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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 Pco<jats:sub>2<\/jats:sub> (Pet<jats:sub>CO<jats:sub>2<\/jats:sub><\/jats:sub>) 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 \u00b1 6 mmHg) was lower ( P &lt; 0.05) by 14% at T3 and 8% at T4, whereas standing MAP (75 \u00b1 7 mmHg) was lower by 16% at T2, 37% at T3, and 15% at T4; 4) Pet<jats:sub>CO<jats:sub>2<\/jats:sub><\/jats:sub> was reduced ( P &lt; 0.05) at all times while supine (\u22123\u20134 Torr) and standing (\u22124\u20135 Torr) during exercise trial; 5) standing MCAv was reduced ( P &lt; 0.05) by 23% at T3 and 30% at T4 during the exercise trial; 6) changes in MCAv with standing always correlated ( P &lt; 0.01) with changes in Pet<jats:sub>CO<jats:sub>2<\/jats:sub><\/jats:sub> ( r = 0.78\u20130.93), but only with changes in MAP at T1, T2, and T3 ( P &lt; 0.05; r = 0.62\u20130.84); 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. <\/jats:p>","DOI":"10.1152\/japplphysiol.00175.2008","type":"journal-article","created":{"date-parts":[[2008,5,16]],"date-time":"2008-05-16T00:59:20Z","timestamp":1210899560000},"page":"213-225","source":"Crossref","is-referenced-by-count":29,"title":["Mechanisms of orthostatic intolerance following very prolonged exercise"],"prefix":"10.1152","volume":"105","author":[{"given":"Samuel J. 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