Abstract
Parasympathetic modulation of heart rate (HR) declined immediately after initiation of an ad lib high fat diet (HFD), and remained depressed during 6–12 wks of developing obesity. Contributions from altered vagal transmission and end organ sensitivity were evaluated following 1 wk or 12 wks of HFD. HR responses were recorded during graded a) vagal nerve stimulations and b) left ventricular methacholine (MCh) infusions. After 1 wk of HFD, vagally mediated bradycardia at 8 Hz was 37.3% greater in overfed rabbits compared to lean controls (−110.9 ± 11.4 vs −80.8 ± 14.1 bpm, respectively, p=NS). After 12 wks of HFD, the bradycardia was 65.8% greater in the obese animals (−111.4 ± 13.9 vs −67.2 ± 8.70 bpm, p ≤ 0.05). MCh infusions were also consistently more effective in the obese rabbits. MCh reduced heart rate more in obese rabbits than in lean controls, with differences of 16.2 and 80.5 bpm, respectively, at low and high doses (0.5 and 3.0 μg/kg). The findings support the hypothesis that obesity lowers parasympathetic transmission and induces a compensatory increase in available neurotransmitter and/or cholinergic sensitivity within the sinoatrial node.
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