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Identifying the cause of fatigue in sport and exercise

This is an excerpt from Exercise Physiology-6th Edition by George A. Brooks,Thomas D. Fahey,Kenneth M. Baldwin.

Before the cause and site of fatigue can be identified, we must define it. Usually, in athletic competition, fatigue means the inability to maintain a given exercise intensity. For instance, in distance running or swimming, when the competitor is unable to keep pace, they are considered to have fatigued for the particular event. However, an athlete is rarely completely fatigued and can usually maintain a lesser power output for some time. In a few circumstances, such as during wilderness hiking, individuals will push themselves until they are completely unable to move. In such cases of complete exhaustion, death can result from exposure.

Sometimes the specific cause and site of a decrement in work performance (fatigue) can be identified. For instance, the depletion of a particular metabolite in a particular fiber type within a specific muscle may be identified. At other times, as in dehydration, the causes of fatigue are diffuse and involve several factors that contribute to the disturbance in homeostasis.

Identifying a factor whose presence is correlated with the onset of fatigue is easier than determining that the presence (or absence) of the factor and fatigue are causally related. For instance, heavy muscular exercise has long been observed to be associated with acid accumulation. Historically, “lactic acid” was assumed to be the cause of fatigue, but glycolysis makes lactate anion, not lactic acid (Brooks 2025). It’s true that lactate concentration is high during and after hard exhausting exercise, but the association is one of correlation rather than cause. Historically, scientists have failed to consider an obvious explanation, that lactate appearance is a strain response in the body’s attempt to mitigate metabolic stress. Moreover, when lactate concentration is high, so are other metabolites (e.g., hydrogen and phosphate ions). In contrast, other metabolites such as glycogen, adenosine triphosphate (ATP), and creatine phosphate (CP) can be low. Is fatigue the result of acidosis and CP depletion, or is some other factor causing lactate and CP levels to change? To reiterate, much of the data relating lactate accumulation to onset of fatigue has been circumstantial, and most reports on lactate describe concentration, not production and disposal rates. Briefly, glycolysis makes lactate, not lactic acid. And lactate production is a strain response to mitigate challenges to ATP and C~P homeostasis. Lactate is not an innocent bystander in the scenario of muscle fatigue; lactate is an active participant in mitigating the onset of fatigue.

Compartmentalization in physiological organization, involving the division of the body into various systems, organs, tissues, and cells and the subdivisions of cells into various subfractions, organelles and reticula, also makes it difficult to identify the fatigue site. For instance, ATP may be depleted at a particular site within a cell (e.g., on the heads of myosin cross bridges) but may be adequate elsewhere. In such a case, it would be extremely difficult to identify ATP depletion as the cause of fatigue, even if a muscle biopsy were performed or nuclear magnetic resonance (NMR) spectroscopy techniques were used. Compartmentalization can mask the site of fatigue.

The effect of exercise at given absolute or relative intensities of V̇O₂max can be more severe on untrained than on trained individuals. For instance, fatigue occurs sooner in an untrained person exercising at 75% of V̇O₂max than in an endurance-trained individual exercising at the same relative work rate, or at a higher absolute work rate that elicits 75% of the trained individual’s V̇O₂max.

It is well known that environment can affect exercise endurance. For example, endurance is reduced during exercise in heat. This reduced endurance is due to the redistribution of cardiac output from contracting muscles and hepatic gluconeogenic areas to include greater cutaneous circulation. High muscle temperatures can also loosen the coupling between oxidation and phosphorylation in mitochondria. In this case, V̇O₂max is unchanged or increased, but ATP production is decreased. To the extent that the exercise is submaximal and there exists a reserve for cardiac output expansion, exercise under conditions of heat can be continued. The stress level, however, is greater.

If the need to circulate blood to exercising muscles, cutaneous areas, and other essential areas exceeds cardiac output, then endurance is reduced. During exercise in hot environments, the rate of sweat loss increases, and body heat is gained over time. Severe sweating results in dehydration and shifts both fluids and electrolytes among body compartments. These shifts, as well as increased body temperature, represent direct irritants to the CNS that can additionally affect an individual’s subjective perception of the exercise.

The physiological status of the individual can also easily affect exercise tolerance. For instance, if an individual exercises to fatigue in the heat on Monday, their ability to repeat that performance later in the day, or on Tuesday, or perhaps even Wednesday may be impaired. Similarly, individuals may have less endurance when they are glycogen depleted than when glycogen levels are normal or supercompensated.

More Excerpts From Exercise Physiology-6th Edition

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