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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

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