Linear relationship between VO2max and VO2max decrement during exposure to acute hypoxia

Abstract

The purpose of these experiments is to test the hypothesis that exercise-induced hypoxemia at sea level in highly trained athletes might be exacerbated during acute hypoxia and therefore result in correspondingly larger decrements in maximal O2 uptake (VO2max) compared with less trained individuals. Thirteen healthy male volunteers were divided into two groups according to their level of fitness: 1) trained endurance athletes (T) (n = 7), with a VO2max range of 56-75 ml.kg-1.min-1 and 2) untrained individuals (UT) (n = 6), with a VO2max range of 33-49 ml.kg-1.min-1. Subjects performed two incremental cycle ergometry tests to determine VO2max under hypoxic conditions [14% O2-86% N2, barometric pressure (PB) = 760 Torr] and normoxic conditions (21% O2-79% N2, PB = 760 Torr). Tests were single blind, randomly administered, and separated by at least 72 h. Mean percent oxyhemoglobin saturation (%SaO2) during maximal exercise under hypoxic conditions was significantly (P less than 0.05) lower in the T group (77%) compared with the UT group (86%). Furthermore, the T group exhibited larger decrements (P less than 0.05) in VO2max (normoxic-hypoxic) compared with the UT group. Finally, a significant linear correlation (r = 0.94) existed between normoxic VO2max (ml.kg-1.min-1) and delta VO2max (normoxic-hypoxic). These data suggest that highly T endurance athletes suffer more severe gas exchange impairments during acute exposure to hypoxia than UT individuals, and this may explain a portion of the observed variance in delta VO2max among individuals during acute altitude or hypoxia exposure.

Oxygen availability and PCr recovery rate in untrained human calf muscle: evidence of metabolic limitation in normoxia

“…However, the translation of these data to a situation where a much greater muscle mass is recruited is actually quite complex and now introduces the potential for central limitations (e.g., cardiac output and or blood flow distribution) that may lead to differing results. Thus, although the current data are in line with the concepts that untrained subjects are probably not O 2 supply limited when studied during whole body exercise breathing ambient air (34), there is actually a continuum of responses (21) and that exercise-trained individuals are more susceptible to reductions in O 2 availability (16), this translation between paradigms should be viewed with caution.…”

“…THE REDUCED OXYGEN AVAILABILITY of severe hypoxia uniformly attenuates human maximal oxidative metabolic rate; however, limitations to maximal oxidative rate in normoxia and the impact of moderate hypoxia appear to be dependent on the exercise training status of the population studied (5,16,24). The clear dependence between O 2 supply and skeletal muscle maximal oxidative rate assessed during maximal exercise in trained human muscle has been previously recognized (24).…”

“…In conclusion, this study has revealed that O 2 availability does not impact maximal oxidative rate in sedentary humans until the O 2 level falls well below that of ambient air, indicating a metabolic limitation in normoxia. oxidative capacity; 31 P-magnetic resonance spectroscopy; exercise THE REDUCED OXYGEN AVAILABILITY of severe hypoxia uniformly attenuates human maximal oxidative metabolic rate; however, limitations to maximal oxidative rate in normoxia and the impact of moderate hypoxia appear to be dependent on the exercise training status of the population studied (5,16,24). The clear dependence between O 2 supply and skeletal muscle maximal oxidative rate assessed during maximal exercise in trained human muscle has been previously recognized (24).…”

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

“…Conversely, athletes from the ML group tend to have a lower cardiovascular response (i.e., Q , heart rate, and stroke volume) together with an increased a-vO 2 difference, allowing them to maintain aerobic energy turnover at submaximal exercise. Such compensatory adjustments between Q and maximal a-vO 2 difference have already been reported after ␤-adrenergic blockade in normoxia but also in severe hypoxia (4,300 m or FI O 2 ϭ ϳ12.5%), where the drug-induced limitation in heart rate and Q were compensated for by elevations in a-vO 2 difference and O 2 extraction at submaximal (50) and maximal exercise (28), allowing maintenance of oxygen uptake. Taken together, these results suggest that factors improving systemic O 2 extraction, either directly or more likely by reflex modification of blood flow redistribution, could compensate for the reduced systemic O 2 delivery.…”

“…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.…”