Matthew N. Cramer

Large differences in peak oxygen uptake do not independently alter changes in core temperature and sweating during exercise.

The independent influence of peak oxygen uptake (Vo(₂ peak)) on changes in thermoregulatory responses during exercise in a neutral climate has not been previously isolated because of complex interactions between Vo(₂ peak), metabolic heat production (H(prod)), body mass, and body surface area (BSA). It was hypothesized that Vo(₂ peak) does not independently alter changes in core temperature and sweating during exercise. Fourteen males, 7 high (HI) Vo(₂ peak): 60.1 ± 4.5 ml·kg⁻¹·min⁻¹; 7 low (LO) Vo(₂ peak): 40.3 ± 2.9 ml·kg⁻¹·min⁻¹ matched for body mass (HI: 78.2 ± 6.1 kg; LO: 78.7 ± 7.1 kg) and BSA (HI: 1.97 ± 0.08 m²; LO: 1.94 ± 0.08 m²), cycled for 60-min at 1) a fixed heat production (FHP trial) and 2) a relative exercise intensity of 60% Vo(₂ peak) (REL trial) at 24.8 ± 0.6°C, 26 ± 10% RH. In the FHP trial, H(prod) was similar between the HI (542 ± 38 W, 7.0 ± 0.6 W/kg or 275 ± 25 W/m²) and LO (535 ± 39 W, 6.9 ± 0.9 W/kg or 277 ± 29 W/m²) groups, while changes in rectal (T(re): HI: 0.87 ± 0.15°C, LO: 0.87 ± 0.18°C, P = 1.00) and aural canal (T(au): HI: 0.70 ± 0.12°C, LO: 0.74 ± 0.21°C, P = 0.65) temperature, whole-body sweat loss (WBSL) (HI: 434 ± 80 ml, LO: 440 ± 41 ml; P = 0.86), and steady-state local sweating (LSR(back)) (P = 0.40) were all similar despite relative exercise intensity being different (HI: 39.7 ± 4.2%, LO: 57.6 ± 8.0% Vo(2 peak); P = 0.001). At 60% Vo(2 peak), H(prod) was greater in the HI (834 ± 77 W, 10.7 ± 1.3 W/kg or 423 ± 44 W/m²) compared with LO (600 ± 90 W, 7.7 ± 1.4 W/kg or 310 ± 50 W/m²) group (all P < 0.001), as were changes in T(re) (HI: 1.43 ± 0.28°C, LO: 0.89 ± 0.19°C; P = 0.001) and T(au) (HI: 1.11 ± 0.21°C, LO: 0.66 ± 0.14°C; P < 0.001), and WBSL between 0 and 15, 15 and 30, 30 and 45, and 45 and 60 min (all P < 0.01), and LSR(back) (P = 0.02). The absolute esophageal temperature (T(es)) onset for sudomotor activity was ∼0.3°C lower (P < 0.05) in the HI group, but the change in T(es) from preexercise values before sweating onset was similar between groups. Sudomotor thermosensitivity during exercise were similar in both FHP (P = 0.22) and REL (P = 0.77) trials. In conclusion, changes in core temperature and sweating during exercise in a neutral climate are determined by H(prod), mass, and BSA, not Vo(₂ peak).

Selecting the correct exercise intensity for unbiased comparisons of thermoregulatory responses between groups of different mass and surface area

We assessed whether comparisons of thermoregulatory responses between groups unmatched for body mass and surface area (BSA) should be performed using a metabolic heat production (prod) in Watts or Watts per kilogram for changes in rectal temperature (ΔTre), and an evaporative heat balance requirement (Ereq) in Watts or Watts per square meter for local sweat rates (LSR). Two groups with vastly different mass and BSA [large (LG): 91.5 ± 6.8 kg, 2.12 ± 0.09 m(2), n = 8; small (SM): 67.6 ± 5.6 kg, 1.80 ± 0.09 m(2), n = 8; P < 0.001], but matched for heat acclimation status, sex, age, and with the same onset threshold esophageal temperatures (LG: +0.37 ± 0.12°C; SM: +0.41 ± 0.17°C; P = 0.364) and thermosensitivities (LG: 1.02 ± 0.54, SM: 1.00 ± 0.38 mg·cm(-2)·min(-1)·°C(-1); P = 0.918) for sweating, cycled for 60 min in 25°C at different levels of prod (500 W, 600 W, 6.5 W/kg, 9.0 W/kg) and Ereq (340 W, 400 W, 165 W/m(2), 190 W/m(2)). ΔTre was different between groups at a prod of 500 W (LG: 0.52 ± 0.15°C, SM: 0.92 ± 0.24°C; P < 0.001) and 600 W (LG: 0.78 ± 0.19°C, SM: 1.14 ± 0.24°C; P = 0.007), but similar at 6.5 W/kg (LG: 0.79 ± 0.21°C, SM: 0.85 ± 0.14°C; P = 0.433) and 9.0 W/kg (LG: 1.02 ± 0.22°C, SM: 1.14 ± 0.24°C; P = 0.303). Furthermore, ΔTre was the same at 9.0 W/kg in a 35°C environment (LG: 1.12 ± 0.30°C, SM: 1.14 ± 0.25°C) as at 25°C (P > 0.230). End-exercise LSR was different at Ereq of 400 W (LG: 0.41 ± 0.18, SM: 0.57 ± 0.13 mg·cm(-2)·min(-1); P = 0.043) with a trend toward higher LSR in SM at 340 W (LG: 0.28 ± 0.06, SM: 0.37 ± 0.15 mg·cm(-2)·min(-1); P = 0.057), but similar at 165 W/m(2) (LG: 0.28 ± 0.06, SM: 0.28 ± 0.12 mg·cm(-2)·min(-1); P = 0.988) and 190 W/m(2) (LG: 0.41 ± 0.18, SM: 0.37 ± 0.15 mg·cm(-2)·min(-1); P = 0.902). In conclusion, when comparing groups unmatched for mass and BSA, future experiments can avoid systematic differences in ΔTre and LSR by using a fixed prod in Watts per kilogram and Ereq in Watts per square meter, respectively.

Local sweating on the forehead, but not forearm, is influenced by aerobic fitness independently of heat balance requirements during exercise

The present study investigated the influence of maximal oxygen uptake ( ) on local steady‐state sudomotor responses to exercise, independently of evaporative requirements for heat balance (Ereq). Eleven fit (F; 61.9 ± 6.0 ml kg−1 min−1) and 10 unfit men (UF; 40.4 ± 3.8 ml kg−1 min−1) cycled for 60 min at an air temperature of 24.5 ± 0.8°C and ambient humidity of 0.9 ± 0.3 kPa at a set metabolic heat production per unit surface area, producing the same Ereq in all participants (BAL trial) and, in a second trial, at 60% of . During the BAL trial, absolute power (F 107 ± 2 and UF 102 ± 2 W; P= 0.126), Ereq (F 175 ± 5 and UF 176 ± 9 W m−2; P= 0.855), steady‐state whole‐body sweat rate (F 0.44 ± 0.02 and UF 0.47 ± 0.02 mg cm−2 min−1; P= 0.385) and local sweat rate on the arm (F 0.29 ± 0.03 and UF 0.35 ± 0.03 mg cm−2 min−1; P= 0.129) were not different between groups; however, local sweat rate on the forehead in UF (1.67 ± 0.20 mg cm−2 min−1) was almost double (P= 0.002) that of F (0.87 ± 0.11 mg cm−2 min−1). Heart rate, ratings of perceived exertion and relative exercise intensity were also significantly greater in UF (P < 0.05). There was a trend towards an elevated minute ventilation in UF (P= 0.052), while end‐tidal was significantly lower in UF (P= 0.028). At 60% , absolute power (F 174 ± 6 and UF 110 ± 5 W; P < 0.001), Ereq (F 291 ± 14 and UF 190 ± 17 W m−2; P < 0.001), steady‐state whole‐body sweat rate (F 0.84 ± 0.05 and UF 0.53 ± 0.03 mg cm−2 min−1; P < 0.001) and local sweat rate on the arm (F 0.75 ± 0.04 and UF 0.35 ± 0.03 mg cm−2 min−1; P < 0.001) and on the forehead (F 2.92 ± 0.42 and UF 1.68 ± 0.23 mg cm−2 min−1; P= 0.022) were all significantly greater in F compared with UF. Heart rate and ratings of perceived exertion were similar at all time points (P > 0.05). Significantly greater minute ventilation (P < 0.001) and end‐tidal responses (P= 0.017) were found in F. In conclusion, aerobic fitness alters local sweating on the forehead, but not the forearm, independently of evaporative requirements for heat balance, and may be the result of differential control of sweating in these skin areas associated with the relative intensity of exercise.

Biophysical aspects of human thermoregulation during heat stress.

Humans maintain a relatively constant core temperature through the dynamic balance between endogenous heat production and heat dissipation to the surrounding environment. In response to metabolic or environmental disturbances to heat balance, the autonomic nervous system initiates cutaneous vasodilation and eccrine sweating to facilitate higher rates of dry (primarily convection and radiation) and evaporative transfer from the body surface; however, absolute heat losses are ultimately governed by the properties of the skin and the environment. Over the duration of a heat exposure, the cumulative imbalance between heat production and heat dissipation leads to body heat storage, but the consequent change in core temperature, which has implications for health and safety in occupational and athletic settings particularly among certain clinical populations, involves a complex interaction between changes in body heat content and the bodys morphological characteristics (mass, surface area, and tissue composition) that collectively determine the bodys thermal inertia. The aim of this review is to highlight the biophysical aspects of human core temperature regulation by outlining the principles of human energy exchange and examining the influence of body morphology during exercise and environmental heat stress. An understanding of the biophysical factors influencing core temperature will enable researchers and practitioners to better identify and treat individuals/populations most vulnerable to heat illness and injury during exercise and extreme heat events. Further, appropriate guidelines may be developed to optimize health, safety, and work performance during heat stress.

Explained variance in the thermoregulatory responses to exercise: the independent roles of biophysical and fitness/fatness-related factors

Individual variation in the thermoregulatory responses to exercise is notoriously large. Although aerobic fitness (V̇o2 max) and body fatness are traditionally considered important predictors of individual core temperature and sweating responses, recent evidence indicates potentially important and independent roles for biophysical factors. Using stepwise regression, we examined the proportion of individual variability in rectal temperature changes (ΔTre), whole body sweat loss (WBSL), and steady-state local sweat rate (LSRss) independently described by 1) biophysical factors associated with metabolic heat production (Hprod) and evaporative heat balance requirements (Ereq) relative to body size and 2) factors independently related to V̇o2 max and body fatness. In a total of 69 trials, 28 males of wide-ranging morphological traits and V̇o2 max values cycled at workloads corresponding to a range of absolute Hprod (410-898 W) and relative intensities (32.2-82.0% V̇o2 max) for 60 min in 24.8 ± 0.7°C and 33.4 ± 12.2% relative humidity. Hprod (in W/kg total body mass) alone described ∼50% of the variability in ΔTre (adjusted to r(2) = 0.496; P < 0.001), whereas surface area-to-mass ratio and body fat percentage (BF%) explained an additional 4.3 and 2.3% of variability, respectively. For WBSL, Ereq (in W) alone explained ∼71% of variance (adjusted to r(2) = 0.713, P < 0.001), and the inclusion of BF% explained an additional 1.3%. Similarly, Ereq (in W/m(2)) correlated significantly with LSRss (adjusted to r(2) = 0.603, P < 0.001), whereas %V̇o2 max described an additional ∼4% of total variance. In conclusion, biophysical parameters related to Hprod, Ereq, and body size explain 54-71% of the individual variability in ΔTre, WBSL, and LSRss, and only 1-4% of additional variance is explained by factors related to fitness or fatness.

Should electric fans be used during a heat wave

Heat waves continue to claim lives, with the elderly and poor at greatest risk. A simple and cost-effective intervention is an electric fan, but public health agencies warn against their use despite no evidence refuting their efficacy in heat waves. A conceptual human heat balance model can be used to estimate the evaporative requirement for heat balance, the potential for evaporative heat loss from the skin, and the predicted sweat rate, with and without an electrical fan during heat wave conditions. Using criteria defined by the literature, it is clear that fans increase the predicted critical environmental limits for both the physiological compensation of endogenous/exogenous heat, and the onset of cardiovascular strain by an air temperature of ∼3-4 °C, irrespective of relative humidity (RH) for the young and elderly. Even above these critical limits, fans would apparently still provide marginal benefits at air temperatures as high as 51.1 °C at 10%RH for young adults and 48.1 °C at 10%RH for the elderly. Previous concerns that dehydration would be exacerbated with fan use do not seem likely, except under very hot (>40 °C) and dry (<10%RH) conditions, when predicted sweat losses are only greater with fans by a minor amount (∼20-30 mL/h). Relative to the peak outdoor environmental conditions reported during ten of the most severe heat waves in recent history, fan use would be advisable in all of these situations, even when reducing the predicted maximum sweat output for the elderly. The protective benefit of fans appears to be underestimated by current guidelines.

Acute limb heating improves macro- and microvascular dilator function in the leg of aged humans

Local heating of an extremity increases blood flow and vascular shear stress throughout the arterial tree. Local heating acutely improves macrovascular dilator function in the upper limbs of young healthy adults through a shear stress-dependent mechanism but has no such effect in the lower limbs of this age group. The effect of acute limb heating on dilator function within the atherosclerotic prone vasculature of the lower limbs of aged adults is unknown. Therefore, the purpose of this study was to test the hypothesis that acute lower limb heating improves macro- and microvascular dilator function within the leg vasculature of aged adults. Nine young and nine aged adults immersed their lower limbs at a depth of ~33 cm into a heated (~42°C) circulated water bath for 45 min. Before and 30 min after heating, macro (flow-mediated dilation)- and microvascular (reactive hyperemia) dilator functions were assessed in the lower limb, following 5 min of arterial occlusion, via Doppler ultrasound. Compared with preheat, macrovascular dilator function was unchanged following heating in young adults (P = 0.6) but was improved in aged adults (P = 0.04). Similarly, microvascular dilator function, as assessed by peak reactive hyperemia, was unchanged following heating in young adults (P = 0.1) but was improved in aged adults (P < 0.01). Taken together, these data suggest that acute lower limb heating improves both macro- and microvascular dilator function in an age dependent manner. NEW & NOTEWORTHY We demonstrate that lower limb heating acutely improves macro- and microvascular dilator function within the atherosclerotic prone vasculature of the leg in aged adults. These findings provide evidence for a potential therapeutic use of chronic lower limb heating to improve vascular health in primary aging and various disease conditions.

A comparison between the technical absorbent and ventilated capsule methods for measuring local sweat rate

This study assessed the accuracy of the technical absorbent (TA) method for measuring local sweat rate (LSR) relative to the well-established ventilated capsule (VC) method during steady-state and nonsteady-state sweating using large and small sample surface areas on the forearm and midback. Forty participants (38 males and two females) cycled at 60% peak oxygen consumption for 75 min in either a temperate [22.3 ± 0.9°C, 32 ± 17% relative humidity (RH)] or warm (32.5 ± 0.8°C, 29 ± 7% RH) environment. Simultaneous bilateral comparisons of 5-min LSR measurements using the TA and VC methods were performed for the back and forearm after 10, 30, 50, and 70 min. LSR values, measured using the TA method, were highly correlated with the VC method at all time points, irrespective of sample surface area and body region (all P < 0.001). On average, ≈ 79% of the variability observed in LSR measured with the VC method was described by the TA method. The mean difference in absolute LSR using the TA method (TA-VC with 95% confidence intervals) was -0.23 [-0.30,-0.16], -0.11 [-0.21,0.00], -0.03 [-0.14,+0.08], and +0.02 [-0.07,+0.11] mg · cm(-2) · min(-1) after 10, 30, 50, and 70 min of exercise, respectively. Duplicate LSR measurements within each method during steady-state sweating were highly correlated (TA: r = 0.96, P < 0.001, n = 20; VC: r = 0.97, P < 0.001, n = 20) with a mean bias of +0.07 ± 0.14 and +0.01 ± 0.10 mg · cm(-2) · min(-1) for TA and VC methods, respectively. The mean smallest detectable difference in LSR was 0.12 and 0.05 mg · min(-1) · cm(-2) for TA and VC methods, respectively. These data support the TA method as a reliable alternative for measuring the rate of sweat appearance on the skin surface.

Compensatory hyperhidrosis following thoracic sympathectomy: A biophysical rationale

A side-effect of endoscopic thoracic sympathectomy (ETS) is compensatory hyperhidrosis (CH), characterized by excessive sweating from skin areas with intact sudomotor function. The physiological mechanism of CH is unknown, but may represent an augmented local sweat rate from skin areas with uninterrupted sympathetic innervation based on evaporative heat balance requirements. For a given combination of activity and climate, the same absolute amount of evaporation (if any) is needed to balance the rate of metabolic heat production both pre- and post-ETS. However, the rate of local sweating per unit of skin surface area with intact sudomotor activity must be greater post-ETS as evaporation must be derived from a smaller skin surface area. Under conditions with high evaporative requirements, greater degradations in sweating efficiency associated with an increased dripping of sweat should also occur post-ETS, further pronouncing the sweat rate required for heat balance. In conclusion, in addition to the potential role of psychological stimuli for increased sudomotor activity, the existence of CH post-ETS can be described by the interplay between fundamental thermoregulatory physiology and altered heat balance biophysics and does not require a postoperative alteration in physiological control.

Comments on point:counterpoint: humans do/do not demonstrate selective brain cooling during hyperthermia.

TO THE EDITOR: Middle cerebral artery blood velocity (MCAVmean) is reduced up to 30% in humans following a passive increase in internal temperature of 1–1.5°C (1). If the diameter of the MCA remains unchanged during heat stress, reductions in MCAVmean are proportional to reductions in cerebral blood flow. In support of selective brain cooling in hyperthermic humans, White et al. (7) suggest that vasodilation of the cerebral vasculature exists, which in turn increases cranial perfusion and maintains the arterial-venous temperature difference. The authors state, “it remains to be explained how MCA velocity, and presumably cranial perfusion, is reduced in hyperthermic humans if mean arterial blood pressure is maintained and MCA caliber remains constant” (4, 7). This argument ignores the potent effects of changes in carbon dioxide partial pressures on cerebral perfusion, with hypercapnia increasing and hypocapnia decreasing cerebral blood flow, respectively (6). During moderate to pronounced passive heat stress, arterial and end-tidal carbon dioxide partial pressures decrease upward to 8 Torr (1, 2). Importantly, an 8-Torr reduction in arterial carbon dioxide partial pressure is estimated to reduce cerebral blood flow by 24% (5) through increases in resistance of the cerebral arterioles “downstream” from the MCA (3). Thus the clear and robust reduction in MCAVmean during passive heat stress is likely due primarily to decreases in carbon dioxide partial pressures causing increases in vascular resistance of cerebral arterioles distal to the MCA.