Augmented muscle sympathetic reactivity in normotensive adults with elevated maximal exercise blood pressure

Elevated peak blood pressure (BP) during exercise is an independent risk factor for future hypertension, but the mechanisms responsible for inter-individual differences in exercise BP remain poorly studied. Forty-four participants (22±5 years; 18 female) completed a maximal exercise test (modified Bruce protocol) with brachial artery BP measured every 90-seconds (automated auscultation). On a subsequent visit, participants underwent measures of carotid-femoral pulse wave velocity (n=37), superficial femoral artery flow-mediated dilation (n=27), and muscle sympathetic nerve activity (MSNA; microneurography, n=44). Hemodynamic and MSNA data were collected at rest, during handgrip exercise (static and rhythmic), and post-exercise circulatory occlusion. Participants were separated by sex and grouped into tertiles based on peak exercise systolic BP (SBP). Peak exercise SBP differed between tertiles (Tertile 1: 168±16 vs. Tertile 2: 194±14 vs. Tertile 3: 223±17 mmHg, P<0.001), despite no differences in resting SBP (P=0.12), diastolic BP (P=0.17), heart rate (P=0.12), superficial femoral artery flow-mediated dilation (P=0.85), carotid-femoral pulse wave velocity (P=0.15), or MSNA (17.8±5.9 vs. 16.8±5.8 vs. 19.0±4.5 bursts/min, P=0.56). MSNA was higher during the final 30-seconds of static handgrip in Tertile 3 compared to both Tertile 1 and 2 (28.8±8.0 vs. 29.3±9.0 vs. 43.7 ± 14.0 bursts/min, both P<0.01) and post-exercise circulatory occlusion (Tertile 1: 28.0±9.3 vs. Tertile 3: 38.5±15.8, P=0.03; Tertile 2: 27.5±9.1 vs. Tertile 3: 38.5±15.8 bursts/min, P=0.01). MSNA did not differ during rhythmic handgrip exercise (all P>0.19). Normotensive adults with higher peak SBP during maximal treadmill exercise have augmented MSNA during activation of the muscle metaboreflex.