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This Article Full Text Full Text (PDF) All Versions of this Article: 105/1/213    most recent 00175.2008v1 Submit a response Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Lucas, S. J. E. Articles by Ainslie, P. N. PubMed PubMed Citation Articles by Lucas, S. J. E. Articles by Ainslie, P. N.

Mechanisms of orthostatic intolerance following very prolonged exercise

¹School of Physical Education and ²Department of Physiology, University of Otago, Dunedin, New Zealand; ³Department of Chemical Pathology, St. George's Healthcare National Health Service Trust, Tooting, London; and ⁴Research Institute for Sport and Exercise Sciences, Liverpool John Moores University, Liverpool, United Kingdom

Submitted 13 February 2008 ; accepted in final form 14 May 2008

Nine men completed a 24-h exercise trial, with physiological testing sessions before (T1, 0630), during (T2, 1640; T3, 0045; T4, 0630), and 48-h afterwards (T5, 0650). 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 and then stood for 6 min, while heart rate variability (spectral analysis of ECG), middle cerebral artery perfusion velocity (MCAv), mean arterial pressure (MAP; Finometer), and end-tidal PCO₂ (PET_CO2) were measured, and venous blood was sampled for cardiac troponin I. During the exercise trial: 1) two, six, and four participants were orthostatically intolerant at T2, T3, and T4, respectively; 2) changes in heart rate variability 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) PET_CO2 was reduced (P < 0.05) at all times while supine (–3–4 Torr) and standing (–4–5 Torr) 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 PET_CO2 (r = 0.78–0.93), but only with changes in MAP at T1, T2, and T3 (P < 0.05; r = 0.62–0.84); and 7) only two individuals showed minor elevations in cardiac troponin I. Recovery was complete within 48 h. During prolonged exercise, postural-induced hypotension and hypocapnia exacerbate cerebral hypoperfusion and facilitate syncope.

syncope; hypotension; cerebrovascular function