The contributions of increases in circulating catecholamines, changes in ce
ntral command, and muscle afferents on baroreflex control of the sinus node
during exercise are unclear. We used a dobutamine infusion to induce hemod
ynamic changes comparable to those of moderate physical exercise in the abs
ence of changes in central command and muscle afferents in 13 healthy subje
cts. Dobutamine (up to 9 mu g/kg body weight per minute) increased systolic
blood pressure, shortened the RR interval, increased systolic blood pressu
re variability, but blunted RR interval variability (P < 0.05 versus placeb
o). Consequently, dobutamine decreased the coherence between variations in
systolic blood pressure and RR interval and decreased arterial baroreflex s
ensitivity from 12 +/- 2 to 3 +/- 1 ms/mm Hg (P < 0.01). The largest increa
ses in systolic blood pressure with dobutamine were paralleled by the great
est impairments in arterial baroreflex sensitivity (0.50 < r < 0.56, P < 0.
01). The chronotropic effects of dobutamine prevented a reflex bradycardia
in response to the blood pressure increase. However, less predominant low-f
requency oscillations in systolic blood pressure (P < 0.0001) suggested pre
served sympathetic withdrawal in response to the blood pressure increase in
duced by dobutamine. In conclusion, this study revealed that a shift in the
operating point of the arterial baroreceptors and the chronotropic effects
of adrenergic stimulation impair baroreflex control of the sinus node duri
ng dobutamine exercise stress testing. Baroreflex control of the sinus node
is not reset when hemodynamic characteristics of exercise are reproduced i
n the absence of modifications in central command and muscles afferents.