Contraction specific changes in passive torque in human skeletal muscle

Abstract

The present investigation examined passive torque and electromyographic response in human skeletal muscle during passive static stretch within 60 s after maximal repetitive eccentric and concentric contractions. Passive torque (Nm) offered by the hamstring muscle group was measured during passive knee extension in a modified dynamometer in 10 subjects. The distal thigh was elevated to 0.52 rad from horizontal and the backrest was positioned at 1.57 rad. The lever arm moved the leg passively at 0.09 rad s-1 from a starting position of 1.48 rad below horizontal to the final position where it remained stationary for 90 s. Gross electrical activity of the human hamstring muscle group was recorded simultaneously. The effect of concentric or eccentric contraction was tested on separate days. Two stretch manoeuvres with a 45 min hiatus were administered on a control and experimental side. The experimental side performed 40 maximal effort repetitive concentric or eccentric hamstring muscle contractions at 1.05 rad s-1 prior to the second stretch. Passive torque during the 90 s stretch declined 30-35% on the experimental and control side in all stretches, P< 0.001, without a significant effect of prior contraction mode. Passive peak and final torques were lower on the experimental side, P < 0.01 after concentric contractions. Passive peak and final torques remained unchanged after eccentric contractions on the experimental side. The low level EMG response of the hamstring muscle during the stretch was unchanged after maximal repetitive concentric or eccentric contractions. These data demonstrate acute contraction specific alteration in passive torque in human skeletal muscle, which cannot be accounted for by EMG activity. Furthermore, the lack of difference on the control side implies that one 90 s stretch has no effect on passive torque of the muscle 45 min later.

Isokinetic eccentric exercise as a model to induce and reproduce pathophysiological alterations related to delayed onset muscle soreness

“…DOMS is accompanied by many other pathophysiological alterations than measured in this study, such as difference in muscle tissue viscoelasticity (41), immune response (33), edema (24), structural and ultrastructural alterations (42,43) and signs of an inflammatory response (30). All these parameters could probably also be used in this model to increase the knowledge of the effect of physiotherapy on these pathophysiological alterations.…”

The acute effects of static stretching on peak torque, mean power output, electromyography, and mechanomyography

“…It is believed that increasing flexibility (increasing joint range of motion) will promote better performances and reduce the risk of injury during strenuous exercise (Shellock and Prentice 1985;Smith 1994). Previous studies have used muscle stretching techniques to examine passive force production (Magnusson 1998;Magnusson et al 1995Magnusson et al , 1996, stressrelaxation characteristics of muscle (McHugh et al 1992;Taylor et al 1990;Toft et al 1989), neuromuscular reflex patterns (Guissard et al 1988;Hutton 1992;Vujnovich and Dawson 1994), factors contributing to muscle damage (Armstrong et al 1993;Lieber et al 1991), and mechanisms of increase in musculotendonous flexibility (Magnusson 1998;Toft et al 1989). Until recently, however, few studies have examined the acute effects of stretching on performance measures (deVries 1963).…”

Ipsilateral resistance exercise prevents exercise-induced central sensitization in the contralateral limb: a randomized controlled trial

“…This might indicate either passive or active hyperemia (improvement in muscle re-perfusion) after maximal voluntary isometric contractions in the IPSI group. RBE in the ipsilateral limb has been explained by adaptations to passive or dynamic elements (Brockett et al 2001;Magnusson et al 1995), intermediate filament remodeling (Fridén et al 1983), attenuated inflammatory response (Pierrynowski et al 1987;Pizza et al 2002), as well as changes in motor unit activation pattern (Warren et al 2000). The present findings suggest that interaction of afferent inputs at an interneuronal level, presumably in the dorsal horn of the reflex pathway could be a potential mechanism for RBE.…”