Parasympathetic neural activity accounts for the lowering of exercise heart rate at high altitude

Background-In chronic hypoxia, both heart rate (HR) and cardiac output (Q) are reduced during exercise. The role of parasympathetic neural activity in lowering HR is unresolved, and its influence on Q and oxygen transport at high altitude has never been studied. Methods and Results-HR, Q, oxygen uptake, mean arterial pressure, and leg blood flow were determined at rest and during cycle exercise with and without vagal blockade with glycopyrrolate in 7 healthy lowlanders after 9 weeks' residence at greater than or equal to 5260 m (ALT). At ALT, glycopyrrolate increased resting HR by 80 bpm (73 +/-4 to 153 +/-4 bpm) compared with 53 bpm (61 +/-3 to 114 +/-6 bpm) at sea level (SL). During exercise at ALT, glycopyrrolate increased HR by approximate to 40 bpm both at submaximal (127 +/-4 to 170 +/-3 bpm; 118 W) and maximal (141 +/-6 to 180 +/-2 bpm) exercise, whereas at SL, the increase was only by 16 bpm (137 +/-6 to 153 +/-4 bpm) at 118 W. with no effect at maximal exercise (181 +/-2 bpm). Despite restoration of maximal IIR to SL values, glycopyrrolate had no influence on Q, which was reduced at ALT. Breathing FIO2=0.55 at peak exercise restored Q and power output to SL values. Conclusions-Enhanced parasympathetic neural activity accounts for the lowering of HR during exercise at ALT without influencing Q. The abrupt restoration of peak exercise Q in chronic hypoxia to maximal SL values when arterial PO2 and SO2 are similarly increased suggests hypoxia-mediated attenuation of Q.