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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 [+ or -] 0.2 vs. 14.6 [+ or -] 3 normalized units (nu), P = 0.0003] and higher high-frequency (97.9 [+ or -] 0.2 vs. 85.0 [+ or -] 3 nu, P = 0.0005) components of pulse interval than untrained rats. Trained HF rats had higher spontaneous baroreceptor sensitivity of HR (1.19 [+ or -] 0.2 vs. 0.51 [+ or -] 0.1 ms/mmHg, P = 0.003) and RSNA [2.69 [+ or -] 0.4 vs. 1.29 [+ or -] 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 [+ or -] 215; untrained HF rats, 1,150 [+ or -] 158; and normal control rats, 2,064 [+ or -] 327 au/mmHg, P = 0.05). In conclusion, exercise training improves AODN sensitivity in HF rats. baroreflex control; autonomic nervous system

Because diabetes mellitus is associated with impairment of testicular function, ultimately leading to reduced fertility, this study was conducted to evaluate the existence of a cause-effect relationship between increased oxidative stress in diabetes and reduced mitochondrial antioxidant capacity. The susceptibility to oxidative stress and antioxidant capacity (in terms of glutathione, coenzyme Q, and vitamin E content) of testis mitochondrial preparations isolated from Goto-Kakizaki (GK) non-insulin-dependent diabetic rats and from Wistar control rats, 1 yr of age, was evaluated. It was found that GK mitochondrial preparations showed a lower susceptibility to lipid peroxidation induced by ADP/[Fe.sup.2+], as evaluated by oxygen consumption and reactive oxygen species generation. The decreased susceptibility to oxidative stress in diabetic rats was associated with an increase in mitochondrial glutathione and coenzyme Q9 contents, whereas vitamin E was not changed. These results demonstrate a higher antioxidant capacity in diabetic GK rats. We suggest this is an adaptive response of testis mitochondria to the increased oxidative damage in diabetes mellitus. diabetes mellitus; sexual dysfunction; oxidative stress; testis mitochondria; glutathione; vitamin E