Submitted on February 13, 2008
Accepted on May 13, 2008
Mechanisms of orthostatic intolerance following very prolonged exercise
Samuel J.E. Lucas1*, James D Cotter2, Carissa Murrell3, Luke Wilson3, J. Greg Anson4, David C. Gaze5, Keith George6, and Philip N. Ainslie3
1 School of Physical Education, University of Otago, Dunedin, New Zealand; Department of Physiology, University of Otago, Dunedin, New Zealand
2 School of Physical Education, University of Otago, Dunedin, Otago, New Zealand
3 Department of Physiology, University of Otago, Dunedin, New Zealand
4 School of Physical Education, University of Otago, Dunedin, New Zealand
5 Department of Chemical Pathology, St George's Healthcare NHS Trust, London, United Kingdom
6 Research Institute for Sport and Exercise Sciences, Liverpool John Moores University, Liverpool, United Kingdom
* To whom correspondence should be addressed. E-mail: sam.lucas{at}otago.ac.nz.
Nine males completed a 24-h exercise trial, with physiological testing sessions before (T1, ~06:30), during (T2, ~16:40; T3, ~00:45; T4, ~06:30) and 48-h afterward (T5, ~06:50). Participants cycled and ran/trekked continuously between test sessions. A 24-h sedentary control trial was undertaken in crossover order. Within testing sessions participants lay supine then stood for 6 min, while heart rate variability (HRV; spectral analysis of ECG), middle cerebral artery perfusion velocity (MCAv), mean arterial pressure (MAP; Finometer) and end-tidal PCO2 (PETCO2) were measured, and venous blood was sampled for cardiac troponin I (cTnI). During the exercise trial: 1) two, six and four participants were orthostatically intolerant at T2, T3 and T4, respectively; 2) changes in HRV were only observed at T2; 3) supine MAP (baseline = 81±6 mmHg) was lower (P<0.05) by 14% at T3 and 8% at T4, whereas standing MAP (75±7 mmHg) was lower by 16% at T2, 37% at T3 and 15% at T4; 4) PETCO2 was reduced (P<0.05) at all times whilst supine (-3-4 mmHg) and standing (-4-5 mmHg) during exercise trial; 5) standing MCAv was reduced (P<0.05) by 23% at T3 and 30% at T4 during the exercise trial; 6) changes in MCAv with standing always correlated (P<0.01) with changes in PETCO2 (r=0.78-0.93), but only with changes in MAP at T1, T2, and T3 (P<0.05; r=0.62 to 0.84), and 7) only two individuals showed minor elevations in cTnI. Recovery was complete within 48 h. During prolonged exercise, postural-induced hypotension and hypocapnia exacerbate cerebral hypo-perfusion and facilitate syncope.
