Answer to O. Jay's Letter to the Editor

Dear Editors

The authors would like to thank Dr Jay for his insightful and constructive comments on our recently-published manuscript in the International Journal of Sports Medicine [2]. Using the 2-compartment thermometry model of “core” (T_es) and “shell” (T_sk) temperatures to calculate body heat storage (S), we recently postulated that “changes in the pattern” of S may serve as a key signal mediating reductions in self-selected work-rate during moderate duration, high intensity exercise in the heat [2], supporting previous observations [9]. These findings were based upon large differences in S observed between the HOT and COOL conditions during the early stages of exercise, and the tendency for this difference to decline during the later stages of exercise. In light of the inadequacies highlighted by Dr. Jay, when estimating S using the thermometry approach, we agree that “changes in the pattern of S” seem unlikely to serve as the key signal mediating early reduction in work-rate during self-paced exercise in the heat. Indeed, our own calculations (using indirect calorimetry) confirm the author's suggestions that S remained consistently higher in the HOT condition relative to COOL throughout the duration of exercise. Nevertheless, it should be noted that these observations do not detract from the overall message communicated in the manuscript, that a pre-exercise elevation in body heat content leads to an anticipatory reduction in work-rate during self-paced exercise in the heat.

In contrast with exercise protocols that require individuals to cycle to volitional exhaustion at a fixed work-rate, during a more externally-valid self-paced time trial, athletes can alter pace in response to various external and internal physiological cues and signals [4]. The concept of pacing to optimise athletic performance is well established. Neverthless, there is considerable debate surrounding the mechanism/s which serve to regulate self-paced exercise [1]. A growing body of literature suggests that exercise intensity is controlled by a central anticipatory control system which serves to regulate the degree of motor unit recruitment in order to prevent catastrophic failures in any physiological system [7]. Evidence supporting the existence of this control mechanism has been frequently cited from studies that have evaluated the influence of heat stress on self-paced endurance performance [8] [10]. Under such conditions, decrements in work-rate during the early stages of exercise (relative to cooler conditions), despite low levels of thermoregulatory strain have led to suggestions that in the heat, anticipatory changes in work-rate serve to prevent body temperature rising to levels associated with the development of fatigue.

In his letter to the editor, Dr. Jay argues that the decrements in 4-km time trial performance in the heat were mediated through an incrementally greater level of hyperthermia-induced central fatigue. It is well established that when exercise is performed at a constant work-rate to exhaustion in the heat, volitional fatigue occurs at a limiting internal body temperature due to a decline in central drive [6]. Closer inspection of the current data, however, indicates that such a mechanism fails to explain the work-rate decrements observed during exercise in the heat. Work-rate was reduced from the onset of exercise in the heat relative to the Cool condition, despite low levels of thermoregulatory strain. Furthermore, a characteristic “U-shaped” work-rate profile was observed during exercise under both Hot and Cool conditions [3]. Consequently, subjects were able to increase their work-rate during the final stages of exercise in the heat despite higher levels of core body temperature. As such, fatigue traditionally associated with an incrementally greater level of hyperthermia-induced central fatigue cannot account for the changes in work-rate observed [2].

It is our opinion that the current findings provide further evidence of the anticipatory feed-forward regulation of exercise intensity and the signals involved in its control during an exercise protocol that is much more valid to real-world athletic events than tests of ‘time-to-exhaustion’ [2]. In contrast with previous studies in which participants immediately commenced exercise on entering the controlled environmental conditions (mediating a rapid elevation in T_sk per se), our participants remained seated for 20 min in the HOT and COOL conditions prior to exercise. This resulted in marked changes in both T_sk and T_m independent of any change in T_es [2]. Interestingly, work-rate in our study was reduced from the outset of the time trial compared with the decrements that have been reported after 10–15 min of exercise when subjects commenced exercise on immediate exposure to high ambient temperatures [8] [9] [10]. These observations suggest that signals arising from marked changes in both T_sk and T_m may serve to mediate decrements in work-rate observed from the onset of exercise [2]. Indeed Dr Jay and colleagues have previously hypothesised that an anticipatory reduction in exercise intensity may occur relative to early changes in brain and/or muscle temperature [5]. Further research is needed to explore the mechanisms involved in the control of self-paced exercise, especially since this type of protocol is more relevant to athletic competitions. The present findings suggest that sensory information arising from thermoreceptors located within different tissue are likely to contribute to such anticipatory control of work-rate.

Warren Gregson

References

• 1 Abbiss CR, Laursen PB. Describing and understanding pacing strategies during athletic competition.  Sports Med. 2008;  38 239-252
• 2 Altareki N, Drust B, Atkinson G, Cable T, Gregson W. Effects of environmental heat stress (35°C) with simulated air movement on the thermoregulatory responses during a 4-km cycling time trial.  Int J Sports Med. 2009;  30 9-15
• 3 Ansley L, Schabort E, St Claire Gibson A, Lambert MI, Noakes TD. Regulation of pacing strategies during successive 4-km time trials.  Med Sci Sports Exerc. 2004;  36 1819-1825
• 4 Atkinson G, Peacock O, St. Claire Gibson A, Tucker R. Distribution of power output during cycling.  Sports Med. 2007;  37 647-667
• 5 Jay O, Kenny GP. Viewpoint. Current evidence does not support an anticipatory regulation of exercise intensity mediated by rate of body heat storage.  J Appl Physiol. 2008;  , (Epub ahead of print; Aug 7). DOI:10.1152/japplphysiol.906312.2008
• 6 Nybo L. Hyperthermia and fatigue.  J Appl Physiol. 2008;  104 871-878
• 7 St Clair Gibson A, Noakes TD. Evidence for complex system integration and dynamic neural regulation of skeletal muscle recruitment during exercise in humans.  Br J Sports Med. 2004;  38 797-806
• 8 Tatterson AJ, Hahn AG, Martin DT, Febbraio MA. Effects of heat stress on physiological responses and exercise performance in elite cyclists.  J Sci Med Sport. 2000;  3 186-193
• 9 Tucker R, Marle T, Lambert EV, Noakes TD. The rate of heat storage mediates an anticipatory reduction in exercise intensity during cycling at a fixed rating of perceived exertion.  J Physiol. 2006;  3 905-915
• 10 Tucker R, Rauch L, Harley YX, Noakes TD. Impaired exercise performance in the heat is associated with an anticipatory reduction in skeletal muscle recruitment.  Pflugers Arch. 2004;  448 422-430

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