KENNY, GLEN P.1; DORMAN, LUCY E.1; WEBB, PAUL2; DUCHARME, MICHEL B.1,3; GAGNON, DANIEL1; REARDON, FRANCIS D.1; HARDCASTLE, STEPHEN G.4; JAY, OLLIE1
Body core temperature in humans is determined by the relative rates of net metabolic heat production and net heat loss via the heat exchange avenues of convection, conduction, radiation, and evaporation. In order for any measure of core temperature to be maintained at any steady-state value during exercise or rest, the difference between the rates of net heat production and net heat loss must be zero (1). After the onset of exercise, the time taken to balance the differential rates of heat production and heat loss is known as the thermal inertia (24) or temporal dissociation (36). At a given rate of heat production, a greater thermal inertia results in a larger change in body heat content and a greater increase in core temperature (33).
Factors unrelated to the elevation in body heat content and therefore core temperature (i.e., of nonthermal origin such as baroreceptors, mechanoreceptors, metaboreceptors, central command, etc.) but engaged during exercise have been shown to modulate the rate of local sweating and skin blood flow (21,22,30,31). Consequently, nonthermal factors may prolong thermal inertia after the onset of exercise subsequent to the secondary influence on heat loss responses, thereby extending the time to achieve a stable core temperature. As in the case of exercise, postexercise local skin blood flow and sweating are also subject to nonthermal influences associated with hemodynamic changes and hydration status (10). Studies show that in parallel to the rapid decrease in metabolic heat production after cessation of exercise, there is a rapid decline in local skin blood flow and sweating to preexercise levels during the early stages of recovery (11,12,16,17). The result is a reduced heat dissipation manifested primarily as a reduction in whole-body evaporative heat loss (18). Consequently, a sustained elevation of core and muscle temperatures (16,17) relative to preexercise rest has been reported for as long as 90 min after the cessation of exercise and by a magnitude that is dependent upon the intensity of the preceding exercise bout (17). For a more comprehensive discussion of the influence of nonthermal factors on exercise and postexercise thermoregulatory control, the reader is referred to comprehensive reviews on this topic (10,22,30).
Recent findings demonstrate that the prolonged elevations in core and muscle tissue temperatures are associated with a greater thermal inertia measured during exercise than recovery (18). Whether or not this pattern of response is altered with repeated exercise and therefore with a progressive increase in body heat storage remains unclear. Previous studies showed that intermittent exercise results in a progressive increase in core temperature, although the magnitude of increase in the postexercise elevation in core temperature is reduced with successive work/rest intervals (2,3,13,15,19,25). From a mechanistic point of view, if the postexercise reduction in heat loss responses is primarily of nonthermal origin, the progressive increase in core temperature with successive work/rest intervals would result in a similar reduction in postexercise heat loss and therefore similar changes in body heat content during each recovery bout. In contrast, if thermal factors predominate, we would expect that the rate of heat loss with each successive recovery bout would decline at a slower rate. The net result would be a greater decrease in body heat content within each successive recovery interval.
Previous studies have reported the temporal changes in local heat loss responses as well as core and muscle temperatures during intermittent exercise for different work-recovery periods (2,3,13,15,19,20,25,28). However, local heat loss responses do not illustrate how much whole-body heat transfer is altered, and core temperature measurements do not accurately represent the magnitude of residual body heat storage (9). It is generally accepted that the only way to accurately estimate the rates of whole-body evaporative and dry heat loss as well as the change in body heat content in humans is by performing simultaneous minute-by-minute measurements of the individual heat balance components by whole-body calorimetry (34). However, due to the limited accessibility of direct calorimeters, the evaluation of dyamic heat balance and cumulative heat storage in humans during intermittent bouts of exercise has not been previously examined.
Therefore, the aim of this study was to investigate heat balance during thermal transients caused by successive exercise bouts by directly measuring the individual components of heat production and heat loss using a whole-body calorimeter regulated to an ambient air temperature of 30°C and 30% relative humidity. We hypothesized that during exercise, although there would be a cumulative increase in body heat storage and core temperature, the incremental change would be progressively less due to an increased thermolytic activity. It was also hypothesized that during recovery, despite a greater thermal drive with successive exercise bouts, the rate of decay of postexercise whole-body heat loss would be similar indicating that the influence of nonthermal factors predominates.
After approval of the experimental protocol from the University of Ottawa Research Ethics Committee and obtaining written informed consent, 10 healthy, nonsmoking normotensive participants (6 males and 4 females) volunteered for the study. Mean ± SD characteristics of these participants were as follows: age = 27 ± 7 yr; height = 1.74 ± 0.07 m; weight = 75.2 ± 14.7 kg; body fat = 18.3% ± 7.3%; body surface area = 1.90 ± 0.21 m2; and maximal oxygen consumption (V˙O2max) = 51.6 ± 8.0 mL·kg−1·min−1. Female subjects had not taken medications except monophasic oral contraceptive, which provided 30-35 μg of ethinyl estrogen and low-dose progestin for 21 d and placebo for 7 d. To control for hormonal effects, we tested female subjects during the early follicular phase of their menstrual cycle.
The modified Snellen direct air calorimeter was used for the purpose of measuring the rate of evaporative (H˙E) and dry heat loss (H˙D), yielding an accuracy of ± 2.3 W for the measurement of rate of total heat loss (H˙L).1 A full peer-reviewed technical description of the fundamental principles and performance characteristics of the Snellen whole-body calorimeter is available (27).
In summary, the calorimeter incorporates a semirecumbent constant load eddy current cycle ergometer. The ergometer pedals are located inside of the calorimeter and mechanically linked by chains to the resistance control unit, regulating rate of external work (W˙) at a predetermined level, outside of the calorimeter so that any heat generated by the unit does not enter the calorimeter. The calorimeter is housed within a climatic chamber slightly pressurized (+8.25 mm Hg) to nullify potential air leakage through the calorimeter walls. Differential air temperature and humidity are measured over the calorimeter by sampling the influent and effluent air. The water content is measured using precision dew point thermometry (RH Systems model 373H, Albuquerque, NM), whereas the air temperature is measured using RTD high-precision thermistors (±0.002°C, Black Stack model 1560; Hart Electronics, American Fork, UT). Air mass flow through the calorimeter is estimated by differential thermometry over a known heat source (2 × 750 W heating elements) placed in the effluent air stream. Differential temperature over the heater is measured using a third aforementioned high-precision thermistor placed downstream from the heater. Air mass flow rate (kg air·min−1) is continuously measured during each trial. Data from the calorimeter were collected continuously at 8-s intervals throughout the trials. The real-time data were displayed and recorded on a personal computer (Dell OPTIPLEX GX270) with LabVIEW software (Version 7.0; National Instruments, Austin, TX).
H˙E (in watts) was calculated from the calorimetry data every minute using the following equation:
Equation (Uncited)Image Tools
where mass flow is the rate of flow of air mass (kg air·s−1), (humidityout − humidityin) is the calorimeter inflow-outflow difference in absolute humidity (g water·kg air−1), and 2427 is the latent heat of vaporization of sweat (J·g sweat−1) at 30°C (38).
H˙D (in watts) from radiation, convection, and conduction was calculated from the calorimetry data every minute using the following equation:
Equation (Uncited)Image Tools
where mass flow is the rate of flow of air mass (kg air·s−1), (temperatureout − temperaturein) is the calorimeter inflow-outflow difference in air temperature (°C), and 1005 is the specific heat of air (J·(kg air·°C)−1).
A 6-L fluted mixing box housed within the calorimeter was used for the concurrent measurement of metabolic energy expenditure (M˙). The indirect calorimetry open-circuit technique used expired gas samples drawn from the mixing box. Expired gas was analyzed for oxygen (O2; error of ±0.01%) and carbon dioxide (CO2; error of ±0.02%) concentrations using electrochemical gas analyzers (AMETEK model S-3A/1 and CD 3A; Applied Electrochemistry, Pittsburgh, PA). Expired air was recycled back into the calorimeter chamber to account for respiratory dry and evaporative heat loss. Before each session, gas mixtures of 4% CO2, 17% O2, and balance nitrogen were used to calibrate the gas analyzers, and a 3-L syringe was used to calibrate the turbine ventilometer (error ±3%, typically <1%). Rate of metabolic energy expenditure (M˙) was calculated from minute-average values for V˙O2 and the respiratory exchange ratio (RER) using the following equation (26):
Equation (Uncited)Image Tools
where ec is the caloric equivalent per liter of oxygen for the oxidation of carbohydrates (21.13 kJ), and ef is the caloric equivalent per liter of oxygen for the oxidation of fat (19.62 kJ).
The calorimeter data were then used to calculate rate of body heat storage (S˙; in watts) and change in body heat content (ΔHb; in kilojoules) using the following equations:
where M˙ is the rate of metabolic heat production, H˙E is the rate of evaporative heat loss, H˙D is the rate of dry heat loss, and W˙ is the rate of external work (all units in watts).
Esophageal temperature (Tes) was measured by placing a pediatric thermocouple probe of approximately 2 mm in diameter (Mon-a-therm Nasopharyngeal Temperature Probe; Mallinckrodt Medical, St. Louis, MO) through the participant's nostril while they were asked to sip water through a straw. The location of the probe tip in the esophagus was estimated to be at the level of the eighth and ninth thoracic vertebrae (23). Rectal temperature (Tre) was measured using a pediatric thermocouple probe (Mon-a-therm General Purpose Temperature Probe; Mallinckrodt Medical) inserted to a minimum of 12 cm past the anal sphincter. Mean skin temperature (T¯sk) was calculated using 12 skin temperatures weighted to the regional proportions as determined by Hardy and DuBois (7): head 7%, hand 4%, upper back 9.5%, chest 9.5%, lower back 9.5%, abdomen 9.5%, bicep 9%, forearm 7%, quadriceps 9.5%, hamstring 9.5%, front calf 8.5%, and back calf 7.5%.
Regional muscle temperature was measured using a flexible multisensor intramuscular temperature probe (Model IT-17:18, type T, time constant of 0.1 s; Physitemp Instruments Inc., Clifton, NJ) inserted into the vastus lateralis (Tvl), triceps brachii (Ttb), and upper trapezius (Tut) (16,17). Using aseptic technique, the skin, subcutaneous tissue, and muscle were anesthetized to a maximum depth of 40 mm by infiltrating ∼3 mL of lidocaine with 2% epinephrine. An 18-gauge, 45-mm nonradiopaque FEP polymer catheter (Medex Canada Inc., Toronto, ON, Canada) was then inserted at an angle and parallel to the long axis of the muscle into the anesthetized tract to the required depth (∼1 cm). The catheter stylet was then withdrawn, and the temperature probe was inserted into the catheter shaft. The probe assembly, including the catheter shaft, was secured to the skin with sterile, waterproof dressing. The implant site for Tvl was approximately midway between, and lateral to, a line joining the anterior superior iliac spine and the superior aspect of the center of the patella. The Ttb probe was inserted approximately midway between, and lateral to, a line joining the greater tubercle of the humerus and the superior aspect of the olecranon of the ulna. The Tut probe was inserted 3 cm superior to the center point between the acromion process and the superior angle of the scapula.
Temperature data were collected using an HP Agilent data acquisition module (model 3497A) at a sampling rate of 15 s and were simultaneously displayed and recorded in spreadsheet format on a personal computer (IBM ThinkCentre M50) with LabVIEW software (Version 7.0; National Instruments).
Heart rate (HR) was monitored using a Polar coded transmitter, recorded continuously and stored with a Polar Advantage interface and Polar Precision Performance software (Polar Electro Oy, Kempele, Finland).
All participants volunteered for three separate testing days. On testing days 1 and 2, body adiposity and V˙O2max were measured respectively. The body composition of each participant was measured using dual energy x-ray absorptiometry by which the body mass is partitioned into fat tissue mass, lean tissue mass, and bone mass. Maximal oxygen consumption was measured during a progressive incremental cycling protocol performed on a Monark cycle ergometer. Subjects were asked to cycle continuously at 80 rpm, at a starting work rate of 40 W for 2 min. The work rate was then increased by 40-W increments every 2 min thereafter until the subject could not maintain the pedaling cadence.
On testing day 3, the calorimetry experimental intermittent exercise protocol was performed. To control for seasonal acclimatization, we performed all experimental trials during the months of January and February. Testing days were separated by a minimum of 72 h. All calorimeter trials were performed at the same time of day. Participants were asked to arrive at the laboratory after eating a small breakfast (i.e., dry toast and juice) but consuming no tea or coffee that morning and also avoiding any major thermal stimuli on their way to the laboratory. Participants were also asked not to drink alcohol or exercise for 24 h before experimentation. For all experimentation, clothing insulation was standardized at ∼0.2 to 0.3 clo (i.e., cotton underwear, shorts, socks, and athletic shoes).
After instrumentation, the participant entered the calorimeter regulated to an ambient air temperature of 30°C and 30% relative humidity. The participant, seated in the semirecumbent position, rested for a 60-min habituation period while a steady-state baseline resting condition was achieved. Subsequently, the participant performed three 30-min bouts of semirecumbent cycling at a constant rate of metabolic heat production (M˙ − W˙) equal to 497 ± 14, 499 ± 4, and 500 ± 10 W for Ex1, Ex2, and Ex3, respectively. The corresponding work rates were 98 ± 8, 97 ± 8, and 96 ± 9 W for Ex1, Ex2, and Ex3, respectively, which equated to a relative work intensity of 50.1% ± 15.1%, 49.8% ± 14.9%, and 50.6% ± 15.6% of their predetermined V˙O2max. Each exercise was separated by 15 min of stationary recovery with the exception that the final recovery (R3) was 60 min in duration.
The observed rate of H˙L for each individual was best fit by a least-squares monoexponential model during each separate exercise and recovery bout as follows:
where H˙L(t) is the rate of net heat loss at a given time (t), H˙L_0 is the H˙L at the onset of exercise, H˙L_END is the H˙L at t = ∞ (i.e., the value required for heat balance (H˙L = M˙ − W˙) based on the assumption that the conditions (30°C, 30% RH) are compensable), amplitude (for exercise) is the difference between H˙L at the onset of the given exercise bout and M˙ − W˙ at the end of the given exercise bout, amplitude (for recovery) is the difference between H˙L at the start of the given recovery bout and M˙ − W˙ at the end of the given recovery bout, and τ is the time constant of the observed exponential growth (exercise) or decay (recovery).
A one-way repeated-measures ANOVA was used to separately analyze the end-exercise and end-recovery data, by using the repeated factors of bout (levels: Ex1, Ex2, and Ex3; or R1, R2, and R3). The dependent variables were M˙ − W˙, H˙L, H˙E, H˙D, and ΔHb as well as Tes, Tre, T¯sk, Tvl, Ttb, and Tut. In addition, values for all of the above variables were compared with preexercise baseline rest throughout the final 60-min recovery period at the end of the experimental protocol (time points: 0, 15, 30, 45, and 60 min). A one-way repeated-measures ANOVA was used to analyze the τ values obtained from empirical modeling by using the same repeated factors of bout. These τ values were further analyzed by comparing within each exercise/recovery cycle (i.e., Ex1/R1; Ex2/R2; Ex3/R3) using paired sample t-tests.
Post hoc comparisons were performed using paired sample t-tests. The level of significance was set at an alpha level of 0.05, and the level was adjusted during multiple comparisons so as to maintain the rate of type I error at 5% using a Holm-Bonferroni correction. All analyses were performed using the statistical software package SPSS 16.0 for Windows (SPSS Inc., Chicago, IL).
The mean simultaneous rates of M˙ − W˙ and H˙L throughout the experimental protocol are given in Figure 1A. After the start of Ex1, M˙ − W˙ increased immediately and was not initially offset by H˙L. As exercise progressed, H˙L increased exponentially primarily due to changes in H˙E (Fig. 1B). Immediately after Ex1, M˙ − W˙ reduced rapidly, returning to levels not significantly different from preexercise rest by the end of R1. At the same time, H˙L also reduced rapidly in an exponential manner. Postexercise changes in H˙L were again predominantly influenced by changes in H˙E (Fig. 1B), with minimal changes observed in H˙D (Fig. 1B). A similar pattern was observed during the Ex2/R2 and Ex3/R3 cycles.
FIGURE 1-Mean whole-...Image Tools
Metabolic heat production was identical between all three exercise bouts as well as between all three recovery periods. However, the exponential response of H˙L with time during exercise was found to change with repeated exercise bouts (P < 0.001). These differences are evidenced (Table 1) by the significantly greater time constants (τ) associated with the exponential increase in H˙L during Ex1 relative to Ex2 (P < 0.001) and Ex3 (P < 0.001). In contrast, no such differences were observed between the exponential changes in H˙L during successive recovery periods (P = 0.832). Within each exercise/recovery cycle, τ of the exponential growth in H˙L during Ex1 was significantly greater than τ of the exponential decay in H˙L during R1 (P < 0.011). No differences were observed for τ between Ex2 and R2 (P = 0.096) and between Ex3 and R3 (P = 0.163). At the end of the 60-min recovery after Ex3, H˙L was only elevated by 33 ± 22 W, with H˙E no longer significantly elevated above preexercise baseline levels.
The ΔHb as measured by calorimetry during Ex1 was significantly greater in comparison to Ex2 and Ex3, but there was no difference in the ΔHb during Ex2 and Ex3 (Fig. 2A). There were no differences in ΔHb between the 15-min recovery periods of R1, R2, and R3 (F2, 18 = 1.0, P = 0.379) (Fig. 2B). The cumulative change in body heat content from preexercise rest throughout the protocol was consequently greater at the end of Ex2 and Ex3 relative to the end of Ex1 (Fig. 3). Likewise, cumulative heat storage was greater at the end of R2 and R3 relative to the end of R1. After 60 min of recovery after the end of Ex3, ΔHb was +188 ± 94 kJ.
Tes was significantly influenced by successive exercise bouts (P = 0.004), but not successive recovery bouts (P = 0.097). A greater Tes 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, Tes reduced similarly with no difference observed between the end of R1, R2, or R3. Tes was significantly elevated above preexercise baseline values for the duration of the experimental protocol, and after 60 min of recovery after Ex3, Tes remained 0.18 ± 0.12°C above baseline.
FIGURE 4-Mean change...Image Tools
Tre was significantly influenced by successive exercise (P < 0.001) and recovery (P < 0.001) bouts. A greater Tre was observed at the end of Ex2 relative to Ex1 and at the end of Ex3 relative to Ex2 (Fig. 4A). During recovery, Tre was progressively higher with each subsequent recovery interval (i.e., R1 < R2 < R3). Tre remained significantly elevated above preexercise baseline rest throughout the experimental protocol. After 60 min of recovery after the end of Ex3, Tre was still 0.28 ± 0.15°C above baseline.
During exercise, Tvl (P = 0.001), Ttb (P = 0.018), and Tut (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, Tvl 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 Tut 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, Ttb was not different between successive recoveries (F2, 18 = 2.2, P = 0.135). After 60 min of recovery after the end of Ex3, Tvl and Ttb remained elevated above resting values by 1.65 ± 0.79°C and 1.17 ± 0.83°C, respectively. In contrast, Tut 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 Tes 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)-Tes 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 (Ta = 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) Cited Here...
1. Belding HS, Hatch TF. Index for evaluating heat stress in terms of resulting physiological strain. Heat Piping Air Cond
2. Belding HS, Hertig BA, Kraning KK. Comparison of man's responses to pulsed and unpulsed environmental heat and exercise. J Appl Physiol
3. Ekblom B, Greenleaf CJ, Greenleaf JE, Hermansen L. Temperature regulation during continuous and intermittent exercise in man. Acta Physiol Scand
4. Franklin PJ, Green DJ, Cable NT. The influence of thermoregulatory mechanisms on post-exercise hypotension in humans. J Physiol
5. Gagge AP, Gonzales RR. Mechanisms of heat exchange. In: Handbook of Physiology Environmental Physiology
. Bethesda (MD): American Physiological Society; 1996. p. 45-84.
6. Gisolfi CV, Wenger CB. Temperature regulation during exercise: old concepts, new ideas. Exerc Sport Sci Rev
7. Hardy JD, DuBois EF. The technique of measuring radiation and convection. J Nutr
8. Jay O, Kenny GP. The determination of changes in body heat content during exercise using calorimetry and thermometry. J Human Environ Syst
9. Jay O, Reardon FD, Webb P, et al. Estimating changes in mean body temperature for humans during exercise using core and skin temperatures is inaccurate even with a correction factor. J Appl Physiol
10. Journeay WS, Carter R 3rd, Kenny GP. Thermoregulatory control following dynamic exercise. Aviat Space Environ Med
11. Journeay WS, Jay O, McInnis NH, Leclair E, Kenny GP. Postexercise heat loss and hemodynamic responses during head-down tilt are similar between genders. Med Sci Sports Exerc
12. Journeay WS, Reardon FD, Martin CR, Kenny GP. Control of cutaneous vascular conductance and sweating during recovery from dynamic exercise in humans. J Appl Physiol
13. Kaciuba-Uscilko H, Kruk B, Szczpaczewska M, et al. Metabolic, body temperature and hormonal responses to repeated periods of prolonged cycle-ergometer exercise in men. Eur J Appl Physiol Occup Physiol
14. Kenny GP, Gagnon D, Jay O, McInnis NH, Journeay WS, Reardon FD. Can supine recovery mitigate the exercise intensity dependent attenuation of post-exercise heat loss responses? Appl Physiol Nutr Metab
15. Kenny GP, Giesbrecht GG, Thoden JS. Post-exercise thermal homeostasis as a function of changes in pre-exercise core temperature. Eur J Appl Physiol Occup Physiol
16. Kenny GP, Jay O. Sex differences in postexercise esophageal and muscle tissue temperature response. Am J Physiol Regul Integr Comp Physiol
17. Kenny GP, Jay O, Zaleski W, Reardon ML, et al. Postexercise hypotension causes a prolonged perturbation in esophageal and active muscle temperature recovery. Am J Physiol Regul Integr Comp Physiol
18. Kenny GP, Webb P, Ducharme MB, Reardon FD, Jay O. Calorimetric measurement of postexercise net heat loss and residual body heat storage. Med Sci Sports Exerc
19. Kraning KK 2nd, Gonzalez RR. Physiological consequences of intermittent exercise during compensable and uncompensable heat stress. J Appl Physiol
20. Kruk B, Szczypaczewska M, Opaszowski B, Kaciuba-Uscilko H, Nazar K. Thermoregulatory and metabolic responses to repeated bouts of prolonged cycle-ergometer exercise in man. Acta Physiol Pol
21. Mack GW, Cordero D, Peters J. Baroreceptor modulation of active cutaneous vasodilation during dynamic exercise in humans. J Appl Physiol
22. Mekjavic IB, Eiken O. Contribution of thermal and nonthermal factors to the regulation of body temperature in humans. J Appl Physiol
23. Mekjavic IB, Rempel ME. Determination of esophageal probe insertion length based on standing and sitting height. J Appl Physiol
24. Murgatroyd PR, Shetty PS, Prentice AM. Techniques for the measurement of human energy expenditure: a practical guide. Int J Obes Relat Metab Disord
25. Nielsen B. Thermoregulatory responses to arm work, leg work and intermittent leg work. Acta Physiol Scand
26. Nishi Y. Measurement of thermal balance in man. In: Cena K, Clark J, editors. Bioengineering, Thermal Physiology and Comfort
. New York (NY): Elsevier; 1981. p. 29-39.
27. Reardon FD, Leppik KE, Wegmann R, Webb P, Ducharme MB, Kenny GP. The Snellen human calorimeter revisited, re-engineered and upgraded: design and performance characteristics. Med Biol Eng Comput
28. Saltin B, Gagge AP, Stolwijk JA. Body temperatures and sweating during thermal transients caused by exercise. J Appl Physiol
29. Saltin B, Hermansen L. Esophageal, rectal, and muscle temperature during exercise. J Appl Physiol
30. Shibasaki M, Kondo N, Crandall CG. Non-thermoregulatory modulation of sweating in humans. Exerc Sport Sci Rev
31. Shibasaki M, Wilson TE, Crandall CG. Neural control and mechanisms of eccrine sweating during heat stress and exercise. J Appl Physiol
32. Thoden JS, Kenny GP, Reardon FD, Jette M, Livingston S. Disturbance of thermal homeostasis during post-exercise hyperthemia. Eur J Appl Physiol Occup Physiol
33. Webb P. Heat storage during exercise, especially in muscle. In: Hodgson RA, Heaney J, editors. Environmenal Ergonomics
. San Diego (CA); 1998. p. 121-4.
34. Webb P. Human Calorimeters
. New York (NY): Praeger; 1985. p. 176.
35. Webb P. The physiology of heat regulation. Am J Physiol
36. Webb P, Annis JA. Bio-thermal responses to varied work programs in men kept thermally neutral by water cooled clothing. NASA Contract Rep NASA CR
37. Webb P, Troutman SJ Jr, Annis JF. Automatic cooling in water cooled space suits. Aerosp Med
38. Wenger CB. Heat of evaporation of sweat: thermodynamic considerations. J Appl Physiol
39. Wilkins BW, Minson CT, Halliwill JR. Regional hemodynamics during postexercise hypotension II. Cutaneous circulation. J Appl Physiol