Chronic endurance exercise training: a condition of inadequate blood pressure regulation and reduced tolerance to LBNP.

We review the hypotheses presented to account for the anecdotal and literature-based reports that chronic endurance exercise training reduces orthostatic tolerance. The findings from cross-sectional investigations of unfit subjects and endurance athletes are examined, as well as limited data from recent investigations of the changes in orthostatic tolerance and blood pressure regulation that occur after 8 d to 8 months of endurance exercise training. Statistical models have not found wide variations in maximal aerobic power (VO2max) to contribute to the prediction of orthostatic responses. However, research data are generally consistent that the orthostatic tolerance of athletes whose VO2max exceeds 65 ml.kg-1.min-1 is lower than that of sedentary control subjects. These two findings suggest that it is exercise training, rather than VO2max, that reduces orthostatic tolerance. Findings from a recent longitudinal investigation corroborate this theory. We conclude that at least four factors associated with exercise training contribute to the development of orthostatic intolerance. These include: a) increased limb compliance (although its effect is likely to be trivial), b) eccentric ventricular hypertrophy, and c) increases in total blood volume, which may attenuate cardiopulmonary baroreflex responsiveness, shift ventricular function to a steeper portion of the ventricular compliance curve, and increase the inhibitory effect of cardiopulmonary baroreceptors on carotid baroreflex responsiveness; and d) an independent effect that reduces carotid and aortic baroreflex responsiveness. These mechanisms mimic changes observed in pathological states such as heart failure and hypertension. Our conclusions are best summarized by Greenleaf et al. (J. Appl. Physiol. 51:298-305, 1981): ""Trained men can run, but they cannot stand.''