Abstract
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.
Key words
muscle damage - spinal excitability - twitch contraction - interpolated twitch technique
