hronic congestive heart failure (CHF) is a complex metabolic syndrome resulting from global hypoperfusion and neurohumoral activation. Sympathoadrenergic hyperactivity and stimulation of the reninangiotensin -aldosterone cascade promote endothelial dysfunction in the macro-and microcirculation, and thus influence the distribution of the terminal blood flow. The increased total peripheral resistance, reduction of blood supply and impaired peripheral vascular dilatation in response to vasodilator stimuli result in atrophy of skeletal muscle and decreased oxidative activity. Physical training could reverse the pathologic changes in patients with CHF and there have been many reports during the past decade that clearly demonstrate the benefits of exercise on functional capacity, ventilation, metabolic status, autonomic control of heart rate (HR) variability and other parameCirculation Journal Vol. 70, January 2006 ters, 1-5 including skeletal muscle performance and impaired endothelial function. 6,7 However, most of the actual training protocols are based on systemic exercise requiring increased cardiac output, which cannot be achieved by all patients, and in general are only suitable for patients with a moderately advanced grade of CHF; less attention has been paid to the development of safe and efficient training programs for patients with severe grades of the disease. Background This study was designed to evaluate the effects of low-frequency electrical stimulation (LFES) on muscle strength and blood flow in patients with advanced chronic heart failure (CHF). Methods and ResultsPatients with CHF (n=15; age 56.5±5.2 years; New York Heart Association III -IV; ejection fraction 18.7±3.3%) were examined before and after 6 weeks of LFES (10 Hz) of the quadriceps and calf muscles of both legs (1 h/day, 7 days/week). Dynamometry was performed weekly to determine maximal muscle strength (Fmax; N) and isokinetic peak torque (PTmax; Nm); blood flow velocity (BFV) was measured at baseline and after 6 weeks of LFES using pulsed-wave Doppler velocimetry of the right femoral artery.

These results suggest that exercise does not worsen renal function and has renal-protective effects in this model of rats. Moreover, the antihypertensive therapy has additional renal-protective effects in this model of rats.

1. Low-voltage electrical stimulation (LVES) in skeletal muscle at a level far below the threshold of muscle contraction has been reported to promote local angiogenesis. However, the mechanism underlying the promotion of local angiogenesis by LVES has not been fully elucidated. In the present study, we evaluated whether angiogenic factors, such as vascular endotherial growth factor (VEGF), hepatocyte growth factor (HGF) and fibroblast growth factor (FGF), as well as other disadvantageous factors, such as inflammation (interleukin (IL)-6) and hypoxia (hypoxia-inducible factor (HIF)-1alpha), contribute to the local angiogenesis produced by LVES. 2. We completely excised bilateral femoral arteries of male Sprague-Dawley rats. After the operation, electrodes were implanted onto the centre of the fascia of the bilateral tibialis anterior (TA) muscles, tunnelled subcutaneously and exteriorized at the level of the scapulae. The right TA muscles of rats were stimulated continuously at a stimulus frequency of 50 Hz, with a 0.1 V stimulus strength and no interval, for 5 days. The left TA muscles served as controls. 3. We found that both VEGF and HGF protein were significantly increased by LVES in stimulated muscles compared with control. The VEGF level of the LVES group was 89.10 +/- 17.19 ng/g, whereas that of the control group was 65.07 +/- 12.88 ng/g, as determined by ELISA (P < 0.05). The HGF level of the LVES and control groups was 8.52 +/- 1.96 and 5.80 +/- 2.14 ng/g, respectively (P < 0.05). In contrast, there was no difference in FGF, IL-6 and HIF-1alpha between the LVES and control groups. 4. These results suggest that LVES in a hindlimb ischaemia model of rats increases not only VEGF, but also HGF, production, which may be the main mechanism responsible for the angiogenesis produced by LVES.

Exercise training and bisoprolol have similar effects concerning resting hemodynamics and baroreflex function in SHR. Although additive effects of exercise training to bisoprolol are not evident under quiet, nonstressful conditions, some additive effects may be obtained under stress such as restrain.

The aim of this study was to evaluate the effects of moderate-intensity regular exercise and/or an angiotensin converting enzyme (ACE) inhibition on tumor necrosis factor-(TNF-) and glucose and lipid