Submitted on October 5, 2001
Accepted on June 7, 2003
Change in spontaneous baroreflex control of pulse interval during heat stress in humans
Kichang Lee1, Dwayne N Jackson2, Douglas L Cordero1, Takeshi Nishiyasu2, Jochen K Peters1, and Gary W Mack1*
1 John B. Pierce Laboratory, New Haven, CT, USA; Department of Epidemiology and Public Health, Yale University School of Medicine, New Haven, CT, USA
2 John B. Pierce Laboratory, New Haven, CT, USA
* To whom correspondence should be addressed. E-mail: mack{at}jbpierce.org.
Spontaneous baroreflex control of pulse interval (PI) was assessed in healthy volunteers under thermoneutral condition and followed by heat stress condition in which +20 mmHg of lower body positive pressure (LBPP) was added for 5 minute at the end of each thermal condition to investigate the effect of the peripheral blood pooling. Subjects rested in the supine position while immersing their lower body in the water bath placed inside LBPP chamber with breathing at 0.20 Hz. Arterial blood pressure (automated brachial auscultation and Finapres), PI (EKG), esophageal temperature, skin temperature, and stroke volume were continuously collected and digitized during each experimental stage. Spontaneous baroreflex function was evaluated by multiple techniques to disclose possible changes in baroreflex control of PI during heat stress; 1) the mean slope of the linear relationship between PI and systolic blood pressure (SBP) with 3 or more simultaneous increasing/or decreasing sequences, 2) the linear relationship between changes in PI and SBP (
PI/SBP) derived using the first differential equation, 3) the linear relationship between changes in PI and SBP with simultaneously increasing/ or decreasing (+PI /+SBP or -PI /-SBP), 4) beat-to-beat changes in both SBP and PI when arterial blood pressure was forced to decrease with application of -60 mmHg of lower body negative pressure, and 5) transfer function analysis. Heat stress increased esophageal temperature by 0.6 ± 0.1°C, decreased PI from 1007 ± 43 to 776 ± 37 msec and stroke volume by 16 ± 5 ml.beat-1. Baroreflex control of PI assessed by several different techniques provides consistent evident of a reduction in baroreflex sensitivity during heat stress. Also, heat stress increased the incident of baroreflex from 5.2 ± 0.8 to 8.6 ± 0.9 sequences per 100 heartbeats. The relationship between baroreflex sensitivity and PI or vagal power (log2 area under the power spectral density plot between 0.15 and 0.4 Hz) showed a significant correlation (r2 = 0.45, r2 = 0.71, respectively, P<0.05). An attenuation in baroreflex sensitivity during heat stress appears related to a shift in autonomic balance (shift in resting PI) rather than heat stress, per se.
