The Impact Of Muscle Oxidative Capacity On Neuromuscular Recovery After Eccentric Damage

After muscle damage, neuromuscular function is compromised, and exercise tolerance is reduced. Whether baseline (BL) muscle oxidative capacity (MOC), a measure of mitochondrial function, is associated with neuromuscular recovery in humans is unknown. PURPOSE: To test the hypothesis that MOC at BL is associated with recovery in neuromuscular efficiency (NME) and torque complexity after muscle damage. METHODS: In 19 healthy adults (23 ± 2 yrs; 9 M/10F), muscle oxygen consumption (mV̇O2) was estimated by near-infrared spectroscopy during repeated arterial occlusions ([heme]diff /2 slope) after intermittent isometric contractions performed at 50% of maximal voluntary contraction (MVC) until task failure. MOC at BL was determined by the recovery kinetics of mV̇O2. Muscle damage was induced by repeated isokinetic eccentric contractions until MVC torque was reduced by 40%. Participants performed MVCs and repeated the task-failure protocol 1 h, 24 h, 48 h, and 7d post-damage. Changes in torque complexity were determined by detrended fluctuation analysis (ΔDFA), approximate (ΔApEn), and sample entropy (ΔSampEn). NME was calculated as muscle torque divided by the root mean square (RMS) of electromyography signals normalized to MVC at BL. Comparisons were made using one-way repeated measures ANOVAs and Tukey’s tests. Relationships were determined by linear regression. RESULTS: MVC was lower 1 h and 24 h (both, p < 0.05), but not 48 h (p = 0.98), post-damage compared to BL. TTF was less 1 h (p < 0.01), but not 24 h (p = 0.08), post-damage compared to BL. NME at task failure was reduced 1 h (0.05 ± 0.03 Nm/%RMS; p < 0.0001) and 24 h (0.10 ± 0.05 Nm/%RMS; p < 0.01), but not 48 h (0.16 ± 0.09; p = 0.99), post-damage compared to BL (0.16 ± 0.04 Nm/%RMS). ΔApEn was reduced 24 h (p < 0.05), but not 1 h (p = 0.21) or 48 h (p = 0.58), compared to BL. There were no significant changes in ΔSampEn post-damage compared to BL (all, p > 0.05). ΔDFA increased 48 h (p < 0.05), but not 1 h (p = 0.08), 24 h (p = 0.45), or 7d (p = 0.64), compared to BL. Higher MOC at BL was associated with greater NME at task failure at BL (p = 0.03; r2 = 0.44) as well as 24 h (p < 0.05; r2 = 0.37) and 48 h (p = 0.01; r2 = 0.55) post damage. CONCLUSION: Muscle damage lowered NME at task failure within 1 h but this effect was reversed by 48 h after damage. The recovery of NME after damage was associated with MOC.