Delayed recovery of velocity-dependent power loss following eccentric actions of the ankle dorsiflexors

Author:

Power Geoffrey A.1,Dalton Brian H.1,Rice Charles L.12,Vandervoort Anthony A.13

Affiliation:

1. Canadian Centre for Activity and Aging, School of Kinesiology, Faculty of Health Sciences,

2. Department of Anatomy and Cell Biology, and

3. School of Physical Therapy, Faculty of Health Sciences, University of Western Ontario, London, Ontario, Canada

Abstract

Unaccustomed eccentric exercise has been shown to impair muscle function, although little is known regarding this impairment on muscle power. The purpose of this study was to investigate changes in neuromuscular properties of the ankle dorsiflexors during and after an eccentric contraction task and throughout recovery in 21 (10 men, 11 women) recreationally active young adults (25.8 ± 2.3 yr). All subjects performed 5 sets of 30 eccentric contractions at 80% of maximum isometric voluntary contraction (MVC) torque. Data were recorded at baseline, during the fatigue task, and for 30 min of recovery. There were no significant sex differences for all fatigue measures; thus data were pooled. After the fatigue task, MVC torque declined by 28% ( P < 0.05) and did not recover fully, and voluntary activation of the dorsiflexors, as assessed by the interpolated twitch technique, was near maximal (>99%) during and after the fatigue task ( P > 0.05). Peak twitch torque was reduced by 21% at 2 min of recovery and progressively decreased to 35% by 30 min ( P < 0.05). Low-frequency torque depression (10-to-50 Hz ratio) was present at 30 s of recovery, increased to 51% by 10 min, and did not recover fully ( P < 0.05). Velocity-dependent concentric power was reduced by 8% immediately after task termination and did not recover fully within 30 min ( P < 0.05). The main findings of an incomplete recovery of MVC torque, low-frequency torque depression, and shortening velocity indicate the presence of muscle damage, which may have altered excitation-contraction coupling and cross-bridge kinetics and reduced the number of functional sarcomeres in series, ultimately leading to velocity-dependent power loss.

Publisher

American Physiological Society

Subject

Physiology (medical),Physiology

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