Hoffman B W, Cresswell A G, Carroll T J, Lichtwark G A
Centre for Sensorimotor Neuroscience, School of Human Movement Studies, The University of Queensland, Brisbane, Queensland, Australia.
Centre for Sensorimotor Neuroscience, School of Human Movement Studies, The University of Queensland, Brisbane, Queensland, Australia
J Appl Physiol (1985). 2014 Jun 1;116(11):1455-62. doi: 10.1152/japplphysiol.01431.2012. Epub 2013 Apr 4.
Extensive muscle damage can be induced in isolated muscle preparations by performing a small number of stretches during muscle activation. While typically these fiber strains are large and occur over long lengths, the extent of exercise-induced muscle damage (EIMD) observed in humans is normally less even when multiple high-force lengthening actions are performed. This apparent discrepancy may be due to differences in muscle fiber and tendon dynamics in vivo; however, muscle and tendon strains have not been quantified during muscle-damaging exercise in humans. Ultrasound and an infrared motion analysis system were used to measure medial gastrocnemius fascicle length and lower limb kinematics while humans walked backward, downhill for 1 h (inducing muscle damage), and while they walked briefly forward on the flat (inducing no damage). Supramaximal tibial nerve stimulation, ultrasound, and an isokinetic dynamometer were used to quantify the fascicle length-torque relationship pre- and 2 h postexercise. Torque decreased 23%, and optimal fascicle length shifted rightward ~10%, indicating that EIMD occurred during the damage protocol even though medial gastrocnemius fascicle stretch amplitude was relatively small (18% of optimal fascicle length) and occurred predominantly within the ascending limb and plateau region of the length-torque curve. Furthermore, tendon contribution to overall muscle-tendon unit stretch was ~91%. The data suggest the compliant tendon plays a role in attenuating muscle fascicle strain during backward walking in humans, thus minimizing the extent of EIMD. As such, in situ or in vitro mechanisms of muscle damage may not be applicable to EIMD of the human gastrocnemius muscle.
在肌肉激活过程中进行少量拉伸,可在离体肌肉标本中诱发广泛的肌肉损伤。虽然通常这些纤维应变很大且发生在较长长度上,但即使进行多次高负荷的拉长动作,在人类中观察到的运动诱导性肌肉损伤(EIMD)程度通常也较小。这种明显的差异可能是由于体内肌肉纤维和肌腱动力学的差异;然而,在人类肌肉损伤运动过程中,肌肉和肌腱应变尚未得到量化。当人类向后下坡行走1小时(诱发肌肉损伤)以及在平地上短暂向前行走(不诱发损伤)时,使用超声和红外运动分析系统测量腓肠肌内侧肌束长度和下肢运动学。使用超强胫神经刺激、超声和等速测力计来量化运动前和运动后2小时的肌束长度 - 扭矩关系。扭矩下降约23%,最佳肌束长度向右移动约10%,这表明即使腓肠肌内侧肌束拉伸幅度相对较小(约为最佳肌束长度的18%)且主要发生在长度 - 扭矩曲线的上升支和平台区段,在损伤方案期间仍发生了EIMD。此外,肌腱对整个肌肉 - 肌腱单元拉伸的贡献约为91%。数据表明,顺应性肌腱在人类向后行走过程中对减轻肌肉肌束应变起作用,从而使EIMD的程度最小化。因此,肌肉损伤的原位或体外机制可能不适用于人类腓肠肌的EIMD。