Buckthorpe Matthew, Pain Matthew T G, Folland Jonathan P
School of Sport, Exercise and Health Sciences, Loughborough University, Loughborough, UK Isokinetic Medical Group, London, UK
School of Sport, Exercise and Health Sciences, Loughborough University, Loughborough, UK.
Exp Physiol. 2014 Jul;99(7):964-73. doi: 10.1113/expphysiol.2013.075614. Epub 2014 Apr 11.
The study aimed to assess the influence of fatigue induced by repeated high-force explosive contractions on explosive and maximal isometric strength of the human knee extensors and to examine the neural and contractile mechanisms for the expected decrement. Eleven healthy untrained males completed 10 sets of voluntary maximal explosive contractions (five times 3 s, interspersed with 2 s rest). Sets were separated by 5 s, during which supramaximal twitch and octet contractions [eight pulses at 300 Hz that elicit the contractile peak rate of force development (pRFD)] were evoked. Explosive force, at specific time points, and pRFD were assessed for voluntary and evoked efforts, expressed in absolute terms and normalized to maximal/peak force. Maximal voluntary contraction force (MVCF) and peak evoked forces were also determined. Surface EMG amplitude was measured from three superficial agonists and normalized to maximal compound action potential area. By set 10, explosive force (47-52%, P < 0.001) and MVCF (42%, P < 0.001) had declined markedly. Explosive force declined more rapidly than MVCF, with lower normalized explosive force at 50 ms (29%, P = 0.038) that resulted in reduced normalized explosive force from 0 to 150 ms (11-29%, P ≤ 0.038). Neural efficacy declined by 34%, whilst there was a 15-28% reduction in quadriceps EMG amplitude during voluntary efforts (all P ≤ 0.03). There was demonstrable contractile fatigue (pRFD: octet, 27%; twitch, 66%; both P < 0.001). Fatigue reduced normalized pRFD for the twitch (21%, P = 0.001) but not the octet (P = 0.803). Fatigue exerted a more rapid and pronounced effect on explosive force than on MVCF, particularly during the initial 50 ms of contraction, which may explain the greater incidence of injuries associated with fatigue. Both neural and contractile fatigue mechanisms appeared to contribute to impaired explosive voluntary performance.
该研究旨在评估反复进行高强度爆发性收缩所诱发的疲劳对人体膝关节伸肌的爆发力和最大等长肌力的影响，并探究预期力量下降的神经和收缩机制。11名健康的未经训练男性完成了10组自愿性最大爆发性收缩（每组3秒，共5组，每组间休息2秒）。组间间隔5秒，在此期间诱发超强单收缩和八联收缩[300赫兹的8个脉冲，可引发收缩力发展的峰值速率（pRFD）]。在特定时间点评估自愿性和诱发性动作的爆发力、pRFD，以绝对值表示并归一化至最大/峰值力量。还测定了最大自主收缩力（MVCF）和诱发峰值力。从三块表层主动肌测量表面肌电图振幅，并归一化至最大复合动作电位面积。到第10组时，爆发力（47 - 52%，P < 0.001）和MVCF（42%，P < 0.001）显著下降。爆发力下降速度比MVCF更快，在50毫秒时归一化爆发力更低（29%，P = 0.038），导致0至150毫秒期间归一化爆发力降低（11 - 29%，P ≤ 0.038）。神经效能下降34%，而在自愿性动作期间股四头肌肌电图振幅降低15 - 28%（所有P ≤ 0.03）。存在明显的收缩性疲劳（pRFD：八联收缩为27%；单收缩为66%；两者P < 0.001）。疲劳使单收缩的归一化pRFD降低（21%，P = 0.001），但八联收缩未降低（P = 0.803）。疲劳对爆发力的影响比对MVCF更迅速、更明显，尤其是在收缩的最初50毫秒内，这可能解释了与疲劳相关的损伤发生率更高的原因。神经和收缩性疲劳机制似乎都导致了爆发性自愿动作表现受损。
