Title

Neural mechanisms that regulate repeated, high-intensity muscular performance – New insights into fatigue?

Document Type

Article

School

School of Medical and Health Sciences

Comments

Kirk, B., Pulverenti, T., Rowe, G., Trajano, G., & Blazevich. A.J. (2017). Neural mechanisms that regulate repeated, high-intensity muscular performance – new insights into fatigue. Paper presented at the International Congress on Soldiers’ Physical Performance (ICSPP) 2017: Research priorities across the service members operational lifecycle? Abstract available in the Journal of Science and Medicine in Sport, 20(2), S42–S43. Abstract available here.

Abstract

Purpose: To determine the site of change within the corticospinal-motoneuronal pathway that underpins the fatigue process during fatiguing high-intensity efforts.

Methods:In experiment 1, 16 resistance trained men performed 6 sets of unilateral isometric calf contractions on the right leg (3 s on/2 s off) reaching a target level of 85% MVC until failure (i.e.

Results: In experiment 1, a significant reduction in maximal isometric strength occurred (12.9%; p < 0.001), which recovered by Post-10. Triceps surae EMG:Mmax was reduced significantly post-exercise (4.4%; p = 0.024) and was fully recovered by Post-10. Corticospinal excitability declined significantly at Post (10.2%; p = 0.010) but recovered by Post-10. Caffeine improved torque (p = 0.003) and EMG:Mmax (p = 0.001) significantly at all time points, but corticospinal excitability was unchanged (p = 0.122). Thus, caffeine had a positive influence on muscle activation and force production, but its effects were not detected at the corticospinal level. In experiment 2, changes in force and EMG:Mmax were similar to experiment 1. T-vib declined significantly at Post (p = 0.019) and recovered by Post-20. However, no change was detected in T-sust (p = 0.246). Caffeine had no significant effect on T-vib (p = 0.437) or T-sust (p = 0.910).

Conclusions: Changes in the corticospinal-motoneuronal pathway appear to contribute, in part, to the loss of force seen during high-intensity efforts. This was demonstrated as a loss in corticospinal excitability and, for the first time, spinal ‘amplifier’ function after repeated high-intensity contractions. Caffeine was shown to improve muscular force output, however the improvement was not linked to changes in corticospinal excitability or spinal ‘amplifier’ function, thus caffeine is likely to exert its effects on other parts of the nervous system. This study highlights that changes in the nervous system contribute to the loss of force during fatiguing high-intensity contractions.

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