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Objective <p>Exercise-induced muscle damage (EIMD) compromises neuromuscular function and reduces exercise tolerance. Whether muscle oxidative capacity (MOC), an index of mitochondrial function, is reduced by EIMD or influences neuromuscular recovery remains unknown.</p> Purpose <p>This study tested the hypotheses that EIMD would reduce MOC and that higher baseline (BL) MOC would be associated with faster recovery of neuromuscular efficiency (NME).</p> Methods <p>Fourteen healthy adults (23 ± 3 yrs; 7M/7F) completed neuromuscular testing, and a subset of nine participants (24 ± 3 yrs; 6M/3F) underwent MOC assessment. MOC was determined from the recovery kinetics of muscle oxygen consumption using near-infrared spectroscopy during repeated arterial occlusions. MOC was determined at BL and 1&#xa0;H, 24&#xa0;H, 48&#xa0;H, and 1 week after damage. EIMD was induced by eccentric contractions until maximal voluntary contraction (MVC) was reduced by 40%. Participants returned 1&#xa0;H, 24&#xa0;H, 48&#xa0;H, and 1 week after damage to perform intermittent isometric contractions to task failure. NME at exercise onset was determined as the ratio of MVC-normalized EMG root mean square (%) to torque output (Nm).</p> Results <p>EIMD did not reduce MOC (BL: 1.93 ± 1.39&#xa0;min<sup>− 1</sup>; 1&#xa0;H: 2.14 ± 2.20&#xa0;min<sup>− 1</sup>). Compared to BL (0.23 ± 0.11 Nm/%), NME was reduced at 1&#xa0;H (0.15 ± 0.07 Nm/%; <i>p</i> &lt; 0.05) and 24&#xa0;H (0.18 ± 0.10 Nm/%; <i>p</i> &lt; 0.01) but not 48&#xa0;H (0.27 ± 0.11 Nm/%; <i>p</i> = 0.99). Higher MOC at BL was associated with faster recovery of NME (<i>p</i> = 0.04; r<sup>2</sup> = 0.44).</p> Conclusion <p>These findings suggest MOC may support neuromuscular recovery despite being unaffected by muscle damage.</p>

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The impact of muscle oxidative capacity on neuromuscular recovery after exercise-induced muscle damage

  • 期刊论文

  • 发表日期：

    2025年12月4日

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  • Colin W. Kipper,
  • Petra Kis,
  • Kylie N. Burleson,
  • Kilyn D. Fredrickson,
  • Jerome Hausselle,
  • Jiyoung Bae,
  • Shane M. Hammer

摘要

Objective

Exercise-induced muscle damage (EIMD) compromises neuromuscular function and reduces exercise tolerance. Whether muscle oxidative capacity (MOC), an index of mitochondrial function, is reduced by EIMD or influences neuromuscular recovery remains unknown.

Purpose

This study tested the hypotheses that EIMD would reduce MOC and that higher baseline (BL) MOC would be associated with faster recovery of neuromuscular efficiency (NME).

Methods

Fourteen healthy adults (23 ± 3 yrs; 7M/7F) completed neuromuscular testing, and a subset of nine participants (24 ± 3 yrs; 6M/3F) underwent MOC assessment. MOC was determined from the recovery kinetics of muscle oxygen consumption using near-infrared spectroscopy during repeated arterial occlusions. MOC was determined at BL and 1 H, 24 H, 48 H, and 1 week after damage. EIMD was induced by eccentric contractions until maximal voluntary contraction (MVC) was reduced by 40%. Participants returned 1 H, 24 H, 48 H, and 1 week after damage to perform intermittent isometric contractions to task failure. NME at exercise onset was determined as the ratio of MVC-normalized EMG root mean square (%) to torque output (Nm).

Results

EIMD did not reduce MOC (BL: 1.93 ± 1.39 min− 1; 1 H: 2.14 ± 2.20 min− 1). Compared to BL (0.23 ± 0.11 Nm/%), NME was reduced at 1 H (0.15 ± 0.07 Nm/%; p < 0.05) and 24 H (0.18 ± 0.10 Nm/%; p < 0.01) but not 48 H (0.27 ± 0.11 Nm/%; p = 0.99). Higher MOC at BL was associated with faster recovery of NME (p = 0.04; r2 = 0.44).

Conclusion

These findings suggest MOC may support neuromuscular recovery despite being unaffected by muscle damage.