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1 Penn State Heart & Vascular Institute, Pennsylvania State University College of Medicine, Hershey, Pennsylvania, United States
2 Penn State Heart & Vascular Institute, Pennsylvania State University College of Medicine, Hershey, United States
* To whom correspondence should be addressed. E-mail: jzl10{at}psu.edu.
This study was undertaken to test the hypothesis that activation of the muscle reflex elicits less sympathetic activation towards skeletal muscle than to internal organs. In decerebrate rats, we examined renal and lumbar (mainly innervating hindlimb blood vessels) sympathetic nerve activities (RSNA and LSNA, respectively) during: 1) 1-min repetitive (1- to 4-s stimulation-to-relaxation) contraction of the triceps surae muscles; 2) repetitive tendon stretch; and 3) repetitive contraction with hindlimb circulatory occlusion. During these interventions, the RSNA and LSNA responded synchronously as tension was developed. The increase in RSNA was greater than that for LSNA (+51±14 vs. +24±5%, p<0.05 in contraction; +46±8 vs. +17±4%, p<0.05 in stretch; +76±20 vs. +39±7%, p<0.05 in contraction with occlusion) during all three interventions; repetitive contraction (n=10, +508±48 g in tension from baseline), tendon stretch (n=12, +454±34 g), and contraction during hindlimb circulatory occlusion (n=9, +473±33 g). Additionally, hindlimb circulatory occlusion significantly enhanced the RSNA and LSNA responses to contraction. These data demonstrate that the RSNA responses to muscle contraction and stretch are greater as compared with the LSNA. We suggest that activation of the muscle afferents induces the differential sympathetic outflow that is directed towards the kidney as opposed to the limbs. This contributes to the distribution of cardiac output observed during exercise. We further suggest that as exercise proceeds muscle metabolites produced in contracting muscle sensitize muscle afferents and enhance sympathetic drive to both limbs and renal beds.
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