Schwiete Carsten, Mester Joachim, Wahl Patrick, Broich Holger, Behringer Michael
Department of Sports Sciences, Goethe University Frankfurt, Frankfurt am Main, Germany.
German Research Centre of Elite Sport, German Sport University Cologne, Cologne, Germany.
Physiol Rep. 2025 Jul;13(13):e70441. doi: 10.14814/phy2.70441.
High-velocity eccentric training elicits exercise-induced muscle damage (EIMD), predominantly attributed to mechanical strain. However, the potential contribution of metabolic stress to muscle damage remains underexplored, especially in trained populations. This study examined whether metabolic changes contribute to EIMD during maximal eccentric hamstring curls. Thirty male participants performed five sets of 15 maximal eccentric leg curls at 210°/s. Muscle oxygenation (SmO₂) and pulmonary gas exchange (VO and VCO₂) were recorded during the intervention. Creatine kinase (CK), muscle soreness, muscle stiffness, muscle contractility, peak torque, and maximal voluntary contraction (MVC) were measured pre-exercise, post, and over 96 h of recovery. Linear mixed models were used to analyze associations between metabolic parameters and damage markers. Peak torque declined significantly after 48 h (-25.64%), muscle stiffness was increased post (p = 0.004); CK peaked at 96 h (p < 0.001). For peak torque and CK, linear mixed models were fitted revealing significant contributions of △VO% (p = 0.04) and △VCO% (p = 0.08) to peak torque. Fixed effects explained 30.6% of the variance. Higher oxygen uptake (△VOrec%) during rest intervals predicted lower CK elevations (p = 0.04). SmO₂ decreased by 13% within sets but had no significant effects on EIMD. Our findings indicate metabolic factors significantly contribute to EIMD in high-velocity eccentric protocols. Greater aerobic demands within sets were associated with greater force deficits, whereas greater oxygen uptake during rest mitigated creatine kinase levels. Enhancing aerobic capacity and fatigue resistance could mitigate muscle damage and improve recovery trajectories in similarly demanding training contexts.
高速离心训练会引发运动诱导的肌肉损伤(EIMD),主要归因于机械应变。然而,代谢应激对肌肉损伤的潜在作用仍未得到充分研究,尤其是在受过训练的人群中。本研究调查了在最大离心腘绳肌卷曲过程中,代谢变化是否会导致EIMD。30名男性参与者以210°/秒的速度进行了五组每组15次的最大离心腿部卷曲。在干预过程中记录肌肉氧合(SmO₂)和肺气体交换(VO和VCO₂)。在运动前、运动后以及恢复的96小时内测量肌酸激酶(CK)、肌肉酸痛、肌肉僵硬、肌肉收缩力、峰值扭矩和最大自主收缩(MVC)。使用线性混合模型分析代谢参数与损伤标志物之间的关联。48小时后峰值扭矩显著下降(-25.64%),运动后肌肉僵硬增加(p = 0.004);CK在96小时达到峰值(p < 0.001)。对于峰值扭矩和CK,拟合线性混合模型显示△VO%(p = 0.04)和△VCO%(p = 0.08)对峰值扭矩有显著贡献。固定效应解释了30.6%的方差。休息间隔期间较高的摄氧量(△VOrec%)预示着较低的CK升高(p = 0.04)。组内SmO₂下降了13%,但对EIMD没有显著影响。我们的研究结果表明,在高速离心训练方案中,代谢因素对EIMD有显著影响。组内更高的有氧需求与更大的力量 deficit 相关,而休息期间更高的摄氧量可减轻肌酸激酶水平。在类似要求的训练环境中,提高有氧能力和疲劳抵抗力可以减轻肌肉损伤并改善恢复轨迹。