Influence of nonthermal baroreceptor modulation of heat loss responses during uncompensable heat stress

Abstract

We evaluated the hypothesis that with increasing levels of hyperthermia, thermal influences would predominate over nonthermal baroreceptor control of cutaneous vascular conductance (CVC) and local sweat rate (LSR). On separate days, eight male participants were positioned in either an upright seated posture (URS) or a 15 degrees head-down tilt (HDT) posture in a thermoneutral condition and during passive heating, until mean body temperature (T(body)) increased by 1.5 degrees C. Hemodynamic [heart rate (HR), cardiac output, mean arterial pressure (MAP)] and thermal responses [T(re), CVC, LSR] were measured continuously. MAP showed a gradual decrease in the early- to mid-stages of heating for both HDT and URS. At a T(body) > 0.6 degrees C, MAP achieved a stable, albeit reduced level from baseline resting for the duration of the heating, whereas MAP decreased significantly throughout the heating period in the URS position (p < 0.001). CVC increased rapidly in the early stages of heating and achieved a stable elevated level in both HDT and URS at the mid-stage of heating (T(body) increase <or= 0.45 degrees C) for the duration of the heating period (i.e., to a T(body) increase of 1.5 degrees C). A similar pattern of response was observed in LSR. A rapid increase in LSR was observed in the early- to mid-stages of heating (T(body) increase <or= 0.75 degrees C), followed by a slower increase until the end of heating. Responses were similar between conditions. We conclude that despite a significant nonthermal drive, as evidenced by a significant difference in MAP between conditions in the late stages of heating, the thermoeffector activity governing CVC and LSR responses are primarily modulated by thermal input.

Responses to hyperthermia. Optimizing heat dissipation by convection and evaporation: Neural control of skin blood flow and sweating in humans

“…Similarly, multiple studies involving a range of techniques designed to elicit baroreflex unloading, including passive heat stress coupled with lower body negative pressure, head up tilt, or infusion of pharmacological agents, have demonstrated no effect on sweating rates during passive heat stress. Kenny et al (2010) observed no difference in sweating or cutaneous blood flow during upright seated versus 15° head-down tilt during passive heating, confirming earlier results. Similarly, Schlader et al (2015) observed an attenuated vasodilation with cardiopulmonary and arterial baroreceptor unloading, but no effect on sweating rate during passive heat stress.…”

Hyperthermia modifies muscle metaboreceptor and baroreceptor modulation of heat loss in humans

“…Previous studies suggested that the contribution of nonthermal factors to modulation of heat loss responses is attenuated with progressive increases in hyperthermia (7,16,17). Specifically, Kondo et al (17) demonstrated that increases in sweat rate during IHG exercise became significantly attenuated with moderate increases in core temperature (ϳ0.3°C).…”

“…Furthermore, SkBF was not measured during this study; as such, there remains a critical gap in our understanding of the role of baroreflex activity on SkBF during post-IHG exercise ischemia. Finally, a number of studies suggest that the relative influence of nonthermal factors in modulating thermoefferent activity can change as a function of the level of hyperthermia (7,16,17). For example, Kondo et al.…”

“…Previous research has established that changes in baroreflex activity alone, induced by postural (e.g., head-down tilt) or mechanical [lower body positive pressure (LBPP)/lower body negative pressure (LBNP)] challenges, can influence skin blood flow (SkBF) (14,15,21,37) and sweating (11,14,16,22). It is plausible, therefore, that the measured reduction of cutaneous vascular conductance and concomitant increases in sweating during the post-IHG exercise period of ischemia may be influenced not only by metaboreflex activity, but also by baroreflex activity or a combination of both reflexes.…”

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

“…Owing to instances of hypotension following volume depletion, body posture was adjusted from an upright seated position to a supine posture (note that seven total subjects were tested, with four seated in the upright position and three supine). Although postural differences with heat stress influence baroreflex control of SkBF (Lind et al 1968), it should be noted that: (i) all analyses were performed within subject, with the position of a given subject consistent between all three trials; (ii) perturbations that unload baroreceptors do not appear to alter thermoregulatory sweat rate (Wilson et al 2005;Kenny et al 2010;Lynn et al 2012); (iii) comparisons within posture still revealed no effect of treatment on P crit for core temperature, metabolic rate, whole-body sweat rate, LSR mean and T sk ; and (iv) the slightly higher P crit for core temperature in the upright seated position (CON, 5.2 ± 0.1 kPa; DEH, 5.0 ± 0.2 kPa; and SAL, 5.2 ± 0.1 kPa; n = 4) compared with the supine posture (CON, 4.9 ± 0.4 kPa; DEH, 4.9 ± 0.1 kPa; and SAL, 5.1 ± 0.1 kPa; n = 3) can be explained by the greater effective skin area from which heat loss could occur while seated.…”