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Central fatigue contributes to the greater reductions in explosive than maximal strength with high‐intensity fatigue
Author(s) -
Buckthorpe Matthew,
Pain Matthew T. G.,
Folland Jonathan P.
Publication year - 2014
Publication title -
experimental physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.925
H-Index - 101
eISSN - 1469-445X
pISSN - 0958-0670
DOI - 10.1113/expphysiol.2013.075614
Subject(s) - isometric exercise , explosive material , turnover , contraction (grammar) , intensity (physics) , explosive strength , medicine , chemistry , physics , physical medicine and rehabilitation , management , quantum mechanics , organic chemistry , economics
New FindingsWhat is the central question of this study? Repeated high‐force contractions of skeletal muscle cause a decline in the force‐generating capacity, referred to as muscle fatigue. The influence of fatigue on explosive strength and the associated contractile and neural mechanisms responsible is not known.What is the main finding and its importance? Fatigue exerts a more pronounced influence on explosive force production than on maximal voluntary force production. Contractile and neural mechanisms were considered responsible.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.