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1Department of Physiology and 2School of Physical Education, University of Otago, Dunedin, New Zealand; 3Department of Integrative Physiology, University of North Texas Health Science Center, Fort Texas, Texas; and 4Research Institute for Sport and Exercise Science, Liverpool John Moores University, Liverpool, United Kingdom
Submitted 10 December 2006 ; accepted in final form 20 March 2007
We examined potential mechanisms (autonomic function, hypotension, and cerebral hypoperfusion) responsible for orthostatic intolerance following prolonged exercise. Autonomic function and cerebral hemodynamics were monitored in seven athletes pre-, post- (<4 h), and 48 h following a mountain marathon [42.2 km; cumulative gain
1,000 m;
15°C; completion time, 261 ± 27 (SD) min]. In each condition, middle cerebral artery blood velocity (MCAv), blood pressure (BP), heart rate (HR), and cardiac output (Modelflow) were measured continuously before and during a 6-min stand. Measurements of HR and BP variability and time-domain analysis were used as an index of sympathovagal balance and baroreflex sensitivity (BRS). Cerebral autoregulation was assessed using transfer-function gain and phase shift in BP and MCAv. Hypotension was evident following the marathon during supine rest and on standing despite increased sympathetic and reduced parasympathetic control, and elevations in HR and cardiac output. On standing, following the marathon, there was less elevation in normalized low-frequency HR variability (P < 0.05), indicating attenuated sympathetic activation. MCAv was maintained while supine but reduced during orthostasis postmarathon [–10.4 ± 9.8% pre- vs. –15.4 ± 9.9% postmarathon (%change from supine); P < 0.05]; such reductions were related to an attenuation in BRS (r = 0.81; P < 0.05). Cerebral autoregulation was unchanged following the marathon. These findings indicate that following prolonged exercise, hypotension and postural reductions in autonomic function or baroreflex control, or both, rather than a compromise in cerebral autoregulation, may place the brain at risk of hypoperfusion. Such changes may be critical factors in collapse following prolonged exercise.
cerebral blood flow velocity; hypotension
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S. J. E. Lucas, J. D. Cotter, C. Murrell, L. Wilson, J. G. Anson, D. Gaze, K. P. George, and P. N. Ainslie Mechanisms of orthostatic intolerance following very prolonged exercise J Appl Physiol, July 1, 2008; 105(1): 213 - 225. [Abstract] [Full Text] [PDF] |
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