Date of Award


Degree Type


Degree Name

Master of Science (Sports Science)


School of Medical and Health Sciences

First Advisor

Professor Anthony Blazevich

Second Advisor

Dr Gabriel Trajano

Field of Research Code

110602, 110699


Fatigue can accumulate sufficiently to limit muscular force production during repeated, forceful muscle contractions, including those that occur in the occupational, clinical and athletic settings. Fatigue during such efforts is likely to result from disturbances to multiple processes in the nervous system and muscle. However, previous research examining the mechanisms underpinning fatigue have typically required subjects to perform low-level constant-force contractions or to repeat maximal efforts in a single set format. Such tasks do not translate well to occupational, daily living or athletic situations where high-intensity, yet submaximal, repeated efforts may be performed in work bouts (or sets) with brief rest periods for recovery. Therefore, the overall aim of the present research was to investigate the neuromuscular mechanisms contributing to force loss after repeated, high-intensity muscular efforts with longer (90 s) periods of rest separating repetitions into sets of contractions.

In Experiment 1, 16 resistance trained men performed 6 sets of unilateral isometric plantar flexor contractions of the right leg (3 s contraction/2 s rest) reaching a target level of 85% maximal voluntary contraction (MVC). Sets were separated by a 90-s inter-set rest and completed to failure (i.e.

In Experiment 1, a significant reduction in maximum voluntary isometric plantar flexion torque (12.2%; p < 0.001) was observed post-exercise, which did not recover by POST-20. Significant reductions in triceps surae EMG/M (-6%; p = 0.024) and MEP/M amplitude (9%; p = 0.01) were found post-exercise but recovered by POST-10. Cortical silent period (an indicator of GABAB-mediated intracortical inhibition) was reduced (-4%; p = 0.016) post-exercise and did not recover by POST-20. In Experiment 2, temporal changes in torque were similar to Experiment 1. Significant reductions in the evoked torque response from 20 Hz (p < 0.001), 80 Hz (p < 0.001) and VFT (p < 0.001) stimulations were observed at POST and did not recover by POST-20, however no changes in 20:80 and 20:VFT ratios were observed. Finally, significant reductions in both Tvib (-13%; p = 0.035) and Tsust (-25%; p = 0.035) were found post-exercise but recovered by POST-10. The ingestion of caffeine allowed for a greater overall torque production and neural drive (EMG/M) but the lack of condition  time interaction effect indicated that it did not clearly affect the time course of fatigue or recovery. Further, no detectable effects were observed compared to the non-caffeine condition in corticospinal excitability, MN excitability or E-C coupling, as shown by the negligible changes in MEP/M amplitude, PIC facilitation, and torque during 20-Hz, 80-Hz and VFT stimulations.

These data suggest that corticospinal tract efficiency and PIC-mediated facilitation of the MN pool can be compromised and are likely to account in part for the force loss immediately following an acute bout of repeated, high-intensity muscular efforts performed in sets (with 90 s rest). However, changes in E-C coupling efficiency (i.e. ‘peripheral fatigue) are likely to explain the ongoing, prolonged loss of force, at least to 20 min post-exercise. Therefore, it is likely that both changes in the nervous system as well as the muscle contribute to the loss of force following repeated, high-intensity muscular efforts.