Central and peripheral contributions to control of heart rate during heat acclimation

Abstract

The contributions of the autonomic nervous system and the cardiac pacing cells in the development of heat-acclimation-induced bradycardia were analyzed, and the effect of heat acclimation on the chronotropic response of the heart to heat stress (40 degrees C) was studied. Rats were acclimated at 34 degrees C for 0, 5, 14, 30 and 60 days. Heart rate (HR) was measured in conscious animals, using chronic subcutaneous electrodes. Sympathetic and parasympathetic influences were studied by IP administration of 0.1 and 1 mg/100 g body weight atropine and propranolol respectively, while intrinsic HR (HRi) was measured following administration of both drugs simultaneously. The effects of carbamylcholine and norepinephrine on the beating rate of isolated rat atria were investigated to study pacemaker responsiveness to neutrotransmitters. Up to day 14 of heat acclimation, bradycardia was attained by tonic parasympathetic acceleration (18%) and temporal sympathetic withdrawal (0.8% on day 14), to compensate for the gradually augmented HRi (2.5% and 8% on days 5 and 14, respectively). Following long-term acclimation HRi declined below pre-acclimation rate. This was associated with resumed sympathetic activity (16% and 10% on days 30 and 60 respectively) while parasympathetic activity continued to be high (18%). Tachycardia, known to occur with severe uncontrolled body hyperthermia, was attenuated following heat acclimation by 42%. It was concluded that during the initial phase of heat acclimation bradycardia is achieved primarily by changes in autonomic influences, while following long-term acclimation, changes in the intrinsic properties of the pacing cells (HRi) and the autonomic system both play a role.

HIF-1α-targeted pathways are activated by heat acclimation and contribute to acclimation-ischemic cross-tolerance in the heart

“…The C group was held at an ambient temperature of 24 Ϯ 1°C; heat acclimation was attained by a continuous exposure to 34 Ϯ 1°C and 30 -40% relative humidity in a light-cycled room (12:12 h) for 30 days (long-term acclimation), as previously described (15). The efficacy of this treatment has been previously validated using the decrease in heart rate as a criterion (18). For characterization of the effects of HS on C and AC rats, the animals were subjected to HS at 41°C for 2 h. During HS, the colonic temperature (T c) was monitored online, using a YL 402 thermistor inserted 6 cm beyond the anal sphincter and attached to a computerized data acquisition system.…”

Relationships of the Cardiac Signal and Heat Acclimated State: Spectral Profiles from ECG Analysis

“…Horowitz and Meiri [7] have previously demonstrated that the decreased HR seen with heat acclimation is in part a function of acceleration of parasympathetic and withdrawal of sympathetic nervous input. In previous work with spectral analysis of HRV, high frequency peaks and the power represented by the area under the curve of the high frequency peak have been used as an indication of parasympathetic activity, and the ratio of low to high frequency power has been used as an indication of sympathetic activity [1,11].…”

“…Although there is individual variability in heat tolerance and ability to acclimate, the following are among the physiological changes generally observed with acclimation in both man [16] and rats [4,6,7,8] There is an increase in plasma volume, tolerance time in the heat, skin blood flow, time interval during which sweating (saliva spreading in rats) can be maintained; there is a decrease in basal heart rate (HR) and HR during heat exposure, core temperature (Tc) during heat exposure, and Tc threshold for sweating (in terms of salivation).…”

“…In anesthetized rats, heart rate increases with increasing Tc, and this modulation is a result of interaction between sympathetic and parasympathetic input [7,15]. This progressive increase in heart rate with increasing Tc results from a combination of increased firing rate of intrinsic cardiac pacemaker cells and the effect of the combination of decreasing parasympathetic and increasing sympathetic input [15].…”

“…The changes in heart rate through the course of acclimation is a dynamic process with early decreases being mediated largely by increased parasympathetic and decreased sympathetic input. Later (beyond 2 weeks) in the course of acclimation, intrinsic heart rate decreases and the role of the autonomic nervous system although still significant may play less of a role in maintaining the bradycardia [7]. Animals subjected to a heat stress test following acclimation have a significantly attenuated tachycardia compared to unacclimated control animals [7,13].…”