Length-dependent changes in voluntary activation, maximum voluntary torque and twitch responses after eccentric damage in humans.

To assess the contribution of central and peripheral factors to changes in maximum voluntary force and its length dependence after eccentric muscle damage, voluntary and twitch torque were measured across a wide angular range, along with voluntary activation using twitch interpolation. Isometric torque from both maximum voluntary contractions (MVCs) and paired twitches to motor nerve stimulation were measured from 60 to 150 deg elbow flexion in 10 deg increments in eight subjects. Optimal angles were determined by curve fitting. Each subject then performed eccentric contractions until voluntary torque had decreased by approximately 40%. Measurements were repeated at 2 h, 1 day and 8 days post-exercise to follow acute and longer-term changes. Before exercise, the optimal angle was in the mid-range (93+/-10 deg; mean+/-s.d.) for MVCs, and at a more extended elbow angle for the twitch (106+/-6 deg, P < 0.05). Voluntary activation was generally high (> 94%) but depended on elbow angle, with activation being approximately 4% lower at the most flexed compared to the most extended angle. Two hours after exercise, MVCs decreased 40%, while twitch torque declined 70%. All subjects showed a shift in optimal angle to longer muscle lengths for MVCs (17+/-16 deg at 2 h, 14+/-7 deg at day 1, P < 0.05). This shift contributed minimally (approximately 3%) to the reduction in torque at 90 deg, as the torque-angle relation was relatively flat around the optimum. The twitch showed a smaller shift (approximately 4 deg) to longer lengths which was not statistically significant. Voluntary activation was significantly impaired in the early stages after exercise (2 h and day 1, P < 0.05), particularly at short muscle lengths. By 8 days after exercise, the optimal angle had returned to pre-exercise values, but MVC, twitch torque and voluntary activation had not fully recovered. Eccentric exercise causes a short-term shift in the optimal angle for MVCs and produces a length-dependent impairment in voluntary activation. Therefore, it appears that both central and peripheral factors limit muscle performance following eccentric damage, with limits to voluntary drive being especially important at short lengths.

Maximal force, voluntary activation and muscle soreness after eccentric damage to human elbow flexor muscles.

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.