CARDIOVASCULAR FUNCTION FOLLOWING REDUCED AEROBIC ACTIVITY

Purpose: The aim of this study was to test the hypothesis that a susta ined reduction of physical activity (deconditioning) would alter the c ardiovascular regulatory function. Methods: Nineteen young, healthy vo lunteers participated in physical deconditioning for a period of 8 wk. Before (pre) and following (post) physical deconditioning, the respon ses of heart rate (HR), mean arterial pressure (MAP, measured by Finap res), 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-s tate phenylephrine (PE) infusion superimposed by LBNP and NP to counte ract the PE increased CVP and carotid sinus pressure, respectively. Re sults: Active physical deconditioning significantly decreased maximal oxygen uptake (-7%) and LBNP tolerance (-13%) without a change in base line hemodynamics. Plasma volume (-3% at P = 0.135), determined by Eva ns Blue dilution, and blood volume (-4% at P = 0.107) were not signifi cantly 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 accompanie d by a greater tachycardia. Deconditioning increased the aortic barore flex 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 (calc ulated from [MAP-CVP]/FBE) to CVP (-2.75 +/- 0.26 vs -4.94 +/- 0.97 PR U/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- a nd postdeconditioning. Conclusions: We concluded that the functional m odification of the cardiac pressure-volume relationship resulted in th e reduced LBNP tolerance, despite the accentuated aortic and cardiopul monary baroreflex function following deconditioning.