Role of skeletal muscles impairment and brain oxygenation in limiting oxidative metabolism during exercise after bed rest.

"Central" and "peripheral" limitations to oxidative metabolism during exercise were evaluated on 10 young males following a 35-day horizontal bed rest (BR). Incremental (IE), moderate- and heavy-intensity constant-load exercises (CLE) were carried out on a cycloergometer before and 1-2 days after BR. Pulmonary gas exchange, cardiac output (Q') (by impedance cardiography), skeletal muscle (vastus lateralis) and brain (frontal cortex) oxygenation (by near-infrared spectroscopy) were determined. After BR, "peak" (values at exhaustion during IE) workload, peak O(2) uptake (V'O(2)peak), peak stroke volume, Q'peak and peak skeletal muscle O(2) extraction were decreased (-18%, -18%, -22%, -19%, -33%, respectively). The gas exchange threshold was ~60% of V'O(2)peak both before and after BR. At the highest workloads brain oxygenation data suggest an increased O(2) extraction, which was unaffected by BR. V'O(2) kinetics during CLE (same % of peak workload before and after BR) were slower (time constant of the "fundamental" component 31.1+/-2.0 s before vs. 40.0+/-2.2 s after BR); the amplitude of the "slow component" was unaffected by BR, thus it would be greater, after BR, at the same absolute workload. A more pronounced "overshoot" of skeletal muscle O(2) extraction during CLE was observed after BR, suggesting an impaired adjustment of skeletal muscle O(2) delivery. The role of skeletal muscles in the impairment of oxidative metabolism during submaximal and maximal exercise after BR was identified. The reduced capacity of peak cardiovascular O(2) delivery did not determine a "competition" for the available O(2) between skeletal muscles and brain.