Congestive heart failure (CHF) induces abnormal regulation of peripheral blood flow during exercise. Previous studies have suggested that a reflex from contracting muscle is disordered in this disease. However, there has been very little investigation of the muscle reflex regulating sympathetic outflows in CHF. Myocardial infarction (MI) was induced by the coronary artery ligation in rats. Echocardiography was performed to determine fractional shortening (FS), an index of the left ventricular function. We examined renal and lumbar sympathetic nerve activities (RSNA and LSNA, respectively) during 1-min repetitive (1- to 4-s stimulation-to-relaxation) contraction or stretch of the triceps surae muscles. During these interventions, the RSNA and LSNA responded synchronously as tension was developed. The RSNA and LSNA responses to contraction were significantly greater in MI rats (n=13) with FS < 30% than in control animals (n=13) with FS > 40% (RSNA: +49±7 vs. +19±4 a.u., P<0.01; LSNA: +28±7 vs. +8±2 a.u., P<0.01) at the same tension development. Stretch also increased the RSNA and LSNA to a large degree in MIs (n=13) than in controls (n=13) (RSNA: +36±6 vs. +19±3 a.u., P<0.05; LSNA: +24±3 vs. +9±2 a.u., P<0.01). The data demonstrate that CHF exaggerates sympathetic nerve responses to muscle contraction as well as stretch. We suggest that muscle afferents-mediated sympathetic outflows contribute to the abnormal regulation of peripheral blood flow seen during exercise in CHF.