Exercise training hypotension: implications for plasma volume, renin, and vasopressin

Abstract

To determine the function of changes in plasma volume (PV), plasma renin activity (PRA), and arginine vasopressin (AVP) in the mechanism of the reduction of resting blood pressure during exercise training, resting supine, sitting, and standing systolic (SBP) and 5th-phase diastolic (DBP) blood pressures were measured in 10 men (19-24 yr) before and after an 8-day (2 h/day) training period on a cycle ergometer. The control group (5 men) exercised at 1.4 1/min [44% peak O2 uptake (VO2 max)] at 23.8 degrees C Tdb and 50% rh, and the acclimation group at 1.5 1/min (46% VO2 max) at 39.8 degrees C Tdb and 50% rh. After acclimation, resting supine and sitting DPB decreased (P less than 0.05) by 6 and 9 mmHg, respectively. There were no significant changes in DBP in the controls or in SBP in either group. After training, PV increased by 12.2% in controls and by 17.6% after acclimation. The resting hypotension could not be attributed to changes in resting levels of PV, AVP, or PRA. However, large decreases in PV and large increases in AVP and especially PRA during acclimation exposures suggest these responses may play a role in the chronic hypotensive response.

Chronic physical activity mitigates cerebral hypoperfusion during central hypovolemia in elderly humans

“…For example, patients with idiopathic orthostatic intolerance show a greater decrease in V MCA and a greater increase in CVR compared with age-and sex-matched healthy adults during graded orthostatic stress simulated by head-up tilt (20). The better maintained cerebral perfusion observed in the elderly ACT group compared with the elderly SED cohort in the present study seems to be contrary to the belief that "trained man can run, but they cannot stand" (12). More incidence of orthostatic intolerance in high-fit younger subjects has been observed compared with their age-matched healthy, average-fit counterparts, which has been reportedly related to a greater cardiac compliance (27) that compromises SV output (25) and a diminished baroreflex sensitivity that compromises tachycardiac and vasoconstrictive responses (33).…”

Endurance Exercise Training in Orthostatic Intolerance

“…Previous studies on the influence of exercise training on orthostatic tolerance reported controversial results, [11][12][13][14]16,28 which may be related to different inclusion criteria, training regimes, methods used for assessment of changes, and a different pathophysiological mechanism, depending on physical capacity: In untrained subjects, symptoms of OI has been related to hypovolemia and a possible cardiac atrophy. 29 In contrast in highly fit subjects, symptoms of OI might be caused by attenuated carotid baroreflex responsiveness and a larger compliance of the heart.…”

“…Greenleaf et al even stated that "trained men can run, but they cannot stand." 11 Another report indicates that chronic endurance training causes orthostatic hypotension. 12 Smith and Raven suggested that the negative effect of training on orthostatic tolerance was caused by long training periods (Ͼ6 months) at very high levels.…”

Cardiovascular function and the veteran athlete

“…The effect of fitness on orthostatic tolerance and syncope remains controversial. A lowered resting orthostatic tolerance has been observed in young highly trained athletes (Levine et al 1991;Raven and Pawelczyk 1993;Ogoh et al 2003), as outlined by the statement ''trained men can run but they cannot stand'' (Greenleaf et al 1981). Others have found orthostatic tolerance to be unchanged (Hernandez et al 2005) or even improved in young highly trained individuals (Convertino 1993;Winker et al 2005).…”