Aortic stiffness contributes to greater pressor responses during static hand grip exercise in healthy young and middle-aged normotensive men

Central arterial stiffness can influence exercise blood pressure (BP) by increasing the rise in arterial pressure per unit increase in aortic inflow. Whether central arterial stiffness influences the pressor response to isometric handgrip exercise (HG) and post-exercise muscle ischemia (PEMI), two common laboratory tests to study sympathetic control of BP, is unknown. We studied 46 healthy non-hypertensive males (23 young and 23 middle-aged) during HG (which increases in cardiac output [Q(center dot)c]) and isolated metaboreflex activation PEMI (no change or decreases in Q(center dot)c). Aortic stiffness (aortic pulse wave velocity [aPWV]; applanation tonometry via SphygmoCor) was measured during supine rest and was correlated to the pressor responses to HG and PEMI. BP (photoplethysmography) and muscle sympathetic nerve activity (MSNA) were continuously recorded at rest, during HG to fatigue (35 % maximal voluntary contraction) and 2-min of PEMI. aPWV was higher in middle-aged compared to young males (7.1 +/- 0.9 vs 5.4 +/- 0.7 m/s, P < 0.001). Middle-aged males also exhibited greater increases in systolic pressure (Delta 30 +/- 11 vs 10 +/- 8 mmHg) and MSNA (Delta 2313 +/- 2006 vs 1387 +/- 1482 %/min) compared to young males during HG (both, P < 0.03); with no difference in the Q.c response (P = 0.090). Responses to PEMI were not different between groups. Sympathetic transduction during these stressors (MSNA-diastolic pressure slope) was not different between groups (P > 0.341). Middle-aged males displayed a greater increase in SBP per unit change of Q(center dot)c during HG (Delta SBP/Delta Q(center dot)c; 21 +/- 18 vs 6 +/- 10 mmHg/L/min, P = 0.004), with a strong and moderate relationship between the change in systolic (r = 0.53, P < 0.001) and diastolic pressure (r = 0.34, P = 0.023) and resting aPWV, respectively; with no correlation during PEMI. Central arterial stiffness can modulate pressor responses during stimuli associated with increases in cardiac output and sympathoexcitation in healthy males.