Jonathan E. Wingo

Skin blood flow and local temperature independently modify sweat rate during passive heat stress in humans

Sweat rate (SR) is reduced in locally cooled skin, which may result from decreased temperature and/or parallel reductions in skin blood flow. The purpose of this study was to test the hypotheses that decreased skin blood flow and decreased local temperature each independently attenuate sweating. In protocols I and II, eight subjects rested supine while wearing a water-perfused suit for the control of whole body skin and internal temperatures. While 34°C water perfused the suit, four microdialysis membranes were placed in posterior forearm skin not covered by the suit to manipulate skin blood flow using vasoactive agents. Each site was instrumented for control of local temperature and measurement of local SR (capacitance hygrometry) and skin blood flow (laser-Doppler flowmetry). In protocol I, two sites received norepinephrine to reduce skin blood flow, while two sites received Ringer solution (control). All sites were maintained at 34°C. In protocol II, all sites received 28 mM sodium nitroprusside to equalize skin blood flow between sites before local cooling to 20°C (2 sites) or maintenance at 34°C (2 sites). In both protocols, individuals were then passively heated to increase core temperature ~1°C. Both decreased skin blood flow and decreased local temperature attenuated the slope of the SR to mean body temperature relationship (2.0 ± 1.2 vs. 1.0 ± 0.7 mg·cm(-2)·min(-1)·°C(-1) for the effect of decreased skin blood flow, P = 0.01; 1.2 ± 0.9 vs. 0.07 ± 0.05 mg·cm(-2)·min(-1)·°C(-1) for the effect of decreased local temperature, P = 0.02). Furthermore, local cooling delayed the onset of sweating (mean body temperature of 37.5 ± 0.4 vs. 37.6 ± 0.4°C, P = 0.03). These data demonstrate that local cooling attenuates sweating by independent effects of decreased skin blood flow and decreased local skin temperature.

Acute volume expansion preserves orthostatic tolerance during whole-body heat stress in humans.

Whole‐body heat stress reduces orthostatic tolerance via a yet to be identified mechanism(s). The reduction in central blood volume that accompanies heat stress may contribute to this phenomenon. The purpose of this study was to test the hypothesis that acute volume expansion prior to the application of an orthostatic challenge attenuates heat stress‐induced reductions in orthostatic tolerance. In seven normotensive subjects (age, 40 ± 10 years: mean ±s.d.), orthostatic tolerance was assessed using graded lower‐body negative pressure (LBNP) until the onset of symptoms associated with ensuing syncope. Orthostatic tolerance (expressed in cumulative stress index units, CSI) was determined on each of 3 days, with each day having a unique experimental condition: normothermia, whole‐body heating, and whole‐body heating + acute volume expansion. For the whole‐body heating + acute volume expansion experimental day, dextran 40 was rapidly infused prior to LBNP sufficient to return central venous pressure to pre‐heat stress values. Whole‐body heat stress alone reduced orthostatic tolerance by ∼80% compared to normothermia (938 ± 152 versus 182 ± 57 CSI; mean ±s.e.m., P < 0.001). Acute volume expansion during whole‐body heating completely ameliorated the heat stress‐induced reduction in orthostatic tolerance (1110 ± 69 CSI, P < 0.001). Although heat stress results in many cardiovascular and neural responses that directionally challenge blood pressure regulation, reduced central blood volume appears to be an underlying mechanism responsible for impaired orthostatic tolerance in the heat‐stressed human.

Cardiovascular Drift Is Related to Reduced Maximal Oxygen Uptake during Heat Stress

INTRODUCTION/PURPOSE This study investigated whether the progressive rise in heart rate (HR) and fall in stroke volume (SV) during prolonged, constant-rate, moderate-intensity exercise (cardiovascular drift, CVdrift) in a hot environment is associated with a reduction in VO(2max). METHODS CVdrift was measured in nine male cyclists between 15 and 45 min of cycling at 60% VO(2max) in 35 degrees C that was immediately followed by measurement of VO(2max). VO(2max) also was measured after 15 min of cycling on a separate day, so that any change in VO(2max) between 15 and 45 min could be associated with the CVdrift that occurred during that time interval. This protocol was performed under one condition in which fluid was ingested and there was no significant body weight change (0.3 +/- 0.4%), and under another in which no fluid was ingested and dehydration occurred (2.5 +/- 1%, P < 0.05). RESULTS Fluid ingestion did not affect CVdrift or change in VO(2max). A 12% increase in HR (151 +/- 9 vs 169 +/- 10 bpm, P < 0.05) and 16% decrease in SV (120 +/- 12 vs 101 +/- 10 mL.beat(-1), P < 0.05) between 15 and 45 min was accompanied by a 19% decrease in VO(2max) (4.4 +/- 0.6 vs 3.6 +/- 0.4 L.min(-1), P < 0.05) despite attainment of a higher maximal HR (P < 0.05) at 45 min (194 +/- 5 bpm) vs 15 min (191 +/- 5 bpm). Submaximal VO(2) increased only slightly over time, but VO(2max) increased from 63 +/- 5% at 15 min to 78 +/- 8% at 45 min (P < 0.05). CONCLUSION We conclude CVdrift during 45 min of exercise in the heat is associated with decreased VO(2max) and increased relative metabolic intensity. The results support the validity of using changes in HR to reflect changes in relative metabolic intensity during prolonged exercise in a hot environment in which CVdrift occurs.

Cerebrovascular responsiveness to steady-state changes in end-tidal CO2 during passive heat stress

This study tested the hypothesis that passive heat stress alters cerebrovascular responsiveness to steady-state changes in end-tidal CO(2) (Pet(CO(2))). Nine healthy subjects (4 men and 5 women), each dressed in a water-perfused suit, underwent normoxic hypocapnic hyperventilation (decrease Pet(CO(2)) approximately 20 Torr) and normoxic hypercapnic (increase in Pet(CO(2)) approximately 9 Torr) challenges under normothermic and passive heat stress conditions. The slope of the relationship between calculated cerebrovascular conductance (CBVC; middle cerebral artery blood velocity/mean arterial blood pressure) and Pet(CO(2)) was used to evaluate cerebrovascular CO(2) responsiveness. Passive heat stress increased core temperature (1.1 +/- 0.2 degrees C, P < 0.001) and reduced middle cerebral artery blood velocity by 8 +/- 8 cm/s (P = 0.01), reduced CBVC by 0.09 +/- 0.09 CBVC units (P = 0.02), and decreased Pet(CO(2)) by 3 +/- 4 Torr (P = 0.07), while mean arterial blood pressure was well maintained (P = 0.36). The slope of the CBVC-Pet(CO(2)) relationship to the hypocapnic challenge was not different between normothermia and heat stress conditions (0.009 +/- 0.006 vs. 0.009 +/- 0.004 CBVC units/Torr, P = 0.63). Similarly, in response to the hypercapnic challenge, the slope of the CBVC-Pet(CO(2)) relationship was not different between normothermia and heat stress conditions (0.028 +/- 0.020 vs. 0.023 +/- 0.008 CBVC units/Torr, P = 0.31). These results indicate that cerebrovascular CO(2) responsiveness, to the prescribed steady-state changes in Pet(CO(2)), is unchanged during passive heat stress.

Sympathetic nerve activity and whole body heat stress in humans.

We and others have shown that moderate passive whole body heating (i.e., increased internal temperature ∼0.7°C) increases muscle (MSNA) and skin sympathetic nerve activity (SSNA). It is unknown, however, if MSNA and/or SSNA continue to increase with more severe passive whole body heating or whether these responses plateau following moderate heating. The aim of this investigation was to test the hypothesis that MSNA and SSNA continue to increase from a moderate to a more severe heat stress. Thirteen subjects, dressed in a water-perfused suit, underwent at least one passive heat stress that increased internal temperature ∼1.3°C, while either MSNA (n = 8) or SSNA (n = 8) was continuously recorded. Heat stress significantly increased mean skin temperature (Δ∼5°C, P < 0.001), internal temperature (Δ∼1.3°C, P < 0.001), mean body temperature (Δ∼2.0°C, P < 0.001), heart rate (Δ∼40 beats/min, P < 0.001), and cutaneous vascular conductance [Δ∼1.1 arbitrary units (AU)/mmHg, P < 0.001]. Mean arterial blood pressure was well maintained (P = 0.52). Relative to baseline, MSNA increased midway through heat stress (Δ core temperature 0.63 ± 0.01°C) when expressed as burst frequency (26 ± 14 to 45 ± 16 bursts/min, P = 0.001), burst incidence (39 ± 13 to 48 ± 14 bursts/100 cardiac cyles, P = 0.03), or total activity (317 ± 170 to 489 ± 150 units/min, P = 0.02) and continued to increase until the end of heat stress (burst frequency: 61 ± 15 bursts/min, P = 0.01; burst incidence: 56 ± 11 bursts/100 cardiac cyles, P = 0.04; total activity: 648 ± 158 units/min, P = 0.01) relative to the mid-heating stage. Similarly, SSNA (total activity) increased midway through the heat stress (normothermia; 1,486 ± 472 to mid heat stress 6,467 ± 5,256 units/min, P = 0.03) and continued to increase until the end of heat stress (11,217 ± 6,684 units/min, P = 0.002 vs. mid-heat stress). These results indicate that both MSNA and SSNA continue to increase as internal temperature is elevated above previously reported values.

Consensus recommendations on training and competing in the heat

Exercising in the heat induces thermoregulatory and other physiological strain that can lead to impairments in endurance exercise capacity. The purpose of this consensus statement is to provide up‐to‐date recommendations to optimize performance during sporting activities undertaken in hot ambient conditions. The most important intervention one can adopt to reduce physiological strain and optimize performance is to heat acclimatize. Heat acclimatization should comprise repeated exercise‐heat exposures over 1–2 weeks. In addition, athletes should initiate competition and training in a euhydrated state and minimize dehydration during exercise. Following the development of commercial cooling systems (e.g., cooling vest), athletes can implement cooling strategies to facilitate heat loss or increase heat storage capacity before training or competing in the heat. Moreover, event organizers should plan for large shaded areas, along with cooling and rehydration facilities, and schedule events in accordance with minimizing the health risks of athletes, especially in mass participation events and during the first hot days of the year. Following the recent examples of the 2008 Olympics and the 2014 FIFA World Cup, sport governing bodies should consider allowing additional (or longer) recovery periods between and during events for hydration and body cooling opportunities when competitions are held in the heat.

Dynamic cerebral autoregulation during passive heat stress in humans

This study tested the hypothesis that passive heating impairs cerebral autoregulation. Transfer function analyses of resting arterial blood pressure and middle cerebral artery blood velocity (MCA V(mean)), as well as MCA V(mean) and blood pressure responses to rapid deflation of previously inflated thigh cuffs, were examined in nine healthy subjects under normothermic and passive heat stress (increase core temperature 1.1 +/- 0.2 degrees C, P < 0.001) conditions. Passive heating reduced MCA V(mean) [change (Delta) of 8 +/- 8 cm/s, P = 0.01], while blood pressure was maintained (Delta -1 +/- 4 mmHg, P = 0.36). Coherence was decreased in the very-low-frequency range during heat stress (0.57 +/- 0.13 to 0.26 +/- 0.10, P = 0.001), but was >0.5 and similar between normothermia and heat stress in the low- (0.07-0.20 Hz, P = 0.40) and high-frequency (0.20-0.35 Hz, P = 0.12) ranges. Transfer gain was reduced during heat stress in the very-low-frequency (0.88 +/- 0.38 to 0.59 +/- 0.19 cm.s(-1).mmHg(-1), P = 0.02) range, but was unaffected in the low- and high-frequency ranges. The magnitude of the decrease in blood pressure (normothermia: 20 +/- 4 mmHg, heat stress: 19 +/- 6 mmHg, P = 0.88) and MCA V(mean) (13 +/- 4 to 12 +/- 6 cm/s, P = 0.59) in response to cuff deflation was not affected by the thermal condition. Similarly, the rate of regulation of cerebrovascular conductance (CBVC) after cuff release (0.44 +/- 0.22 to 0.38 +/- 0.13 DeltaCBVC units/s, P = 0.16) and the time for MCA V(mean) to recover to precuff deflation baseline (10.0 +/- 7.9 to 8.7 +/- 4.9 s, P = 0.77) were not affected by heat stress. Counter to the proposed hypothesis, similar rate of regulation responses suggests that heat stress does not impair the ability to control cerebral perfusion after a rapid reduction in perfusion pressure, while reduced transfer function gain and coherence in the very-low-frequency range during heat stress suggest that dynamic cerebral autoregulation is improved during spontaneous oscillations in blood pressure within this frequency range.

Effect of Ambient Temperature on Cardiovascular Drift and Maximal Oxygen Uptake

PURPOSE This study tested the hypothesis that the magnitude of cardiovascular (CV) drift and decrease in maximal oxygen uptake (V[spacing dot above]O2max) would be greater at 35 degrees C than at 22 degrees C. METHODS The increase in HR and decrease in stroke volume (SV) between 15 and 45 min of cycling at 59.2 +/- 1.9% V[spacing dot above]O2max (CV drift) was measured in hot (HEAT, 35 degrees C) and cool (COOL, 22 degrees C) ambient temperatures in 10 endurance-trained men (age = 23 +/- 3 yr, V[spacing dot above]O2max = 64.7 +/- 8.7 mL.kg.min). V[spacing dot above]O2max was measured immediately after the 45 min of cycling and again under both ambient temperature conditions on separate days after 15 min of cycling. This design permitted assessment of V[spacing dot above]O2max between the same time points that CV drift occurred. Fluid to replace sweat losses was provided during all trials. RESULTS CV drift and the associated decrease in V[spacing dot above]O2max was greater (P < 0.05) in HEAT versus COOL. HR increased 11% (P < 0.05), SV decreased 11% (P < 0.05), and V[spacing dot above]O2max fell 15% (P < 0.05) between 15 and 45 min in HEAT, whereas HR and SV changed less (+2% and -2% for HR and SV, respectively, P < 0.05), and there was no significant decrease in V[spacing dot above]O2max (5%, P > 0.05) between 15 and 45 min in COOL. CONCLUSION These data demonstrate the magnitude of CV drift during prolonged submaximal exercise, and the accompanying decrease in V[spacing dot above]O2max measured immediately thereafter is greater in a hot than in a cool environment.

Effects of heat stress on dynamic cerebral autoregulation during large fluctuations in arterial blood pressure

Impaired cerebral autoregulation during marked reductions in arterial blood pressure may contribute to heat stress-induced orthostatic intolerance. This study tested the hypothesis that passive heat stress attenuates dynamic cerebral autoregulation during pronounced swings in arterial blood pressure. Mean arterial blood pressure (MAP) and middle cerebral artery blood velocity were continuously recorded for approximately 6 min during normothermia and heat stress (core body temperature = 36.9 +/- 0.1 degrees C and 38.0 +/- 0.1 degrees C, respectively, P < 0.001) in nine healthy individuals. Swings in MAP were induced by 70-mmHg oscillatory lower body negative pressure (OLBNP) during normothermia and at a sufficient lower body negative pressure to cause similar swings in MAP during heat stress. OLBNP was applied at a very low frequency ( approximately 0.03 Hz, i.e., 15 s on-15 s off) and a low frequency ( approximately 0.1 Hz, i.e., 5 s on-5 s off). For each thermal condition, transfer gain, phase, and coherence function were calculated at both frequencies of OLBNP. During very low-frequency OLBNP, transfer function gain was reduced by heat stress (0.55 +/- 0.20 and 0.31 +/- 0.07 cm x s(-1) x mmHg(-1) during normothermia and heat stress, respectively, P = 0.02), which is reflective of improved cerebrovascular autoregulation. During low-frequency OLBNP, transfer function gain was similar between thermal conditions (1.19 +/- 0.53 and 1.01 +/- 0.20 cm x s(-1) x mmHg(-1) during normothermia and heat stress, respectively, P = 0.32). Estimates of phase and coherence were similar between thermal conditions at both frequencies of OLBNP. Contrary to our hypothesis, dynamic cerebral autoregulation during large swings in arterial blood pressure during very low-frequency (i.e., 0.03 Hz) OLBNP is improved during heat stress, but it is unchanged during low-frequency (i.e., 0.1 Hz) OLBNP.

Cardiovascular drift during heat stress: implications for exercise prescription.

Cardiovascular drift, the progressive increase in heart rate and decrease in stroke volume that begins after approximately 10 min of prolonged moderate-intensity exercise, is associated with decreased maximal oxygen uptake, particularly during heat stress. Consequently, the increased heart rate reflects an increased relative metabolic intensity during prolonged exercise in the heat when cardiovascular drift occurs, which has implications for exercise prescription.