Profound strength loss is a marker of exercise-induced muscle damage; however, there is a large intersubject variability in the response, even when subjects are exposed to standardized exercise protocols. We sought to identify factors including neural drive and peripheral function underlying variability in early development of muscle strength loss after lengthening actions. We objectively characterized subjects on the basis of postexercise strength loss and analyzed voluntary and stimulated muscle function before and after exercise to test the hypothesis that greater strength loss would be associated with greater losses in peripheral, but not central, function.
Forty-six subjects were tested. Central measures were integrated electromyographic activity (iEMG), compound muscle action potential (CMAP), and central activation ratio (CAR). Peripheral measures were maximal isometric and eccentric voluntary action torques and stimulated tetanic and twitch torques. Subjects performed 50 maximal lengthening (eccentric) actions of the elbow flexors. Isometric strength was assessed pre- and postexercise and for 4 d after exercise. Central and peripheral functions were assessed before and 5 min after exercise.
Cluster analysis of isometric strength loss at 0 and 24 h after exercise generated three groups: higher responders (HR) (N = 21; 49% average loss), lower responders (LR) (N = 22; 23% average loss), and nonresponders (N = 3; no loss). Maximal eccentric torque losses were greater in the HR group than in the LR group. Greater dysfunction was found for all peripheral measures (torque after tetanic stimuli; torque after twitch stimuli) in the HR group, whereas central measures (iEMG, CMAP, and CAR) were not different between groups (P > 0.05).
Greater voluntary strength loss after lengthening exercise was associated with greater impairment of peripheral function, but similar central function, suggesting that the mechanism(s) driving variations in strength loss after lengthening actions are localized within the periphery.
Department of Kinesiology, Totman Building, University of Massachusetts, Amherst, MA
Address for correspondence: Monica J. Hubal, Research Center for Genetic Medicine, Children's National Medical Center, 111 Michigan Avenue NW, Washington, DC 20010; E-mail: email@example.com.
Submitted for publication February 2006.
Accepted for publication October 2006.