Individual Variation in the Reduction of Heart Rate and Performance at Lactate Thresholds in Acute Normobaric Hypoxia

Friedmann, B; Frese, Falko; Menold, Elmar; Bärtsch, Peter

doi:10.1055/s-2004-821326

Cited by 21 publications

(31 citation statements)

References 28 publications

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“…Although previous studies (Levine et al, 1992;Desplanches et al, 1993;Beidleman et al, 2003) showed that training in hypoxia improves aerobic performance in hypoxia, we attribute this difference between HG and NG to the fact that HG might have been somewhat better trained prior to the study. HG reached almost the same values for P max and Vo 2 max as NG, despite being tested at an Fio 2 ¼ 0.15, which is expected to decrease both P max and Vo 2 max by about 15% to 20% (Friedmann et al, 2005).…”

Section: Discussionmentioning

confidence: 76%

“…To be able to train subjects at the same relative workload in both groups, ergometry was performed at an Fio 2 ¼ 0.15 (ambient Po 2 equivalent to 3000 m) in the HG and in normal room air (altitude <100 m) in the NG. Since performance decreases at Fio 2 ¼ 0.15 (Friedmann et al, 2005) by 15% to 20%, ergometry was started at 40 W, with an increment of 40 W every 3 min in HG; starting load and increments were 50 W in NG. The adjustment of workloads resulted in similar test durations in both groups and helped to conceal the test condition from subjects with prior experience in such testing.…”

Section: Preexaminationmentioning

confidence: 99%

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Training in Normobaric Hypoxia and Its Effects on Acute Mountain Sickness after Rapid Ascent to 4559 m

Schommer

Wiesegart

Menold

et al. 2010

High Altitude Medicine & Biology

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In a randomized, placebo-controlled, double-blind study, we tested a 4-week program in normobaric hypoxia that is commercially offered for the prevention of acute mountain sickness (AMS). Twenty-two male and 18 female healthy subjects [mean age 33 +/- 7 (SD) years] exercised 70 min, 3 x /week for 3 weeks on a bicycle ergometer at workloads of 60% VO2max either in normoxia (normoxia group, NG) or in normobaric hypoxia (hypoxia group, HG), corresponding to altitudes of 2500, 3000, and 3500 m during weeks 1, 2, and 3, respectively. Four passive exposures of 90 min in normoxia (NG) or hypoxia corresponding to 4500 m (HG) followed in week 4. Five days after the last session, subjects ascended within 24 h from sea level to 4559 m (one overnight stay at 3611 m) and stayed there for 24 h. AMS was defined as LL (Lake Louise score) > or =5 and AMS-C > or =0.70. The AMS incidence (70% in NG vs. 60% in HG, p = 0.74), LL scores (7.1 +/- 4.3 vs. 5.9 +/- 3.4, p = 0.34), and AMS-C scores (1.50 +/- 1.22 vs. 0.93 +/- 0.81, p = 0.25) at the study endpoint were not significantly different between the groups. However, the incidence of AMS at 3611 m (6% vs. 47%, p = 0.01) and the functional LL score at 4559 m were lower in HG. SpO2 at 3611 m, heart rate during ascents, and arterial blood gases at 4559 m were not different between groups. We conclude that the tested program does not reduce the incidence of AMS within a rapid ascent to 4559 m, but our data show that it prevents AMS at lower altitudes. Whether such a program would prevent AMS at higher altitudes, but with slower ascent, remains to be tested.

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Section: Discussionmentioning

confidence: 76%

Section: Preexaminationmentioning

confidence: 99%

Training in Normobaric Hypoxia and Its Effects on Acute Mountain Sickness after Rapid Ascent to 4559 m

Schommer

Wiesegart

Menold

et al. 2010

High Altitude Medicine & Biology

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“…The physiological response of human body to hypoxia is variabial (Angermann et al 2006;Friedmann et al 2005). In past studies, however, all the subjects were given the same hypoxic gas without concerning the individual variability.…”

Section: Discussionmentioning

confidence: 99%

The effect of acute hypoxia on left ventricular function during exercise

Yan

et al. 2007

Eur J Appl Physiol

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The eVect of acute hypoxia on the human left ventricular function during exercise was evaluated by 2D and Doppler echocardiography on 11 healthy male college students. Each subject completed 6-min moderate intensity (100 W) supine cycling exercises in normoxia and hypoxia, respectively. The concentration of inspired O 2 was adjusted to keep arterial hemoglobin O 2 concentration (SpO 2 ) at 88-92% during hypoxia. Doppler indices obtained were compared between normoxia and hypoxia. The left ventricular myocardial diastolic function was increased during exercise in hypoxia compared with normoxia. The peak velocity of early Wlling wave increased at rest (P < 0.05) and during exercise (P < 0.05 at second minute, and P < 0.01 at sixth minute) in hypoxia. The heart rate (P < 0.01) and cardiac output (P < 0.001) were elevated markedly at rest during hypoxia. The left ventricular systolic function variables, such as stroke volume, ejection fraction, and end-systolic volume were relatively unaltered during hypoxia compared with normoxia. The results suggest that acute hypoxia increases the left ventricular myocardial diastolic function during moderate intensity supine cycling exercise without aVecting the systolic function.

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“…Although this phenomenon is well described, a wide interindividual variability in the magnitude of reduction of V O 2max at a given level of hypoxia has been reported by several laboratories (8,14,28,31,37). Of note is the observation that the hypoxia-induced reduction in V O 2max is greater in endurance athletes than in sedentary subjects (28).…”

mentioning

confidence: 96%

Impairment of maximal aerobic power with moderate hypoxia in endurance athletes: do skeletal muscle mitochondria play a role?

Ponsot

Dufour

Doutreleau

et al. 2010

American Journal of Physiology-Regulatory, Integrative and Comp

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This study investigates the role of central vs. peripheral factors in the limitation of maximal oxygen uptake (V O2max) with moderate hypoxia [inspired fraction (FI O 2 ) ϭ14.5%]. Fifteen endurance-trained athletes performed maximal cycle incremental tests to assess V O2max, maximal cardiac output (Q max), and maximal arteriovenous oxygen (a-vO2) difference in normoxia and hypoxia. Muscle biopsies of vastus lateralis were taken 1 wk before the cycling tests to evaluate maximal muscle oxidative capacity (V max) and sensitivity of mitochondrial respiration to ADP (Km) on permeabilized muscle fibers in situ. Those athletes exhibiting the largest reduction of V O2max in moderate hypoxia (Severe Loss group: Ϫ18 Ϯ 2%) suffered from significant reductions in Q max (Ϫ4 Ϯ 1%) and maximal a-vO2 difference (Ϫ14 Ϯ 2%). Athletes who well tolerated hypoxia, as attested by a significantly smaller drop of V O2max with hypoxia (Moderate Loss group: Ϫ7 Ϯ 1%), also display a blunted Q max (Ϫ9 Ϯ 2%) but, conversely, were able to maintain maximal a-vO 2 difference (ϩ1 Ϯ 2%). Though V max was similar in the two experimental groups, the smallest reduction of V O2max with moderate hypoxia was observed in those athletes presenting the lowest apparent Km for ADP in the presence of creatine (KmϩCr). In already-trained athletes with high muscular oxidative capacities, the qualitative, rather than quantitative, aspects of the mitochondrial function may constitute a limiting factor to aerobic ATP turnover when exercising at low FIO 2 , presumably through the functional coupling between the mitochondrial creatine kinase and ATP production. This study suggests a potential role for peripheral factors, including the alteration of cellular homeostasis in active muscles, in determining the tolerance to hypoxia in maximally exercising endurance-trained athletes.exercise; cardiac output HYPOXIC ENVIRONMENTS HAVE repeatedly been observed to depress maximal oxygen uptake (V O 2max ) during whole body exercise in humans, and the magnitude of this reduction is thought to be proportional to the hypoxia-induced diminution of arterial oxygen content (15). Although this phenomenon is well described, a wide interindividual variability in the magnitude of reduction of V O 2max at a given level of hypoxia has been reported by several laboratories (8,14,28,31,37). Of note is the observation that the hypoxia-induced reduction in V O 2max is greater in endurance athletes than in sedentary subjects (28). However, the mechanisms involved in the fitness-specific limitation of maximal aerobic metabolism with moderate hypoxia [inspired fraction (FI O 2 ) ϭ ϳ14.5% or 2,000 -3,000 m] remain unclear, as changes in oxygen extraction may play a role to maintain arteriovenous oxygen (a-vO 2 ) difference and aerobic power. For instance, despite being the two determinants of V O 2max during whole body exercise in athletes, little is known about the respective contribution of cardiac output (Q ) and a-vO 2 difference in the individual hypoxia tolerance, especially within a hom...

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Individual Variation in the Reduction of Heart Rate and Performance at Lactate Thresholds in Acute Normobaric Hypoxia

Cited by 21 publications

References 28 publications

Training in Normobaric Hypoxia and Its Effects on Acute Mountain Sickness after Rapid Ascent to 4559 m

Training in Normobaric Hypoxia and Its Effects on Acute Mountain Sickness after Rapid Ascent to 4559 m

The effect of acute hypoxia on left ventricular function during exercise

Impairment of maximal aerobic power with moderate hypoxia in endurance athletes: do skeletal muscle mitochondria play a role?

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