Maximal-effort knee-extension exercise impairs skeletal muscle oxidative capacity and V̇o2 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 V̇o₂ recovery ([Formula: see text]). Healthy young adults completed isokinetic (120°·s^-1), maximal voluntary dynamic contractions (MVDCs) lasting 24 (baseline [Formula: see text]) and 240 s (postfatiguing exercise [Formula: see text]). Vastus lateralis [Formula: see text] 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 V̇o₂ (pV̇o₂), muscle V̇o₂ (mV̇o₂), and surface electromyography (sEMG) measures of muscle activation were also measured throughout the 240-s trial. Compared with the 24-s trial, [Formula: see text] following 240 s of MVDCs was impaired by ∼25% (part A; P = 0.005) and ∼16% (part B; P = 0.017). Moreover, both pV̇o₂ and mV̇o₂ 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 also that mitochondrial O₂ consumption is uncoupled from power output and ATP demand during fatiguing exercise.NEW & NOTEWORTHY We measured rates of skeletal muscle V̇o₂ recovery ([Formula: see text]) at baseline and following fatiguing exercise using near-infrared diffuse correlation spectroscopy (NIRS-DCS). Regardless of whether [Formula: see text] was measured via the conventional repeated arterial occlusion method (part A) or a novel NIRS-DCS "free-flow" method (part B), fatiguing exercise impaired [Formula: see text] by ∼15%-25%. Because ATP demand rapidly declines post exercise, the slow [Formula: see text] recovery observed here suggests fatiguing exercise may uncouple the functional relationship between mitochondrial O₂ consumption and ATP synthase activity.