Background and Aim: The relationship between inspiratory muscle weakness and exercise intolerance in patients with heart failure has not been established, especially in elderly patients. The aim of this study was to investigate the relationship between inspiratory muscle strength and exercise tolerance according to age in elderly patients with heart failure. Methods: A total of 25 hospitalized patients were allocated to younger group (age<75) or older group (age>75). Medical records were reviewed with regard to echocardiograms (EF, LVDd/Ds), laboratory data (BNP), chest X-ray (CTR). We assessed inspiratory muscle strength (PImax), knee extensor muscle strength (KEMS), six-minute walk distance (6MWD) and normal / maximal gate speed. The correlation between 6MWD and other values was tested by Pearson's product-moment correlation coefficient in each group. Differences between 2 groups were compared with using stu-dent's t-test. A P-value of <.05 was considered to be statistically significant. Results: 6MWD was significantly correlated with PImax (r=0.74), KEMS (r=0.81), normal gate speed (r=0.71), maximal gate speed (r=0.68) in younger group. On the other hand, 6MWD was significantly correlated with only KEMS (r=0.57) and maximal gate speed (r=0.63) in older group. The value of 6MWD was shorter and the value of gate speed was slower in older group compared with those values in younger group (p<.05). Conclusion: These results suggested that inspiratory muscle weakness might be associated with exercise intolerance in younger patients with heart failure. Meanwhile, muscle strength and gate speed might be important as a determining factor of exercise tolerance in elderly patients with heart failure. Background: Although Chinese pulmonary function testing (PFT)

Several investigators have demonstrated that diabetes is associated with autonomic and myocardial dysfunction. Exercise training is an efficient non-pharmacological treatment for cardiac and metabolic diseases. The aim of the present study was to investigate the effects of exercise training on hemodynamic and autonomic diabetic dysfunction. After 1 week of diabetes induction (streptozotocin, 50 mg/kg, iv), male Wistar rats (222 ± 5 g, N = 18) were submitted to exercise training for 10 weeks on a treadmill. Arterial pressure signals were obtained and processed with a data acquisition system. Autonomic function and intrinsic heart rate were studied by injecting methylatropine and propranolol. Left ventricular function was assessed in hearts perfused in vitro by the Langendorff technique. Diabetes (D) bradycardia and hypotension (D: 279 ± 9 bpm and 91 ± 4 mmHg vs 315 ± 11 bpm and 111 ± 4 mmHg in controls, C) were attenuated by training (TD: 305 ± 7 bpm and 100 ± 4 mmHg). Vagal tonus was decreased in the diabetic groups and sympathetic tonus was similar in all animals. Intrinsic heart rate was lower in D (284 ± 11 bpm) compared to C and TD (390 ± 8 and 342 ± 14 bpm, respectively). Peak systolic pressure developed at different pressures was similar for all groups, but +dP/dt max was decreased and -dP/dt max was increased in D. In conclusion, exercise training reversed hypotension and bradycardia and improved myocardial function in diabetic rats. These changes represent an adaptive response to the demands of training, supporting a positive role of physical activity in the management of diabetes.

Several investigators have demonstrated that streptozotocin (STZ) diabetes induces changes in the autonomic control of the cardiovascular system. Changes in cardiovascular function may be related to peripheral neuropathy. The aim of the present study was to analyze changes in heart rate (HR) and arterial pressure (AP) as well as baroreflex and chemoreflex sensitivity in STZ-induced diabetic male Wistar rats (STZ, 50 mg/kg, iv, 15 days). Intra-arterial blood pressure signals were obtained for control and diabetic rats (N = 9, each group). Data were processed in a data acquisition system (CODAS, 1 kHz). Baroreflex sensitivity was evaluated by measuring heart rate changes induced by arterial pressure variation produced by phenylephrine and sodium nitroprusside injection. Increasing doses of potassium cyanide (KCN) were used to evaluate bradycardic and pressor responses evoked by chemoreflex activation. STZ induced hyperglycemia (447 ± 49 vs 126 ± 3 mg/dl), and a reduction in AP (99 ± 3 vs 118 ± 2 mmHg), resting HR (296 ± 11 vs 355 ± 16 bpm) and plasma insulin levels (16 ± 1 vs 57 ± 11 µU/ml). We also observed that the reflex bradycardia (-1.68 ± 0.1 vs -1.25 ± 0.1 bpm/mmHg, in the diabetic group) and tachycardia (-3.68 ± 0.5 vs -1.75 ± 0.3 bpm/mmHg, in the diabetic group) produced by vasopressor and depressor agents were impaired in the diabetic group. Bradycardia evoked by chemoreflex activation was attenuated in diabetic rats

In CHF patients with IMW, IMT results in a significant increase in OUES.