Bishop, David ORCID: 0000-0002-6956-9188 (2012) Fatigue during intermittent-sprint exercise. Clinical and Experimental Pharmacology and Physiology, 39 (9). pp. 836-841. ISSN 0305-1870 (print) 1440-1681 (online)

Abstract

Summary: There is a reversible decline in force production by muscles when they are contracting at or near their maximum capacity. The task-dependent nature of fatigue means that the mechanisms of fatigue may differ between different types of contractions. This paper examines how fatigue manifests during whole-body, intermittent-sprint exercise and discusses the potential muscular and neural mechanisms that underpin this fatigue. Fatigue is defined as a reversible, exercise-induced reduction in maximal power output (e.g. during cycling exercise) or speed (e.g. during running exercise), even though the task can be continued. The small changes in surface electromyogram (EMG), along with a lack of change in voluntary muscle activation (estimated from both percutaneous motor nerve stimulations and trans-cranial magnetic stimulation), indicate that there is little change in neural drive to the muscles following intermittent-sprint exercise. This, along with the observation that the decrease in EMG is much less than that which would be predicted from the decrease in power output, suggests that peripheral mechanisms are the predominant cause of fatigue during intermittent-sprint exercise. At the muscle level, limitations in energy supply, including phosphocreatine hydrolysis and the degree of reliance on anaerobic glycolysis and oxidative metabolism, and the intramuscular accumulation of metabolic by-products, such as hydrogen ions, emerge as key factors responsible for fatigue.

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