Mechanisms producing tachycardia in conscious baboons during environmental heat stress

Abstract

The involvement of changes in sympathetic activity, changes in cardiac efferent vagal activity, and nonautonomic mechanisms in producing the rise in heart rate (HR) during heat stress-induced hyperthermia was studied in seven unanesthetized, chronically instrumented baboons (Papio anubis and P. cynocephalus). The experimental protocol consisted of subjecting the baboon to environmental heating (EH) of sufficient intensity (40-45 degrees C) to raise arterial blood temperature (Tbl) 2-3 degrees C in 1-2 h while in one of four states: 1) normal (control), 2) beta-adrenergic receptor blockade induced by propranolol, 3) cholinergic receptor blockade induced by atropine, and 4) combined beta- and cholinergic receptor blockade induced by propranolol and atropine together. HR rose linearly with Tbl during EH in all four states (correlation coefficient greater than or equal to 0.97 in all cases) with average HR-Tbl regression coefficients (slopes) being 20.5 +/- 1.2 (SE) beats X min-1 . degrees C for the normal state, 12.2 +/- 0.5 beats X min-1 . degrees C-1 for the beta-blockade state, 13.3 +/- 1.1 beats X min-1 . degrees C for the cholinergic blockade state, and 8.4 +/- 0.8 beats X min-1 . degrees C-1 for the combined beta- and cholinergic receptor blockade state. Thus nonautonomic mechanisms account for about 40% of the tachycardia in heat-stressed baboons with the remaining 60% produced by combined vagal withdrawal and sympathetic activation. Furthermore application of a multiplicative model of autonomic control of HR to these data suggests that about 75% of the autonomic component is produced by vagal withdrawal.

Self-paced exercise in hot and cool conditions is associated with the maintenance of %V̇o2peak within a narrow range

“…Accordingly, it has been suggested that the increase in heart rate during sustained constant-load exercise in the heat is only partly related to the reduction in V O 2peak , with the remainder of the increase associated with other factors (2). The greater increase in heart rate is proposed to occur as a result of an elevation in sympathetic nervous activity and vagal withdrawal, as well as via the direct effect of blood temperature on the sinoatrial node (i.e., pacemaker tissue located in the right atrium) (16,21,22). The latter has been shown to produce an increase in heart rate of 7-8 beats·min Ϫ1 ·°C Ϫ1 (14,16,21).…”

“…The greater increase in heart rate is proposed to occur as a result of an elevation in sympathetic nervous activity and vagal withdrawal, as well as via the direct effect of blood temperature on the sinoatrial node (i.e., pacemaker tissue located in the right atrium) (16,21,22). The latter has been shown to produce an increase in heart rate of 7-8 beats·min Ϫ1 ·°C Ϫ1 (14,16,21). Hence, with progressive increases in ambient and concomitantly core temperature, the increase in heart rate during exercise-heat stress may be more pronounced for a given increase in %V O 2peak than in cooler conditions (2).…”

Influences of Skin and Core Temperature on Cardiovascular Responses during Exercise

“…Under these conditions the influence of temperature on heart rate has been determined in living humans, indicating that HR increased with a slope of 7 beats for every 1°C increase in T c [37]. Internal body temperature has been demonstrated to directly impact IHR in baboons [28] with similar results. Gorman et al, determined that 40% of tachycardia, in heat stressed baboons was produced from non-autonomic sources [28,37].…”

“…Gorman et al, determined that 40% of tachycardia, in heat stressed baboons was produced from non-autonomic sources [28,37]. In addition, after beta adrenergic and cholinergic receptor blockade, it was established that HR increased with a slope of 8 beats for every 1°C increase in T c [28].…”

“…As T c increases, blood flow is diverted to the skin to facilitate heat removal from the core [69] and cardiac output (Q) must increase to maintain blood pressure and oxygen delivery to the brain. In addition, elevations in T c can directly increase heart rate (HR) by speeding the firing-rate of action potentials of the sinoatrial node [28], and can increase the force of heart contractions leading to increased stroke volume (SV). High T c has even been proposed as direct cause of fatigue controlled by the CNS in an effort to prevent the body from reaching dangerously high temperatures.…”