title: Maximal force, voluntary activation and muscle soreness after eccentric damage to human elbow flexor muscles.
abstract: Muscle damage reduces voluntary force after eccentric exercise but impaired neural drive to the muscle may also contribute. To determine whether the delayed-onset muscle soreness, which develops approximately 1 day after exercise, reduces voluntary activation and to identify the possible site for any reduction, voluntary activation of elbow flexor muscles was examined with both motor cortex and motor nerve stimulation. We measured maximal voluntary isometric torque (MVC), twitch torque, muscle soreness and voluntary activation in eight subjects before, immediately after, 2 h after, 1, 2, 4 and 8 days after eccentric exercise. Motor nerve stimulation and motor cortex stimulation were used to derive twitch torques and measures of voluntary activation. Eccentric exercise immediately reduced the MVC by 38 +/- 3% (mean +/- s.d., n = 8). The resting twitch produced by motor nerve stimulation fell by 82 +/- 6%, and the estimated resting twitch by cortical stimulation fell by 47 +/- 15%. While voluntary torque recovered after 8 days, both measures of the resting twitch remained depressed. Muscle tenderness occurred 1-2 days after exercise, and pain during contractions on days 1-4, but changes in voluntary activation did not follow this time course. Voluntary activation assessed with nerve stimulation fell 19 +/- 6% immediately after exercise but was not different from control values after 2 days. Voluntary activation assessed by motor cortex stimulation was unchanged by eccentric exercise. During MVCs, absolute increments in torque evoked by nerve and cortical stimulation behaved differently. Those to cortical stimulation decreased whereas those to nerve stimulation tended to increase. These findings suggest that reduced voluntary activation contributes to the early force loss after eccentric exercise, but that it is not due to muscle soreness. The impairment of voluntary activation to nerve stimulation but not motor cortical stimulation suggests that the activation deficit lies in the motor cortex or at a spinal level.
authors.affiliation: Prince of Wales Medical Research Institute, University of New South Wales, Barker Street, Randwick, Sydney, NSW 2031, Australia.
authors.forename: O
authors.initials: O
authors.lastname: Prasartwuth
authors.forename: J L
authors.initials: JL
authors.lastname: Taylor
authors.forename: S C
authors.initials: SC
authors.lastname: Gandevia
mesh_terms: D000328:Adult; D001917:Brachial Plexus / Q000166:cytology / Q000502:physiology; D004551:Elbow Joint / Q000502:physiology; D004558:Electric Stimulation; D004576:Electromyography; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009044:Motor Cortex / Q000166:cytology / Q000502:physiology; D009046:Motor Neurons / Q000502:physiology; D009119:Muscle Contraction / Q000502:physiology*; D018482:Muscle, Skeletal / Q000293:injuries* / Q000294:innervation / Q000502:physiology*; D010146:Pain / Q000503:physiopathology*; D019415:Torque; D014836:Volition / Q000502:physiology