During self-paced exercise, the exercise work rate is regulated by the brain based on the integration of numerous signals from various physiological systems. It has been proposed that the brain regulates the degree of muscle activation and thus exercise intensity specifically to prevent harmful physiological disturbances. It is presently proposed how the rating of perceived exertion (RPE) is generated as a result of the numerous afferent signals during exercise and serves as a mediator of any subsequent alterations in skeletal muscle activation levels and exercise intensity. A conceptual model for how the RPE mediates feedforward, anticipatory regulation of exercise performance is proposed, and this model is applied to previously described research studies of exercise in various conditions, including heat, hypoxia and reduced energy substrate availability. Finally, the application of this model to recent novel studies that altered pacing strategies and performance is described utilising an RPE clamp design, central nervous system drugs and the provision of inaccurate duration or distance feedback to exercising athletes.We have previously described studies of pacing strategy using various experimental interventions, including faster and slower starts, higher temperatures, hypoxia, hyperoxia and altered energy substrate availability. 1 We have proposed the presence of a complex, regulatory system that mediates changes to skeletal muscle motor unit activation and work rate in order both to optimise performance and prevent potentially harmful changes to homeostasis. We subsequently develop a model to explain how this regulatory system might utilise the subjective rating of perceived exertion (RPE) as a means of integrating afferent information and a variety of other cues in order to achieve these objectives during exercise. THE RPE DURING CONSTANT WORKLOAD EXERCISE: THE LIMIT VARIABLE FOR VOLITIONAL PERFORMANCE TO FATIGUEOften measured as an index of subjective perception of effort during exercise, the RPE has been causally linked to physiological variables such as muscular force, 2 heart rate, ventilation, respiratory rate, oxygen uptake and blood lactate concentrations.3 Borg 4 has stated that the RPE is the ''single best indicator of physical strain'', and ''integrates various information, including the many signals elicited from the peripheral working muscles and joints, from the central cardiovascular and respiratory functions, and from the central nervous system''. The RPE also incorporates other mediators, most notably psychological and affective components.5 6 The overall sensation of exertion measured during exercise is thus the conscious/ verbal manifestation of the integration of these psychological and physiological cues (see Hampson et al 7 for a complete review). The biological link between the subjective sensation of effort and the physiological changes occurring during exercise is of crucial importance, because it provides a mechanism by which the RPE could, in theory, contribute to the regul...

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.

The aim of the present study was to examine the regulation of exercise intensity in hot environments when exercise is performed at a predetermined, fixed subjective rating of perceived exertion (RPE). Eight cyclists performed cycling trials at 15• C (COOL), 25• C (NORM) and 35 • C (HOT) (65% humidity throughout), during which they were instructed to cycle at a Borg rating of perceived exertion (RPE) of 16, increasing or decreasing their power output in order to maintain this RPE. Power output declined linearly in all three trials and the rate of decline was significantly higher in HOT than in NORM and COOL (2.35 ± 0.73 W min −1 , 1.63 ± 0.70 and 1.61 ± 0.80 W min −1 , respectively, P < 0.05). The rate of heat storage was significantly higher in HOT for the first 4 min of the trials only, as a result of increasing skin temperatures. Thereafter, no differences in heat storage were found between conditions. We conclude that the regulation of exercise intensity is controlled by an initial afferent feedback regarding the rate of heat storage, which is used to regulate exercise intensity and hence the rate of heat storage for the remainder of the anticipated exercise bout. This regulation maintains thermal homeostasis by reducing the exercise work rate and utilizing the subjective RPE specifically to ensure that excessive heat accumulation does not occur and cellular catastrophe is avoided.