Influence of duty cycle on the time course of muscle fatigue and the onset of neuromuscular compensation during exhaustive dynamic isolated limb exercise.

Am J Physiol Regul Integr Comp Physiol

Biomechanics Laboratory, Departments of Health and Human Performance and Organismal Biology and Ecology, University of Montana, Missoula, Montana

Published: July 2015

We investigated the influence of altered muscle duty cycle on the performance decrements and neuromuscular responses occurring during constant-load, fatiguing bouts of knee extension exercise. We experimentally altered the durations of the muscularly inactive portion of the limb movement cycle and hypothesized that greater relative durations of inactivity within the same movement task would 1) reduce the rates and extent of muscle performance loss and 2) increase the forces necessary to trigger muscle fatigue. In each condition (duty cycle = 0.6 and 0.3), male subjects [age = 25.9 ± 2.0 yr (SE); mass = 85.4 ± 2.6 kg], completed 9-11 exhaustive bouts of two-legged knee extension exercise, at force outputs that elicited failure between 4 and 290 s. The novel duty cycle manipulation produced two primary results; first, we observed twofold differences in both the extent of muscle performance lost (DC0.6 = 761 ± 35 N vs. DC0.3 = 366 ± 49 N) and the time course of performance loss. For example, exhaustive trials at the midpoint of these force ranges differed in duration by more than 30 s (t0.6 = 36 ± 2.6 vs. t0.3 = 67 ± 4.3 s). Second, both the minimum forces necessary to exceed the peak aerobic capacity and initiate a reliance on anaerobic metabolism, and the forces necessary to elicit compensatory increases in electromyogram activity were 300% greater in the lower vs. higher duty cycle condition. These results indicate that the fatigue-induced compensatory behavior to recruit additional motor units is triggered by a reliance on anaerobic metabolism for ATP resynthesis and is independent of the absolute level or fraction of the maximum force produced by the muscle.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4491536PMC
http://dx.doi.org/10.1152/ajpregu.00356.2014DOI Listing

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