T es was significantly influenced by successive exercise bouts (P = 0.004), but not successive recovery bouts (P = 0.097). A greater T es was observed at the end of Ex2 and Ex3 in comparison to Ex1, but no differences were seen between Ex2 and Ex3 (Fig. 4A). During recovery, T es reduced similarly with no difference observed between the end of R1, R2, or R3. T es was significantly elevated above preexercise baseline values for the duration of the experimental protocol, and after 60 min of recovery after Ex3, T es remained 0.18 ± 0.12°C above baseline.
T re was significantly influenced by successive exercise (P < 0.001) and recovery (P < 0.001) bouts. A greater T re was observed at the end of Ex2 relative to Ex1 and at the end of Ex3 relative to Ex2 (Fig. 4A). During recovery, T re was progressively higher with each subsequent recovery interval (i.e., R1 < R2 < R3). T re remained significantly elevated above preexercise baseline rest throughout the experimental protocol. After 60 min of recovery after the end of Ex3, T re was still 0.28 ± 0.15°C above baseline.
During exercise, T vl (P = 0.001), T tb (P = 0.018), and T ut (P = 0.001) all became significantly greater with successive exercise bouts (Fig. 4B). For all muscle temperatures, significantly greater values were observed at the end of Ex2 and Ex3 in comparison to Ex1, but no differences were seen between Ex2 and Ex3. During recovery, T vl was greater at the end of R2 (P = 0.024) and R3 (P = 0.027) in comparison to R1, but no difference was observed between R2 and R3 (P = 0.157). Likewise T ut was greater at the end of R2 (P = 0.015) and R3 (P = 0.024) in comparison to R1, but no difference was observed between R2 and R3 (P = 0.331). In contrast, T tb was not different between successive recoveries (F 2, 18 = 2.2, P = 0.135). After 60 min of recovery after the end of Ex3, T vl and T tb remained elevated above resting values by 1.65 ± 0.79°C and 1.17 ± 0.83°C, respectively. In contrast, T ut only remained elevated above baseline values for 30 min of postexercise recovery after the end of Ex3.
Mean skin temperature
T¯ sk at the end of each successive exercise bout was not significantly different (P = 0.059). Similarly during recovery, no significant differences were observed in T¯ sk between the end of R1, R2, or R3 (P = 0.080). After Ex3, T¯ sk returned to levels not significantly greater than baseline after 15 min of recovery in R3 (Fig. 4C).
Preexercise baseline resting HR was 65 ± 3 beats·min−1. HR was 141 ± 12, 145 ± 9, and 148 ± 10 beats·min−1 at the end of Ex1, Ex2, and Ex3, respectively. No differences were observed between these HR values at the end of exercise (P = 0.054). At the end of R1, R2, and R3, HR was 80 ± 5, 82 ± 7, and 82 ± 6 beats·min−1 (P = 0.189), respectively. Similarly, no differences were observed between these HR values at the end of recovery. However, HR was significantly greater than preexercise baseline rest throughout Ex1, R1, Ex2, R2, Ex3, and R3 (all P values <0.05).
A key finding of this study was that the additional amount of heat stored in the body (i.e., ΔHb) subsequent to the first exercise/rest cycle was significantly less during the second and the third exercise/rest cycles. This reduction in the net change in body heat content was predominantly due to a greater rate of increase in whole-body net heat loss for a similar rate of net heat production in both Ex2 and Ex3 relative to Ex1. The net change in body heat content during each recovery period was similar despite cumulative residual heat storage and elevated core and muscle tissue temperatures. At the cessation of exercise, the rate of metabolic heat production was reduced similarly across all recovery periods, reaching resting levels within 10 min. This was paralleled by a rapid reduction in net whole-body heat loss that was similar during all three recovery bouts despite a progressively greater thermal drive.
Thermal inertia and changes in M˙ − W˙ and H˙L during exercise
Changes in body core temperature are a direct result of a thermal imbalance between the rate of heat production and the rate of total heat dissipation to the surrounding environment (6). In the present study, we show a rapid increase in the rate of heat production to the predetermined sustained elevated value of ∼500 W. As shown in previous studies (35,37), the exponential increase in the rate of heat loss lagged significantly behind that for the increase in the rate of heat production resulting in net body heat storage in each of the three exercise bouts. The slow response, reflected by a larger τ value, is known as the thermal inertia (24) or temporal dissociation (36). However, we show that after accounting for differences in amplitude between exercise bouts (primarily due to different values at the beginning of exercise), this exponential increase in H˙L becomes faster with successive exercise bouts. Specifically, the τ for H˙L (i.e., the time taken for ∼63% of the change in H˙L from the start of exercise to the asymptotic point (M˙ − W˙) during Ex1 of 12.3 ± 2.3 min was significantly longer than τ during Ex2 (7.2 ± 1.6 min) and Ex3 (7.1 ± 1.6 min). Consequently, the difference in the amount of heat stored during both Ex2 (135 ± 60 kJ) and Ex3 (124 ± 78 kJ) was significantly less in comparison to Ex1 (256 ± 76 kJ; Fig. 2A). The smaller τ value for H˙L observed in Ex2 and Ex3 indicates that the thermal inertia is reduced when the body is already warm and much of the heat already stored during the first exercise/recovery cycle remains. Our findings are consistent with previous reports suggesting that the time to onset of local sweating (20) and skin vasodilation (15) is shortened in successive exercise bouts. In addition to thermal controllers of sweating and skin blood flow, many nonthermal factors modulate the skin blood flow and sweating response (21,22,30,31). In the context of our observations, the more rapid increase in H˙L observed in Ex2 and Ex3 in comparison to Ex1 most likely reflects the greater thermal drive. However, the similarity in H˙L response between Ex2 and Ex3 despite a cumulative increase in body heat content and core temperature may be indicative of a possible non-thermal-mediated influence on heat loss responses. Further studies are required to evaluate these possible mechanisms.
Thermal inertia and changes in M˙ − W˙ and H˙L during postexercise recovery
In contrast to the differences in thermal inertia observed during exercise, no difference in thermal inertia was observed across all three recovery periods. Specifically, the τ for H˙L during R1 of 6.5 ± 1.1 min was similar to the τ during R2 (5.9 ± 1.3 min) and R3 (6.0 ± 1.2 min). Consequently, similar changes in body heat content were measured during the 15-min recovery period (−82 ± 48, −91 ± 48, and −88 ± 54 kJ for R1, R2, and R3, respectively; Fig. 2B). The reduction in postexercise net heat loss at an air temperature of 30°C (30% RH) was predominantly due to rapid reductions in the rate of whole-body evaporative heat loss. Specifically, the evaporation observed after 10 min of recovery in R1, R2, and R3, respectively, was only 22.8% ± 7.6%, 4.7% ± 9.8%, and 1.5% ± 12.0% of the evaporation at the end of the preceding exercise bout. Meanwhile, metabolic heat production returned to preexercise resting levels within 10 min of recovery in all three recovery bouts.
Underlying mechanisms for differences between exercise and postexercise thermoregulatory control
Studies show that the metabolic heat production during exercise results in body heat storage and a corresponding increase in core and muscle tissue temperatures that persists for a prolonged period after exercise (4,17,18,29,32,39), the magnitude of which is determined by the relative intensity of the physical activity performed (17). Further, Kenny et al. (15) showed that although the postexercise elevation in T es achieved a higher absolute temperature with successive exercise bouts, the magnitude of increase was less in the subsequent exercise/recovery cycles (i.e., 0.48°C, 0.15°C, and 0.11°C for Ex1/R1, Ex2/R2, and Ex3/R3, respectively). This was paralleled by a rapid decrease in local heat loss responses to baseline resting values within the first ∼10 min of recovery. On the basis that the postexercise metabolic rate was similar for each recovery interval, the authors speculated that the progressive increase in internal body temperature was the result of a possible resetting of the skin blood flow (or sweating)-T es relationship postexercise. This apparent perturbation in postexercise thermoregulatory control has subsequently been ascribed to nonthermal factors thought to be associated with a postexercise hypotension response (10,16,17).
Consistent with previous reports, we show that this postexercise elevation is not associated with an increase in metabolic heat production due to a residual increase in tissue metabolism (15,32). Rather, we show that despite a persistent and progressive elevation in core and muscle tissue temperatures, H˙E reduced rapidly in the early stages of recovery, which was also accompanied by minimal H˙D. Furthermore, despite a greater thermal drive with successive exercise bouts, the rate of decay of whole-body heat transfer after cessation of exercise is similar between recovery bouts despite cumulative residual heat storage and elevated core and muscle tissue temperatures. This is evidenced by our findings that the τ for H˙L during R1 was similar to the τ during R2 and R3. If thermal factors predominated, we would expect that the rate of heat loss with each successive recovery bout would have declined at a slower rate. In such case, the net result would be a greater decrease in body heat content within each successive recovery bout. Due to technical limitations in the present study, it was not possible to measure mean arterial pressure and local heat loss responses in the direct calorimeter. As such, we cannot confirm the level of influence of nonthermal factors such as those associated with postexercise blood pressure regulation (10,16,17) on whole-body heat loss response. Although our data do not allow a discussion of the effects of these nonthermal factors, they may well be involved in modulating the rate of whole-body heat loss during successive exercise/recovery cycles. Further research is needed to understand the interplay between thermal and nonthermal factors during thermal transients caused by successive bouts of exercise of varying duration and/or intensity under different ambient conditions.
In the context of our current observations, it is evident that differences in thermoregulatory control during and after exercise may potentially have a pronounced effect on the magnitude of change in body heat content and core temperature during intermittent work. We show that despite a cumulative increase in body heat content and core and muscle tissue temperatures with successive moderate intensity exercise bouts performed in a warm dry ambient condition, the rate of heat dissipation remains unchanged across the three recovery periods. Even after a 60-min recovery following the third exercise bout, core and muscle temperatures remained significantly elevated above baseline resting. In work conditions requiring higher intensity work efforts and/or performed in hot and/or more humid ambient conditions, this may result in greater levels of thermal strain thereby increasing the risk of thermal injury. Countermeasures may be necessary to attenuate the increase in body heat content. Although for some jobs this may be easily achieved by decreasing work intensity, reducing work time, extending the rest period, or a combination of these, certain jobs may require a task to be performed at a specific intensity and/or duration. In such cases, implementing countermeasures performed during recovery from exercise, which have been shown to enhance heat dissipation such as the use of a simple postural manipulation (i.e., supine recovery) (14) or active/passive recoveries (12), may prove beneficial.
The whole-body calorimeter does not presently allow us to verify that dripping of sweat did not occur. However, the environmental conditions (i.e., hot-dry environment and an air mass flow of ∼9 kg air·min−1) were selected to ensure a high evaporative driving force (8) and therefore complete evaporation of all secreted sweat at the body surface. Although local sweat rate and skin blood flow were not measured in the present study, we measured evaporative heat loss by calorimetry, which is considered to be the best way of accurately determining whole-body sweat rate (5). Under the environment conditions tested (T a = 30°C, RH = 30%), whole-body evaporation of sweat represents by far the most dominant avenue for heat dissipation during exercise and recovery (18). By experimental design, all subjects performed the three successive exercise bouts at a constant rate of heat production of ∼500 W, with any fatigue-induced changes in mechanical efficiency offset by adjusting the W˙ to maintain a constant rate M˙ − W˙. Therefore, any differences in heat loss responses between the three exercise bouts were independent of changes in heat production.
We show that for intermittent exercise separated by short bouts of rest, the cumulative increase in body heat storage and core temperature increases with successive exercise bouts; however, the magnitude of increase became progressively less. This was a consequence of an increased thermolytic activity in the second and the third exercise bouts relative to the first. Despite the greater thermal drive at the end of the second and the third exercise bout relative to the first, the decline in postexercise whole-body heat dissipation was similarly rapid during all three recovery periods. These observations suggest that factors of nonthermal origin may play an important role in modulating thermal control of postexercise whole-body heat loss in intermittent exercise bouts.
This research was supported by the Natural Sciences and Engineering Research Council (Grant # RGPIN-298159-2004, grant held by Dr. Glen Kenny) and the Workplace Safety and Insurance Board of Ontario (WSIB grant #06005, grant held by Dr. Glen Kenny and Dr. Ollie Jay). Dr. Glen Kenny was supported by a University of Ottawa Research Chair Award. The provision of financial support does not in any way infer or imply endorsement of the research findings by either agency. The results of the present study do not constitute endorsement by ACSM.
1Rate of total heat loss (H˙L) is the sum of concurrent rates of evaporative (H˙E) and dry (H˙D) heat loss (i.e., H˙L = H˙E + H˙D)
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Keywords:©2009The American College of Sports Medicine
BODY HEAT STORAGE; CALORIMETRY; HEAT STRESS; THERMOREGULATION