Sympathetic reserve, serum potassium, and orthostatic intolerance after endurance exercise and implications for neurocardiogenic syncope.

Abstract

To elucidate the mechanisms of orthostatic intolerance (OI) after endurance exercise which are incompletely understood. We investigated beat-to-beat haemodynamic and autonomic parameters in 51 male athletes during supine rest and after active standing the day before and 2 h after a marathon run. None of the subjects before the marathon [non-orthostatic intolerance (Non-OI)], but 14 after the marathon [orthostatic intolerance (OI)] exhibited with pre-syncope. There were no differences between OI and Non-OI before the marathon. After the marathon, only Non-OI was able to increase sympathetic modulation to resistance vessels from already increased basal levels in response to standing; OI could not. OI instead exhibited a decrease in total peripheral resistance and a paradoxical increase in parasympathetic sinus node modulation. We observed a significant correlation between serum potassium before the race and the maximally achieved sympathetic drive after the marathon (r = 0.55, P = 0.001). Post-exercise OI is associated with a 'high basal sympathetic modulation of vasomotor tone in combination with a diminished orthostatic sympathetic response' to resistance vessels. This situation may mimic the OI in some clinical conditions, which are also known to be associated with increased 'basal' sympathetic tone. The role of serum potassium deserves further study.