Key points are not available for this paper at this time.
Exercise-induced muscle injury is commonly accompanied by a reduction of muscular strength. It has been suggested that this reduction in voluntary force is attributable to "peripheral" and "central" mechanisms within the neuromuscular system. The quadriceps muscle of 15 subjects was damaged with four bouts of 25 maximal voluntary concentric-eccentric contractions at a speed of 60°/s. In a time period of 7 days, we investigated the contribution of agonist muscle activation and contractile properties (CP) to changes in isometric maximum voluntary torque (iMVT). In order to provide a comprehensive assessment, the neural drive to muscles was estimated with the interpolated twitch technique and root mean square of the EMG signal. CP were evaluated by analysing the twitch torque signal induced by single and doublet stimulation. Furthermore, we measured changes in alpha motoneuron excitability of vastus medialis at the spinal level due to muscle soreness using the H reflex technique. The iMVT was impaired at post, 24 h and 48 h, while rate of torque development and voluntary activation (VA) were only decreased immediately after the intervention. CP were impaired immediately after exercise and at 24 h. Maximal H reflex (Hmax), maximal M wave (Mmax) and the Hmax/Mmax-ratio were not affected. Sensation of muscle soreness assessment revealed impairments at 24 h, 48 h and 72 h. Data suggest that reduced VA and altered CP contribute to the force loss immediately after concentric-eccentric exercise. Thereafter, the impairment of CP seems to be mainly responsible for the reduced iMVT. In addition, there is no evidence for an association between muscle soreness and VA as well as between muscle soreness and spinal excitability.
Behrens et al. (Tue,) studied this question.