| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
1 Physiology, University of Otago, New Zealand
2 Physical Education, University of Otago, Dunedin, New Zealand
3 School of Physical Education, University of Otago, Dunedin, New Zealand; Physical Education, University of Otago, Dunedin, New Zealand
4 Integrativr Physiology, University of North Texas Health Science Center, Fort Worth, Texas, United States
5 Research Institute for Sport and Exercise Sciences, Liverpool John Moores University, Liverpool, United Kingdom
* To whom correspondence should be addressed. E-mail: philip.ainslie{at}stonebow.otago.ac.nz.
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 
1000 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 prior to and during a 6-min stand. Measurements of HR and BP variability and time-domain analysis were used as an index of sympatho-vagal balance and baroreceptor 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 upon standing despite increased sympathetic and reduced parasympathetic control, and elevations in HR and cardiac output. Upon standing, following the marathon, there was less elevation in normalized low- frequency HR variability (P<0.05), indicating attenuated sympathetic activation. MCAv was maintained whilst supine but reduced during orthostasis post-marathon (-10.4 ± 9.8% pre-, vs. -15.4 ± 9.9% post- [% 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 and/or baroreflex control, 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.
This article has been cited by other articles:
|
|
 |
|
  K. N. Thomas, J. D. Cotter, S. D. Galvin, M. J. A. Williams, C. K. Willie, and P. N. Ainslie Initial orthostatic hypotension is unrelated to orthostatic tolerance in healthy young subjects J Appl Physiol, August 1, 2009; 107(2): 506 - 517. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P. N. Ainslie and J. Duffin Integration of cerebrovascular CO2 reactivity and chemoreflex control of breathing: mechanisms of regulation, measurement, and interpretation Am J Physiol Regulatory Integrative Comp Physiol, May 1, 2009; 296(5): R1473 - R1495. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
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]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| Visit Other APS Journals Online |
