Fatigue during prolonged exercise is often described as an acute impairment of exercise performance that leads to an inability to produce or maintain a desired power output. The original central fatigue hypothesis emphasizes that an exercise-induced increase in serotonin is responsible for the development of fatigue. However, several pharmacological studies attempted and failed to alter exercise capacity through changes in serotonergic neurotransmission in humans, indicating that the role of serotonin is often overrated. Recent studies, implying the inhibition of the reuptake of both dopamine and noradrenaline, were capable of detecting changes in performance, specifically when ambient temperature was high. As dopamine and noradrenaline innervate areas of the hypothalamus, changes in the catecholaminergic concentrations may also be expected to be involved with the regulation of body core temperature during exercise in the heat. Evidence from different studies suggests that it is very unlikely that one neurotransmitter system is responsible for the appearance of central fatigue. It has been shown that when the catecholaminergic systems are manipulated during exercise in the heat, there is a discrepancy between the rise in core temperature and the perception of effort, the same phenomenon will also have an influence on the pacing strategy used by the athletes. Pacing is the efficient use of energetic resources during exercise, so that all energy stores are used before finishing a race, but not so far from the end of a race that a meaningful slowdown can occur. Three basic types of pacing - positive, negative and even pacing - have been identified, all depending on the duration of the event and the consequences of slowing down. It appears that intramuscular substrate/metabolic changes are more likely to be determining of changes in muscular power output in short duration events, while core temperature elevation is more central important in mid-duration events and the availability of carbohydrates as a substrate is being critical in long term events (>90 minutes). The component that appears to integrate all variables described above is the rating of perceived exertion (RPE). Pacing strategy in normal temperatures is quite straightforward, but also depends on exercise duration and the developed performance template. Most studies investigating longer duration events find a fast start that is followed by an even pace strategy in the middle part and an end sprint in the final minutes of the race. During exercise in the heat, fatigue seems to occur upon the attainment of a critical core/brain temperature of 39.5 - 40.0°C. This critical core temperature serves as a protective mechanism preventing potential damage to body tissues by limiting further heat production. Also, a reduction in power output and muscle activation occurs long before these critical core temperatures are reached, indicating that athletes and exercisers can anticipate the exercise intensity and heat stress they will be exposed to. Several studies showed that drugs acting on brain dopamine change the initial anticipatory setting of work rate by elevating arousal and motivational levels. This results in a mismatch between the actual and template RPE. Consequently, this leads to an increased work rate and heat production, until the conscious RPE returns to anticipated levels for the time trial in the heat. Taken together it appears that performance enhancing or deteriorating effects of central nervous system drugs on endurance performance are reflected by changes in pacing strategy.
Meeusen, R., & Roelands, B. (2014). Exercise in the heat: What does the brain tell us? In Science of Sport, Exercise and Physical Activity in the Tropics (pp. 19–28). Nova Science Publishers, Inc.