OBJECTIVE: High dietary salt has been demonstrated to inhibit angiogenesis in skeletal muscle. The purpose of this study was to determine whether high salt impairs steady state muscle performance following a chronic stimulation protocol. METHODS: Sprague-Dawley rats were placed on a control diet (CD, 0.4% NaCl) or high salt diet (HSD, 4.0% NaCl) prior to implantation of an electrical muscle stimulator. In chronically stimulated animals, hind limb muscles were stimulated to contract eight hours daily for seven days. Sham animals received a stimulator that was never activated. RESULTS: Following chronic stimulation, tibialis anterior (TA) muscles of animals on CD demonstrated an 84.6% increase in force of contraction at the end of an acute stimulation bout relative to sham animals fed CD. Decreased muscle fatigue was associated with an increase in capillaries per TA fiber (C:F). Chronic stimulation in HSD rats induced a smaller improvement (52.2%) in final force compared to HSD sham rats. This impairment of muscle performance in high salt-fed rats correlated with inhibited angiogenesis. Infusion of angiotensin II in HSD animals restored angiogenesis and muscle fatigue to CD levels. CONCLUSIONS: This study suggests that angiogenic inhibition by high salt is associated with impaired skeletal muscle performance following chronic stimulation.
OBJECTIVE: High dietary salt has been demonstrated to inhibit angiogenesis in skeletal muscle. The purpose of this study was to determine whether high salt impairs steady state muscle performance following a chronic stimulation protocol. METHODS:Sprague-Dawley rats were placed on a control diet (CD, 0.4% NaCl) or high salt diet (HSD, 4.0% NaCl) prior to implantation of an electrical muscle stimulator. In chronically stimulated animals, hind limb muscles were stimulated to contract eight hours daily for seven days. Sham animals received a stimulator that was never activated. RESULTS: Following chronic stimulation, tibialis anterior (TA) muscles of animals on CD demonstrated an 84.6% increase in force of contraction at the end of an acute stimulation bout relative to sham animals fed CD. Decreased muscle fatigue was associated with an increase in capillaries per TA fiber (C:F). Chronic stimulation in HSDrats induced a smaller improvement (52.2%) in final force compared to HSD sham rats. This impairment of muscle performance in high salt-fed rats correlated with inhibited angiogenesis. Infusion of angiotensin II in HSD animals restored angiogenesis and muscle fatigue to CD levels. CONCLUSIONS: This study suggests that angiogenic inhibition by high salt is associated with impaired skeletal muscle performance following chronic stimulation.
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