Proceedings of The Physiological Society

University of Oxford (2011) Proc Physiol Soc 23, C20

Oral Communications

The influence of systemic sympathetic activity on cerebral blood flow and cerebrovascular reactivity at rest and during exercise: Alterations with ageing.

S. J. Lucas1,2, K. N. Thomas2,3, S. D. Galvin3, P. N. Ainslie4

1. Department of Physiology, University of Otago, Dunedin, New Zealand. 2. School of Physical Education, University of Otago, Dunedin, New Zealand. 3. Department of Medical and Surgical Sciences, University of Otago, Dunedin, New Zealand. 4. Department of Health and Human Kinetics, Faculty of Health and Social Development, University of British Columbia Okanagan, Kelowna, British Columbia, Canada.


Cerebral blood flow (CBF) is regulated by several factors, including arterial PCO2 and arterial blood pressure (BP). To a lesser extent, CBF may also be influenced directly or indirectly by changes in cardiac output and sympathetic nerve activity (SNA). Given that SNA is known to be an important regulator of MAP via its effect on peripheral vascular resistance and cardiac output, we examined the effect of age on the influence of systemic sympathetic activity on regulating cerebral perfusion at rest and during exercise. Eight younger (aged: 26±5 y) and eight older (aged: 56±3 y) participants were tested at supine rest and during a 10-min exercise test (at 50% heart rate range) before (control) and 90 min following the administration of selective α1-blockade (Prazosin; 1 mg/20 kg body weight). Continuous measures of middle cerebral artery blood flow velocity (MCAv, Transcranial Doppler); MAP (intra-arterial and/or Finometer); heart rate (HR, ECG) and end-tidal PCO2 (PETCO2) were obtained during steady-state eupcapnia (room air) and hypercapnia (7% CO2; 93% O2) conditions at rest and during exercise. At supine rest, α1-adrenoreceptor blockade decreased MAP by a comparable extent in both younger (82 to 68 mmHg) and older (97 to 80 mmHg) participants. In the control condition, exercise-induced MAP increases were similar for both groups (Δ17 vs. 24 mmHg; P=0.45). Following blockade, exercise-induced increases were abolished in the young (Δ5 mmHg; P=0.24 vs. rest) yet remained in the old (Δ15 mmHg; P<0.01 vs. rest). Following blockade, MCAv was reduced (P<0.01) for both young and old at rest [76 to 65 cm/s (young) and 60 to 48 cm/s (old)]. Exercise-induced increases in MCAv were abolished in the young following blockade (Δ18 vs. 1 cm/s; interaction effect: P<0.01), whilst the older group’s response was unaffected (Δ5 vs. 2 cm/s; interaction effect: P=0.66). Unexpectedly, CBF responsiveness to hypercapnia was reduced in the young during exercise (3.1 to 2.2 cm/s /mmHg), whilst the older group showed the expected increase (2.3 to 3.0 cm/s /mmHg). Following blockade, hypercapnia CBF responsiveness increased for both groups at rest and during exercise (P<0.05). The reliance on α1 sympathetically driven vasoconstriction during exercise is critical in the young but seems to be a redundant mechanism in order to maintain MAP with advancing age. Regardless of the pathway, exercise-induced elevations in MAP with ageing would seem beneficial in the regulation of MCAv. Furthermore, these data provide evidence for sympathetically mediated constraint on CBF-CO2 responsiveness during rest and exercise.

Where applicable, experiments conform with Society ethical requirements