Revisiting the influence of individual factors on heat exchange during exercise in dry heat using direct calorimetry.

NEW FINDINGS: What is the central question of this study? The aim was to identify the greatest contributor(s) to the variation in whole-body heat exchange, as assessed using direct calorimetry, among young men and women with heterogeneous characteristics during exercise at increasing metabolic heat production rates in dry heat. What is the main finding and its importance? The evaporative heat loss requirement, body morphology and aerobic fitness made the greatest contributions to the individual variation in evaporative and dry heat exchange, with the variance explained being exercise intensity dependent. These findings provide a foundation on which to build our ability to explain the individual variation in heat exchange during exercise-induced heat stress. ABSTRACT: Numerous individual factors (e.g. fitness, sex, body morphology) are known to independently modulate heat exchange during exercise in the heat. However, in our view, the individual factor(s) making the greatest contribution to the variation in heat exchange among men and women remains poorly understood, despite several studies. We therefore sought to revisit this question by assessing whole-body dry and evaporative heat exchange using direct calorimetry in a heterogeneous sample of 100 young men (n = 57) and women (n = 43). Participants performed three 30 min bouts of cycling at very light (men/women; 300/250 W), light (400/325 W) and moderate (500/400 W) metabolic heat production rates, separated by a 15 min recovery, in dry heat (40°C, ∼12% relative humidity). Positive associations were observed between the evaporative heat loss requirement (metabolic heat production ± dry heat exchange) and evaporative heat loss (all P < 0.01), especially during moderate exercise (men, r = 0.62; women, r = 0.82), which explained 19-67% of individual variation. Peak aerobic power (in millilitres per kilogram per minute) was also positively related to evaporative heat loss in both sexes, albeit only during light and moderate exercise (r = 0.33-0.43; all P < 0.05), explaining a further 5-9% of individual variation. Dry heat exchange shared negative associations with body mass and surface area during all exercise bouts in both sexes (r = -0.29 to -0.55; all P < 0.05), explaining 9-30% of individual variation. We therefore demonstrate that the evaporative heat loss requirement, peak aerobic power and body morphology are the greatest contributors to the variation in whole-body heat exchange among young men and women exercising in dry heat, with the strength of those relationships being heat-load dependent.

Self-reported physical activity level does not alter whole-body total heat loss independently of aerobic fitness in young adults during exercise in the heat.

We evaluated whether self-reported physical activity (PA) level modulates whole-body total heat loss (WB-THL) as assessed using direct calorimetry in 10 young adults (aged 22 ± 3 years) matched for rate of peak oxygen consumption (an index for aerobic fitness), but of low and high self-reported PA, during 3 incremental cycling bouts (∼39%, 52%, and 64% peak oxygen consumption) in the heat (40 °C). We showed that level of self-reported PA does not appear to influence WB-THL independently of peak oxygen consumption.

Postexercise whole-body sweating increases during muscle metaboreceptor activation in young men.

We assessed the effect of metaboreceptor activation on whole-body evaporative heat loss (WB-EHL) in 12 men (aged 24 ± 4 years) in the early-to-late stages of a 60-min exercise recovery in the heat. Metaboreceptor activation induced by 1-min isometric-handgrip (IHG) exercise followed by 5-min forearm ischemia to trap metabolites increased WB-EHL by 25%-31% and 26%-34% during the ischemic period relative to IHG-only and control (natural recovery only), respectively, throughout recovery. We show that metaboreceptor activation enhances WB-EHL in recovery.

Fitness-related differences in the rate of whole-body evaporative heat loss in exercising men are heat-load dependent.

NEW FINDINGS: What is the central question of this study? Aerobic fitness modulates heat loss, but the heat-load threshold at which fitness-related differences in heat loss occur in young healthy men remains unclear. What is the main finding and its importance? We demonstrate using direct calorimetry that aerobic fitness modulates heat loss in a heat-load-dependent manner, with fitness-related differences occurring between young men who have low and high fitness when the heat load is ∼≥500 W. Although aerobic fitness has been known for some time to modulate heat loss, our findings define the precise heat-load threshold at which fitness-related differences occur. The effect of aerobic fitness (defined as rate of peak oxygen consumption) on heat loss during exercise is thought to be related to the level of heat stress. However, it remains unclear at what combined exercise and environmental (net) heat-load threshold these fitness-related differences occur. To identify this, we assessed whole-body heat exchange (dry and evaporative) by direct calorimetry in young (22 ± 3 years) men matched for physical characteristics with low (Low-fit; 39.8 ± 2.5 ml O2  kg-1  min-1 ), moderate (Mod-fit; 50.9 ± 1.2 ml O2  kg-1  min-1 ) and high aerobic fitness (High-fit; 62.0 ± 4.4 ml O2  kg-1  min-1 ; each n = 8), during three 30 min bouts of cycling in dry heat (40°C, 12% relative humidity) at increasing rates of metabolic heat production of 300 (Ex1), 400 (Ex2) and 500 W (Ex3), each followed by a 15 min recovery period. Each group was exposed to a similar net heat load (metabolic plus ∼100 W dry heat gain; P = 0.83) during each exercise bout [∼400 (Ex1), ∼500 (Ex2) and ∼600 W (Ex3); P < 0.01]. Although evaporative heat loss was similar between groups during Ex1 (P = 0.33), evaporative heat loss was greater in the High-fit (Ex2, 466 ± 21 W; Ex3, 557 ± 26 W) compared with the Low-fit group (Ex2, 439 ± 22 W; Ex3, 511 ± 20 W) during Ex2 and Ex3 (P ≤ 0.03). Conversely, evaporative heat loss for the Mod-fit group did not differ from either the High-fit or Low-fit group during all exercise bouts (P ≥ 0.09). We demonstrate that aerobic fitness modulates heat loss in a heat-load-dependent manner, such that young, highly fit men display greater heat-loss capacity only at heat loads ∼≥500 W compared with their lesser trained counterparts.

Fitness-related differences in the rate of whole-body total heat loss in exercising young healthy women are heat-load dependent.

NEW FINDINGS: What is the central question of this study? Aerobic fitness modulates heat loss, albeit the heat load at which fitness-related differences occur in young healthy women remains unclear. What is the main finding and its importance? We demonstrate using direct calorimetry that fitness modulates heat loss in a heat-load dependent manner, with differences occurring between young women of low and high fitness and matched physical characteristics when the metabolic heat load is at least 400 W in hot, dry conditions. Although fitness has been known for some time to modulate heat loss, our findings define the metabolic heat load at which fitness-related differences occur. ABSTRACT: Aerobic fitness has recently been shown to alter heat loss capacity in a heat-load dependent manner in young men. However, given that sex-related differences in heat loss capacity exist, it is unclear whether this response is consistent in women. We therefore assessed whole-body total heat loss in young (21 ± 3 years old) healthy women matched for physical characteristics, but with low (low-fit; 35.8 ± 4.5 ml O2  kg-1  min-1 ) or high aerobic fitness (high-fit; 53.1 ± 5.1 ml O2  kg-1  min-1 ; both n = 8; indexed by peak oxygen consumption), during three 30 min bouts of cycling performed at increasing rates of metabolic heat production of 250 (Ex1), 325 (Ex2) and 400 W (Ex3), each separated by a 15 min recovery, in hot, dry conditions (40°C, 11% relative humidity). Whole-body total heat loss (evaporative ± dry heat exchange) and metabolic heat production were measured using direct and indirect calorimetry, respectively. Body heat content was measured as the temporal summation of heat production and loss. Total heat loss did not differ during Ex1 (low-fit, 215 ± 16 W; high-fit, 231 ± 20 W; P > 0.05) and Ex2 (low-fit, 278 ± 15 W; high-fit, 301 ± 20 W; P > 0.05), but was lower in the low-fit (316 ± 21 W) compared with the high-fit women (359 ± 32 W) during Ex3 (P < 0.01). Consequently, the low-fit group stored 1.3-fold more heat (429 ± 61 kJ) throughout the three exercise bouts relative to the high-fit group (330 ± 113 kJ; P < 0.05). We show that aerobic fitness independently modulates heat loss capacity during exercise in hot, dry conditions in women separated by a peak oxygen consumption of ∼17 ml O2  kg-1  min-1 starting at a metabolic heat load of 400 W.

The recommended Threshold Limit Values for heat exposure fail to maintain body core temperature within safe limits in older working adults.

PURPOSE: The American Conference of Governmental and Industrial Hygienists (ACGIH®) Threshold Limit Values (TLV® guidelines) for work in the heat consist of work-rest (WR) allocations designed to ensure a stable core temperature that does not exceed 38°C. However, the TLV® guidelines have not been validated in older workers. This is an important shortcoming given that adults as young as 40 years demonstrate impairments in their ability to dissipate heat. We therefore evaluated body temperature responses in older adults during work performed in accordance to the TLV® recommended guidelines. METHODS: On three occasions, 9 healthy older (58 ± 5 years) males performed a 120-min work-simulated protocol in accordance with the TLV® guidelines for moderate-to-heavy intensity work (360 W fixed rate of heat production) in different wet-bulb globe temperatures (WBGT). The first was 120 min of continuous (CON) cycling at 28.0°C WBGT (CON[28°C]). The other two protocols were 15-min intermittent work bouts performed with different WR cycles and WBGT: (i) WR of 3:1 at 29.0°C (WR3:1[29°C]) and (ii) WR of 1:1 at 30.0°C (WR1:1[30°C]). Rectal temperature was measured continuously. The rate of change in mean body temperature was determined via thermometry (weighting coefficients: rectal, 0.9; mean skin temperature, 0.1) and direct calorimetry. RESULTS: Rectal temperature exceeded 38°C in all participants in CON[28°C] and WR3:1[29°C] whereas a statistically similar proportion of workers exceeded 38°C in WR1:1[30°C] (χ2; P = 0.32). The average time for rectal temperature to reach 38°C was: CON[28°C], 53 ± 7; WR3:1[29°C], 79 ± 11; and WR1:1[30°C], 100 ± 29 min. Finally, while a stable mean body temperature was not achieved in any work condition as measured by thermometry (i.e., >0°C·min-1; all P<0.01), heat balance as determined by direct calorimetry was achieved in WR3:1[29°C] and WR1:1[30°C] (both P ≥ 0.08). CONCLUSION: Our findings indicate that the TLV® guidelines do not prevent body core temperature from exceeding 38°C in older workers. Furthermore, a stable core temperature was not achieved within safe limits (i.e., ≤38°C) indicating that the TLV® guidelines may not adequately protect all individuals during work in hot conditions.

Temperature of Ingested Water during Exercise Does Not Affect Body Heat Storage.

PURPOSE: The objective of this study was to examine the effect of ingested water temperature on heat balance during exercise as assessed by direct calorimetry. METHODS: Ten healthy males (25 ± 4 yr) cycled at 50% V˙O2peak (equivalent rate of metabolic heat production (M-W) of 523 ± 84 W) for 75 min under thermocomfortable conditions (25°C, 25% relative humidity) while consuming either hot (50°C) or cold (1.5°C) water. Four 3.2 mL·kg⁻¹ boluses of hot or cold water were consumed 5 min before and at 15, 30, and 45 min after the onset of exercise. Total heat loss (HL = evaporative heat loss (HE) ± dry heat exchange (HD)) and M-W were measured by direct and indirect calorimetry, respectively. Change in body heat content (ΔHb) was calculated as the temporal summation of M-W and HL and adjusted for changes in heat transfer from the ingested fluid (Hfluid). RESULTS: The absolute difference for HL (209 ± 81 kJ) was similar to the absolute difference of Hfluid (204 ± 36 kJ) between conditions (P = 0.785). Furthermore, the difference in HL was primarily explained by the corresponding changes in HE (hot: 1538 ± 393 kJ; cold: 1358 ± 330 kJ) because HD was found to be similar between conditions (P = 0.220). Consequently, no difference in ΔHb was observed between the hot (364 ± 152 kJ) and cold (363 ± 134 kJ) conditions (P = 0.971) during exercise. CONCLUSION: We show that ingestion of hot water elicits a greater HL relative to cold water ingestion during exercise. However, this response was only compensated for the heat of the ingested fluid as evidenced by similar ΔHb between conditions. Therefore, our findings indicate that relative to cold water ingestion, consuming hot water does not provide a thermoregulatory advantage. Both hot and cold water ingestion results in the same amount of heat stored during prolonged moderate-intensity exercise.

Adenosine receptor inhibition attenuates the suppression of postexercise cutaneous blood flow.

The time-dependent contributions of active vasodilation (e.g. nitric oxide) and noradrenergic vasoconstriction to the postexercise suppression of cutaneous perfusion despite persistent hyperthermia remain unknown. Moreover, adenosine receptors have been shown to mediate the decrease in cutaneous perfusion following passive heating. We examined the time-dependent modulation of nitric oxide synthase, noradrenergic vasoconstriction and adenosine receptors on postexercise cutaneous perfusion. Eight males performed 15 min of high-intensity (85% VO2 max) cycling followed by 60 min of recovery in temperate ambient conditions (25°C). Four microdialysis probes were inserted into the forearm skin and continuously infused with: (1) lactated Ringer solution (Control); (2) 10 mm N(G)-nitro-l-arginine methyl ester (l-NAME; nitric oxide synthase inhibitor); (3) 10 mm bretylium tosylate (BT; inhibitor of noradrenergic vasoconstriction); or (4) 4 mm theophylline (THEO; adenosine receptor inhibitor). Cutaneous vascular conductance (CVC) was expressed as a percentage of maximum and was calculated as perfusion units (laser Doppler) divided by mean arterial pressure. End-exercise CVC was similar in Control, THEO and BT (P > 0.1), but CVC with l-NAME (39 ± 4%) was lower than Control (59 ± 4%, P < 0.01). At 20 min of recovery, Control CVC (22 ± 3%) returned to baseline levels (19 ± 2%, P = 0.11). Relative to Control, CVC was reduced by l-NAME for the first 10 min of recovery whereas CVC was increased with BT for the first 30 min of recovery (P < 0.03). In contrast, CVC with THEO was elevated throughout the 60 min recovery period (P ≤ 0.01) compared to Control. We show that adenosine receptors appear to have a major role in postexercise cutaneous perfusion whereas nitric oxide synthase and noradrenergic vasoconstriction are involved only earlier during recovery.