Proceedings of The Physiological Society

Europhysiology 2018 (London, UK) (2018) Proc Physiol Soc 41, PCA148

Poster Communications

Lifelong endurance training modifies sympathetic baroreflex control of neural vasoconstrictor tone at rest

D. J. Wakeham1,2, R. N. Lord1, J. S. Tablot1, B. Curry1, T. Dawkins1, L. L. Simpson3,4, R. Shave5, J. Moore3, C. J. Pugh1

1. Cardiff School of Sport and Health Sciences, Cardiff Metropolitan University, Cardiff, United Kingdom. 2. Institute of Research Excellence in Sport and Exercise, Cardiff Metropolitan University, Cardiff, United Kingdom. 3. School of Sport Health and Exercise Sciences, Bangor University, Bangor, United Kingdom. 4. Institute of Research Excellence in Sport and Exercise, Bangor University, Bangor, United Kingdom. 5. Centre for Heart, Lung, and Vascular Health, School of Health and Exercise Sciences, University of British Columbia Okanagan, Kelowna, British Columbia, Canada.


Changes in blood pressure during middle age are associated with elevated muscle sympathetic nerve activity (MSNA), alterations in the sympathetic baroreflex, and stiffening of the barosensitive aortic and carotid arteries. It is well known that lifelong endurance-training attenuates the age-related increase in arterial stiffness; however, the impact on sympathetic baroreflex function (i.e. operating pressure, set point and gain) is less clear. We examined sympathetic baroreflex control of MSNA in age-matched recreationally active middle-aged men (n = 10: age, 53 [52-55] years), and determined whether this differed from that of lifelong (29 [28-40] years of training) endurance-trained runners (n = 13: age, 57 [54-59] years). Indices of spontaneous sympathetic baroreflex function were determined from beat-by-beat changes in diastolic blood pressure (DBP, photoplethysmography) and the corresponding MSNA (microneurography) during six minutes of supine rest. Aortic (Carotid-Femoral Pulse Wave Velocity via applanation tonometry) and carotid (β Stiffness Index via B-mode ultrasound) stiffness were also measured. Data presented are means [95% confidence intervals] and were compared using independent t-tests. Resting heart rate (electrocardiogram) was lower in runners (43 [38-47] vs 56 [49-62] bpm, P < 0.01) but mean brachial artery pressure was not different (93 [90-96] vs 95 [89-101] mmHg, P = 0.54). Aortic (6.8 [6.2-7.3] vs 7.5 [6.9-8.1] m/s-1, P = 0.02) and carotid artery stiffness (4.06 [3.25-4.88] vs 5.06 [3.94-6.19] AU, P = 0.04) were also lower in runners. Spontaneous sympathetic baroreflex operating DBP was similar (77 [74-81] vs 79 [73-85] mmHg, P = 0.57), as was MSNA burst frequency (31 [27-34] vs 28 [19-38] bursts/min-1, P = 0.55) and sympathetic baroreflex gain (i.e. responsiveness) (-6.1 [-8.0 - -4.1] vs -6.9 [-9.8 - -4.0] %/mmHg, P = 0.55). However, the corresponding MSNA burst incidence (i.e.' set point') was higher in runners (72 [63-81] vs 50 [33-66] bursts/100hb-1, P < 0.01). In conclusion, lifelong endurance runners had lower stiffness in barosensitive arteries, and an upward setting of the sympathetic baroreflex; meaning there was a higher likelihood of a burst of MSNA for a similar operating DBP. This was evident despite no difference in the responsiveness of MSNA to spontaneous fluctuations in blood pressure. We suggest that the greater MSNA burst incidence in lifelong runners is necessary to maintain resting blood pressure in the context of the training-induced bradycardia, skeletal muscle angiogenesis and possible reductions in α-adrenergic sensitivity. Investigation is required to explore the mechanisms that underpin modified sympathetic baroreflex function following lifelong endurance training.

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