, Remacha AF, Ventura R, Sarda MP, Segura J, Rodriguez FA.
We investigated changes induced by four weeks of intermittent hypobaric hypoxia
(IHH) at a simulated altitude of 4000-5500 m in highly trained athletes. Serum
erythropoietin increased significantly (p<0.001) after the sessions of
IHH, but reticulocyte and red cell parameters did not. Our IHH protocol stimulated
endogenous erythropoietin secretion without producing the subsequent erythropoietic
response.
Publication Types:
· Letter
Effects of intermittent
hypoxia on pulmonary haemodynamics: animal models versus studies in humans.
Zielinski J.
2nd Dept of Respiratory Medicine,
The aim of this review was to analyse the effects
of intermittent hypoxia (IH) on pulmonary haemodynamics, comparing results
of animal experiments with results of clinical studies. In animal investigations
even short hypoxic exposure, continuously or in short repeated episodes mimicking
obstructive sleep apnoea (OSA), leads to pulmonary artery remodelling and
to pulmonary hypertension (PH). Results of investigations on effects of nocturnal
IH on pulmonary haemodynamics in patients with chronic obstructive pulmonary
disease (COPD) are discordant. Earlier studies reported the development of
mild PH in subjects desaturating during sleep, while more recent investigations
did not confirm those findings. Alveolar IH developing during apnoeic episodes
during sleep in OSA patients is a disease-induced model to study its effects
on pulmonary haemodynamics. In the majority of studies in OSA patients
pulmonary arterial pressure remained within normal values. PH was found in
patients with OSA accompanied by COPD and/or extreme obesity. People commuting
between lowland and high altitude due to their employment, are also repeatedly
exposed to IH. Results of clinical investigations suggest that it did not
lead to the development of permanent PH. The mechanisms of discrepancies between
effects of intermittent hypoxia in animal models and in humans remain to be
studied.
Publication Types:
· Review
· Review, Tutorial
Effects
of hypoxic interval training on cycling performance.
Roels B, Millet GP, Marcoux CJ, Coste O, Bentley DJ, Candau RB.
UPRES EA 3759 Faculty of Sport Sciences, 700 avenue
Pic St Loup, 34090
PURPOSE: The aim of this study was to test the hypothesis that intermittent
hypoxic interval training improves sea level cycling performance more than
equivalent training in hypoxia or normoxia. METHODS: Thirty-three well-trained
cyclists and triathletes (25.9 +/- 2.7 yr, VO(2max) 66.1 +/- 6.1 mL.min(-1).kg(-1))
were divided into three groups: intermittent hypoxic (IHT, N = 11, P(I)O(2)
of 100 mm Hg), intermittent hypoxic interval training (IHIT, N = 11) and normoxia
(Nor, N = 11, P(I)O(2) of 160 mm Hg) and completed a 7-wk training program,
consisting of two high-intensity (100 or 90% relative peak power output) interval
training sessions each week. Each interval training session was performed
in a laboratory on the subject's own bicycle, in normoxic or hypoxic conditions
for the Nor and the IHT group, respectively. The
IHIT group performed warm-up and cool-down plus recovery from each interval
in hypoxic conditions. In contrast to IHT, interval exercise bouts were performed
in normoxic conditions. RESULTS: Mean power output during a 10-min cycle time
trial improved after the first 4 wk of training by 5.2 +/- 3.9, 3.7 +/- 5.9,
and 5.0 +/- 3.4% for IHIT, IHT, and Nor, respectively, without significant
differences between groups. Moreover, mean power output did not show any significant
improvement in the following 3 wk in any group. VO(2max) (L.min(-1)) increased only in IHIT during the training
period (8.7 +/- 9.1%; P < 0.05). No changes in cycling efficiency or in
hematological variables (P > 0.05) were observed. CONCLUSION: Four weeks
of interval training induced an improvement in endurance performance. However,
short-term exposure to hypoxia (approximately 114 min.wk(-1))
did not elicit a greater increase in performance or any hematological modifications.
Dynamic electrophysiological
examination in patients with lumbar spinal stenosis: is it useful in clinical
practice?
Adamova B, Vohanka S, Dusek L.
Department of Neurology,
Neurogenic claudication (NC) is typical of lumbar
spinal stenosis (LSS). One suspected pathophysiological mechanism underlying
NC is intermittent hypoxia of cauda equina fibres resulting from venous pooling,
which may lead to ischaemic nerve conduction failure and to transient clinical
and electrophysiological changes after exercise. The aim of this study was
to evaluate the appearance of significant transient electrophysiological abnormalities
after walking exercise in patients with LSS and to establish the contribution
of dynamic electrophysiological examination in the differential diagnostics
of patients with LSS. The study participants were 36 consecutive patients
with LSS demonstrated by computed tomography (CT). The control groups included,
respectively, 28 patients with diabetes mellitus and clinically manifested
polyneuropathy, and 32 healthy volunteers. The LSS patients were divided into
four subgroups based on the clinical severity of the disease (with respect
to the presence or absence of NC in the history and pareses on neurological
examination). Soleus H-reflex, tibial F-wave and motor evoked potentials (MEPs)
to abductor hallucis muscle were examined in all groups, before and after
quantified walking on a treadmill. The electrophysiological parameters measured
after an exercise treadmill test (ETT) in LSS patients and in both control
groups were compared with the same parameters obtained before ETT. The study
shows that the electrophysiological parameters reveal minimal but statistically
significant changes after walk loading in patients with LSS (a prolongation
of the minimal latency of the tibial F-wave and of the latency of the soleus
H-reflex). The changes in these parameters were demonstrated not only in patients
with NC but also in patients without NC. More pronounced changes were found
in LSS patients exhibiting chronic lower extremity pareses. Conclusions: From
among a large battery of electrophysiological tests, only the minimal latency
of the tibial F-wave and the latency of the soleus H-reflex exhibit changes
after walk loading in patients with LSS. These are minimal but statistically
significant. Dynamic electrophysiological examination can illustrate the pathophysiology
of NC in LSS, but from a practical point of view its contribution to the differential
diagnostics of LSS or diabetic polyneuropathy is limited by an absence of
established cut-off values.
Effects of
Intermittent Hypoxia on Heart Rate Variability during Rest and Exercise.
Povea C, Schmitt L, Brugniaux J,
Nicolet G, Richalet JP,
Fouillot JP.
Universite Paris 13, Faculte de Medecine,
Povea, Camilo; Laurent Schmitt; Julien Brugniaux; Gerard Nicolet; Jean-Paul
Richalet; and Jean-Pierre Fouillot. Effects of intermittent
hypoxia on heart rate variability during rest and exercise. High Alt.
Med. Biol. 6:215-225, 2005.-Changes in heart rate variability induced by an
intermittent exposure to hypoxia were evaluated in
athletes unacclimatized to altitude. Twenty national elite athletes trained
for 13 days at 1200 m and either lived and slept
at 1200 m (live low, train low, LLTL) or between 2500 and 3000 m (live high,
train low, LHTL). Subjects were investigated at 1200 m prior to and at the
end of the 13-day training camp. Exposure to acute hypoxia (11.5% O(2))
during exercise resulted in a significant decrease in spectral components
of heart rate variability in comparison with exercise in normoxia: total power
(p < 0.001), low-frequency component. LF (p < 0.001),
high-frequency component, HF (p < 0.05). Following acclimatization,
the LHTL group increased its LF component (p < 0.01) and LF/HF ratio during
exercise in hypoxia after the training period. In parallel, exposure to intermittent
hypoxia caused an increased ventilatory response to hypoxia. Acclimatization
modified the correlation between the ventilatory response to hypoxia at rest
and the difference in total power between normoxia and hypoxia (r (2) = 0.65,
p < 0.001). The increase in total power, LF component, and LF/HF ratio
suggests that intermittent hypoxic training increased the response of the
autonomic nervous system mainly through increased sympathetic activity.
Exercise training improves
lung gas exchange, attenuates acute hypoxic pulmonary hypertension, but does
not prevent pulmonary hypertension of prolonged hypoxia.
Favret F, Henderson KK,
Allen J, Richalet JP,
Gonzalez NC.
A.R.P.E., EA2363 reponses cellulaires et fonctionnelles
a l'hypoxie, Universite Paris 13,
We have previously shown an attenuation of hypoxic pulmonary hypertension
by exercise training ET (15), although the mechanism was not determined. The
present study examined the effect of ET on the pulmonary arterial pressure
(Pap) response of rats to short and long term hypoxia. After 3 weeks of treadmill
training, male rats were divided into two groups: one (HT) was placed in hypobaric
hypoxia (380 Torr); the second remained in normoxia (NT). Both groups continued
to train in normoxia for 10 days, after which they were studied at rest and
during hypoxic and normoxic exercise. Sedentary normoxic (NS) and hypoxic
(HS) littermates were exposed to the same environments as their trained counterparts.
Resting and exercise hypoxic PaO2 were higher in NT and HT than in NS and
HS, respectively, although alveolar ventilation of trained rats was not higher.
Lower A-a PO2 and higher effective lung diffusing capacity for O2 (DLO2) in
NT vs NS and in HT vs HS suggest ET improved efficacy of gas exchange. Pulmonary
arterial pressure (Pap) and Pap/cardiac output (Pap/Q) were lower in NT than
NS in hypoxia, indicating ET attenuates the initial vasoconstriction of hypoxia.
However, ET had no effect on chronic hypoxic pulmonary hypertension: Pap and
Pap/Q in hypoxia were similar in HS vs HT. However, right ventricular weight
was lower in HT than in HS, although Pap was not different. Since ET attenuates
the initial pulmonary vasoconstriction of hypoxia, development of pulmonary
hypertension may be delayed in HT rats, and the time during which right ventricular
afterload is elevated may be shorter in this group. ET effects may improve
the response to acute hypoxia by increasing efficacy of gas exchange and lowering
right ventricular work.
Eighteen days of "Living
High - Training Low" stimulate erythropoiesis
and enhance aerobic performance in elite middle-distance runners.
Brugniaux JV,
Schmitt L, Robach P, Nicolet G, Fouillot JP,
Moutereau S,
Lasne F, Pialoux V, Saas P, Chorvot MC, Cornolo J, Olsen NV, Richalet JP.
Laboratoire, Universite Paris 13,
The efficiency of "Living High - Training Low" (LHTL) remains controversial,
despite its wide utilization. This study aimed to verify if maximal and/or
submaximal aerobic performance were modified by LHTL and whether these effects
persist for 15 days after returning to normoxia. Finally we tried to elucidate
if the mechanisms involved were only related to changes in oxygen carrying
capacity. Eleven elite middle-distance runners were tested before (PRE), at
the end (POST1) and 15 days after the end (POST2) of a 18-day LHTL session. Hypoxic group (LHTL, n=5) spent 14h
per day in hypoxia (6 nights at 2,500m and 12 nights at 3,000m) while control
group (CON, n=6) slept in normoxia (1,200m). Both LHTL and CON trained at
1,200m. V O2max and maximal aerobic power were improved at POST1 and POST2
for LHTL only (+7.1% and +3.4 % for V O2max, +8.4% and +4.7% for maximal aerobic
power, respectively). Similarly V O2 and ventilation at ventilatory threshold
increased in LHTL only (+18.1% and +12.2% at POST1, +15.9% and +15.4% at POST2,
respectively). Heart rate during a 10-minute run at 19.5 km/h decreased for
LHTL at POST2 (-4.4%). Despite the stimulation of erythropoiesis in LHTL shown
by the 27.4%-increase in serum transferrin receptor and the 10.1%-increase
in total hemoglobin mass, red cell volume was not significantly increased
at POST1 (+9.2%, n.s.). Therefore, both maximal and submaximal aerobic performance
in elite runners was increased by LHTL mainly link to an improvement in oxygen
transport in early return to normoxia and probably to other process at POST2.
Depressurization in military
aircraft: rates, rapidity, and health effects for 1055 incidents.
Files
DS, Webb JT, Pilmanis AA.
Department of Graduate Education, USAF School of Aerospace Medicine, Brooks
City-Base, TX 78235, USA. douglas.files@brooks.af.mil
INTRODUCTION: Aircraft cabin depressurization is a rare event but one which
demands attention because of the grave potential for aircrew incapacity in
flight. The purpose of the current study was to determine rates of depressurization
incidents for
| Eur J Appl Physiol. 2005 Jun;94(3):298-304. Epub 2005 Mar 12. |
Living high-training low altitude
training: effects on mucosal immunity.
Tiollier E, Schmitt L, Burnat P, Fouillot JP,
Robach P, Filaire E, Guezennec C,
Richalet JP.
Departement de physiologie, IMASSA, 91223 Bretigny-sur-Orge
Cedex,
Secretory immunoglobulin A (sIgA) is the major immunoglobulin
of the mucosal immune system. Whereas the suppressive effect of heavy training
on mucosal immunity is well documented, little is known regarding the influence
of hypoxia exposure on sIgA during altitude training. This investigation examined
the impact of an 18-day Living high-training low (LHTL) training camp on sIgA
levels in 11 (six females and five males) elite cross-country skiers. Subjects
from the control group (n=5) trained and lived at 1,200 m of altitude, whereas,
subjects from the LHTL group (n=6) trained at 1,200 m, but lived at a simulated
altitude of 2,500, 3,000 and 3,500 m (3x6-day, 11 h day(-1))
in hypoxic rooms. Saliva samples were collected before, after each 6-day phases
and 2 weeks thereafter (POST). Salivary sIgA, protein and cortisol were measured.
There was a downward trend in sIgA concentrations over the study, which reached
significance in LHTL (P<0.01), but not in control (P=0.08). Salivary IgA
concentrations were still lower baseline at POST (P<0.05). Protein concentration
increased in LHTL (P<0.05) and was negatively correlated with sIgA concentration
after the 3,000 and 3,500 m-phase and at POST (P<0.05 all). Cortisol concentrations
were unchanged over the study and no relationship was found between cortisol
and sIgA. In summary, data were strongly suggestive of a cumulative negative
effect of physical exercise and hypoxia on sIgA levels during LHTL training.
Two weeks of active recovery did not allow for proper sIgA recovery. The mechanism
underlying this depression of sIgA could be mediated by neural factors.
Publication Types:
· Clinical Trial
· Randomized Controlled Trial
A three-week traditional altitude training increases hemoglobin
mass and red cell volume in elite biathlon athletes.
Heinicke K, Heinicke I, Schmidt W, Wolfarth B.
Division of Physiology, Department of Medicine, University of California,
San Diego, La Jolla, 92093, USA. kheinicke@ucsd.edu
It is well known that altitude training stimulates
erythropoiesis, but only few data are available concerning the direct altitude
effect on red blood cell volume (RCV) in world class endurance athletes during
exposure to continued hypoxia. The purpose of this study was to evaluate the
impact of three weeks of traditional altitude training at 2050 m on total
hemoglobin mass (tHb), RCV and erythropoietic activity in highly-trained endurance
athletes. Total hemoglobin mass, RCV, plasma volume (PV), and blood volume
(BV) from 6 males and 4 females, all members of a world class biathlon team,
were determined on days 1 and 20 during their stay at altitude as well as
16 days after returning to sea-level conditions (800 m, only males) by using
the CO-rebreathing method. In males tHb (14.0 +/- 0.2 to 15.3 +/- 1.0 g/kg,
p < 0.05) and RCV (38.9 +/- 1.5 to 43.5 +/- 3.9 ml/kg, p < 0.05) increased
at altitude and returned to near sea-level values 16 days after descent. Similarly
in females, tHb (13.0 +/- 1.0 to 14.2 +/- 1.3 g/kg, p < 0.05) and RCV (37.3
+/- 3.3 to 42.2 +/- 4.1 ml/kg, p < 0.05) increased. Compared to their sea-level
values, the BV of male and female athletes showed a tendency to increase at
the end of the altitude training period, whereas PV was not altered. In male
athletes, plasma erythropoietin concentration increased up to day 4 at altitude
(11.8 +/- 5.0 to 20.8 +/- 6.0 mU/ml, p < 0.05)
and the plasma concentration of the soluble transferrin receptor was elevated
by about 11 % during the second part of the altitude training period, both
parameters indicating enhanced erythropoietic activity. In conclusion, we
show for the first time that a three-week traditional
altitude training increases erythropoietic activity even in world class endurance
athletes leading to elevated tHb and RCV. Considering the relatively fast
return of tHb and RCV to sea-level values after hypoxic exposure, our data
suggest to precisely schedule training at altitude
and competition at sea level.
Altitude training experiences
and perspectives: survey of 67 professional pilots.
Hackworth C,
Peterson L, Jack D, Williams C.
Federal Aviation Administration Civil Aerospace Medical
Institute,
INTRODUCTION: Pilots and crewmembers of flights exceeding 7620 m/mean sea
level (msl) are required to complete ground training in high-altitude physiology,
including hypoxia training. However, regulations do not require altitude chamber
training (ACT). METHOD: An anonymous questionnaire concerning their experiences
and perceptions of hypoxia training was filled out by 67 pilots attending
an aviation safety conference. All pilots had logged professional business
flight hours in the previous 6 mo. RESULTS: There were 62 pilots who reported
receiving hypoxia training, and of these, 71% reported having initial ACT.
Most of the pilots surveyed agreed that all pilots should receive introductory
hypoxia training (92%), recurrent hypoxia training (86%), initial ACT (85%),
and recurrent ACT (70%). Initial ACT received lower endorsements for private
(32%) or recreational (10%) pilots than for commercial (74%) and air transport
(90%) pilots. When asked if ACT should be based on the altitude capability
of an aircraft, 59% responded affirmatively. Apparently, the perceived need
for ACT was based on the likelihood of flying at higher altitudes and not
simply the level of certification. When asked if the current regulations (i.e.,
not requiring ACT) addressing high-altitude flying (above 7620 m/msl) are
sufficient, 52% of the current sample disagreed or strongly disagreed. DISCUSSION:
Generally, these professional pilots perceived that pilot training should
include introductory hypoxia training, recurrent hypoxia training, and ACT.
Exceptions were initial ACT for recreational pilots and private pilots. Generalizability
of these results may be affected by the specificity and size of the sample.
Distributing the survey to a wider audience of pilots would provide additional
information regarding perceptions of hypoxia training.
Going
high with type 1 diabetes.
Leal
C.
Institut d'Estudis de Medicina de Muntanya,
This review aims to identify the main issues facing
a healthy and well-controlled type-1 diabetic mountaineer at high altitude.
Most of the problems are self-managed by the diabetic climber although the
risk of serious morbidity or even death remains. Given the scarce evidence
on diabetes at altitude, an extensive search of the literature, including
case reports and anecdotes was carried out to reach the recommendations.
Publication Types:
· Review
Effect
of endurance training on the VO2-work rate relationship in normoxia and hypoxia.
Prieur F, Benoit H, Busso T, Castells J, Denis C.
Laboratory of Multidisciplinary Analysis in Physical Activities,
UFR STAPS of Lievin,
PURPOSE: We postulated that the relationship between VO2 and work rate (VO2-WR
relationship) during incremental exercise is dependent on O2 availability,
and that training-induced adaptations alter this relationship. We therefore
studied the effect of endurance training on VO2 response during incremental
exercise in normoxia and hypoxia (FIO2=0.134). METHODS: Before and after training
(6 d.wk, 4 wk), eight subjects performed incremental exercises under normoxia
and hypoxia and one constant-work rate exercise in normoxia at 80% of pretraining
VO2max. The slopes of the VO2-WR relationship during incremental exercise
were calculated using all the points (whole slope) or only points before the
lactate threshold (pre-LT slope). The difference between VO2max measured and
VO2max expected from the pre-LT slope (DeltaVO2) was determined, as was the
difference between VO2 at minute 10 and VO2 at minute 4 during the constant-work
rate exercise (DeltaVO2(10'-4')). RESULTS: In normoxia, training induced a
significant decrease in the whole slope (11.0+/-1.0 vs 9.9+/-0.4 mL.min.W,
P<0.05). In hypoxia, training induced a significant increase in the pre-LT
slope (8.7+/-1.2 vs 9.8+/-0.7 mL.min.W; P<0.05) and the whole slope (8.5+/-1.2
vs 9.4+/-0.5 mL.min.W; P<0.05). A significant correlation between the decrease
of DeltaVO2 and the decrease of DeltaVO2(10'-4')
with training was found in normoxia (P<0.01, r=0.79). CONCLUSIONS: Taken
together, these results indicate that adaptations induced by endurance training
are associated with more efficient incremental and constant-workload exercise
performed in normoxia. Moreover, training contributes to improved
O2 delivery during moderate exercise performed in hypoxia, and to enhanced
near-maximal exercise tolerance.
· Review, Multicase
Individual
variation in the erythropoietic response to altitude training in elite junior
swimmers.
Friedmann B,
Frese F, Menold E, Kauper F, Jost J, Bartsch P.
Department of Sports Medicine, Medical Clinic and Policlinic,
OBJECTIVES: Inter-individual variations in sea level performance after altitude
training have been attributed, at least in part, to an inter-individual variability
in hypoxia induced erythropoiesis. The aim of the present study was to examine
whether the variability in the increase in total haemoglobin mass after training
at moderate altitude could be predicted by the erythropoietin response after
4 h exposure to normobaric hypoxia at an ambient Po(2) corresponding to the
training altitude. METHODS: Erythropoietin levels were measured in 16 elite
junior swimmers before and after 4 h exposure to normobaric hypoxia (Fio(2) 0.15, approximately 2500 m) as well as repeatedly during
3 week altitude training (2100-2300 m). Before and after the altitude training,
total haemoglobin mass (CO rebreathing) and performance in a stepwise increasing
swimming test were determined. RESULTS: The erythropoietin increase (10-185%)
after 4 h exposure to normobaric hypoxia showed considerable inter-individual
variation and was significantly (p<0.001) correlated with the acute erythropoietin
increase during altitude training but not with the change in total haemoglobin
mass (significant increase of approximately 6% on average). The change in
sea level performance after altitude training was not related to the change
in total haemoglobin mass. CONCLUSIONS: The results of the present prospective
study confirmed the wide inter-individual variability in erythropoietic response
to altitude training in elite athletes. However, their erythropoietin response
to acute altitude exposure might not identify those athletes who respond to
altitude training with an increase in total haemoglobin mass.
Why doesn't exercise grow
the lungs when other factors do?
Wagner PD.
Division of Physiology, Department of Medicine, University of California,
San Diego, 9500 Gilman Drive, DEPT 0623A, La Jolla, CA 92093, USA. pdwagner@ucsd.edu
Exercise training enhances every component of the O(2)
transport and metabolic system--except the lungs. Consequently, the lungs
can contribute to the limitation of VO(2)max. Only
hypoxia early in life and substantial lung resection reproducibly stimulate
growth in normal lungs across species. Possible pathways involve genes activated
by hypoxia or mechanical strain, or both, including growth factors, hormones,
nitric oxide, and retinoids.
Publication Types:
· Review
· Review, Tutorial
[Mechanisms of adaptation to
intermittent hypoxic training course in sportsmen of high qualification]
[Article in Ukrainian]
Radziievs'kyi PO.
Boris Grinchenko Kyiv Municipal Pedagogical University.
Normobaric intermittent hypoxic training (IHT) is an effective method for
improvement of the FRS state, increase of the aerobic productivity, as well
as general and special capacity for work in sportsmen of high qualification.
High efficacy of IHT in improving all aspects of sportsmen FRS is a result
of alternating the hypoxic influences and normoxic intervals between them
during which the level of plastic processes remains increased, oxygen tension
in arterial blood and tissues increases to nonnoxic values. After IHT course,
the state of organ respiration improves, the respiration volume, a part of
alveolar ventilation in the minute volume of respiration, oxygen saturation
of arterial blood, hemoglobin content in blood--increase as well as economy
and efficacy of oxygen regimes of organism, general and special (especially
important) physical capacity for work.
Chronic intermittent hypoxia
and incremental cycling exercise independently depress muscle in vitro maximal
Na+-K+-ATPase activity in well-trained athletes.
Aughey RJ, Gore CJ, Hahn AG, Garnham AP, Clark SA, Petersen AC,
Roberts AD, McKenna MJ.
School of Human Movement, Recreation and Performance (FO22) Victoria University
of Technology, P.O. Box 14428, MCMC, Melbourne, Victoria 8001, Australia.
Athletes commonly attempt to enhance performance by training in normoxia but
sleeping in hypoxia [live high and train low (LHTL)]. However, chronic hypoxia
reduces muscle Na(+)-K(+)-ATPase content, whereas
fatiguing contractions reduce Na(+)-K(+)-ATPase activity, which each may impair
performance. We examined whether LHTL and intense exercise would decrease
muscle Na(+)-K(+)-ATPase activity and whether these
effects would be additive and sufficient to impair performance or plasma K(+)
regulation. Thirteen subjects were randomly assigned to two fitness-matched
groups, LHTL (n = 6) or control (Con, n = 7). LHTL slept at simulated moderate
altitude (3,000 m, inspired O(2) fraction = 15.48%)
for 23 nights and lived and trained by day under normoxic conditions in
Publication Types:
· Clinical Trial
· Randomized Controlled Trial
Effects of
hypoxic interval training on cycling performance.
Roels B, Millet GP, Marcoux CJ, Coste O, Bentley DJ, Candau RB.
UPRES EA 3759 Faculty of Sport Sciences, 700 avenue
Pic St Loup, 34090
PURPOSE: The aim of this study was to test the hypothesis that intermittent
hypoxic interval training improves sea level cycling performance more than
equivalent training in hypoxia or normoxia. METHODS: Thirty-three well-trained
cyclists and triathletes (25.9 +/- 2.7 yr, VO(2max) 66.1 +/- 6.1 mL.min(-1).kg(-1))
were divided into three groups: intermittent hypoxic (IHT, N = 11, P(I)O(2)
of 100 mm Hg), intermittent hypoxic interval training (IHIT, N = 11) and normoxia
(Nor, N = 11, P(I)O(2) of 160 mm Hg) and completed a 7-wk training program,
consisting of two high-intensity (100 or 90% relative peak power output) interval
training sessions each week. Each interval training session was performed
in a laboratory on the subject's own bicycle, in normoxic or hypoxic conditions
for the Nor and the IHT group, respectively. The
IHIT group performed warm-up and cool-down plus recovery from each interval
in hypoxic conditions. In contrast to IHT, interval exercise bouts were performed
in normoxic conditions. RESULTS: Mean power output during a 10-min cycle time
trial improved after the first 4 wk of training by 5.2 +/- 3.9, 3.7 +/- 5.9,
and 5.0 +/- 3.4% for IHIT, IHT, and Nor, respectively, without significant
differences between groups. Moreover, mean power output did not show any significant
improvement in the following 3 wk in any group. VO(2max) (L.min(-1)) increased only in IHIT during the training
period (8.7 +/- 9.1%; P < 0.05). No changes in cycling efficiency or in
hematological variables (P > 0.05) were observed. CONCLUSION: Four weeks
of interval training induced an improvement in endurance performance. However,
short-term exposure to hypoxia (approximately 114 min.wk(-1))
did not elicit a greater increase in performance or any hematological modifications.
Chronic intermittent hypoxia
and incremental cycling exercise independently depress muscle in vitro maximal
Na+-K+-ATPase activity in well-trained athletes.
Aughey RJ, Gore CJ, Hahn AG, Garnham AP, Clark SA, Petersen AC,
Roberts AD, McKenna MJ.
School of Human Movement, Recreation and Performance (FO22) Victoria University
of Technology, P.O. Box 14428, MCMC, Melbourne, Victoria 8001, Australia.
Athletes commonly attempt to enhance performance by training in normoxia but
sleeping in hypoxia [live high and train low (LHTL)]. However, chronic hypoxia
reduces muscle Na(+)-K(+)-ATPase content, whereas
fatiguing contractions reduce Na(+)-K(+)-ATPase activity, which each may impair
performance. We examined whether LHTL and intense exercise would decrease
muscle Na(+)-K(+)-ATPase activity and whether these
effects would be additive and sufficient to impair performance or plasma K(+)
regulation. Thirteen subjects were randomly assigned to two fitness-matched
groups, LHTL (n = 6) or control (Con, n = 7). LHTL slept at simulated moderate
altitude (3,000 m, inspired O(2) fraction = 15.48%)
for 23 nights and lived and trained by day under normoxic conditions in
Publication Types:
· Clinical Trial
· Randomized Controlled Trial
Effects
of hypoxic interval training on cycling performance.
Roels B, Millet GP, Marcoux CJ, Coste O, Bentley DJ, Candau RB.
UPRES EA 3759 Faculty of Sport Sciences, 700 avenue
Pic St Loup, 34090
PURPOSE: The aim of this study was to test the hypothesis that intermittent
hypoxic interval training improves sea level cycling performance more than
equivalent training in hypoxia or normoxia. METHODS: Thirty-three well-trained
cyclists and triathletes (25.9 +/- 2.7 yr, VO(2max) 66.1 +/- 6.1 mL.min(-1).kg(-1))
were divided into three groups: intermittent hypoxic (IHT, N = 11, P(I)O(2)
of 100 mm Hg), intermittent hypoxic interval training (IHIT, N = 11) and normoxia
(Nor, N = 11, P(I)O(2) of 160 mm Hg) and completed a 7-wk training program,
consisting of two high-intensity (100 or 90% relative peak power output) interval
training sessions each week. Each interval training session was performed
in a laboratory on the subject's own bicycle, in normoxic or hypoxic conditions
for the Nor and the IHT group, respectively. The
IHIT group performed warm-up and cool-down plus recovery from each interval
in hypoxic conditions. In contrast to IHT, interval exercise bouts were performed
in normoxic conditions. RESULTS: Mean power output during a 10-min cycle time
trial improved after the first 4 wk of training by 5.2 +/- 3.9, 3.7 +/- 5.9,
and 5.0 +/- 3.4% for IHIT, IHT, and Nor, respectively, without significant
differences between groups. Moreover, mean power output did not show any significant
improvement in the following 3 wk in any group. VO(2max) (L.min(-1)) increased only in IHIT during the training
period (8.7 +/- 9.1%; P < 0.05). No changes in cycling efficiency or in
hematological variables (P > 0.05) were observed. CONCLUSION: Four weeks
of interval training induced an improvement in endurance performance. However,
short-term exposure to hypoxia (approximately 114 min.wk(-1))
did not elicit a greater increase in performance or any hematological modifications.
Exercise training in chronic
heart failure: effects on pro-inflammatory markers.
Niebauer J, Clark AL, Webb-Peploe KM,
Coats AJ.
Cardiac Medicine,
BACKGROUND: Acute bouts of exercise have been shown to induce inflammatory
cytokine activation and peripheral hypoxia in patients with chronic heart
failure (CHF). In this study, we set out to investigate the impact of chronic
exercise training on pro-inflammatory cytokines and markers of endothelial
damage. METHODS AND RESULTS: We measured tumor necrosis factor alpha (TNFalpha),
its soluble TNF-receptors 1 and 2, interleukin 6 (IL-6), soluble e-selectin,
soluble intracellular adhesion molecule-1 (sICAM) and sCD14 in 18 patients
with CHF and 9 age-matched controls in a randomized cross-over study of 8
weeks of exercise training (5 days/week, submaximal bicycle ergometer training,
30 min/day; calisthenics 9 min/day) versus 8 weeks of rest. At baseline, patients
had a lower peak Vo(2) (p=0.009) and a trend for
higher levels of e-selectin (p=0.08) and sCD14 (p=0.06), in addition to significantly
elevated levels of sICAM (p=0.02), TNFalpha (p=0.02) and TNF-R2 (p=0.002);
TNF-R1 and IL-6 were not elevated. Although exercise training was effective
and led to an increase in peak Vo(2) in CHF (p<0.003),
there was no activation of any of the above variables observed, neither in
patients nor controls. CONCLUSIONS: Chronic heart failure is associated with
increased levels of TNFalpha and markers of endothelial damage. Whereas acute
bouts of exercise have been reported to lead to an increase in pro-inflammatory
cytokines and markers of endothelial damage, these effects are not seen when
exercise is performed chronically.
Publication Types:
· Clinical Trial
Exercise training prevents the
inflammatory response to hypoxia in cremaster venules.
Orth TA, Allen JA, Wood JG, Gonzalez NC.
Dept. of Molecular and Integrative Physiology,
Systemic hypoxia produces microvascular inflammation in several tissues, including
skeletal muscle. Exercise training (ET) has been shown to reduce the inflammatory
component of several diseases. Alternatively, ET could influence hypoxia-induced
inflammation by improving tissue oxygenation or increasing mechanical antiadhesive
forces at the leukocyte-endothelial interface. The effect of 5 wk of treadmill
ET on hypoxia-induced microvascular inflammation was studied in the cremaster
microcirculation of rats using intravital microscopy. In untrained rats, hypoxia
(arterial
· Randomized Controlled Trial
| Eur J Appl Physiol. 2005 Jun;94(3):298-304. Epub 2005 Mar 12. |
Living high-training low altitude
training: effects on mucosal immunity.
Tiollier E, Schmitt L, Burnat P, Fouillot JP,
Robach P, Filaire E, Guezennec C,
Richalet JP.
Departement de physiologie, IMASSA, 91223 Bretigny-sur-Orge
Cedex,
Secretory immunoglobulin A (sIgA) is the major immunoglobulin
of the mucosal immune system. Whereas the suppressive effect of heavy training
on mucosal immunity is well documented, little is known regarding the influence
of hypoxia exposure on sIgA during altitude training. This investigation examined
the impact of an 18-day Living high-training low (LHTL) training camp on sIgA
levels in 11 (six females and five males) elite cross-country skiers. Subjects
from the control group (n=5) trained and lived at 1,200 m of altitude, whereas,
subjects from the LHTL group (n=6) trained at 1,200 m, but lived at a simulated
altitude of 2,500, 3,000 and 3,500 m (3x6-day, 11 h day(-1))
in hypoxic rooms. Saliva samples were collected before, after each 6-day phases
and 2 weeks thereafter (POST). Salivary sIgA, protein and cortisol were measured.
There was a downward trend in sIgA concentrations over the study, which reached
significance in LHTL (P<0.01), but not in control (P=0.08). Salivary IgA
concentrations were still lower baseline at POST (P<0.05). Protein concentration
increased in LHTL (P<0.05) and was negatively correlated with sIgA concentration
after the 3,000 and 3,500 m-phase and at POST (P<0.05 all). Cortisol concentrations
were unchanged over the study and no relationship was found between cortisol
and sIgA. In summary, data were strongly suggestive of a cumulative negative
effect of physical exercise and hypoxia on sIgA levels during LHTL training.
Two weeks of active recovery did not allow for proper sIgA recovery. The mechanism
underlying this depression of sIgA could be mediated by neural factors.
Publication Types:
· Clinical Trial
· Randomized Controlled Trial
Going high
with type 1 diabetes.
Leal
C.
Institut d'Estudis de Medicina de Muntanya,
This review aims to identify the main issues facing
a healthy and well-controlled type-1 diabetic mountaineer at high altitude.
Most of the problems are self-managed by the diabetic climber although the
risk of serious morbidity or even death remains. Given the scarce evidence
on diabetes at altitude, an extensive search of the literature, including
case reports and anecdotes was carried out to reach the recommendations.
Publication Types:
· Review
· Review, Multicase
Effect of endurance
training on the VO2-work rate relationship in normoxia and hypoxia.
Prieur F, Benoit H, Busso T, Castells J, Denis C.
Laboratory of Multidisciplinary Analysis in Physical Activities,
UFR STAPS of Lievin,
PURPOSE: We postulated that the relationship between VO2 and work rate (VO2-WR
relationship) during incremental exercise is dependent on O2 availability,
and that training-induced adaptations alter this relationship. We therefore
studied the effect of endurance training on VO2 response during incremental
exercise in normoxia and hypoxia (FIO2=0.134). METHODS: Before and after training
(6 d.wk, 4 wk), eight subjects performed incremental exercises under normoxia
and hypoxia and one constant-work rate exercise in normoxia at 80% of pretraining
VO2max. The slopes of the VO2-WR relationship during incremental exercise
were calculated using all the points (whole slope) or only points before the
lactate threshold (pre-LT slope). The difference between VO2max measured and
VO2max expected from the pre-LT slope (DeltaVO2) was determined, as was the
difference between VO2 at minute 10 and VO2 at minute 4 during the constant-work
rate exercise (DeltaVO2(10'-4')). RESULTS: In normoxia, training induced a
significant decrease in the whole slope (11.0+/-1.0 vs 9.9+/-0.4 mL.min.W,
P<0.05). In hypoxia, training induced a significant increase in the pre-LT
slope (8.7+/-1.2 vs 9.8+/-0.7 mL.min.W; P<0.05) and the whole slope (8.5+/-1.2
vs 9.4+/-0.5 mL.min.W; P<0.05). A significant correlation between the decrease
of DeltaVO2 and the decrease of DeltaVO2(10'-4')
with training was found in normoxia (P<0.01, r=0.79). CONCLUSIONS: Taken
together, these results indicate that adaptations induced by endurance training
are associated with more efficient incremental and constant-workload exercise
performed in normoxia. Moreover, training contributes to improved
O2 delivery during moderate exercise performed in hypoxia, and to enhanced
near-maximal exercise tolerance.
O2 arterial desaturation
in endurance athletes increases muscle deoxygenation.
Legrand R, Ahmaidi S, Moalla W, Chocquet D, Marles A, Prieur F, Mucci P.
Laboratory of Multidisciplinary Analysis of Physical Activity,
Faculty of Sport Sciences,
PURPOSE: The aim of this study was to compare the muscle deoxygenation measured
by near infrared spectroscopy in endurance athletes who presented or not with
exercise-induced hypoxemia (EIH) during a maximal incremental test in normoxic
conditions. METHODS: Nineteen male endurance sportsmen performed an incremental
test on a cycle ergometer to determine maximal oxygen consumption (VO2max)
and the corresponding power output (P(max)). Arterial
O2 saturation (SaO2) was measured noninvasively with a pulse oxymeter at the
earlobe to detect EIH, which was defined as a drop in SaO2 > 4% between
rest and the end of the exercise. Muscle deoxygenation of the right vastus
lateralis was monitored by near infrared spectroscopy and was expressed in
percentage according to the ischemia-hyperemia scale. RESULTS: Ten athletes
exhibited arterial hypoxemia (EIH group) and the nine others were nonhypoxemic
(NEIH group). Training volume, competition level, VO2max, Pmax, and lactate
concentration were similar in the two groups. Nevertheless, muscle deoxygenation
at the end of the exercise was significantly greater in the EIH group (P <
0.05). CONCLUSION: Greater muscle deoxygenation at maximal exercise in hypoxemic
athletes seems to be due, at least in part, to reduced oxygen delivery--that is, exercise-induced hypoxemia--to
working muscle added to the metabolic demand. In addition, our finding is
also consistent with the hypothesis of greater muscle oxygen extraction in
order to counteract reduced O2 availability.
A three-week
traditional altitude training increases hemoglobin mass and red cell volume
in elite biathlon athletes.
Heinicke K, Heinicke I, Schmidt W, Wolfarth B.
Division of Physiology, Department of Medicine, University of California,
San Diego, La Jolla, 92093, USA. kheinicke@ucsd.edu
It is well known that altitude training stimulates
erythropoiesis, but only few data are available concerning the direct altitude
effect on red blood cell volume (RCV) in world class endurance athletes during
exposure to continued hypoxia. The purpose of this study was to evaluate the
impact of three weeks of traditional altitude training at 2050 m on total
hemoglobin mass (tHb), RCV and erythropoietic activity in highly-trained endurance
athletes. Total hemoglobin mass, RCV, plasma volume (PV), and blood volume
(BV) from 6 males and 4 females, all members of a world class biathlon team,
were determined on days 1 and 20 during their stay at altitude as well as
16 days after returning to sea-level conditions (800 m, only males) by using
the CO-rebreathing method. In males tHb (14.0 +/- 0.2 to 15.3 +/- 1.0 g/kg,
p < 0.05) and RCV (38.9 +/- 1.5 to 43.5 +/- 3.9 ml/kg, p < 0.05) increased
at altitude and returned to near sea-level values 16 days after descent. Similarly
in females, tHb (13.0 +/- 1.0 to 14.2 +/- 1.3 g/kg, p < 0.05) and RCV (37.3
+/- 3.3 to 42.2 +/- 4.1 ml/kg, p < 0.05) increased. Compared to their sea-level
values, the BV of male and female athletes showed a tendency to increase at
the end of the altitude training period, whereas PV was not altered. In male
athletes, plasma erythropoietin concentration increased up to day 4 at altitude
(11.8 +/- 5.0 to 20.8 +/- 6.0 mU/ml, p < 0.05)
and the plasma concentration of the soluble transferrin receptor was elevated
by about 11 % during the second part of the altitude training period, both
parameters indicating enhanced erythropoietic activity. In conclusion, we
show for the first time that a three-week traditional
altitude training increases erythropoietic activity even in world class endurance
athletes leading to elevated tHb and RCV. Considering the relatively fast
return of tHb and RCV to sea-level values after hypoxic exposure, our data
suggest to precisely schedule training at altitude
and competition at sea level.
Altitude negates the benefits
of aerobic training on the vascular adaptations in rats.
Reboul C, Tanguy S, Dauzat M, Obert P.
Dynamics of Cardio-Vascular Incoherences, Faculty of Medicine
INTRODUCTION: This study questioned the effect of living and training at moderate
altitude on aortic vasoreactivity. Considering that chronic hypoxia exposure
and endurance training are able to generate opposite effects on the systemic
vascular reactivity, it was hypothesized that endurance training benefits
on the vascular function could be limited by chronic hypoxia. METHODS: Sea-level
native rats were randomly assigned to N (living in normoxia), NT (living and
training 5 d.wk for 5 wk in normoxia), CH (living in hypoxia, 2800 m), and
CHT (living and training 5 d.wk for 5 wk in hypoxia, 2800 m) groups. Concentration
response curves to epinephrine, norepinephrine, endothelin-1, acetylcholine,
and sodium nitro-prusside were assessed on aortic isolated rings. Left ventricular
resting and maximal (during Tyrode's infusion) stroke volumes were evaluated
by Doppler-echocardiography and used as indexes of chronic aortic volume overload.
RESULTS: The main finding was that favorable aortic vasoreactivity adaptations
consecutive to sea-level training were not observed when training was conducted
at altitude. An improvement in the endothelium-dependent vasorelaxation (maximal
relaxation, R(max), N = 60.4 +/- 10.0 vs NT = 91.7
+/- 3.2%; P < 0.05) and a reduced sensitivity to ET-1 were observed in
NT rats. Such an enhancement in endothelium-dependent vasorelaxation was not
found in CHT rats (R(max): 48.4 +/- 7.8%). Moreover,
a higher sensitivity to ET-1 was reported in this group. Altitude-induced
limitation in aortic blood flow and shear stress could play a major role in
the explanation of these specific altitude-training adaptations. CONCLUSION:
If extrapolated to the peripheral vascular bed, our results have practical
significance for aerobic performance as aortic vasoreactivity adaptations
after altitude training could contribute to limit blood delivery to exercising
muscles.
Acute sleep responses in a normobaric
hypoxic tent.
Pedlar C, Whyte G, Emegbo S, Stanley N, Hindmarch I,
Godfrey R.
English Institute of Sport, St. Mary's College High Performance
Centre,
PURPOSE: Sleeping in a hypoxic environment is becoming increasingly popular
among athletes attempting to simulate a "live high, train low" training
regime. The purpose of this study was to investigate the acute effects (one
night) of sleeping in a normobaric hypoxic tent (NH) (PO(2)
= 110 mm Hg approximately 2500 m) upon markers of sleep physiology and quality,
compared with sleep in a normal ambient environment (BL) (PO(2) = 159 mm Hg
approximately sea level) and sleep in a normobaric normoxic tent (NN) (PO(2)
= 159 mm Hg). METHODS: Eight male recreational athletes (age 34.5 +/- 6.9
yr; stature 169.1 +/- 8.7 cm; mass 69.3 +/- 8.2 kg; VO(2max)
56.4 +/- 8.3 mL.kg(-1).min(-1)) participated in the study using a randomized,
double-blind crossover design. Polysomnographic studies were undertaken to
measure sleep stages, arterial oxygen saturation (SpO(2)),
heart rate (HR), and the Respiratory Disturbance Index (RDI). The Leeds Sleep
Evaluation Questionnaire (LSEQ) was used to measure subjective sleep quality.
RESULTS: NH (89.9 +/- 4.8%) resulted in a significantly lower (P < 0.05)
SpO(2) compared with both BL (95.7 +/- 1.5%) and NN (93.5 +/-
4.0%). Heart rate was significantly higher (P < 0.05) in NH (51.5 +/- 7.6
beats.min(-1)) compared with NN (48.3 +/- 6.9 beats.min(-1))
but was similar versus BL (50.3 +/- 4.3 beats.min(-1)). RDI (counts.h) and
RDI (total counts) were lowest in BL (3.5 +/- 2.5; 18.1 +/- 7.9) and highest
in NH (36.8 +/- 42.7; 221.9 +/- 254.5). The difference in RDI (counts.h(-1) and total counts) between NH and BL was significant
(P < 0.05). The LSEQ revealed that subjects' "behavior following waking"
score was significantly (P < 0.05) lower in NH (40.9 +/- 9.2) compared
with BL (52.3 +/- 8.3). CONCLUSION: This study presents evidence that sleep
in a normobaric hypoxic tent at a simulated altitude of 2500 m may affect
sleep parameters in some individuals. This type of analysis may be useful
in the early identification of poorly responding individuals to simulated
altitude environments.
Endurance training limits the
functional alterations of heart rat mitochondria submitted to in vitro anoxia-reoxygenation.
Ascensao A, Magalhaes J,
Soares JM, Ferreira R, Neuparth MJ,
Marques F, Oliveira PJ,
Duarte JA.
Department of Sport Biology, Faculty of Sport Sciences, University of Porto,
Rua Dr. Placido Costa, 91, 4200-450 Porto, Portugal.
BACKGROUND: Studies analysing the effect of endurance training on heart mitochondrial
function submitted to in vitro anoxia-reoxygenation (A-R) are missing. The
present study aimed to investigate the effect of moderate endurance treadmill
training (14 weeks) against rat heart mitochondrial dysfunction induced by
in vitro A-R. METHODS: Respiratory parameters (state 3, state 4, ADP/O and
respiratory control ratio-RCR) and oxidative damage markers (carbonyl groups
and malondialdehyde) were determined in isolated mitochondria before and after
1 min anoxia followed by 4 min reoxygenation. Levels of heat shock protein
60 kDa (HSP60) and 70 kDa (HSP70) were measured before A-R in mitochondria
and whole muscle homogenate, respectively. RESULTS: A-R significantly impaired
the rate of state 3 and state 4 respiration, as well
as the RCR and ADP/O in the sedentary group. However, mitochondrial state
3 respiration was significantly higher in trained
than in the sedentary group both before and after A-R. The impairments in
RCR, ADP/O ratio and state 4 induced by A-R in sedentary group were significantly
attenuated in endurance-trained group. The inhibition of state 4 induced by
GDP was significantly higher in trained than in sedentary group. Oxidative
modifications of mitochondrial proteins and phospholipids were found in sedentary
group after A-R, although limited in trained group. Increased levels of mitochondrial
HSP60 and tissue HSP70 accompanied the lower decrease in the respiratory function
after A-R observed in trained group. CONCLUSION: We therefore concluded that
endurance training limited the impairments on rat heart mitochondria caused
by the oxidant insult inflicted by in vitro A-R.
Heart rate
responses during a breath-holding competition in well-trained divers.
Lemaitre F, Bernier F, Petit I, Renard N, Gardette B, Joulia F.
Centre d'Etudes des Transformations des Activites Physiques et Sportives (CETAPS),
UPRES JE n 2318, Faculte des Sciences du Sport et de l'Education Physique
de Rouen, Universite de Rouen, France. frederic.lamaitre@univ-rouen.fr
The diving response elicited by breath-holding (BH)
and immersion mainly consists of bradycardia, decreased cardiac output, and
peripheral vasoconstriction. These responses reduce oxygen consumption and
thereby prolong the duration of the dive. They may also lead to cardiac arrhythmias
or hypoxia, however, which in turn may play a role in the occurrence of syncope
during BH. The aim of the present study was to analyze the cardiac responses
to prolonged breath-holding in elite divers during a competition. Heart rate
behaviour and the incidence of arrhythmia were recorded in 16 well-trained
breath-hold divers (BHD) using a cardio-frequency meter (for 15 divers) and
a Holter (for one diver) during maximal static breath-holding. Anthropometric,
spirometric, and training characteristics such as percentage of body fat,
pulmonary volumes and years of BH training were also determined. Forced vital
capacity (FVC) and forced expiratory volume in one second (FEV (1)) were higher
than the predicted values (+7.7%, p<0.05 and+6.6%, p<0.05, respectively).
During the static BH, divers presented apneic bradycardia (-44%) correlated
with static BH times (p<0.05); this was associated with cardiac arrhythmias
(supraventricular extrasystoles and ventricular extrasystoles) in the Holter-equipped
subject. These results are in agreement with those obtained in laboratory
conditions and confirm the existence of cardiac arrhythmias in well-trained
BHD.
Sleep in athletes undertaking
protocols of exposure to nocturnal simulated altitude at 2650 m.
Kinsman TA, Gore CJ, Hahn AG, Hopkins WG, Hawley JA, McKenna MJ, Clark SA, Aughey RJ, Townsend NE,
Chow CM.
Department of Physiology, Australian Institute of Sport
A popular method to attempt to enhance performance is for athletes to sleep
at natural or simulated moderate altitude (SMA) when training daily near sea
level. Based on our previous observation of periodic breathing in athletes
sleeping at SMA, we hypothesised that athletes' sleep quality would also suffer
with hypoxia. Using two typical protocols of nocturnal SMA (2650 m), we examined
the effect on the sleep physiology of 14 male endurance-trained athletes.
The selected protocols were Consecutive (15 successive exposure nights) and
Intermittent (3x 5 successive exposure nights, interspersed with 2 normoxic
nights) and athletes were randomly assigned to follow either one. We monitored
sleep for two successive nights under baseline conditions (B; normoxia, 600
m) and then at weekly intervals (nights 1, 8 and 15 (N1, N8 and N15, respectively))
of the protocols. Since there was no significant difference in response between
the protocols being followed (based on n=7, for each group) we are unable
to support a preference for either one, although the likelihood of a Type
II error must be acknowledged. For all athletes (n=14), respiratory disturbance
and arousal responses between B and N1, although large in magnitude, were
highly individual and not statistically significant. However, SpO2 decreased
at N1 versus B (p<0.001) and remained lower on N8 (p<0.001) and N15
(p<0.001), not returning to baseline level. Compared to B, arousals were
more frequent on N8 (p=0.02) and N15 (p=0.01). The percent of rapid eye movement
sleep (REM) increased from N1 to N8 (p=0.03) and N15 (p=0.01). Overall, sleeping
at 2650 m causes sleep disturbance in susceptible athletes, yet there was
some improvement in REM sleep over the study duration.
Hypoxia symptoms reported during
helicopter operations below 10,000 ft: a retrospective survey.
Smith A.
BAE Systems,
INTRODUCTION: During routine aviation medicine training, rotary-wing aircrew
are instructed that the impact of hypoxia on them from flying in unpressurized
cabins up to 10,000 ft (3048 m) above mean sea level (AMSL) is relatively
small and has few implications for aviation safety. Such reassurance is based
on data derived from experiments conducted on resting subjects and may not
reflect the true impact of hypoxia in aircrew engaged in operational tasks.
METHOD: A survey listing common symptoms of hypoxia was distributed to Australian
Army helicopter aircrew who had operated at altitudes
up to 10,000 ft AMSL. RESULTS: There were 53 surveys that were returned (71%
response), representing 25 loadmasters, 23 pilots, and 5 aircrewman technicians.
All respondents were Australian Army aircrew. One or more symptoms consistent
with hypoxia were reported by 86.6% of non-pilot aircrew and 60.9% of pilots.
60% of non-pilot aircrew reported four or more symptoms, compared with only
17% of pilots. The most commonly reported symptoms were difficulty with calculations
(45%), feeling light-headed (38%), delayed reaction time (38%), and mental
confusion (36%). Loadmasters reported more symptoms (mean 5.4) than pilots
(mean 2.2) (p < 0.001). From the narratives provided (n = 21), aircrew
experienced potentially operationally significant symptoms at a mean altitude
of 8462 ft (2579 m). CONCLUSION: The helicopter aircrew surveyed reported
symptoms consistent with hypoxia at altitudes within the so-called physiological
zone; loadmasters reported more effects than pilots. It may be inappropriate
to emphasize the benign nature of the physiological zone during aviation medicine
training of a non-resting population such as helicopter aircrew.
Exercise training improves lung
gas exchange, attenuates acute hypoxic pulmonary hypertension, but does not
prevent pulmonary hypertension of prolonged hypoxia.
Favret F, Henderson KK,
Allen J, Richalet JP,
Gonzalez NC.
A.R.P.E., EA2363 reponses cellulaires et fonctionnelles
a l'hypoxie, Universite Paris 13,
We have previously shown an attenuation of hypoxic pulmonary hypertension
by exercise training ET (15), although the mechanism was not determined. The
present study examined the effect of ET on the pulmonary arterial pressure
(Pap) response of rats to short and long term hypoxia. After 3 weeks of treadmill
training, male rats were divided into two groups: one (HT) was placed in hypobaric
hypoxia (380 Torr); the second remained in normoxia (NT). Both groups continued
to train in normoxia for 10 days, after which they were studied at rest and
during hypoxic and normoxic exercise. Sedentary normoxic (NS) and hypoxic
(HS) littermates were exposed to the same environments as their trained counterparts.
Resting and exercise hypoxic PaO2 were higher in NT and HT than in NS and
HS, respectively, although alveolar ventilation of trained rats was not higher.
Lower A-a PO2 and higher effective lung diffusing capacity for O2 (DLO2) in
NT vs NS and in HT vs HS suggest ET improved efficacy of gas exchange. Pulmonary
arterial pressure (Pap) and Pap/cardiac output (Pap/Q) were lower in NT than
NS in hypoxia, indicating ET attenuates the initial vasoconstriction of hypoxia.
However, ET had no effect on chronic hypoxic pulmonary hypertension: Pap and
Pap/Q in hypoxia were similar in HS vs HT. However, right ventricular weight
was lower in HT than in HS, although Pap was not different. Since ET attenuates
the initial pulmonary vasoconstriction of hypoxia, development of pulmonary
hypertension may be delayed in HT rats, and the time during which right ventricular
afterload is elevated may be shorter in this group. ET effects may improve
the response to acute hypoxia by increasing efficacy of gas exchange and lowering
right ventricular work.
Effects of
Intermittent Hypoxia on Heart Rate Variability during Rest and Exercise.
Povea C, Schmitt L, Brugniaux J,
Nicolet G, Richalet JP,
Fouillot JP.
Universite Paris 13, Faculte de Medecine,
Povea, Camilo; Laurent Schmitt; Julien Brugniaux; Gerard Nicolet; Jean-Paul
Richalet; and Jean-Pierre Fouillot. Effects of intermittent
hypoxia on heart rate variability during rest and exercise. High Alt.
Med. Biol. 6:215-225, 2005.-Changes in heart rate variability induced by an
intermittent exposure to hypoxia were evaluated in
athletes unacclimatized to altitude. Twenty national elite athletes trained
for 13 days at 1200 m and either lived and slept
at 1200 m (live low, train low, LLTL) or between 2500 and 3000 m (live high,
train low, LHTL). Subjects were investigated at 1200 m prior to and at the
end of the 13-day training camp. Exposure to acute hypoxia (11.5% O(2))
during exercise resulted in a significant decrease in spectral components
of heart rate variability in comparison with exercise in normoxia: total power
(p < 0.001), low-frequency component. LF (p < 0.001),
high-frequency component, HF (p < 0.05). Following acclimatization,
the LHTL group increased its LF component (p < 0.01) and LF/HF ratio during
exercise in hypoxia after the training period. In parallel, exposure to intermittent
hypoxia caused an increased ventilatory response to hypoxia. Acclimatization
modified the correlation between the ventilatory response to hypoxia at rest
and the difference in total power between normoxia and hypoxia (r (2) = 0.65,
p < 0.001). The increase in total power, LF component, and LF/HF ratio
suggests that intermittent hypoxic training increased the response of the
autonomic nervous system mainly through increased sympathetic activity.
Acute Effect
of Exercise-Hypoxia Challenge on GLUT4 Protein Expression in Rat Cardiac Muscle.
Chiu LL, Tsai YL, Lee WC, Cho YM, Ho HY, Chen SM, Chen MT, Kuo CH.
Laboratory of Exercise Biochemistry,
Chiu, Li-Ling, Ying-Lan Tsai, Wen-Chih Lee, Yu-Min Cho,
Hsin-Yi Ho, Shu-Man Chen, Mu- Tsung Chen, and Chia-Hua Kuo. Acute effect of exercise-hypoxia challenge on GLUT4 protein expression
in rat cardiac muscle. High Alt. Med. Biol. 6:256-267, 2005.-Altitude
training is a frequently used method for enhancing endurance performance in
athletes. But its acute effect on carbohydrate metabolism in cardiac muscle
is unknown. In this study, we determined the acute effect of an exercise-hypoxia
challenge on glycogen storage and GLUT4 protein expression in heart muscle.
Sixteen male Sprague-Dawley rats were assigned to one of two groups: control
(CTRL) and exercise-hypoxia (EX+HY). The exercise protocol consisted of swimming
for 180 min twice, with a 45-min rest interval. Five hours after the exercise,
the EX+HY rats were exposed to a 14% O(2) systemic hypoxia under normobaric condition for 12 h.
After this hypoxia exposure, the EX+HY and control rats were given glucose
orally (1 g/kg body weight) with stomach tube and recovered under normal condition
for 16 h. Ventricular portion of the heart was used to determine the levels
of glycogen, GLUT4 mRNA, and GLUT4 protein after recovery. We found that myocardial
glycogen level was lowered by the exercise-hypoxia challenge (51% below control,
p < 0.05), while GLUT4 mRNA was dramatically elevated (approximately 400%
of the control level, p < 0.05). The acute exercise-hypoxia treatment did
not affect GLUT1 protein level in the same tissue. The novel finding of the
study was that the exercise-hypoxia treatment significantly induced GLUT4
gene expression in the cardiac muscle. This acute response appears to be associated
with a sustained glycogen depletion of the muscle
Chronic intermittent hypoxia
and incremental cycling exercise independently depress muscle in vitro maximal
Na+-K+-ATPase activity in well-trained athletes.
Aughey RJ, Gore CJ, Hahn AG, Garnham AP, Clark SA, Petersen AC,
Roberts AD, McKenna MJ.
School of Human Movement, Recreation and Performance (FO22) Victoria University
of Technology, P.O. Box 14428, MCMC, Melbourne, Victoria 8001, Australia.
Athletes commonly attempt to enhance performance by training in normoxia but
sleeping in hypoxia [live high and train low (LHTL)]. However, chronic hypoxia
reduces muscle Na(+)-K(+)-ATPase content, whereas
fatiguing contractions reduce Na(+)-K(+)-ATPase activity, which each may impair
performance. We examined whether LHTL and intense exercise would decrease
muscle Na(+)-K(+)-ATPase activity and whether these
effects would be additive and sufficient to impair performance or plasma K(+)
regulation. Thirteen subjects were randomly assigned to two fitness-matched
groups, LHTL (n = 6) or control (Con, n = 7). LHTL slept at simulated moderate
altitude (3,000 m, inspired O(2) fraction = 15.48%)
for 23 nights and lived and trained by day under normoxic conditions in
Publication Types:
· Clinical Trial
· Randomized Controlled Trial
Chronic intermittent hypoxia
increases infarction in the isolated rat heart.
Joyeux-Faure M,
Stanke-Labesque F,
Lefebvre B, Beguin P, Godin-Ribuot D,
Ribuot C, Launois SH, Bessard G, Levy P.
Laboratoire HP2, Hypoxie Physio-Pathologie, Faculte de Pharmacie, Domaine
de la Merci, 38706 La Tronche, France. marie.faure@ujf-grenoble.fr
Coronary heart disease is frequently associated with obstructive sleep apnea
syndrome and treating obstructive sleep apnea appears to significantly improve
the outcome in coronary heart disease. Thus we have developed a rat model
of chronic intermittent hypoxia (IH) to study the influence of this condition
on myocardial ischemia-reperfusion tolerance and on functional vascular reactivity.
Wistar male rats were divided in three experimental groups (n = 12 each) subjected
to chronic IH (IH group), normoxia (N group), or control conditions (control
group). IH consisted of repetitive cycles of 1 min (40 s with inspired O(2)
fraction 5% followed by 20 s normoxia) and was applied for 8 h during daytime,
for 35 days. Normoxic cycles were applied in the same conditions, inspired
O(2) fraction remaining constant at 21%. On day 36,
mean arterial blood pressure (MABP) was measured before isolated hearts were
submitted to an ischemia-reperfusion protocol. The thoracic aorta and left
carotid artery were also excised for functional reactivity studies. MABP was
not significantly different between the three experimental groups. Infarct
sizes (in percent of ventricles) were significantly higher in IH group (46.9
+/- 3.6%) compared with N (26.1 +/- 2.8%) and control (21.7 +/- 2.1%) groups.
Vascular smooth muscle function was similar in aorta and carotid arteries
from all groups. The endothelium-dependent relaxation in response to acetylcholine
was also similar in aorta and carotid arteries from all groups. Chronic IH
increased heart sensitivity to infarction, independently of a significant
increase in MABP, and did not affect vascular reactivity of aorta and carotid
arteries.
Exercise training in chronic
heart failure: effects on pro-inflammatory markers.
Niebauer J, Clark AL, Webb-Peploe KM,
Coats AJ.
Cardiac Medicine,
BACKGROUND: Acute bouts of exercise have been shown to induce inflammatory
cytokine activation and peripheral hypoxia in patients with chronic heart
failure (CHF). In this study, we set out to investigate the impact of chronic
exercise training on pro-inflammatory cytokines and markers of endothelial
damage. METHODS AND RESULTS: We measured tumor necrosis factor alpha (TNFalpha),
its soluble TNF-receptors 1 and 2, interleukin 6 (IL-6), soluble e-selectin,
soluble intracellular adhesion molecule-1 (sICAM) and sCD14 in 18 patients
with CHF and 9 age-matched controls in a randomized cross-over study of 8
weeks of exercise training (5 days/week, submaximal bicycle ergometer training,
30 min/day; calisthenics 9 min/day) versus 8 weeks of rest. At baseline, patients
had a lower peak Vo(2) (p=0.009) and a trend for
higher levels of e-selectin (p=0.08) and sCD14 (p=0.06), in addition to significantly
elevated levels of sICAM (p=0.02), TNFalpha (p=0.02) and TNF-R2 (p=0.002);
TNF-R1 and IL-6 were not elevated. Although exercise training was effective
and led to an increase in peak Vo(2) in CHF (p<0.003),
there was no activation of any of the above variables observed, neither in
patients nor controls. CONCLUSIONS: Chronic heart failure is associated with
increased levels of TNFalpha and markers of endothelial damage. Whereas acute
bouts of exercise have been reported to lead to an increase in pro-inflammatory
cytokines and markers of endothelial damage, these effects are not seen when
exercise is performed chronically.
Publication Types:
· Clinical Trial
Exercise training prevents the
inflammatory response to hypoxia in cremaster venules.
Orth TA, Allen JA, Wood JG, Gonzalez NC.
Dept. of Molecular and Integrative Physiology,
Systemic hypoxia produces microvascular inflammation in several tissues, including
skeletal muscle. Exercise training (ET) has been shown to reduce the inflammatory
component of several diseases. Alternatively, ET could influence hypoxia-induced
inflammation by improving tissue oxygenation or increasing mechanical antiadhesive
forces at the leukocyte-endothelial interface. The effect of 5 wk of treadmill
ET on hypoxia-induced microvascular inflammation was studied in the cremaster
microcirculation of rats using intravital microscopy. In untrained rats, hypoxia
(arterial
· Randomized Controlled Trial
| Eur J Appl Physiol. 2005 Jun;94(3):298-304. Epub 2005 Mar 12. |
Living high-training low altitude
training: effects on mucosal immunity.
Tiollier E, Schmitt L, Burnat P, Fouillot JP,
Robach P, Filaire E, Guezennec C,
Richalet JP.
Departement de physiologie, IMASSA, 91223 Bretigny-sur-Orge
Cedex,
Secretory immunoglobulin A (sIgA) is the major immunoglobulin
of the mucosal immune system. Whereas the suppressive effect of heavy training
on mucosal immunity is well documented, little is known regarding the influence
of hypoxia exposure on sIgA during altitude training. This investigation examined
the impact of an 18-day Living high-training low (LHTL) training camp on sIgA
levels in 11 (six females and five males) elite cross-country skiers. Subjects
from the control group (n=5) trained and lived at 1,200 m of altitude, whereas,
subjects from the LHTL group (n=6) trained at 1,200 m, but lived at a simulated
altitude of 2,500, 3,000 and 3,500 m (3x6-day, 11 h day(-1))
in hypoxic rooms. Saliva samples were collected before, after each 6-day phases
and 2 weeks thereafter (POST). Salivary sIgA, protein and cortisol were measured.
There was a downward trend in sIgA concentrations over the study, which reached
significance in LHTL (P<0.01), but not in control (P=0.08). Salivary IgA
concentrations were still lower baseline at POST (P<0.05). Protein concentration
increased in LHTL (P<0.05) and was negatively correlated with sIgA concentration
after the 3,000 and 3,500 m-phase and at POST (P<0.05 all). Cortisol concentrations
were unchanged over the study and no relationship was found between cortisol
and sIgA. In summary, data were strongly suggestive of a cumulative negative
effect of physical exercise and hypoxia on sIgA levels during LHTL training.
Two weeks of active recovery did not allow for proper sIgA recovery. The mechanism
underlying this depression of sIgA could be mediated by neural factors.
Publication Types:
· Clinical Trial
· Randomized Controlled Trial
Going high
with type 1 diabetes.
Leal
C.
Institut d'Estudis de Medicina de Muntanya,
This review aims to identify the main issues facing
a healthy and well-controlled type-1 diabetic mountaineer at high altitude.
Most of the problems are self-managed by the diabetic climber although the
risk of serious morbidity or even death remains. Given the scarce evidence
on diabetes at altitude, an extensive search of the literature, including
case reports and anecdotes was carried out to reach the recommendations.
Publication Types:
· Review
· Review, Multicase
Effect of endurance
training on the VO2-work rate relationship in normoxia and hypoxia.
Prieur F, Benoit H, Busso T, Castells J, Denis C.
Laboratory of Multidisciplinary Analysis in Physical Activities,
UFR STAPS of Lievin,
PURPOSE: We postulated that the relationship between VO2 and work rate (VO2-WR
relationship) during incremental exercise is dependent on O2 availability,
and that training-induced adaptations alter this relationship. We therefore
studied the effect of endurance training on VO2 response during incremental
exercise in normoxia and hypoxia (FIO2=0.134). METHODS: Before and after training
(6 d.wk, 4 wk), eight subjects performed incremental exercises under normoxia
and hypoxia and one constant-work rate exercise in normoxia at 80% of pretraining
VO2max. The slopes of the VO2-WR relationship during incremental exercise
were calculated using all the points (whole slope) or only points before the
lactate threshold (pre-LT slope). The difference between VO2max measured and
VO2max expected from the pre-LT slope (DeltaVO2) was determined, as was the
difference between VO2 at minute 10 and VO2 at minute 4 during the constant-work
rate exercise (DeltaVO2(10'-4')). RESULTS: In normoxia, training induced a
significant decrease in the whole slope (11.0+/-1.0 vs 9.9+/-0.4 mL.min.W,
P<0.05). In hypoxia, training induced a significant increase in the pre-LT
slope (8.7+/-1.2 vs 9.8+/-0.7 mL.min.W; P<0.05) and the whole slope (8.5+/-1.2
vs 9.4+/-0.5 mL.min.W; P<0.05). A significant correlation between the decrease
of DeltaVO2 and the decrease of DeltaVO2(10'-4')
with training was found in normoxia (P<0.01, r=0.79). CONCLUSIONS: Taken
together, these results indicate that adaptations induced by endurance training
are associated with more efficient incremental and constant-workload exercise
performed in normoxia. Moreover, training contributes to improved
O2 delivery during moderate exercise performed in hypoxia, and to enhanced
near-maximal exercise tolerance.
O2 arterial desaturation
in endurance athletes increases muscle deoxygenation.
Legrand R, Ahmaidi S, Moalla W, Chocquet D, Marles A, Prieur F, Mucci P.
Laboratory of Multidisciplinary Analysis of Physical Activity,
Faculty of Sport Sciences,
PURPOSE: The aim of this study was to compare the muscle deoxygenation measured
by near infrared spectroscopy in endurance athletes who presented or not with
exercise-induced hypoxemia (EIH) during a maximal incremental test in normoxic
conditions. METHODS: Nineteen male endurance sportsmen performed an incremental
test on a cycle ergometer to determine maximal oxygen consumption (VO2max)
and the corresponding power output (P(max)). Arterial
O2 saturation (SaO2) was measured noninvasively with a pulse oxymeter at the
earlobe to detect EIH, which was defined as a drop in SaO2 > 4% between
rest and the end of the exercise. Muscle deoxygenation of the right vastus
lateralis was monitored by near infrared spectroscopy and was expressed in
percentage according to the ischemia-hyperemia scale. RESULTS: Ten athletes
exhibited arterial hypoxemia (EIH group) and the nine others were nonhypoxemic
(NEIH group). Training volume, competition level, VO2max, Pmax, and lactate
concentration were similar in the two groups. Nevertheless, muscle deoxygenation
at the end of the exercise was significantly greater in the EIH group (P <
0.05). CONCLUSION: Greater muscle deoxygenation at maximal exercise in hypoxemic
athletes seems to be due, at least in part, to reduced oxygen delivery--that is, exercise-induced hypoxemia--to
working muscle added to the metabolic demand. In addition, our finding is
also consistent with the hypothesis of greater muscle oxygen extraction in
order to counteract reduced O2 availability.
A three-week
traditional altitude training increases hemoglobin mass and red cell volume
in elite biathlon athletes.
Heinicke K, Heinicke I, Schmidt W, Wolfarth B.
Division of Physiology, Department of Medicine, University of California,
San Diego, La Jolla, 92093, USA. kheinicke@ucsd.edu
It is well known that altitude training stimulates
erythropoiesis, but only few data are available concerning the direct altitude
effect on red blood cell volume (RCV) in world class endurance athletes during
exposure to continued hypoxia. The purpose of this study was to evaluate the
impact of three weeks of traditional altitude training at 2050 m on total
hemoglobin mass (tHb), RCV and erythropoietic activity in highly-trained endurance
athletes. Total hemoglobin mass, RCV, plasma volume (PV), and blood volume
(BV) from 6 males and 4 females, all members of a world class biathlon team,
were determined on days 1 and 20 during their stay at altitude as well as
16 days after returning to sea-level conditions (800 m, only males) by using
the CO-rebreathing method. In males tHb (14.0 +/- 0.2 to 15.3 +/- 1.0 g/kg,
p < 0.05) and RCV (38.9 +/- 1.5 to 43.5 +/- 3.9 ml/kg, p < 0.05) increased
at altitude and returned to near sea-level values 16 days after descent. Similarly
in females, tHb (13.0 +/- 1.0 to 14.2 +/- 1.3 g/kg, p < 0.05) and RCV (37.3
+/- 3.3 to 42.2 +/- 4.1 ml/kg, p < 0.05) increased. Compared to their sea-level
values, the BV of male and female athletes showed a tendency to increase at
the end of the altitude training period, whereas PV was not altered. In male
athletes, plasma erythropoietin concentration increased up to day 4 at altitude
(11.8 +/- 5.0 to 20.8 +/- 6.0 mU/ml, p < 0.05)
and the plasma concentration of the soluble transferrin receptor was elevated
by about 11 % during the second part of the altitude training period, both
parameters indicating enhanced erythropoietic activity. In conclusion, we
show for the first time that a three-week traditional
altitude training increases erythropoietic activity even in world class endurance
athletes leading to elevated tHb and RCV. Considering the relatively fast
return of tHb and RCV to sea-level values after hypoxic exposure, our data
suggest to precisely schedule training at altitude
and competition at sea level.
Altitude negates the benefits
of aerobic training on the vascular adaptations in rats.
Reboul C, Tanguy S, Dauzat M, Obert P.
Dynamics of Cardio-Vascular Incoherences, Faculty of Medicine
INTRODUCTION: This study questioned the effect of living and training at moderate
altitude on aortic vasoreactivity. Considering that chronic hypoxia exposure
and endurance training are able to generate opposite effects on the systemic
vascular reactivity, it was hypothesized that endurance training benefits
on the vascular function could be limited by chronic hypoxia. METHODS: Sea-level
native rats were randomly assigned to N (living in normoxia), NT (living and
training 5 d.wk for 5 wk in normoxia), CH (living in hypoxia, 2800 m), and
CHT (living and training 5 d.wk for 5 wk in hypoxia, 2800 m) groups. Concentration
response curves to epinephrine, norepinephrine, endothelin-1, acetylcholine,
and sodium nitro-prusside were assessed on aortic isolated rings. Left ventricular
resting and maximal (during Tyrode's infusion) stroke volumes were evaluated
by Doppler-echocardiography and used as indexes of chronic aortic volume overload.
RESULTS: The main finding was that favorable aortic vasoreactivity adaptations
consecutive to sea-level training were not observed when training was conducted
at altitude. An improvement in the endothelium-dependent vasorelaxation (maximal
relaxation, R(max), N = 60.4 +/- 10.0 vs NT = 91.7
+/- 3.2%; P < 0.05) and a reduced sensitivity to ET-1 were observed in
NT rats. Such an enhancement in endothelium-dependent vasorelaxation was not
found in CHT rats (R(max): 48.4 +/- 7.8%). Moreover,
a higher sensitivity to ET-1 was reported in this group. Altitude-induced
limitation in aortic blood flow and shear stress could play a major role in
the explanation of these specific altitude-training adaptations. CONCLUSION:
If extrapolated to the peripheral vascular bed, our results have practical
significance for aerobic performance as aortic vasoreactivity adaptations
after altitude training could contribute to limit blood delivery to exercising
muscles.
Acute sleep responses in a normobaric
hypoxic tent.
Pedlar C, Whyte G, Emegbo S, Stanley N, Hindmarch I,
Godfrey R.
English Institute of Sport, St. Mary's College High Performance
Centre,
PURPOSE: Sleeping in a hypoxic environment is becoming increasingly popular
among athletes attempting to simulate a "live high, train low" training
regime. The purpose of this study was to investigate the acute effects (one
night) of sleeping in a normobaric hypoxic tent (NH) (PO(2)
= 110 mm Hg approximately 2500 m) upon markers of sleep physiology and quality,
compared with sleep in a normal ambient environment (BL) (PO(2) = 159 mm Hg
approximately sea level) and sleep in a normobaric normoxic tent (NN) (PO(2)
= 159 mm Hg). METHODS: Eight male recreational athletes (age 34.5 +/- 6.9
yr; stature 169.1 +/- 8.7 cm; mass 69.3 +/- 8.2 kg; VO(2max)
56.4 +/- 8.3 mL.kg(-1).min(-1)) participated in the study using a randomized,
double-blind crossover design. Polysomnographic studies were undertaken to
measure sleep stages, arterial oxygen saturation (SpO(2)),
heart rate (HR), and the Respiratory Disturbance Index (RDI). The Leeds Sleep
Evaluation Questionnaire (LSEQ) was used to measure subjective sleep quality.
RESULTS: NH (89.9 +/- 4.8%) resulted in a significantly lower (P < 0.05)
SpO(2) compared with both BL (95.7 +/- 1.5%) and NN (93.5 +/-
4.0%). Heart rate was significantly higher (P < 0.05) in NH (51.5 +/- 7.6
beats.min(-1)) compared with NN (48.3 +/- 6.9 beats.min(-1))
but was similar versus BL (50.3 +/- 4.3 beats.min(-1)). RDI (counts.h) and
RDI (total counts) were lowest in BL (3.5 +/- 2.5; 18.1 +/- 7.9) and highest
in NH (36.8 +/- 42.7; 221.9 +/- 254.5). The difference in RDI (counts.h(-1) and total counts) between NH and BL was significant
(P < 0.05). The LSEQ revealed that subjects' "behavior following waking"
score was significantly (P < 0.05) lower in NH (40.9 +/- 9.2) compared
with BL (52.3 +/- 8.3). CONCLUSION: This study presents evidence that sleep
in a normobaric hypoxic tent at a simulated altitude of 2500 m may affect
sleep parameters in some individuals. This type of analysis may be useful
in the early identification of poorly responding individuals to simulated
altitude environments.
Endurance training limits the
functional alterations of heart rat mitochondria submitted to in vitro anoxia-reoxygenation.
Ascensao A, Magalhaes J,
Soares JM, Ferreira R, Neuparth MJ,
Marques F, Oliveira PJ,
Duarte JA.
Department of Sport Biology, Faculty of Sport Sciences, University of Porto,
Rua Dr. Placido Costa, 91, 4200-450 Porto, Portugal.
BACKGROUND: Studies analysing the effect of endurance training on heart mitochondrial
function submitted to in vitro anoxia-reoxygenation (A-R) are missing. The
present study aimed to investigate the effect of moderate endurance treadmill
training (14 weeks) against rat heart mitochondrial dysfunction induced by
in vitro A-R. METHODS: Respiratory parameters (state 3, state 4, ADP/O and
respiratory control ratio-RCR) and oxidative damage markers (carbonyl groups
and malondialdehyde) were determined in isolated mitochondria before and after
1 min anoxia followed by 4 min reoxygenation. Levels of heat shock protein
60 kDa (HSP60) and 70 kDa (HSP70) were measured before A-R in mitochondria
and whole muscle homogenate, respectively. RESULTS: A-R significantly impaired
the rate of state 3 and state 4 respiration, as well
as the RCR and ADP/O in the sedentary group. However, mitochondrial state
3 respiration was significantly higher in trained
than in the sedentary group both before and after A-R. The impairments in
RCR, ADP/O ratio and state 4 induced by A-R in sedentary group were significantly
attenuated in endurance-trained group. The inhibition of state 4 induced by
GDP was significantly higher in trained than in sedentary group. Oxidative
modifications of mitochondrial proteins and phospholipids were found in sedentary
group after A-R, although limited in trained group. Increased levels of mitochondrial
HSP60 and tissue HSP70 accompanied the lower decrease in the respiratory function
after A-R observed in trained group. CONCLUSION: We therefore concluded that
endurance training limited the impairments on rat heart mitochondria caused
by the oxidant insult inflicted by in vitro A-R.
Heart rate
responses during a breath-holding competition in well-trained divers.
Lemaitre F, Bernier F, Petit I, Renard N, Gardette B, Joulia F.
Centre d'Etudes des Transformations des Activites Physiques et Sportives (CETAPS),
UPRES JE n 2318, Faculte des Sciences du Sport et de l'Education Physique
de Rouen, Universite de Rouen, France. frederic.lamaitre@univ-rouen.fr
The diving response elicited by breath-holding (BH)
and immersion mainly consists of bradycardia, decreased cardiac output, and
peripheral vasoconstriction. These responses reduce oxygen consumption and
thereby prolong the duration of the dive. They may also lead to cardiac arrhythmias
or hypoxia, however, which in turn may play a role in the occurrence of syncope
during BH. The aim of the present study was to analyze the cardiac responses
to prolonged breath-holding in elite divers during a competition. Heart rate
behaviour and the incidence of arrhythmia were recorded in 16 well-trained
breath-hold divers (BHD) using a cardio-frequency meter (for 15 divers) and
a Holter (for one diver) during maximal static breath-holding. Anthropometric,
spirometric, and training characteristics such as percentage of body fat,
pulmonary volumes and years of BH training were also determined. Forced vital
capacity (FVC) and forced expiratory volume in one second (FEV (1)) were higher
than the predicted values (+7.7%, p<0.05 and+6.6%, p<0.05, respectively).
During the static BH, divers presented apneic bradycardia (-44%) correlated
with static BH times (p<0.05); this was associated with cardiac arrhythmias
(supraventricular extrasystoles and ventricular extrasystoles) in the Holter-equipped
subject. These results are in agreement with those obtained in laboratory
conditions and confirm the existence of cardiac arrhythmias in well-trained
BHD.
Sleep in athletes undertaking
protocols of exposure to nocturnal simulated altitude at 2650 m.
Kinsman TA, Gore CJ, Hahn AG, Hopkins WG, Hawley JA, McKenna MJ, Clark SA, Aughey RJ, Townsend NE,
Chow CM.
Department of Physiology, Australian Institute of Sport
A popular method to attempt to enhance performance is for athletes to sleep
at natural or simulated moderate altitude (SMA) when training daily near sea
level. Based on our previous observation of periodic breathing in athletes
sleeping at SMA, we hypothesised that athletes' sleep quality would also suffer
with hypoxia. Using two typical protocols of nocturnal SMA (2650 m), we examined
the effect on the sleep physiology of 14 male endurance-trained athletes.
The selected protocols were Consecutive (15 successive exposure nights) and
Intermittent (3x 5 successive exposure nights, interspersed with 2 normoxic
nights) and athletes were randomly assigned to follow either one. We monitored
sleep for two successive nights under baseline conditions (B; normoxia, 600
m) and then at weekly intervals (nights 1, 8 and 15 (N1, N8 and N15, respectively))
of the protocols. Since there was no significant difference in response between
the protocols being followed (based on n=7, for each group) we are unable
to support a preference for either one, although the likelihood of a Type
II error must be acknowledged. For all athletes (n=14), respiratory disturbance
and arousal responses between B and N1, although large in magnitude, were
highly individual and not statistically significant. However, SpO2 decreased
at N1 versus B (p<0.001) and remained lower on N8 (p<0.001) and N15
(p<0.001), not returning to baseline level. Compared to B, arousals were
more frequent on N8 (p=0.02) and N15 (p=0.01). The percent of rapid eye movement
sleep (REM) increased from N1 to N8 (p=0.03) and N15 (p=0.01). Overall, sleeping
at 2650 m causes sleep disturbance in susceptible athletes, yet there was
some improvement in REM sleep over the study duration.
Hypoxia symptoms reported during
helicopter operations below 10,000 ft: a retrospective survey.
Smith A.
BAE Systems,
INTRODUCTION: During routine aviation medicine training, rotary-wing aircrew
are instructed that the impact of hypoxia on them from flying in unpressurized
cabins up to 10,000 ft (3048 m) above mean sea level (AMSL) is relatively
small and has few implications for aviation safety. Such reassurance is based
on data derived from experiments conducted on resting subjects and may not
reflect the true impact of hypoxia in aircrew engaged in operational tasks.
METHOD: A survey listing common symptoms of hypoxia was distributed to Australian
Army helicopter aircrew who had operated at altitudes
up to 10,000 ft AMSL. RESULTS: There were 53 surveys that were returned (71%
response), representing 25 loadmasters, 23 pilots, and 5 aircrewman technicians.
All respondents were Australian Army aircrew. One or more symptoms consistent
with hypoxia were reported by 86.6% of non-pilot aircrew and 60.9% of pilots.
60% of non-pilot aircrew reported four or more symptoms, compared with only
17% of pilots. The most commonly reported symptoms were difficulty with calculations
(45%), feeling light-headed (38%), delayed reaction time (38%), and mental
confusion (36%). Loadmasters reported more symptoms (mean 5.4) than pilots
(mean 2.2) (p < 0.001). From the narratives provided (n = 21), aircrew
experienced potentially operationally significant symptoms at a mean altitude
of 8462 ft (2579 m). CONCLUSION: The helicopter aircrew surveyed reported
symptoms consistent with hypoxia at altitudes within the so-called physiological
zone; loadmasters reported more effects than pilots. It may be inappropriate
to emphasize the benign nature of the physiological zone during aviation medicine
training of a non-resting population such as helicopter aircrew.
Effects of
Intermittent Hypoxia on Heart Rate Variability during Rest and Exercise.
Povea C, Schmitt L, Brugniaux J,
Nicolet G, Richalet JP,
Fouillot JP.
Universite Paris 13, Faculte de Medecine,
Povea, Camilo; Laurent Schmitt; Julien Brugniaux; Gerard Nicolet; Jean-Paul
Richalet; and Jean-Pierre Fouillot. Effects of intermittent
hypoxia on heart rate variability during rest and exercise. High Alt.
Med. Biol. 6:215-225, 2005.-Changes in heart rate variability induced by an
intermittent exposure to hypoxia were evaluated in
athletes unacclimatized to altitude. Twenty national elite athletes trained
for 13 days at 1200 m and either lived and slept
at 1200 m (live low, train low, LLTL) or between 2500 and 3000 m (live high,
train low, LHTL). Subjects were investigated at 1200 m prior to and at the
end of the 13-day training camp. Exposure to acute hypoxia (11.5% O(2))
during exercise resulted in a significant decrease in spectral components
of heart rate variability in comparison with exercise in normoxia: total power
(p < 0.001), low-frequency component. LF (p < 0.001),
high-frequency component, HF (p < 0.05). Following acclimatization,
the LHTL group increased its LF component (p < 0.01) and LF/HF ratio during
exercise in hypoxia after the training period. In parallel, exposure to intermittent
hypoxia caused an increased ventilatory response to hypoxia. Acclimatization
modified the correlation between the ventilatory response to hypoxia at rest
and the difference in total power between normoxia and hypoxia (r (2) = 0.65,
p < 0.001). The increase in total power, LF component, and LF/HF ratio
suggests that intermittent hypoxic training increased the response of the
autonomic nervous system mainly through increased sympathetic activity.
Acute Effect
of Exercise-Hypoxia Challenge on GLUT4 Protein Expression in Rat Cardiac Muscle.
Chiu LL, Tsai YL, Lee WC, Cho YM, Ho HY, Chen SM, Chen MT, Kuo CH.
Laboratory of Exercise Biochemistry,
Chiu, Li-Ling, Ying-Lan Tsai, Wen-Chih Lee, Yu-Min Cho,
Hsin-Yi Ho, Shu-Man Chen, Mu- Tsung Chen, and Chia-Hua Kuo. Acute effect of exercise-hypoxia challenge on GLUT4 protein expression
in rat cardiac muscle. High Alt. Med. Biol. 6:256-267, 2005.-Altitude
training is a frequently used method for enhancing endurance performance in
athletes. But its acute effect on carbohydrate metabolism in cardiac muscle
is unknown. In this study, we determined the acute effect of an exercise-hypoxia
challenge on glycogen storage and GLUT4 protein expression in heart muscle.
Sixteen male Sprague-Dawley rats were assigned to one of two groups: control
(CTRL) and exercise-hypoxia (EX+HY). The exercise protocol consisted of swimming
for 180 min twice, with a 45-min rest interval. Five hours after the exercise,
the EX+HY rats were exposed to a 14% O(2) systemic hypoxia under normobaric condition for 12 h.
After this hypoxia exposure, the EX+HY and control rats were given glucose
orally (1 g/kg body weight) with stomach tube and recovered under normal condition
for 16 h. Ventricular portion of the heart was used to determine the levels
of glycogen, GLUT4 mRNA, and GLUT4 protein after recovery. We found that myocardial
glycogen level was lowered by the exercise-hypoxia challenge (51% below control,
p < 0.05), while GLUT4 mRNA was dramatically elevated (approximately 400%
of the control level, p < 0.05). The acute exercise-hypoxia treatment did
not affect GLUT1 protein level in the same tissue. The novel finding of the
study was that the exercise-hypoxia treatment significantly induced GLUT4
gene expression in the cardiac muscle. This acute response appears to be associated
with a sustained glycogen depletion of the muscle
Exercise training improves lung
gas exchange, attenuates acute hypoxic pulmonary hypertension, but does not
prevent pulmonary hypertension of prolonged hypoxia.
Favret F, Henderson KK,
Allen J, Richalet JP,
Gonzalez NC.
A.R.P.E., EA2363 reponses cellulaires et fonctionnelles
a l'hypoxie, Universite Paris 13,
We have previously shown an attenuation of hypoxic pulmonary hypertension
by exercise training ET (15), although the mechanism was not determined. The
present study examined the effect of ET on the pulmonary arterial pressure
(Pap) response of rats to short and long term hypoxia. After 3 weeks of treadmill
training, male rats were divided into two groups: one (HT) was placed in hypobaric
hypoxia (380 Torr); the second remained in normoxia (NT). Both groups continued
to train in normoxia for 10 days, after which they were studied at rest and
during hypoxic and normoxic exercise. Sedentary normoxic (NS) and hypoxic
(HS) littermates were exposed to the same environments as their trained counterparts.
Resting and exercise hypoxic PaO2 were higher in NT and HT than in NS and
HS, respectively, although alveolar ventilation of trained rats was not higher.
Lower A-a PO2 and higher effective lung diffusing capacity for O2 (DLO2) in
NT vs NS and in HT vs HS suggest ET improved efficacy of gas exchange. Pulmonary
arterial pressure (Pap) and Pap/cardiac output (Pap/Q) were lower in NT than
NS in hypoxia, indicating ET attenuates the initial vasoconstriction of hypoxia.
However, ET had no effect on chronic hypoxic pulmonary hypertension: Pap and
Pap/Q in hypoxia were similar in HS vs HT. However, right ventricular weight
was lower in HT than in HS, although Pap was not different. Since ET attenuates
the initial pulmonary vasoconstriction of hypoxia, development of pulmonary
hypertension may be delayed in HT rats, and the time during which right ventricular
afterload is elevated may be shorter in this group. ET effects may improve
the response to acute hypoxia by increasing efficacy of gas exchange and lowering
right ventricular work.