Purpose: We compared arterial, aortic, and carotid-cardiac baroreflex sensi
tivity in eight average fit (maximal oxygen uptake, (V) over dot (2max) = 4
2.2 +/- 1.9 mL.kg(-1).min(-1)) and eight high fit ((V) over dot (2max) = 61
.9 +/- 2.2 mL.kg(-1).min(-1)) healthy young adults. Methods: Arterial and a
ortic (ABR) baroreflex functions were assessed utilizing hypo- and hyper-te
nsive challenges induced by graded bolus injections of sodium nitroprusside
(SN) and phenylephrine (PE), respectively. Carotid baroreflex (CBR) sensit
ivity was determined using ramped 5-s pulses of both pressure and suction d
elivered to the carotid sinus via a neck chamber collar, independent of dru
g administration. Results: During vasoactive drug injection, mean arterial
pressure (MAP) was similarly altered in average fit (AF) and high fit II-IF
) groups. However, the heart rate (HR) response range of the arterial baror
eflex was significantly attenuated (P < 0.05) in HF (31 +/- 4 beats min-l)
compared with AF individuals (46 +/- 4 beats min(-1)). When sustained neck
suction and pressure were applied to counteract altered carotid sinus press
ure during SN and PE administration, isolating the ABR response, the respon
se range remained diminished (P 4 0.05) in the HF population (24 +/- 3 beat
s min(-1)) compared with the AF group (41 +/- 4 beats.min(-1)). During CBR
perturbation, the HF (14 +/- 1 beats.min(-1)) and AF (16 +/- 1 beats.min(-1
)) response ranges were similar. The arterial baroreflex response range was
significantly less than the simple sum of the CBR and ABR (HF, 38 +/- 3 be
ats.min(-1) and AF, 57 +/- 4 beats.min(-1)) in both fitness groups. Conclus
ions: These data confirm that reductions in arterial-cardiac reflex sensiti
vity are mediated by diminished ABR function. More importantly, these data
suggest that the integrative relationship between the ABR and CBR contribut
ing to arterial baroreflex control of HR is inhibitory in nature and not al
tered by exercise training.