Does attenuated skin blood flow lower sweat rate and the critical environmental limit for heat balance during severe heat exposure?

Abstract

What is the central question of this study? Does attenuated skin blood flow diminish sweating and reduce the critical environmental limit for heat balance, which indicates maximal heat loss potential, during severe heat stress? What is the main finding and its importance? Isosmotic hypovolaemia attenuated skin blood flow by ∼20% but did not result in different sweating rates, mean skin temperatures or critical environmental limits for heat balance compared with control and volume-infusion treatments, suggesting that the lower levels of skin blood flow commonly observed in aged and diseased populations may not diminish maximal whole-body heat dissipation. Attenuated skin blood flow (SkBF) is often assumed to impair core temperature (T_c ) regulation. Profound pharmacologically induced reductions in SkBF (∼85%) lead to impaired sweating, but whether the smaller attenuations in SkBF (∼20%) more often associated with ageing and certain diseases lead to decrements in sweating and maximal heat loss potential is unknown. Seven healthy men (28 ± 4 years old) completed a 30 min equilibration period at 41°C and a vapour pressure (P_a ) of 2.57 kPa followed by incremental steps in P_a of 0.17 kPa every 6 min to 5.95 kPa. Differences in heat loss potential were assessed by identifying the critical vapour pressure (P_crit ) at which an upward inflection in T_c occurred. The following three separate treatments elicited changes in plasma volume to achieve three distinct levels of SkBF: control (CON); diuretic-induced isosmotic dehydration to lower SkBF (DEH); and continuous saline infusion to maintain SkBF (SAL). The T_c , mean skin temperature (T_sk ), heart rate, mean laser-Doppler flux (forearm and thigh; LDF_mean ), mean local sweat rate (forearm and thigh; LSR_mean ) and metabolic rate were measured. In DEH, a 14.2 ± 5.7% lower plasma volume resulted in a ∼20% lower LDF_mean in perfusion units (PU) (DEH, 139 ± 23 PU; CON, 176 ± 22 PU; and SAL, 186 ± 22 PU; P = 0.034). However, LSR_mean and whole-body sweat losses were unaffected by treatment throughout (P > 0.482). The P_crit for T_c was similar between treatments (CON, 5.05 ± 0.30 kPa; DEH, 4.93 ± 0.16 kPa; and SAL, 5.12 ± 0.10 kPa; P = 0.166). Furthermore, no differences were observed in the skin-air temperature gradient, metabolic rate or changes in T_c (P > 0.197). In conclusion, a ∼20% reduction in SkBF alters neither sweat rate nor the upper limit for heat loss from the skin during non-encapsulated passive heat stress.

Keywords: core temperature; cutaneous vascular conductance; heat loss potential; heat stress; sweat.

Figure 1

Representative core temperature data from the incremental humidity protocol, demonstrating the determination of acritical ambient vapour pressure (P_crit). After 30-min baseline at 41°C with 2.57 kPa (30%RH), ambient vapour pressure was elevated by 0.17 kPa (~2% RH) every 6 min while air temperature remained fixed. Core temperature stayed relatively stable despite the rising ambient vapour pressure. At P_crit, core temperature inflects and rises rapidly. The value of P_crit is identified as the intersection of the two slopes (Slope 1, pre-inflection; Slope 2, post-inflection), determined via segmental regression analysis.

Figure 2

Laser-Doppler derived skin blood flow responses in a control condition without treatment (CON), following diuretic following diuretic-induced dehydration (DEH), and with continuous saline infusion (SAL). Four indices of skin blood flow are presented: mean absolute laser-Doppler flux (LDF_mean), mean laser-Doppler flux expressed as a percentage of maximum values (%LDF_max), mean cutaneous vascular conductance (CVC_mean), and mean cutaneous vascular conductance expressed as a percentage of maximum values (%CVC_max). Analyses were performed for seven subjects up to ~5 kPa (84 min), after which early termination criteria were met at different times. A significant main effect of treatment was observed for LDF_mean, %LDF_max, and %CVC_max (P < 0.05). A trend towards an effect of treatment on CVC_mean was also observed.

Figure 3

Local sweating and skin temperature responses throughout the incremental humidity protocol in a control condition without treatment (CON), following diuretic-induced dehydration (DEH), and with continuous saline infusion (SAL). LSR_mean, mean local sweat rate (2 sites: forearm, thigh); T_sk, mean skin temperature; P_a, ambient vapour pressure. Analysis was performed up to ~5 kPa (84 min) in seven subjects. Beyond this point, early termination criteria were met at different times. No treatment effect was observed for LSR_mean and T_sk.

Figure 4

The skin-air temperature gradient and the corresponding rate of dry heat exchange throughout the incremental humidity protocol in a control condition without treatment (CON), following diuretic-induced dehydration (DEH), and with continuous saline infusion (SAL). T_sk, mean skin temperature; T_a, ambient temperature; P_a, ambient vapour pressure. Data are for seven subjects. Note that negative values for dry heat exchange indicate dry heat gain. No effect of treatment was observed for T_sk − T_a and dry heat exchange (P > 0.193).

Figure 5

Critical ambient vapour pressures (P_crit) for core temperature in a control condition without treatment (CON), following diuretic-induced dehydration (DEH), and with continuous saline infusion (SAL) for seven subjects. No effect of treatment on P_crit for core temperature was observed (P = 0.166).

Figure 6

Mean arterial pressure (MAP) and heart rate responses during the incremental humidity protocol in a control condition without treatment (CON), following diuretic following diuretic-induced dehydration (DEH), and with continuous saline infusion (SAL). ΔMAP, change in mean arterial pressure from baseline; P_a, ambient vapour pressure. Analyses were performed for seven subjects up to ~5 kPa (84 min), after which early termination criteria were met at different times. A significant main effect of treatment was observed for heart rate, but not ΔMAP.