Exercise training improves aortic depressor nerve sensitivity in rats with ischemia-induced heart failure

Abstract

Exercise training improves arterial baroreflex control in heart failure (HF) rabbits. However, the mechanisms involved in the amelioration of baroreflex control are unknown. We tested the hypothesis that exercise training would increase the afferent aortic depressor nerve activity (AODN) sensitivity in ischemic-induced HF rats. Twenty ischemic-induced HF rats were divided into trained (n = 11) and untrained (n = 9) groups. Nine normal control rats were also studied. Power spectral analysis of pulse interval, systolic blood pressure, renal sympathetic nerve activity (RSNA), and AODN were analyzed by means of autoregressive parametric spectral and cross-spectral algorithms. Spontaneous baroreflex sensitivity of heart rate (HR) and RSNA were analyzed during spontaneous variation of systolic blood pressure. Left ventricular end-diastolic pressure was higher in HF rats compared with that in the normal control group (P = 0.0001). Trained HF rats had a peak oxygen uptake higher than untrained rats and similar to normal controls (P = 0.01). Trained HF rats had lower low-frequency [1.8 +/- 0.2 vs. 14.6 +/- 3 normalized units (nu), P = 0.0003] and higher high-frequency (97.9 +/- 0.2 vs. 85.0 +/- 3 nu, P = 0.0005) components of pulse interval than untrained rats. Trained HF rats had higher spontaneous baroreceptor sensitivity of HR (1.19 +/- 0.2 vs. 0.51 +/- 0.1 ms/mmHg, P = 0.003) and RSNA [2.69 +/- 0.4 vs. 1.29 +/- 0.3 arbitrary units (au)/mmHg, P = 0.04] than untrained rats. In HF rats, exercise training increased spontaneous AODN sensitivity toward normal levels (trained HF rats, 1,791 +/- 215; untrained HF rats, 1,150 +/- 158; and normal control rats, 2,064 +/- 327 au/mmHg, P = 0.05). In conclusion, exercise training improves AODN sensitivity in HF rats.

Effects of Long-Term Exercise Training on Autonomic Control in Myocardial Infarction Patients

“…Laterza et al 22 found that exercise training improved BRS and decreased MSNA in never-treated hypertensive patients. Moreover, evidence in the infarct model in rats is consistent with the concept that the increase in BRS is attributed to enhancement in aortic depressor nerve discharge, 21 which is suggestive of amelioration in blood vessel elasticity. It is well known that MI impairs not only reflexes from cardiac receptors but also activates sympathetic afferent fibers in the myocardium, which significantly contribute to sympathoexcitation.…”

“…The improvement of baroreflex control in these 2 different territories (heart and vessels) suggests that exercise training affects the afferent components or bulbar nuclei of the baroreflex pathway. In fact, Rondon et al 21 demonstrated an improvement in aortic depressor nerve sensitivity after exercise training in rats with ischemiainduced heart failure.…”

Aerobic exercise training in heart failure: impact on sympathetic hyperactivity and cardiac and skeletal muscle function

“…The same investigators also demonstrated that this response was mainly parasympathetic-mediated since atropine blocked the improved baroreflex control of heart rate by exercise training (36). In addition, we also demonstrated that improved baroreflex control of renal sympathetic nerve activity in a rat model of myocardial infarction was associated with increased aortic depressor nerve sensitivity (13).…”

“…The beneficial effects of exercise training in HF are associated with neural control of the cardiovascular system (12,13). These effects include reduction of sympathetic outflow in exercised humans (14,15) and animals (16)(17)(18) with HF.…”

Hemodynamic Changes and Autonomic Nervous System After Acute Myocardial Infarction in Rats Submitted to Left Coronary Artery Ligation

“…Evidence has been provided that both the baroreflex control of HR and the HRV may be impaired after myocardial infarction, identifying subgroups of patients with a high susceptibility to malignant ventricular arrhythmias 26 . Previously, we show that the baroreflex control of HR is normal in anesthetized rats 30 days after a myocardial infarction and that these rats had higher spontaneous baroreceptor sensitivity of HR when submitted to exercise training compared to untrained rats 27,28 . Also, the sympathetic tone was higher during the tachycardic phase after myocardial infarction.…”