title: 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.
authors.affiliation: Heart Institute (Instituto do Coração), University of São Paulo, Brazil.
authors.forename: Eduardo
authors.initials: E
authors.lastname: Rondon
authors.forename: Maria S
authors.initials: MS
authors.lastname: Brasileiro-Santos
authors.forename: Edson D
authors.initials: ED
authors.lastname: Moreira
authors.forename: Maria U P B
authors.initials: MU
authors.lastname: Rondon
authors.forename: Katt C
authors.initials: KC
authors.lastname: Mattos
authors.forename: Marcele A
authors.initials: MA
authors.lastname: Coelho
authors.forename: Gustavo J J
authors.initials: GJ
authors.lastname: Silva
authors.forename: Patricia C
authors.initials: PC
authors.lastname: Brum
authors.forename: Patricia
authors.initials: P
authors.lastname: Fiorino
authors.forename: Maria C
authors.initials: MC
authors.lastname: Irigoyen
authors.forename: Eduardo M
authors.initials: EM
authors.lastname: Krieger
authors.forename: Holly R
authors.initials: HR
authors.lastname: Middlekauff
authors.forename: Carlos E
authors.initials: CE
authors.lastname: Negrão
mesh_terms: D000465:Algorithms; D000818:Animals; D001011:Aorta / Q000294:innervation* / Q000502:physiology*; D017704:Baroreflex / Q000502:physiology*; D001794:Blood Pressure / Q000502:physiology; D002303:Cardiac Output, Low / Q000209:etiology / Q000503:physiopathology*; D006339:Heart Rate / Q000502:physiology; D007668:Kidney / Q000294:innervation / Q000502:physiology; D008297:Male; D017202:Myocardial Ischemia / Q000150:complications / Q000503:physiopathology*; D010805:Physical Conditioning, Animal / Q000502:physiology*; D011311:Pressoreceptors / Q000502:physiology; D051381:Rats; D017208:Rats, Wistar; D013564:Sympathetic Nervous System / Q000502:physiology