Central arterial impedance and physical activity-induced changes in stroke volume in hypertension

Abstract

Regular physical activity is recommended as part of the management of hypertension. However, physical activity in hypertension is often symptom limited, an effect that may in-part be attributed to an inability to increase stroke volume (SV) and hence cardiac output (CO). The extent to which this effect is determined by impedance to flow in the proximal aorta generated by increases in aortic stiffness is uncertain. In 56 hypertensives recruited from a hypertension referral clinic (age=56.9±12.8 years) with resting BP values <160/100 mm Hg, I assessed the extent to which proximal aortic characteristic impedance (Zc) determines the impact of modest physical activity (stationary supine bicycle or handgrip) on activity-induced increases in SV. Haemodynamic effects were determined from aortic velocity and diameter assessments in the left ventricular outflow tract (echocardiography) and central arterial pressure measurements (applanation tonometry and SphygmoCor software). Average resting blood pressures (BP) on medication were 140±18 mm Hg systolic and 79±9 mm Hg diastolic BP, with 60.7% controlled to target. Physical activity resulted in an increase in SV (128±43 to 161±68 mls/beat, p=0.0001) and CO (p<0.0001) and a decrease in systemic vascular resistance (SVR) (p<0.005). The increase in SV was strongly and inversely associated with Zc (p<0.0001) and SVR (p<0.0001) at baseline and directly correlated with decreases in SVR with activity (p<0.0001). However, in the same regression model, activity-induced decreases in SVR contributed far more to increases in SV (partial r=-0.755, CI=-0.880 to -0.604) than did variations in Zc either at baseline (partial r=- 0.344, CI=-0.556 to -0.083) or immediately after physical activity (partial r=-0.165, CI=-0.411 to 0.107)(p<0.05 for comparison of partial r values). In conclusion, although the function of the proximal aorta (stiffness) does contribute to the extent to which flow increases with physical activity in hypertension, the contribution is modest in comparison to the impact of activity on arteriolar function (vasodilator effects).