Maximal-effort knee-extension exercise impairs skeletal muscle oxidative capacity and V <scp>o</scp> <sub>2</sub> recovery in vivo

In the present study, we examined how fatiguing exercise affects O<sub>2</sub>-based measures of skeletal muscle oxidative capacity in vivo by measuring changes in the rate constant of muscle V̇o<sub>2</sub> recovery ([Formula: see text]). Healthy young adults completed isokinetic (120°·s<sup>-1</sup>), 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 (<i>part A</i>, <i>n</i> = 14) or a novel NIRS-DCS "free-flow" method (<i>part B</i>, <i>n</i> = 13). Pulmonary V̇o<sub>2</sub> (pV̇o<sub>2</sub>), muscle V̇o<sub>2</sub> (mV̇o<sub>2</sub>), 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% (<i>part A</i>; <i>P</i> = 0.005) and ∼16% (<i>part B</i>; <i>P</i> = 0.017). Moreover, both pV̇o<sub>2</sub> and mV̇o<sub>2</sub> 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 O<sub>2</sub>-based measures of skeletal muscle oxidative capacity, but also that mitochondrial O<sub>2</sub> consumption is uncoupled from power output and ATP demand during fatiguing exercise.<b>NEW & NOTEWORTHY</b> We measured rates of skeletal muscle V̇o<sub>2</sub> 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 (<i>part A</i>) or a novel NIRS-DCS "free-flow" method (<i>part B</i>), 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 O<sub>2</sub> consumption and ATP synthase activity.

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Journal
Journal of Applied Physiology
Published
2025-09-18
DOI
https://doi.org/10.1152/japplphysiol.00517.2025
Primary Topic
Cardiovascular and exercise physiology
Type
article
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article

Maximal-effort knee-extension exercise impairs skeletal muscle oxidative capacity and V o 2 recovery in vivo

Andrew P. Oneglia, Miles F. Bartlett, Sauyeh Zamani, Delaney Davis et al.
Journal of Applied Physiology
Cardiovascular and exercise physiology
article

Maximal-effort knee-extension exercise impairs skeletal muscle oxidative capacity and V o 2 recovery in vivo

Andrew P. Oneglia, Miles F. Bartlett, Sauyeh Zamani, Delaney Davis, Michael D. Nelson, Mark D. Ricard, Ashfaq Siddiqui
article en

Abstract

In the present study, we examined how fatiguing exercise affects O<sub>2</sub>-based measures of skeletal muscle oxidative capacity in vivo by measuring changes in the rate constant of muscle V̇o<sub>2</sub> recovery ([Formula: see text]). Healthy young adults completed isokinetic (120°·s<sup>-1</sup>), 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 (<i>part A</i>, <i>n</i> = 14) or a novel NIRS-DCS "free-flow" method (<i>part B</i>, <i>n</i> = 13). Pulmonary V̇o<sub>2</sub> (pV̇o<sub>2</sub>), muscle V̇o<sub>2</sub> (mV̇o<sub>2</sub>), 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% (<i>part A</i>; <i>P</i> = 0.005) and ∼16% (<i>part B</i>; <i>P</i> = 0.017). Moreover, both pV̇o<sub>2</sub> and mV̇o<sub>2</sub> 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 O<sub>2</sub>-based measures of skeletal muscle oxidative capacity, but also that mitochondrial O<sub>2</sub> consumption is uncoupled from power output and ATP demand during fatiguing exercise.<b>NEW & NOTEWORTHY</b> We measured rates of skeletal muscle V̇o<sub>2</sub> 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 (<i>part A</i>) or a novel NIRS-DCS "free-flow" method (<i>part B</i>), 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 O<sub>2</sub> consumption and ATP synthase activity.

Journal of Applied PhysiologyVol. 139(5)
The University of Texas at Arlington (US), Bartlett Public Library District (US)
Openalex Percentile: Top 60%
Cardiovascular and exercise physiology
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