Whole-body heating slows carotid baroreflex response in human subjects

Abstract

Heat stress increases sympathetic activity and decreases parasympathetic activity to the heart. To test the hypothesis that carotid baroreflex responses of heart rate (HR) and systemic blood pressure become slowed with altered autonomic nerve activities during whole-body heat stress, we determined changes in HR and mean arterial pressure (MAP) in response to approximately 5 s of 40 mmHg neck pressure (NP) and of -65 mmHg neck suction (NS) in normothermia and during whole-body heating produced by a hot water-perfused suit. The NP and NS stimuli were triggered by R waves of an ECG during held expiration in the supine position. Whole-body heating did not alter the onset time of the HR and MAP responses during NP and NS. Whole-body heating significantly increased the time from onset of the HR response until peak of the response during NP (2.53 +/- 0.33 s in normothermia and 3.46 +/- 0.28 s during heating, P<0.05) and NS (1.20 +/- 0.23 s and 2.24 +/- 0.29 s, P<0.05). Whole-body heating significantly increased the time from onset of the MAP response until peak of the response during NP (4.31+/-0.46 s in normothermia, 6.67 +/- 0.56 s during heating, P<0.05) but not during NS (5.06 +/- 0.47 s and 4.50 +/- 0.60 s). These findings suggest that heat stress prolongs the response time of carotid-cardiac and carotid-vasomotor baroreflexes.

Influence of ageing on carotid baroreflex peak response latency in humans

“…Overall, our findings suggest that older individuals exhibit sluggish cardiovascular responses to simulated carotid hypertension, which may be due, in part, to age-related reductions in resting cardiac parasympathetic tone. Previous work in young subjects has observed delayed carotid-cardiac responses during heat stress (Yamazaki & Sone, 2005) and dynamic exercise (Strange et al 1990;Linnarsson et al 1996;Sundblad & Linnarsson, 1996). These studies suggested that such delays were attributable to the reductions in cardiac parasympathetic nerve activity (Keyl et al 2001) and/or the increases in SNA (Yang et al 1994;Sundblad & Linnarsson, 1996) that are typically elicited by these stimuli (Robinson et al 1966;Mitchell, 1990;Kenney et al 1995;Niimi et al 1997).…”

“…In young healthy individuals, a delay in the latency of the peak cardiac baroreflex response has been reported during both heat stress (Yamazaki & Sone, 2005) and dynamic exercise (Strange et al 1990; Linnarsson et al 1996; Sundblad & Linnarsson, 1996). Although not directly tested in these studies, it was suggested that the mechanism for this prolonged response is the increase in cardiac sympathetic tone (Yang et al 1994; Sundblad & Linnarsson, 1996) and/or reduction in cardiac parasympathetic tone (Keyl et al 2001) that are elicited by these stimuli (Robinson et al 1966; Mitchell, 1990; Kenney et al 1995; Niimi et al 1997).…”

“…Data and statistical analysis A 5 min data segment was used for the calculation of baseline cardiovascular variables and heart rate variability. Reflex changes in HR and mean BP were calculated from pre‐stimulus values and the response plotted on a beat‐to‐beat scale with peak response latency defined as the elapsed time to the peak response beat, as described previously (Potts & Raven, 1995; Yamazaki & Sone, 2005). The time to peak change in HR and mean BP in response to individual trials of NP and NS were averaged for each subject and then combined to provide a group mean.…”

Reliability of Surface Emg Measurements of the Quadriceps During Maximal Isometric Contractions Following Water Immersion

“…Water immersion is commonly used for rehabilitation, 1 therapeutic purposes, 22 passive induction or prevention of hyperthermic 20,23 or hypothermic stress, 21 and more recently as a mode of recovery from exercise. 24 The anomalous properties of water may improve 3 or reduce subsequent muscle functioning, 19 depending upon immersion techniques.…”

Heat stress and orthostatic tolerance

“…The rise suggests that the capacity for a tachycardiac response to the rapid onset of hypotension is reduced and the capacity for a bradycardiac response to sudden hypertension is increased. To address whether the reduced responsiveness of HR to rapid hypotensive stimulation is due to a slowing of the response, Yamazaki et al 60) examined the effect of whole-body heating on the response time of HR and blood pressure following 5 s of neck pressure (NP) at 40 mmHg during supine rest. Whole-body heating increased significantly from the onset of NP until the peak of the tachycardiac response (3.93±0.35 s in normothermia and 5.20±0.24 s during heating), and from the onset of NP until the peak of the blood pressure response (6.75±0.51 s in normothermia and 9.39±0.62 s during heating).…”