title: Mechanisms of orthostatic intolerance following very prolonged exercise.
abstract: Nine men completed a 24-h exercise trial, with physiological testing sessions before (T1, approximately 0630), during (T2, approximately 1640; T3, approximately 0045; T4, approximately 0630), and 48-h afterwards (T5, approximately 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 Pco(2) (Pet(CO(2))) 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(CO(2)) 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(CO(2)) (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.
authors.affiliation: School of Physical Education, University of Otago, Dunedin, New Zealand. sam.lucas@otago.ac.nz
authors.forename: Samuel J E
authors.initials: SJ
authors.lastname: Lucas
authors.forename: James D
authors.initials: JD
authors.lastname: Cotter
authors.forename: Carissa
authors.initials: C
authors.lastname: Murrell
authors.forename: Luke
authors.initials: L
authors.lastname: Wilson
authors.forename: J Greg
authors.initials: JG
authors.lastname: Anson
authors.forename: David
authors.initials: D
authors.lastname: Gaze
authors.forename: Keith P
authors.initials: KP
authors.lastname: George
authors.forename: Philip N
authors.initials: PN
authors.lastname: Ainslie
mesh_terms: D000328:Adult; D001794:Blood Pressure / Q000502:physiology; D002245:Carbon Dioxide / Q000378:metabolism; D002560:Cerebrovascular Circulation / Q000502:physiology; D003627:Data Interpretation, Statistical; D004562:Electrocardiography; D015444:Exercise / Q000502:physiology*; D006331:Heart Diseases / Q000378:metabolism / Q000503:physiopathology; D006339:Heart Rate / Q000502:physiology; D006801:Humans; D007024:Hypotension, Orthostatic / Q000503:physiopathology*; D008297:Male; D011187:Posture / Q000502:physiology; D011311:Pressoreceptors / Q000502:physiology; D016683:Supine Position / Q000502:physiology; D013564:Sympathetic Nervous System / Q000502:physiology; D019210:Troponin I / Q000378:metabolism; D014630:Vagus Nerve / Q000502:physiology
chemical_list: D019210:Troponin I; D002245:Carbon Dioxide