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Thesis Format

Integrated Article

Degree

Doctor of Philosophy

Program

Kinesiology

Supervisor

Rice, Charles L

Abstract

Muscle contractility is influenced by its activation history. For example, prolonged muscle activation (e.g., minutes) reduces force; termed muscle fatigue. Conversely, brief (e.g., seconds) activation enhances submaximal force; termed post-activation potentiation (PAP). Prior muscle activation is required for both effects and thus there is a coexistence between these processes.

Here, fatigue and PAP were investigated independently, and concurrently in humans by using voluntary and electrically stimulated isometric (study two) and dynamic contractions (studies one & four), and with single motor unit recordings using intramuscular electromyography (studies two & four). For study three, isolated intact single myofibers from mice were used to make assessments of force changes and intracellular calcium transients.

Study one demonstrated that during voluntary fatiguing contractions, PAP mechanisms delayed power loss in response to stimulated low frequencies of muscle excitation (submaximal) despite a decline in stimulated high frequencies of excitation (maximal). During recovery, power in response to stimulated low frequencies was preferentially impaired. However, inducing PAP ameliorated this power loss. Therefore, the concurrent effects of fatigue and PAP are frequency-dependent, and PAP mitigates power loss of low frequencies during recovery.

Study two investigated the effect of PAP during recovery from fatigue on motor unit (MU) firing rates. During recovery, MU firing rates increased as submaximal torque generation was impaired compared to baseline. However, inducing PAP during the recovery state mitigated the requirement of higher MU firing rates. Therefore, firing rates are responsive to opposing influences on the contractile state and can make compensatory rate adjustments dependent on the active state of the muscle.

Study three, in single myofibers, showed the preferential force loss of low frequencies of excitation (submaximal) during recovery was due to reduced cytosolic Ca2+. However, inducing post-tetanic potentiation in this state recovered submaximal force by increasing cytosolic Ca2+. Therefore, adjustments in force due to activation history are principally accomplished by opposing adjustments in cytosolic Ca2+.

Study four demonstrated that compared to baseline inducing PAP increased MU recruitment thresholds, but decreased firing rates during contractions at 50 and 75% peak power. Therefore, MUs make compensatory adjustments in relation to the active state of the muscle during tasks requiring a high-power output.

Summary for Lay Audience

During high-intensity contractions the force generating capacity of muscle is reduced, known as fatigue. Conversely, after a high-intensity contraction subsequent low force contractions can become enhanced for a short duration, known as post-activation potentiation (PAP). Due to the common factors affected by prior muscle activation, muscle can display opposing but concurrent effects of fatigue and PAP to adjust force outputs in relation to activation by the central nervous system.

Study one indicated that following repetitive maximal contractions power output in response to low submaximal activation demonstrated PAP. However, this can occur with a concurrent reduction of high levels of activation due to fatiguing processes. Therefore, the effect of PAP can be utilized, and during recovery when submaximal contraction is impaired, inducing PAP can minimize this power loss. Therefore, the concurrent effects of fatigue and PAP are contractile intensity dependent.

In study two the effect of inducing PAP during recovery from fatigue on motor unit firing rates was explored. The motor unit (MU) is defined as a motoneuron and the muscle fibers the neuron connects to; ultimately controlling contraction. During recovery, MU firing rates were higher to compensate for impaired submaximal force generation. However, inducing PAP in this state mitigated the requirement of higher MU firing rates as the muscle became more sensitive to neural input. Therefore, the MU made compensatory adjustments based on the force generating capacity of the muscle.

For study three the effect of inducing PAP during recovery from fatigue was investigated in single muscle fibers from mice to provide insights at the cellular level. Specifically, measurements of intracellular Ca2+ were made, which is a principal regulator of muscle contraction. Submaximal force impairments following fatigue were due to reduced Ca2+, however, when PAP was induced force recovered by increasing Ca2+. Therefore, fatigue and PAP both impact force generation by opposing effects on intracellular Ca2+.

In study four the value of PAP during high powered contractions was assessed through MU recordings. Results demonstrated that inducing PAP increased MU recruitment thresholds (i.e., activated later in contraction), but decreased firing rates during high-powered contractions. Therefore, adaptations occur at the MU level during PAP because the muscle becomes more sensitive to neural input.

Overall, muscle activation leads to competing effects of the neuromuscular system at various structural levels reflected by opposing adjustments in force, power, MU activity and intracellular Ca2+ relative to the task demand.

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