Augmented sympathetic neurovascular transduction following acute exercise in normotensive adults

Introduction: The effects of an acute bout of aerobic exercise on sympathetic neurovascular interactions in normotensive adults remain unclear. Pharmacological work has previously demonstrated unchanged α-adrenergic receptor sensitivity, however, assessments under closed-loop conditions have not been conducted. The objective of the current study is to evaluate sympathetic neurovascular transduction following acute exercise in normotensive adults. We hypothesize that acute exercise will decrease sympathetic neurovascular transduction. Methods: Using a randomized cross-over design, eight young healthy participants (four female) performed either: 1) 60 minutes of cycling exercise at 60% VO2max, or 2) 60 minutes of a seated control, separated by a minimum of 1-month. Ninety minutes following both interventions, a 10-minute neuro-cardiovascular assessment was preformed in the supine position. Beat-to-beat heart rate (electrocardiography), blood pressure (finger photoplethysmography), muscle sympathetic nerve activity (MSNA; fibular nerve microneurography), and superficial femoral artery blood flow (Duplex ultrasound) were quantified; femoral vascular conductance (FVC) was calculated as blood flow/mean arterial pressure. Sympathetic-FVC transduction was quantified using the signal-averaging technique, whereby FVC responses to each MSNA burst were serially tracked over 15 cardiac cycles and averaged to derive the nadir change in FVC. Lastly, following measurements performed on the control visit, a subset of participants (n=4) submerged the lower limb into 40°C water to the level of the malleolus, to assess sympathetic-FVC transduction following acute increases in skin blood flow. Results: Compared to control, heart rate (60±8 vs. 66±8 beats/min), superficial femoral artery blood flow (68±25 vs. 104±42 mL/min), and femoral vascular conductance (0.9±0.3 vs. 1.4±0.5 mL/min/mmHg) were elevated following exercise (all P<0.02), while mean arterial pressure (76±4 vs. 78±7 mmHg; P=0.41) and MSNA burst frequency (18±6 vs. 18±5 bursts/min; P=0.85) were not different. The reduction in FVC following a sympathetic burst was increased following exercise (-0.12±0.04 vs. -0.17±0.06 mL/min/mmHg; P=0.04). A greater increase in FVC following exercise was associated with greater magnitude increase in sympathetic-FVC transduction (r=-0.65; P=0.08). However, the increase in FVC following lower limb heating (0.9±0.3 vs. 2.1 mL/min/mmHg; P<0.01) was not associated with parallel changes in sympathetic-FVC transduction (-0.07±0.04 vs. -0.07±0.04 mL/min/mmHg; P=0.92). Conclusion: Sympathetic-FVC transduction is acutely elevated following aerobic exercise, which was associated with the magnitude of post-exercise vasodilation. Considering that sympathetic-FVC transduction was unchanged during lower limb heating, these preliminary observations suggest that augmented sympathetic neurovascular transduction is facilitated by a blood flow-independent mechanism. This research was supported by a Natural Science and Engineering Research Council (NSERC) of Canada Discovery Grant (P.J.M) and a Canadian Institutes of Health Research Fredrick Banting and Charles Best Canada Graduate Scholarship (M.N). This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.