Thesis Defence: Duration-dependent effects of static stretching on neuromuscular outcomes
December 10 at 8:30 am - 12:30 pm
Noah Pemberton, supervised by Dr. Chris McNeil, will defend their thesis titled “Duration-dependent effects of static stretching on neuromuscular outcomes” in partial fulfillment of the requirements for the degree of Master of Science in Health and Exercise Sciences.
An abstract for Noah Pemberton’s thesis is included below.
Defences are open to all members of the campus community as well as the general public. Registration is not required for in-person defences.
Abstract
Static stretching (SS) is a popular warm-up activity prior to exercise as it increases range of motion and reduces injury risk. However, SS >60s has been suggested to be detrimental to torque production during a subsequent exercise bout, with altered neural excitability having a possible role. To investigate if total SS duration influences maximal strength, voluntary activation (VA), and motor pathway excitability, participants underwent separate sessions of either three or six 15-s maximally-tolerable passive stretches of the quadriceps via an isokinetic dynamometer. Prior to as well as ~30s following SS, single stimuli were delivered to the motor cortex, thoracic spine, and femoral nerve during 7-s isometric quadriceps contractions at 15% maximal voluntary contraction (MVC) torque to permit evaluation of excitability at cortical, spinal, and peripheral levels, respectively. To measure maximal strength and VA before and ~40s after SS, participants performed 2-s MVCs with femoral nerve stimulation. Based on data from the first nine participants (six females), there were no interactions or main effects of protocol for any variable, but there were significant effects of time for MVC torque as well as cortical and corticospinal excitability. MVC torque was reduced ~10% (p=0.011), whereas cortical and corticospinal excitability increased ~53% (p=0.033) and ~27% (p=0.004), respectively. Irrespective of total duration, SS led to impaired strength that was not due to reduced VA or offset by increased cortical excitability. Our findings lead us to conclude that the primary mechanisms of post-SS torque depression are likely within the musculotendinous unit.
