Slowed oxygen uptake kinetics in hypoxia correlate with the transient peak and reduced spatial distribution of absolute skeletal muscle deoxygenation

摘要

It remains unclear whether an overshoot in skeletal muscle deoxygenation (HHb; reflecting a microvascular kinetic mismatch of O2 delivery to consumption) contributes to the slowed adjustment of oxidative energy provision at the onset of exercise. We progressively reduced the fractional inspired O2 concentration (FI,O2) to investigate the relationship between slowed pulmonary O2 uptake (V?O2) kinetics and the dynamics and spatial distribution of absolute [HHb]. Seven healthy men performed 8 min cycling transitions during normoxia (FI,O2=0.21), moderate hypoxia (FI,O2=0.16) and severe hypoxia (FI,O2=0.12). uptake was measured using a flowmeter and gas analyser system. Absolute [HHb] was quantified by multichannel, time-resolved near-infrared spectroscopy from the rectus femoris and vastus lateralis (proximal and distal regions), and corrected for adipose tissue thickness. The phase II time constant was slowed (P 0.05) as decreased (normoxia, 17 ± 3 s; moderate hypoxia, 22 ± 4 s; and severe hypoxia, 29 ± 9 s). The [HHb] overshoot was unaffected by hypoxia, but the transient peak [HHb] increased with the reduction in (P 0.05). Slowed kinetics in hypoxia were positively correlated with increased peak [HHb] in the transient (r2= 0.45; P 0.05), but poorly related to the [HHb] overshoot. A reduction of spatial heterogeneity in peak [HHb] was inversely correlated with slowed kinetics (r2= 0.49; P 0.05). These data suggest that aerobic energy provision at the onset of exercise may be limited by the following factors: (i) the absolute ratio (i.e. peak [HHb]) rather than the kinetic ratio (i.e. [HHb] overshoot) of microvascular O2 delivery to consumption; and (ii) a reduced spatial distribution in the ratio of microvascular O2 delivery to consumption across the muscle.