The Assessment of Muscular Effort, Fatigue, and Physiological Adaptation Using EMG and Wavelet Analysis.

Peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC-1α) is a transcription factor co-activator that helps coordinate mitochondrial biogenesis within skeletal muscle following exercise. While evidence gleaned from submaximal exercise suggests that intracellular pathways associated with the activation of PGC-1α, as well as the expression of PGC-1α itself are activated to a greater extent following higher intensities of exercise, we have recently shown that this effect does not extend to supramaximal exercise, despite corresponding increases in muscle activation amplitude measured with electromyography (EMG). Spectral analyses of EMG data may provide a more in-depth assessment of changes in muscle electrophysiology occurring across different exercise intensities, and therefore the goal of the present study was to apply continuous wavelet transforms (CWTs) to our previous data to comprehensively evaluate: 1) differences in muscle electrophysiological properties at different exercise intensities (i.e. 73%, 100%, and 133% of peak aerobic power), and 2) muscular effort and fatigue across a single interval of exercise at each intensity, in an attempt to shed mechanistic insight into our previous observations that the increase in PGC-1α is dissociated from exercise intensity following supramaximal exercise. In general, the CWTs revealed that localized muscle fatigue was only greater than the 73% condition in the 133% exercise intensity condition, which directly matched the work rate results. Specifically, there were greater drop-offs in frequency, larger changes in burst power, as well as greater changes in burst area under this intensity, which were already observable during the first interval. As a whole, the results from the present study suggest that supramaximal exercise causes extreme localized muscular fatigue, and it is possible that the blunted PGC-1α effects observed in our previous study are the result of fatigue-associated increases in muscle acidosis. This should be explored in future research using further combinations of EMG and muscle biochemistry and histology.