Abstract
This study tested the relationship between the magnitude of muscle damage and both central and peripheral modulations during and after eccentric contractions of plantar flexors. Eleven participants performed 10 sets of 30 maximal eccentric contractions of the plantar flexors at 45°·s−1. Maximal voluntary torque, evoked torque (peripheral component) and voluntary activation (central component) were assessed before, during, immediately after (POST) and 48 h after (48 h) the eccentric exercise. Voluntary eccentric torque progressively decreased (up to −36%) concomitantly to a significant alteration of evoked torque (up to −34%) and voluntary activation (up to −13%) during the exercise. Voluntary isometric torque (−48 ± 7%), evoked torque (−41 ± 14%) and voluntary activation (−13 ± 11%) decreased at POST, but only voluntary isometric torque (−19 ± 6%) and evoked torque (−10 ± 18%) remained depressed at 48 h. Neither changes in voluntary activation nor evoked torque during the exercise were related to the magnitude of muscle damage markers, but the evoked torque decrement at 48 h was significantly correlated with the changes in voluntary activation (r = −0.71) and evoked torque (r = 0.77) at POST. Our findings show that neuromuscular responses observed during eccentric contractions were not associated with muscle damage. Conversely, central and peripheral impairments observed immediately after the exercise reflect the long-lasting reduction in force-generating capacity.
Highlights
Eccentric contraction represents a motor action whereby the muscle-tendon unit is forcibly lengthened while the muscle is activated
The present study evaluated voluntary activation and evoked torque as indexes of central and peripheral components, respectively, during and after isokinetic eccentric contractions of plantar flexors
Our results showed a progressive decrease in voluntary torque concomitantly to a significant impairment of both central and peripheral components during eccentric contractions
Summary
Eccentric contraction represents a motor action whereby the muscle-tendon unit is forcibly lengthened while the muscle is activated. In parallel, compared with concentric and isometric contractions, lower surface electromyographic (EMG) activity and voluntary activation have been reported during eccentric contractions (Westing et al, 1991; Babault et al, 2001) This non-maximal motor unit recruitment showed evidences of an unique neural strategy during eccentric contractions (Enoka, 1996), arising from spinal (e.g., facilitation of pre- and post-synaptic inhibitions), and supra-spinal (e.g., cortical excitability enhancement) components (see Duchateau and Baudry, 2014 for a review). It is well-established that unaccustomed or repetitive. Whilst functional (e.g., drop in muscle strength, muscle soreness) and physiological (e.g., muscle fiber disruptions, inflammatory processes) events associated with muscle damage have been well-described (Mair et al, 1992; Faulkner et al, 1993; Paulsen et al, 2012), neuromuscular causes of exercise-induced muscle damage remain not fully understood
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