Affiliation:
1. From the Copenhagen Muscle Research Center, Rigshospitalet, University of Copenhagen, Denmark (R.B., J.-A.L.C., G.R., H.S., B.S.), and the Department of Medicine, University of California, San Diego (P.D.W.).
Abstract
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 ≥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 ≈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 HR to SL values, glycopyrrolate had no influence on Q, which was reduced at ALT. Breathing F
io
2
=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 P
o
2
and S
o
2
are similarly increased suggests hypoxia-mediated attenuation of Q.
Publisher
Ovid Technologies (Wolters Kluwer Health)
Subject
Physiology (medical),Cardiology and Cardiovascular Medicine
Cited by
126 articles.
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