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Thesis Format

Monograph

Degree

Master of Science

Program

Kinesiology

Supervisor

Rice, Charles L.

Abstract

Following short duration, high intensity muscle activation, there is an enhancement of muscle contractile properties, termed postactivation potentiation (PAP). Corticospinal inhibition, assessed by an increased silent period (SP), was shown previously to increase following voluntary or electrically evoked PAP. Although these changes coexist, the direct effect of PAP on corticospinal inhibition has not been systematically evaluated. In 10 participants, SP duration was measured pre and post 10s maximal and submaximal, voluntary and electrically stimulated contractions. Following maximal contractions, mean twitch torque was enhanced ~180% with no enhancement at submaximal levels (~102%). The SP duration was prolonged following all conditions: ~12% post maximal voluntary and stimulated contractions, and ~5% post submaximal voluntary and involuntary contractions. These findings show that corticospinal inhibition is increased not only when the muscle is enhanced by PAP, but also following submaximal efforts inducing no PAP. Therefore, likely indicating that increases in corticospinal inhibition arise likely from afferent feedback relating to activation of the muscle rather than changes in intrinsic contractile states (PAP) per se.

Summary for Lay Audience

Muscle function is enhanced following a short duration (<10s) high force (>75% maximal force) contraction for up to 10 minutes. This enhancement is called postactivation potentiation (PAP) and it can be induced after either voluntary, or involuntary contraction. Whether PAP in the muscle has any direct effect on neural drive from the motor cortex is not known. Magnetic brain stimulation of the motor cortex causes a twitch-like response at the muscle known as a motor evoked potential (MEP). After the MEP, neural drive to the muscle is briefly interrupted ~100-300ms, this is known as the silent period (SP). The duration of the SP is used as a measure of inhibition in the motor pathway of the central nervous system. The purpose of this study was to observe changes in inhibition (SP) following high intensity contractions that cause PAP and contrast it with low intensity contractions that do not cause PAP enhancement. In 10 participants (4 females, 6 males) the SP response was measured before and after voluntary and electrically stimulated contraction of the muscle for 10s either inducing PAP, or not. Regardless of PAP, an increase in SP time occurred in all conditions. These results indicate that PAP enhancement does not in itself directly cause increased inhibition and is more likely the activation of the muscle causing this greater inhibition in central nervous system.

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