Purpose: Previous studies have shown a rapid reduction in postexercise local sweating and blood flow despite elevated core temperatures. However, local heat loss responses do not illustrate how much whole-body heat dissipation is reduced, and core temperature measurements do not accurately represent the magnitude of residual body heat storage. Whole-body evaporative (H˙E) and dry (H˙D) heat loss as well as changes in body heat content (ΔHb) were measured using simultaneous direct whole-body and indirect calorimetry.
Methods: Eight participants cycled for 60 min at an external work rate of 70 W followed by 60 min of recovery in a calorimeter at 30°C and 30% relative humidity. Core temperature was measured in the esophagus (Tes), rectum (Tre), and aural canal (Tau). Regional muscle temperature was measured in the vastus lateralis (Tvl), triceps brachii (Ttb), and upper trapezius (Tut).
Results: After 60 min of exercise, average ΔHb was +273 ± 57 kJ, paralleled by increases in Tes, Tre, and Tau of 0.84 ± 0.49, 0.67 ± 0.36, and 0.83 ± 0.53°C, respectively, and increases in Tvl, Ttb, and Tut of 2.43 ± 0.60, 2.20 ± 0.64, and 0.80 ± 0.20°C, respectively. After a 10-min recovery, metabolic heat production returned to pre-exercise levels, and H˙E was only 22.9 ± 6.9% of the end-exercise value despite elevations in all core temperatures. After a 60-min recovery, ΔHb was +129 ± 58 kJ paralleled by elevations of Tes = 0.19 ± 0.13°C, Tre = 0.20 ± 0.03°C, Tau = 0.18 ± 0.04°C, Tvl = 1.00 ± 0.43°C, Ttb = 0.92 ± 0.46°C, and Tut = 0.31 ± 0.27°C. Despite this, H˙E returned to preexercise levels. Only minimal changes in H˙D occurred throughout.
Conclusion: We confirm a rapid reduction in postexercise whole-body heat dissipation by evaporation despite elevated core temperatures. Consequently, only 53% of the heat stored during 60 min of exercise was dissipated after 60 min of recovery, with the majority of residual heat stored in muscle tissue.
1Laboratory of Human Bioenergetics and Environmental Physiology, School of Human Kinetics, University of Ottawa, Ottawa, Ontario, CANADA; 2Yellow Springs, OH; and 3Defence R&D Canada, Quebec City, Quebec, CANADA
Address for correspondence: Glen P. Kenny, Ph.D., School of Human Kinetics, University of Ottawa, 125 University, Montpetit Hall, Ottawa, Ontario, Canada K1N 6N5; E-mail: email@example.com.
Submitted for publication January 2008.
Accepted for publication March 2008.
At the cessation of exercise, numerous studies have shown that local skin blood flow and sweating return to preexercise levels during the early stages of recovery despite sustained elevations in core temperature (3,12-14,16,17,19,25,30,37). As such, the association between postexercise local heat loss responses and core temperature appears to be different. The underlying mechanism for this apparent perturbation of postexercise thermoregulatory control is suggested to be due to nonthermal factors thought to be associated with blood pressure regulation (12,16-19,25,37).
The primary evidence for the disturbance in postexercise thermoregulation has been based on the rapid reduction in local measurements of heat loss responses. Local sweat rates of the forearm (4,20,25,37,39), forehead (15), upper back (13,16,19,25), and chest (2,38,39) using the ventilated capsule techniques have been used to indicate changes in evaporation. Such measurements reflect changes in localized sudomotor activity only, and if these reductions are counterbalanced by increased sweat rate at other sites of the body, postexercise whole-body evaporative heat loss may not be compromised. As such, a rapid reduction in whole-body evaporative heat loss during postexercise recovery has not yet been proven. Similarly, skin blood flow to local areas such as the forearm, the chest (23,37,39), and the thigh (19,37) has been used to indicate changes in thermal conductivity. In addition, skin blood flow has been used as an index of dry heat loss postexercise, although a rapid reduction in whole-body dry heat loss after exercise has also not yet been proven.
In order for any measure of core temperature to be maintained at a steady state value corresponding to a set-point level, the difference between the rates of net production and the net heat loss must be zero. 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 (27) or temporal dissociation (34). If thermal inertia is indeed greater during exercise than recovery as suggested by previous observations of a rapid decline in heat loss responses (12-14,16,17,19,25,30,37), the change in body heat content (ΔHb) accumulated during exercise will cause a prolonged elevation in postexercise core temperature. The magnitude of ΔHb during postexercise recovery has only ever been estimated using correlate estimations of core, skin, and muscle temperature. Although these data may provide an insight into regional tissue heat distribution, such measurements have been recently demonstrated to be a poor indicator of changes in ΔHb (9,10). The magnitude of residual whole-body heat storage associated with these local temperature elevations during postexercise recovery is therefore not known.
It is generally accepted that the only way to accurately estimate the rates of whole-body evaporative and dry heat loss as well as ΔHb in humans is by performing simultaneous minute-by-minute measurements of the individual heat balance components by whole-body calorimetry (32). As such, the rate of metabolic heat production is measured by respiratory gas analysis under constant extracorporal ambient conditions, whereas the rate of net heat loss from the body is determined from the direct measurement of the rates of sensible (radiation, conduction, and convection) and insensible (evaporation from sweating and respiration) heat loss using a direct calorimeter. Therefore, the aim of the present study was to determine the rates of whole-body evaporative and dry heat loss as well as the change in ΔHb during 60 min of moderate intensity exercise followed by 60 min of postexercise recovery under constant ambient conditions of negative heat absorption. It was hypothesized that a rapid reduction in whole-body evaporative and dry heat loss would occur during postexercise recovery. It was further hypothesized that the rate of decay of whole-body heat loss (evaporative + dry) during recovery would be faster relative to the rate of increase in whole-body heat loss after the onset of exercise, resulting in a residual elevation in ΔHb at the end of recovery as well as sustained elevations in core and muscle tissue temperatures.
After approval of the experimental protocol from the University of Ottawa Research Ethics Committee and obtaining written informed consent, eight healthy, nonsmoking, normotensive participants (six males, two females) volunteered for the study. Mean characteristics of these participants were as follows: age = 28 yr (SD 10), height = 1.73 m (SD 0.10), weight = 74.8 kg (SD 18.5), body fat = 19.3% (SD 7.2), body surface area = 1.88 m2 (SD 0.28), and peak oxygen consumption (V˙O2peak) 47.2 mL·kg−1·min−1 (SD 6.6).
All participants undertook two separate testing sessions. On the first day, an incremental cycle ergometer V˙O2peak test was performed. On the second day, the calorimetry experimental protocol was performed. 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 go 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 significant 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, sports bra (for women), and athletic shoes).
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 in the region bounded by the left ventricle and the aorta corresponding to the level of the eighth and the ninth thoracic vertebrae (26). 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 sphincter. Aural canal temperature (Tau) was measured using a tympanic thermocouple probe (Mon-a-therm Tympanic; Mallinckrodt Medical) placed in the aural canal until resting against the tympanic membrane, after which it was withdrawn slightly. The tympanic probe was held in position and isolated from the external environment with cotton and ear protectors. Skin temperature was measured at 12 points over the body surface using 0.3-mm-diameter T-type (copper-constantan) thermocouples integrated into heat-flow sensors (Concept Engineering, Old Saybrook, CT). Thermocouples were attached using surgical tape (Blenderm; 3M, St Paul, MN). Mean skin temperature (T¯sk) was calculated using the 12 skin temperatures weighted to the regional proportions as determined by Hardy and DuBois (8): 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; Physitemp Instruments Inc., Clifton, NJ; time constant of 0.1 s) inserted into the vastus lateralis (Tvl), triceps brachii (Ttb), and upper trapezius (Tut). Using aseptic technique, the skin, the subcutaneous tissue, and the 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 (2.5 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 tothe skin with sterile, waterproof dressing (17,19). The implant site for the vastus lateralis 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 (17,19). The triceps brachii muscle temperature 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 (17,19). The upper trapezius muscle temperature probe was inserted 3 cm superior tothe center point between the acromion process and the superior angle of the scapula.
All temperature data were collected using an HP Agilent data acquisition module (Model 3497A) at a sampling rate of 15 s. Data were simultaneously displayed and recorded in spreadsheet format on a personal computer (IBM ThinkCentre M50) with LabVIEW software (Version 7.0; National Instruments, TX).
The net rate of metabolic heat production (metabolic rate minus external work rate; M˙ − W˙) was measured by indirect calorimetry and cycle ergometry. The rates of evaporative (H˙E) and dry (H˙D) heat exchange of the body with the environment was measured by direct calorimetry. The rate of net heat loss (H˙L) was calculated every minuteusing the sum of H˙E and H˙D. The rate of body heat storage (S˙) was subsequently calculated every minute by subtracting H˙L from (M˙ − W˙), and the total change in ΔHb from the onset of exercise was calculated using the following equation:
The measurement technique was identical with that described in a previous publication (9). In summary, indirect calorimetry used the open circuit technique using expired gas samples drawn from a 6-L fluted mixing box yielding an error of ± 0.25% for rate of metabolic heat production. Expired gas was analyzed using electrochemical gas analyzers (AMETEK Models S-3A/1 and CD 3A; Applied Electrochemistry, Pittsburgh, PA) calibrated before each trial using gas mixtures of 4% CO2, 17% O2, and balance N2. The turbine ventilometer was calibrated using a3-L syringe. A modified Snellen whole-body air calorimeter was used for the purpose of measuring whole-body changes in evaporative and dry heat loss, yielding an error of ±2.3 W for the measurement of rate of net heatloss. The calorimeter was previously calibrated for rateof dry heat loss using a humanoid manikin heat source made of constant power zone heater cable (5.905 kΩ·m−1; Easy Heat ZH8-1CBR, New Castle, IN) and for rate of evaporative heat loss using a precision tubing pump (Cole-Palmer, Masterflex 7550-30, Pump head 77200-50) delivering 5 mL·min−1 (± 0.01 mL·min−1) of water to a heated 1200-W hot plate. A modified constant workload eddy current cycle ergometer located outside the calorimeter and mechanically connected to pedals within the calorimeter provided the measurement for W˙. Hygrometric response time of the calorimeter was <20 s, giving a low overall thermal inertia under the present conditions where evaporation is the primary avenue of heat loss. A full technical description of the fundamental principles and performance characteristics of the Snellen calorimeter is available (28).
After instrumentation, the participant entered the calorimeter regulated to an ambient air temperature of 30.0 ± 0.1°C and 30 ± 5% relative humidity. The participant, seated in the semirecumbent position, rested for a 45-min habituation period until a steady state baseline resting condition was achieved. Subsequently, the participant cycled at 70 W of external work for 60 min followed by 60 min of stationary recovery while remaining in the semirecumbent position inside the calorimeter.
The observed rate of net heat loss (H˙L) for each individual was best fit by a least-squares monoexponential model during 60 min of exercise and 60 min of postexercise recovery as follows:
where H˙L(t) is the rate of total body 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 the end of postexercise recovery; amplitude is the difference between H˙L at the onset and end of exercise (for a 60-min exercise) and between the end of exercise and end of recovery (for a 60-min recovery); and τ is the time constant of the observed exponential growth (exercise) or decay (recovery).
A one-way repeated-measures ANOVA was used to analyze the postexercise recovery data using the repeated factor of time (levels: preexercise rest and 0, 2, 5, 10, 15, 30, 45, and 60 min of recovery). The dependent variables used were M˙ − W˙, H˙L, H˙E, H˙D, Tre, Tes, Tau, T¯sk, Ttb and Tut. In the event of a main effect of time, paired t-tests were used to compare values at each postexercise time point to preexercise resting values. The changes in ΔHb from preexercise rest to end-exercise and from end-exercise to end-recovery were compared using a paired t-test. The level of significance was set at 0.05, and alpha level was adjusted during multiple comparisons so as to maintain the rate of Type I error at 5% during the Bonferroni post hoc analysis (P ≤ 0.05n−1, where n = number of comparisons). All analyses were performed using the statistical software package SPSS 15.0 for Windows (SPSS Inc., Chicago, IL).
The change in ΔHb during exercise and recovery is illustrated by the shaded gray area in Figure 1A. At the end of 60 min of exercise, ΔHb was +273 kJ (SD57). The ΔHb that dissipated the during 60-min recovery was only 144 kJ (SD 34), significantly less than the heat stored during exercise (P < 0.001). At the end of recovery, residual body heat storage relative to the start of exercise was +129 kJ (SD 58). In other words, only 53.0% (SD 17.3) of the heat stored during the 60-min exercise was dissipated during the 60-min recovery.
The mean simultaneous rates of net heat production (M˙ − W˙) and net heat loss (H˙L) and the resultant difference between these two rates (S˙) throughout pre-exercise rest, 60min of exercise and 60 min of postexercise recovery, are given in Figures 1A and B. After the start of exercise, M˙− W˙ increased immediately and was not initially offset by H˙L, thus giving a pronounced increase in S˙ during the early stages of exercise. As exercise progressed, H˙L increased exponentially, primarily due to changes in the rate of evaporative heat loss (H˙E) (Fig. 2) with S˙ approaching zero by the end of the 60-min exercise bout. Immediately after exercise stopped, M˙ − W˙ reduced rapidly, returning to levels not significantly different from preexercise rest (P> 0.05) after 10 min of recovery. At the same time, H˙L also reduced rapidly during the early stages of postexercise recovery returning to levels not significantly different from preexercise rest (P > 0.05) after 45 min of recovery. Again, S˙ approached zero by the end of 60-min recovery. Postexercise changes in H˙L were again predominantly influenced by changes in H˙E (Fig. 2). Relative to the total elevation in H˙E at the end of 60 min of exercise, 78.8% (SD 10.8) of this value remained after 2 min of postexercise recovery, 46.4% (SD 10.9) after 5 min of recovery, and 22.9% (SD 6.9) after 10 min of recovery. H˙E was not significantly different from preexercise rest (P > 0.05) after 30 min of recovery. At the end of 60-min postexercise recovery, only 3.2% (SD 3.6) of the end-exercise elevation in H˙E remained. During postexercise recovery, there was a slight transient rise in H˙D, with a small (+9.2 W) elevation of H˙D observed after 60 min of recovery in comparison to preexercise rest. No significant differences were observed for H˙D. In summary, changes in net heat loss throughout were dominated by changes in evaporation, and evaporation reduced rapidly during postexercise recovery. In addition, the difference in the rates between net heat production and net heat loss approached zero at the end of both the 60-min exercise and the 60-min recovery.
The change in H˙L with time was accurately described by an exponential growth function during the 60-min exercise period and by an exponential decay function during the 60-min postexercise recovery period. Mean adjusted R2 was 0.97 (SD 0.01) for the exercise H˙E data and 0.94 (SD 0.04) for the postexercise recovery H˙L data (P ≤ 0.001 for each adjusted R2 value). For the two separate exponential models, individual values for H˙L_0 (exercise), H˙L_END (recovery), amplitude, and τ are given in Table 1. The amplitude of increase in H˙L from preexercise rest to end-exercise was not significantly different from the amplitude of decrease in H˙L from end-exercise to end-postexercise recovery (P > 0.05). However, the τ of the exponential growth of H˙L during exercise was significantly greater than the τ of the exponential decay of H˙L during postexercise recovery (P = 0.012). In summary, the time taken for a balance in the rates between net heat production and net heat loss during exercise was significantly longer than during recovery.
At the end of the 60-min exercise, Teswas elevated by 0.79°C (SD 0.48), Tre was elevated by 0.67°C (SD 0.36), Tau was elevated by 0.83°C (SD 0.53), and T¯sk was elevated by 0.47°C (SD 0.22). All indices of core temperature remained significantly greater than preexercise rest throughout recovery, with elevations of 0.19°C (SD 0.12), 0.20°C (SD 0.09), and 0.18°C (SD 0.11) observed for Tes (P = 0.006), Tre (P < 0.001), and Tau (P=0.010), respectively, after the 60-min postexercise (Fig. 3A). T¯sk was no longer significantly above pre-exercise levels after 15 min of recovery (P > 0.05; Fig. 3A).
After 60 min of exercise, Tvl was elevated by 2.43°C (SD0.60), Ttb was elevated by 2.20°C (SD 0.64), and Tut was elevated by 0.80°C (SD 0.20). Relative to preexercise rest, significant elevations of 1.00 (SD 0.43) and 0.92°C (SD 0.46) were evident after the 60-min postexercise recovery for Tvl and Ttb, respectively, whereas Tut only remained significantly elevated for 30 min of recovery (Fig. 3B).
The purpose of the present study was to determine the rates of whole-body evaporative and dry heat loss as well as the change in ΔHb using whole-body direct calorimetry during 60 min of moderate intensity exercise followed by 60 min of postexercise recovery while concurrently measuring core body and muscle temperatures. The findings confirm that whole-body heat dissipation rapidly reduces during the early stages of postexercise recovery despite sustained elevations in core and muscle temperatures. The reduction in postexercise net heat loss at an ambient air temperature of 30°C was predominantly due to rapid changes in the rate of whole-body evaporative heat loss with only ∼20% of the evaporation at end-exercise observed after 10 min of recovery. Meanwhile, metabolic heat production returned to preexercise resting levels within 10 min of recovery. By the end of the 60-min recovery, only 53% of the heat stored during exercise was dissipated.
Time course of dynamic heat balance during exercise and recovery.
By definition, the amount of heat stored in the body (i.e., change in ΔHb, the gray-shaded area in Fig. 1A) is the accumulative difference in the rates between metabolic heat production and whole-body net heat loss (H˙L) by combined evaporative (from sweat and respiration) and dry (conduction or convection and radiation) heat exchange. Heat production was instantly elevated after the onset of exercise (Fig. 1A) due to the liberation of energy supplying the demands of the working muscle groups. Because exercise intensity remained constant and there were no observable reductions in mechanical efficiency, heat production also remained constant throughout the 60-min exercise bout. In parallel, H˙L increased exponentially with a time constant (τ) of 11.7 min (SD 2.9), which is similar to the τ value of ∼10 min previously reported (24,33). Although heat production was no longer elevated above preexercise baseline resting values after 10 min of recovery, the decline in heat production after the cessation of exercise was slower than the increase observed after the onset of exercise. Despite this, the time taken for H˙L to decrease by ∼63% of the total reduction of H˙L seen during recovery (7.2 min) was significantly shorter than the time taken for an increase of H˙L of the same amount during exercise (τ = 11.7 min). As a consequence, only 53% of the exercise-induced increase in body heat content had dissipated after the 60-min recovery. The relative contribution of the slower postexercise reduction in metabolic heat production to the observed residual ΔHb was therefore approximately 9% or one-sixth of the relative effects of the rapid postexercise reduction in H˙L.
Distribution of residual heat storage in the body.
Heat and temperature tend to vary dependently in any system, and for a body of constant mass and specific heat, temperature is the measured variable (1). Therefore, the local tissue measurements in our study provide an insight into the distribution of residual body heat storage seen during postexercise recovery. Sustained elevations in all tissue temperatures were evident at the end of the 60-min recovery (Figs. 3A and B). However, active (vastus lateralis) and inactive (triceps brachii) muscle temperatures (Fig. 3B) showed greater elevations (∼1.0°C) relative to preexercise rest than all core temperature measurements (∼0.2°C) (Fig. 3A). Generally speaking, the body "core" is the collective tissues occupying the deep visceral or splanchnic region. In a typical person at rest, ∼30% of total body mass is visceral "core" mass (35), whereas ∼40% is muscle mass (31). During exercise, a large proportion of blood, which constitutes approximately two-thirds of visceral mass at rest, is redistributed to the skin and the working muscles (11,29). During postexercise recovery, a significant portion of this blood remains pooled in previously active musculature (19). Collectively, these facts suggest that tissue mass of the muscles is much greater than that of the body "core". Because the average specific heat of muscle (3.639 kJ·kg−1·K−1) (6) is comparable to that of visceral "core" mass (3.724 kJ·kg−1·K−1) (40), a disproportionate amount of residual ΔHb after 60-min recovery appears to be stored in muscle mass (elevated by∼1.0°C) relative to the body "core" mass (elevated by∼0.2°C).
Core temperature set-point control theory (7) states that elevations of skin blood flow and sweating proportional to elevations in core temperature should occur via a hypothalamic negative feedback loop to maintain an enhanced rate of dry and evaporative heat loss. However, despite a persistent elevation in core body temperature, whole-body evaporative heat loss (H˙E) reduced rapidly in the early stages of recovery, which was also accompanied by minimal rates of dry heat loss (H˙D). This apparent perturbation in postexercise thermoregulatory control has been previously ascribed to nonthermal factors thought to be associated with a postexercise hypotension response (12,16-19,23,37). Some adjustments to the controlled "passive system" (i.e., the physical human body and the heat transfer phenomena occurring in it and at its surface (5)) will occur after exercise primarily due to changes in blood flow distribution. However, it is believed that the primary adjustment occurs in the controlling "active system (36)" such that the core temperature at onset of local sweating and cutaneous vasodilation is elevated (16,21,22). Future research is necessary to investigate the influence of specific nonthermal factors such as baroreceptor, mechanoreceptor, and metaboreceptor activity on the rate of whole-body heat loss and residual body heat storage during postexercise recovery.
Previous studies have only ever demonstrated postexercise reductions in local sudomotor and vasomotor activity of specific body regions (12-14,16,17,19,25,30,37). For the first time, we clearly show that despite a persistent elevation in core body temperature whole-body net heat loss (H˙L) reduced rapidly in the early stages of recovery. Under the environmental conditions tested (T = 30°C, RH = 30%), whole-body evaporation of sweat was by far the most dominant avenue for heat dissipation during exercise and recovery. Although dry heat loss was minimal throughout due to the small gradient between T¯sk and ambient air temperature, the pronounced postexercise reduction in local skin blood flow previously demonstrated (12-14,16,17,19,25,30,37) likely reduced core-to-skin thermal conductivity and contributed to the rapid postexercise reduction observed in H˙E. Under environmental conditions giving a more pronounced gradient between T¯sk and ambient air temperature, rapid postexercise reductions in skin blood flow would likely impair dry heat loss during recovery. However, further work is required to demonstrate this effect at different ambient temperatures.
After 60 min of cycling at a moderate exercise intensity, whole-body heat dissipation was rapidly reduced after the end of exercise despite residual elevations in all core temperature measurements. After 10 min of recovery, whole-body evaporative heat loss reduced to almost ∼20% of the evaporation measured at the end of exercise, with minimal changes in whole-body dry heat loss. Relative to the exercise period, the decay of whole-body heat dissipation was approximately 1.6 times faster during recovery. Consequently, only 53% of the heat stored during 60 min of exercise was dissipated after 60 min of recovery. Muscle temperatures indicate a high per unit-mass residual heat storage in active and inactive muscle with vastus lateralis and triceps brachii temperatures elevated by 1.0 and 0.8°C, respectively, after 60 min of recovery. The present findings confirm the rapid reduction in postexercise heat loss that may be due to a nonthermal modulation of the thermal control of sweating and skin blood flow.
This research was supported by the Natural Sciences and Engineering Research Council (RGPIN-298159-2004, grant held by Dr. Glen Kenny) and the US Army Medical Research and Material Command's Office of the Congressionally Directed Medical Research Programs (DAMD17-02-2-0063, funding support held by Dr. Glen Kenny). The provision of financial support does not in any way infer or imply endorsement of the research findings by either agency. Dr. Glen Kenny was supported by a University of Ottawa Research Chair Award. The results of the present study do not constitute endorsement by ACSM.
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Keywords:©2008The American College of Sports Medicine
HEAT BALANCE; CALORIMETRY; HEAT PRODUCTION; HEAT STRESS; THERMOREGULATION