This article examines how pacing strategies during exercise are controlled by information processing between the brain and peripheral physiological systems. It is suggested that, although several different pacing strategies can be used by athletes for events of different distance or duration, the underlying principle of how these different overall pacing strategies are controlled is similar. Perhaps the most important factor allowing the establishment of a pacing strategy is knowledge of the endpoint of a particular event. The brain centre controlling pace incorporates knowledge of the endpoint into an algorithm, together with memory of prior events of similar distance or duration, and knowledge of external (environmental) and internal (metabolic) conditions to set a particular optimal pacing strategy for a particular exercise bout. It is proposed that an internal clock, which appears to use scalar rather than absolute time scales, is used by the brain to generate knowledge of the duration or distance still to be covered, so that power output and metabolic rate can be altered appropriately throughout an event of a particular duration or distance. Although the initial pace is set at the beginning of an event in a feedforward manner, no event or internal physiological state will be identical to what has occurred previously. Therefore, continuous adjustments to the power output in the context of the overall pacing strategy occur throughout the exercise bout using feedback information from internal and external receptors. These continuous adjustments in power output require a specific length of time for afferent information to be assessed by the brain's pace control algorithm, and for efferent neural commands to be generated, and we suggest that it is this time lag that crates the fluctuations in power output that occur during an exercise bout. These non-monotonic changes in power output during exercise, associated with information processing between the brain and peripheral physiological systems, are crucial to maintain the overall pacing strategy chosen by the brain algorithm of each athlete at the start of the exercise bout.

Exercise in the heat causes "central fatigue", associated with reduced skeletal muscle recruitment during sustained isometric contractions. A similar mechanism may cause fatigue during prolonged dynamic exercise in the heat. The aim of this study was to determine whether centrally regulated skeletal muscle recruitment was altered during dynamic exercise in hot (35 degrees C) compared with cool (15 degrees C) environments. Ten male subjects performed two self-paced, 20-km cycling time-trials, one at 35 degrees C (HOT condition) and one at 15 degrees C (COOL condition). Rectal temperature rose significantly in both conditions, reaching maximum values at 20 km of 39.2+/-0.2 degrees C in HOT and 38.8+/-0.1 degrees C in COOL (P<0.005 HOT vs. COOL). Core temperatures at all other distances were not different between conditions. Power output and integrated electromyographic activity (iEMG) of the quadriceps muscle began to decrease early in the HOT trial, when core temperatures, heart rates and ratings of perceived exertion (RPE) were similar in both conditions. iEMG was significantly lower in HOT than in COOL at 10 and 20 km, while power output was significantly reduced in the period from 80% to 100% of the trial duration in the HOT compared with COOL condition. Thus, reduced power output and iEMG activity during self-paced exercise in the heat occurs before there is any abnormal increase in rectal temperature, heart rate or perception of effort. This adaptation appears to form part of an anticipatory response which adjusts muscle recruitment and power output to reduce heat production, thereby ensuring that thermal homeostasis is maintained during exercise in the heat.

Increasing inspiratory oxygen tension improves exercise performance. We tested the hypothesis that this is partly due to changes in muscle activation levels while perception of exertion remains unaltered. Eleven male subjects performed two 20-km cycling time-trials, one in hyperoxia (HI, FiO2 40%) and one in normoxia (NORM, FiO2 21%). Every 2 km we measured power output, heart rate, blood lactate, integrated vastus lateralis EMG activity (iEMG) and ratings of perceived exertion (RPE). Performance was improved on average by 5% in HI compared to NORM (P < 0.01). Changes in heart rate, plasma lactate concentration and RPE during the trials were similar. For the majority of the time-trials, power output was maintained in HI, but decreased progressively in NORM (P < 0.01) while it increased in both trials for the last kilometre (P < 0.0001). iEMG was proportional to power output and was significantly greater in HI than in NORM. iEMG activity increased significantly in the final kilometer of both trials (P < 0.001). This suggests that improved exercise performance in hyperoxia may be the result of increased muscle activation leading to greater power outputs. The finding of identical RPE, lactate and heart rate in both trials suggests that pacing strategies are altered to keep the actual and perceived exercise stress at a similar level between conditions. We suggest that a complex, intelligent system regulates exercise performance through the control of muscle activation levels in an integrative manner under conditions of normoxia and hyperoxia.