We previously demonstrated that nonfatiguing rhythmic forearm exercise at 25% maximal voluntary contraction (12 2-s contractions/min) evokes sympathoexcitation without significant engagement of metabolite-sensitive muscle afferents (B.A. Batman, J.C. Hardy, U.A. Leuenberger, M.B. Smith, Q.X. Yang and L.I. Sinoway. J. Appl. Physiol. 76: 1077-1081, 1994). This is in contrast to the sympathetic nervous system responses observed during fatiguing static forearm exercise where metabolite-sensitive afferents are the key determinants of sympathetic activation. In this report we examined whether forearm exercise training would attenuate sympathetic nervous system responses to rhythmic forearm exercise. We measured heart rate, mean arterial blood pressure (MAP), muscle sympathetic nerve activity (microneurography), plasma norepinephrine (NE), and NE spillover and clearance (tritiated NE kinetics) during nonfatiguing rhythmic forearm exercise before and after a 4-wk unilateral forearm training paradigm. Training had no effect on forearm mass, maximal voluntary contraction, or heart rate but did attenuate the increase in MAP (increase in MAP: from 15.2 +/- 1.8 before training to 11.4 +/- 1.4 mmHg after training; P < 0.017), muscle sympathetic nerve activity (increase in bursts: from 10.8 +/- 1.4 before training to 6.2 +/- 1.1 bursts/min after training; P < 0.030), and the NE spillover (increases in arterial spillover: from 1.3 +/- 0.2 before training to 0.6 +/- 0.2 nmol.min-1.m-2 after training, P < 0.014; increase in venous spillover: from 2.0 +/- 0.6 before training to 1.0 +/- 0.5 nmol.min-1.m-2 after training, P < 0.037) seen in response to exercise performed by the trained forearm. Thus forearm training reduces sympathetic responses during a nonfatiguing rhythmic handgrip paradigm that does not engage muscle metaboreceptors. We speculate that this effect is due to a conditioning-induced reduction in mechanically sensitive muscle afferent discharge.

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These results support the conclusion that two dimensional echo/Doppler techniques can be used to estimate rapidly and non-invasively the degree of left ventricular damage produced in living rats with myocardial infarction when compared to non-infarcted controls.