Maximal-effort knee-extension exercise impairs skeletal muscle oxidative capacity and VO2 recovery in vivo.

In the present study, we examined how fatiguing exercise affects O₂-based measures of skeletal muscle oxidative capacity in vivo by measuring changes in the rate constant of muscle VO₂ recovery (k_VO2). Healthy young adults completed isokinetic (120º∙s^-1), maximal voluntary dynamic contractions (MVDCs) lasting 24- (baseline k_VO2) and 240 s (post-fatiguing exercise k_VO2). Vastus lateralis k_VO2 was measured using near-infrared diffuse correlation spectroscopy (NIRS-DCS) via the conventional repeated arterial occlusion method (Part-A, n=14) or a novel NIRS-DCS 'free-flow' method (Part-B, n=13). Pulmonary VO₂ (pVO₂), muscle VO₂ (mVO₂), and surface electromyography (sEMG) measures of muscle activation were also measured throughout the 240-s trial. Compared to the 24-s trial, k_VO2 following 240s of MVDCs was impaired by ~25% (Part-A; p=0.005) and ~16% (Part-B; p=0.017). Moreover, both pVO₂ and mVO₂ rapidly increased to maximal levels, where they remained for the duration of the 240-s trial, despite sEMG activity and peak MVDC power declining. These results demonstrate that fatiguing exercise not only impairs O₂-based measures of skeletal muscle oxidative capacity, but that mitochondrial O₂-consumption is uncoupled from power output and ATP demand during fatiguing exercise.