It has been proposed that self-paced exercise in the heat is regulated by an anticipatory reduction in work rate based on the rate of heat storage. However, performance may be impaired by the development of hyperthermia and concomitant rise in cardiovascular strain increasing relative exercise intensity. This study evaluated the influence of thermal strain on cardiovascular function and power output during self-paced exercise in the heat. Eight endurance-trained cyclists performed a 40 km simulated time trial in hot (35• C) and thermoneutral conditions (20 • C), while power output, mean arterial pressure, heart rate, oxygen uptake and cardiac output were measured. Time trial duration was 64.3 ± 2.8 min (242.1 W) in the hot condition and 59.8 ± 2.6 min (279.4 W) in the thermoneutral condition (P < 0.01). Power output in the heat was depressed from 20 min onwards compared with exercise in the thermoneutral condition (P < 0.05). Rectal temperature reached 39.8 ± 0.3 (hot) and 38.9 ± 0.2• C (thermoneutral; P < 0.01). From 10 min onwards, mean skin temperature was ∼7.5• C higher in the heat, and skin blood flow was significantly elevated (P < 0.01). Heart rate was ∼8 beats min −1 higher throughout hot exercise, while stroke volume, cardiac output and mean arterial pressure were significantly depressed compared with the thermoneutral condition (P < 0.05). Peak oxygen uptake measured during the final kilometre of exercise at maximal effort reached 77 (hot) and 95% (thermoneutral) of pre-experimental control values (P < 0.01). We conclude that a thermoregulatory-mediated rise in cardiovascular strain is associated with reductions in sustainable power output, peak oxygen uptake and maximal power output during prolonged, intense self-paced exercise in the heat.

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.

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).

No abstract

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.

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.

For thermal physiologists, calorimetry is an important methodological tool to assess human heat balance during heat or cold exposures. A whole body direct calorimeter remains the gold standard instrument for assessing human heat balance; however, this equipment is rarely available to most researchers. A more widely accessible substitute is partitional calorimetry, a method by which all components of the conceptual heat balance equation—metabolic heat production, conduction, radiation, convection, and evaporation—are calculated separately based on fundamental properties of energy exchange. Since partitional calorimetry requires relatively inexpensive equipment (vs. direct calorimetry) and can be used over a wider range of experimental conditions (i.e., different physical activities, laboratory or field settings, clothed or seminude), it allows investigators to address a wide range of problems such as predicting human responses to thermal stress, developing climatic exposure limits and fluid replacement guidelines, estimating clothing properties, evaluating cooling/warming interventions, and identifying potential thermoregulatory dysfunction in unique populations. In this Cores of Reproducibility in Physiology (CORP) review, we summarize the fundamental principles underlying the use of partitional calorimetry, present the various methodological and arithmetic requirements, and provide typical examples of its use. Strategies to minimize estimation error of specific heat balance components, as well as the limitations of the method, are also discussed. The goal of this CORP paper is to present a standardized methodology and thus improve the accuracy and reproducibility of research employing partitional calorimetry.

Two studies were performed to 1) characterize changes in local sweat rate (LSR) following fluid ingestion of different temperatures during exercise, and 2) identify the potential location of thermoreceptors along the gastrointestinal tract that independently modify sudomotor activity. In study 1, 12 men cycled at 50% Vo2peak for 75 min while ingesting 3.2 ml/kg of 1.5°C, 37°C, or 50°C fluid 5 min before exercise; and after 15, 30, and 45-min of exercise. In study 2, 8 men cycled at 50% Vo2peak for 75 min while 3.2 ml/kg of 1.5°C or 50°C fluid was delivered directly into the stomach via a nasogastric tube (NG trials) or was mouth-swilled only (SW trials) after 15, 30, and 45 min of exercise. Rectal (Tre), aural canal (Tau), and mean skin temperature (Tsk); and LSR on the forehead, upper-back, and forearm were measured. In study 1, Tre, Tau, and Tsk were identical between trials, but after each ingestion, LSR was significantly suppressed at all sites with 1.5°C fluid and was elevated with 50°C fluid compared with 37°C fluid (P < 0.001). The peak difference in mean LSR between 1.5°C and 50°C fluid after ingestion was 0.29 ± 0.06 mg·min(-1)·cm(-2). In study 2, LSR was similar between 1.5°C and 50°C fluids with SW trials (P = 0.738), but lower at all sites with 1.5°C fluid in NG trials (P < 0.001) despite no concurrent differences in Tre, Tau, and Tsk. These data demonstrate that 1) LSR is transiently altered by cold and warm fluid ingestion despite similar core and skin temperatures; and 2) thermoreceptors that independently and acutely modulate sudomotor output during fluid ingestion probably reside within the abdominal area, but not the mouth.