Acute passive muscle stretching has been widely shown to attenuate maximal and rapid force production during subsequent muscle actions. It has been suggested that this stretch-induced force loss is facilitated by multiple mechanisms including peripherally-mediated mechanical changes in the muscle-tendon unit and centrally-mediated decreases in voluntary neural drive. A growing body of compelling evidence has made it increasingly apparent that impaired voluntary neural drive is the primary factor underpinning stretch-induced force loss. Accordingly, disfacilitation and/or inhibition of neural activity at the supraspinal and spinal levels would theoretically underpin the decreases in neural drive after stretching. With regard to supraspinal changes, increased stretching-related inhibitory sensory feedback could acutely mitigate motor cortical activity by increasing the magnitude of intracortical inhibition and thus reduce the level descending cortical drive reaching muscle. On the other hand, impaired neural drive could stem from changes at the spinal level by alterations in the amount excitatory and inhibitory afferent feedback to the spinal cord. Reductions in the amount of excitatory afferent feedback are particularly interesting as this could impair the development of intrinsic facilitatory processes of spinal motoneurones that augment muscular force production, specifically persistent inward currents. However, the potential impact of supraspinal and spinal mechanisms to stretch-induced force loss has not been explicitly studied and this impedes our ability to identify methods and interventions to overcome the force decrement after acute muscle stretching.
Therefore, the overall aim of this research is to investigate the neural effects contributing to force loss after acute passive muscle stretching, with particular attention to changes in supraspinal and spinal activity. This research will be comprised of three studies. The aim of the first study will be to examine the effect of acute passive muscle stretching on corticospinal excitability and facilitatory spinal reflexes using transcranial magnetic stimulation (TMS) and electrically evoked Hoffmann-reflex (H-reflex) techniques. The aim of the second study will be to determine the relative contribution of separate cortical and spinal responses after acute passive stretching to stretch-induced force loss whilst changes in cortically and spinally evoked potentials are assessed using transcranial magnetic stimulation and cervicomedullary stimulation, respectively. Finally, a third study will examine the effect of caffeine ingestion on spinal excitability and motoneurone facilitation as well as its ability to offset the stretch-induced force loss if ingested prior to stretching using H-reflex measurements and a combined tendon vibration-peripheral nerve stimulation protocol.
The results of this research will provide important information regarding changes in neuromechanical control of muscular force production after stretching and aid in the development of interventions that can diminish the deleterious effects of muscle stretching on muscular force.
Mr Timothy Pulverenti
Professor Anthony Blazevich
Neuroscience Research Australia (Aus), Dr Gabriel Trajano
The University of Western Australia (Aus), Professor Gary Thickbroom
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