This study seeks to confirm the progressive changes in cardiac output and h
eart rate previously reported with 8 h exposures to constant hypoxia, and t
o examine the role of sympathetic mechanisms in generating these changes. R
esponses of ten subjects to four 8 h protocols were compared: (1) air breat
hing with placebo; (2) isocapnic hypoxia (end-tidal P-O2 = 50 mmHg) with pl
acebo; (3) isocapnic hypoxia with beta-blockade; and (4) air breathing with
beta-blockade. Regular measurements of heart rate and cardiac output (usin
g ultrasonography and N2O rebreathing techniques) were made with subjects s
eated in the upright position. The sensitivity of heart rate to rapid varia
tions in hypoxia (G(HR)) and heart rate in the absence of hypoxia were meas
ured at times 0, 4 and 8 h. No significant progressive effect of hypoxia on
cardiac output was detected. There was a gradual rise in heart rate with h
ypoxia of 11 +/- 2 beats min(-1) in the placebo protocol and of 10 +/- 2 be
ats min(-1) in the beta-blockade protocol over 8 h, compared to the air bre
athing protocols. The rise in heart rate was progressive (P < 0.001) and ac
companied by progressive increases in both G(HR) (P < 0.001) and heart rate
measured in the absence of hypoxia (P < 0.05). No significant effect of be
ta-blockade was detected on any of these progressive changes. We conclude t
hat sympathetic mechanisms that act via beta-receptors play little role in
the progressive changes in heart rate observed over 8 h of moderate hypoxia
.