Mechanoreceptor contribution to efferent autonomic outflow is incompletely understood. To determine the effects of mechanoreceptor stimulation on autonomic reflexes, we compared autonomic responses in 34 subjects using a cross-over, counter-balanced design, in which hemodynamic, electromyographic, metabolic, and autonomic data were gathered during rest, passive, and active movement protocols. Because metaboreceptors and ventilatory responses influence autonomic outflow we verified and controlled for these influences during all protocols through comparisons of breath-by-breath gas exchange measurements. Verification of active and passive movements was made via electromyographic recordings of the moving legs. Spectral analysis of R-R variability was used to assess autonomic activity, and low to high frequency ratios were considered representative of sympathovagal balance. A repeated measures analysis of variance revealed significant modulating effects of mechanoreceptor stimulation on sympathovagal balance during passive movement upon efferent autonomic outflow (p < 0.01) independent of central command, chemoreceptor, and metaboreceptor stimulation. Furthermore, breathing frequency and volume were identical for both movement protocols. Therefore, findings in this investigation suggest that modulating influences are being exerted by mechanoreceptor stimulation on autonomic outflow to the heart.

Loss of autonomic balance characterized by increased sympathetic activity and decreased vagal activity has been implicated as a major cardiovascular risk factor. Aspirin's cardioprotective abilities involve a multitude of physiologic processes. However, the effects of aspirin on cardiac autonomic activity are unknown. In a double-blind crossover study, 22 subjects randomly received either aspirin or placebo in the amounts of 325 mg with each meal (three times per day) over a 2.5-day period. The total amount of aspirin ingested was 2,275 mg, which resulted in plasma levels of 3.3 mg/dl. At the conclusion of each treatment, subjects were evaluated for autonomic physiology activity using standard autonomic tests. Power spectral analyses of the electrocardiograms were used to delineate autonomic function. A 2 x 4 repeated measures analysis of variance revealed significant and favorable changes in autonomic activity after the use of aspirin. Specifically, at rest high-frequency (HF) power was significantly higher (mean, 1,090 + 1,463.5 msec2) compared with the placebo (mean, 692 742 msec2) (p<0.05). Low-frequency (LF) power was significantly reduced (mean, 963 745 msec2) after aspirin compared with placebo (mean, 1,100 906 msec2). After the aspirin treatment, a significantly lower LF-to-HF power ratio (mean, 1.7 2 msec2) was noted at rest when compared with the placebo (mean, 2.5 2.7 msec2) (p <0.05). Similar significant trends were seen during the sustained isometric contraction after aspirin therapy for HF power (mean 210 2.15 msec2) compared with placebo (mean, 213 184 msec2) (p <0.05). Accordingly, the LF-to-HF power ratio was lower as well when compared to placebo treatment (mean, 2.3 3.5 msec2) (mean, 5.3 8.4 msec2) (p <0.05). No differences were found in breathing rates for hemodynamic variables between any of the protocols. The significant reduction of LF-to-HF ratio, a marker of sympathovagal balance, for both protocols appeared to be largely due to a withdrawal of LF modulation and concomitant but lesser increase in HF modulation. Favorable alterations in autonomic outflow through prostaglandin inhibition may be one of the mechanisms by which low therapeutic amounts of aspirin provide prophylactic cardioprotection.