Abstract
In severe hypoxia, single-leg peak oxygen uptake (VO2peak) is reduced mainly due to the inability to increase cardiac output (CO). Whether moderate altitude allows CO to increase during single-leg cycling, thereby restoring VO2peak, has not been extensively investigated. Five healthy subjects performed an incremental, maximal, two-legged cycle ergometer test, and on separate days a maximal incremental one-leg cycling test in normoxia and in moderate hypoxia (fraction of inspired oxygen (FiO2) = 15%). Oxygen uptake, heart rate, blood pressure responses, power output, and CO (PhysioFlow) were measured during all tests. Moderate hypoxia lowered single-leg peak power output (154 ± 31 vs. 128 ± 26 watts, p = 0.03) and oxygen uptake (VO2) (36.8 ± 6.6 vs. 33.9 ± 6.9 mL/min/kg, p = 0.04), despite higher peak CO (16.83 ± 3.10 vs. 18.96 ± 3.59 L/min, p = 0.04) and systemic oxygen (O2) delivery (3.37 ± 0.84 vs. 3.47 ± 0.89 L/min, p = 0.04) in hypoxia compared to normoxia. Arterial–venous O2 difference (a–vDO2) was lower in hypoxia (137 ± 21 vs. 112 ± 19 mL/l, p = 0.03). The increases in peak CO from normoxia to hypoxia were negatively correlated with changes in mean arterial pressure (MABP) (p < 0.05). These preliminary data indicate that the rise in CO was not sufficient to prevent single-leg performance loss at moderate altitude and that enhanced baroreceptor activity might limit CO increases in acute hypoxia, likely by reducing sympathetic activation. Since the systemic O2 delivery was enhanced and the calculated a–vDO2 reduced in moderate hypoxia, a potential diffusion limitation cannot be excluded.
Highlights
During exercise involving a large muscle mass, maximal oxygen uptake (VO2max ) and exercise performance are mainly limited by cardiac output (CO)and the ability to deliver oxygen (O2 ) to the working muscles
Resting SpO2 values were higher in normoxia compared to hypoxia, whereas a lower resting HR was observed in normoxia (Table 2)
Data indicate that the CO increase was not sufficient to prevent the decline in Ppeak and VO2peak in hypoxia, and that the individual magnitude of VO2peak reduction was closely associated with individual CO responses
Summary
During exercise involving a large muscle mass (e.g., two-leg cycling), maximal oxygen uptake (VO2max ) and exercise performance are mainly limited by cardiac output (CO)and the ability to deliver oxygen (O2 ) to the working muscles. During exercise involving a large muscle mass (e.g., two-leg cycling), maximal oxygen uptake (VO2max ) and exercise performance are mainly limited by cardiac output (CO). Besides CO and the oxygen content of the arterial blood (CaO2 ), blood flow to and O2 extraction of contracting skeletal muscles are determinants of VO2max [1,2,3,4]. On the contrary, when exercising with a small muscle mass (e.g., single-leg cycling, arm or knee-extensor exercise), CO is not considered the limiting factor for VO2max attainment, since maximal CO values are generally not achieved [5,6,7]. If not compensated by an increased CO and/or O2 extraction, aerobic capacity may be impaired, even when exercising with a small muscle mass.
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