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Baroreflex-Mediated Heart Rate and Vascular Resistance Responses 24 h after Maximal Exercise


Medicine & Science in Sports & Exercise: June 2003 - Volume 35 - Issue 6 - pp 970-977
BASIC SCIENCES: Original Investigations

CONVERTINO, V. A. Baroreflex-Mediated Heart Rate and Vascular Resistance Responses 24 h after Maximal Exercise. Med. Sci. Sports Exerc., Vol. 35, No. 6, pp. 970–977, 2003.

Introduction. Plasma volume, heart rate (HR) variability, and stimulus-response relationships for baroreflex control of forearm vascular resistance (FVR) and HR were studied in eight healthy men after and without performing a bout of maximal exercise to test the hypotheses that acute expansion of plasma volume is associated with 1) reduction in baroreflex-mediated HR response, and 2) altered operational range for central venous pressure (CVP).

Methods. The relationship between stimulus (ΔCVP) and vasoconstrictive reflex response (ΔFVR) during unloading of cardiopulmonary baroreceptors was assessed with lower-body negative pressure (LBNP, 0, −5, −10, −15, −20 mm Hg). The relationship between stimulus (Δmean arterial pressure (MAP)) and cardiac reflex response (ΔHR) during loading of arterial baroreceptors was assessed with steady-state infusion of phenylephrine (PE) designed to increase MAP by 15 mm Hg alone and during application of LBNP (PE+LBNP) and neck pressure (PE+LBNP+NP). Measurements of vascular volume and autonomic baroreflex responses were conducted on two different test days, each separated by at least 1 wk. On one day, baroreflex response was tested 24 h after graded cycle exercise to volitional exhaustion. On another day, measurement of baroreflex response was repeated with no exercise (control). The order of exercise and control treatments was counterbalanced.

Results. Baseline CVP was elevated (P = 0.04) from a control value of 10.5 ± 0.4 to 12.3 ± 0.4 mm Hg 24 h after exercise. Average ΔFVR/ΔCVP during LBNP was not different (P = 0.942) between the exercise (−1.35 ± 0.32 pru·mm Hg−1) and control (−1.32 ± 0.36 pru·mm Hg−1) conditions. However, maximal exercise caused a shift along the reflex response relationship to a higher CVP and lower FVR. HR baroreflex response (ΔHR/ΔMAP) to PE+LBNP+NP was lower (P = 0.015) after maximal exercise (−0.43 ± 0.15 beats·min−1·mm Hg−1) compared with the control condition (−0.83 ± 0.14 beats·min−1·mm Hg−1).

Conclusion. Expansion of vascular volume after acute exercise is associated with altered operational range for CVP and reduced HR response to arterial baroreceptor stimulation.

Increased incidence of orthostatic hypotension and intolerance in humans is associated with vascular hypovolemia and attenuated cardiovascular reflex functions (3,11,15,16,18–22,31,33,37). Specifically, attenuation of the carotid-cardiac baroreflex has accompanied orthostatic compromise reported in healthy human subjects (9,11,21–23,33) and occurred independent of reductions in blood volume (11,44). On the other hand, reduced circulating blood volume appears to be a primary underlying cause for the accentuated tachycardia and peripheral vasoconstriction that accompanies given arterial and cardiopulmonary baroreceptor stimulation (10,44). It is therefore not surprising that blood volume and carotid-cardiac baroreflex sensitivity have been reported to be independent predictors of orthostatic tolerance (19,33). Thus, any treatment that would prove effective in increasing cardiac and vasoconstrictive baroreflex responses or reserves, and/or blood volume could prove effective as a therapeutic countermeasure against development of orthostatic hypotension and intolerance.

Performance of a single bout of graded exercise designed to elicit maximal effort has ameliorated hemodynamic compromise and/or orthostatic hypotension and intolerance in human subjects exposed to extended spaceflight, bed rest, or wheelchair confinement (11,21,22,36,43). This effect may not be surprising because the short-term impacts of maximal exercise included expansion (25) or restoration (13) of blood volume, and increased sensitivity of the carotid-cardiac baroreflex (8,21,22,29,42). However, we are unaware of any data that describe the effect of acute maximal exercise on the reflex HR response to arterial baroreceptor stimulation and vascular response to cardiopulmonary baroreceptor stimulation. Because reserves for eliciting tachycardia and peripheral vasoconstriction are reduced by hypovolemia (10,44), we hypothesized that expanded blood volume associated with acute maximal exercise would cause a reduced reflex response (i.e., greater reserve) of HR and peripheral vascular resistance to arterial and cardiopulmonary baroreceptor stimulation, respectively. The purpose of this investigation was to test this hypothesis.

U.S. Army Institute of Surgical Research, Fort Sam Houston, TX

Address for correspondence: Victor A. Convertino, Ph.D., U.S. Army Institute of Surgical Research, 3400 Rawley E. Chambers Avenue, Building 3611, Fort Sam Houston, TX 78234-6315; E-mail:

Submitted for publication September 2002.

Accepted for publication January 2003.

©2003The American College of Sports Medicine