Cardiovascular function following reduced aerobic activity. Med. Sci. Sports Exerc., Vol. 30, No. 7, pp. 1041-1052, 1998.
Purpose: The aim of this study was to test the hypothesis that a sustained reduction of physical activity (deconditioning) would alter the cardiovascular regulatory function.
Methods: Nineteen young, healthy volunteers participated in physical deconditioning for a period of 8 wk. Before (pre) and following (post) physical deconditioning, the responses of heart rate (HR), mean arterial pressure (MAP, measured by Finapres), central venous pressure (CVP), stroke volume (SV, Doppler), and forearm blood flow (FBF, plethysmography) were determined during lower body negative pressure (LBNP). The carotid baroreflex (CBR) function was assessed using a train of pulsatile neck pressure (NP) and suction, and the aortic baroreflex control of HR was assessed during steady-state phenylephrine (PE) infusion superimposed by LBNP and NP to counteract the PE increased CVP and carotid sinus pressure, respectively.
Results: Active physical deconditioning significantly decreased maximal oxygen uptake (−7%) and LBNP tolerance (−13%) without a change in baseline hemodynamics. Plasma volume (−3% at P = 0.135), determined by Evans Blue dilution, and blood volume (−4% at P = 0.107) were not significantly altered. During LBNP −20 to −50 torr, there was a significantly greater drop of SV per unit decrease in CVP in the post- (14.7 ± 1.6%/mm Hg) than predeconditioning (11.2 ± 0.7%/mm Hg) test accompanied by a greater tachycardia. Deconditioning increased the aortic baroreflex sensitivity (pre vs post: −0.61 ± 0.12 vs −0.84 ± 0.14 bpm·mm−1 Hg, P = 0.009) and the slope of forearm vascular resistance (calculated from [MAP-CVP]/FBF) to CVP (−2.75 ± 0.26 vs −4.94 ± 0.97 PRU/mm Hg, P = 0.086). However, neither the CBR-HR (−0.28 ± 0.03 vs −0.39 ± 0.10 bpm·mm−1 Hg) nor the CBR-MAP (−0.37 ± 0.16 vs −0.25 ± 0.07 mm Hg/mm Hg) gains were statistically different between pre- and postdeconditioning.
Conclusions: We concluded that the functional modification of the cardiac pressure-volume relationship resulted in the reduced LBNP tolerance, despite the accentuated aortic and cardiopulmonary baroreflex function following deconditioning.
Department of Integrative Physiology and the Cardiovascular Research Institute, University of North Texas Health Science Center at Fort Worth, TX 76107
Submitted for publication August 1996.
Accepted for publication May 1998.
We thank all our subjects for their cheerful cooperation in completing the experiments and appreciate the clinical assistance from Brian Foresman, D.O., Frederick Schaller, D.O., and Lon Walder, D.O. This study was supported in part by NASA-RTOP award NAS9-611, NASA-NSCORT NAGW 3853, and NIH grants HL 45547 and 43202.
Address for reprint requests: Peter B. Raven, Ph.D., Department of Integrative Physiology, University of North Texas Health Science Center, 3500 Camp Bowie Blvd., Fort Worth, TX 76107-2699.
Address for correspondence: Xiangrong Shi, Ph.D., Department of Integrative Physiology and the Cardiovascular Research Institute, University of North Texas Health Science Center, 3500 Camp Bowie Boulevard, Fort Worth, TX 76107-2699.