MODULATION OF HUMAN SYMPATHETIC PERIODICITY BY MILD, BRIEF HYPOXIA AND HYPERCAPNIA

We determined the influence of brief mild normocapnic hyperoxia, hypox ia, and hyperoxic hypercapnia on human muscle sympathetic nerve activi ty and R-R intervals, as quantified by both time- and frequency-domain analyses. We obtained measurements in nine healthy young adult men an d women during uncontrolled and frequency (but not tidal volume) contr olled breathing. Responses were evaluated with forward selection and b ackward elimination statistical models, with muscle sympathetic nerve activity as the dependent variable, and power spectral techniques. Hyp eroxia and hypoxia did not alter arterial pressure; hypercapnia increa sed diastolic pressure modestly. Average R-R intervals tended to incre ase during hyperoxia, and decrease during hypoxia and hypercapnia. Dur ing uncontrolled breathing, changes of inspiratory gases exerted only minor effects on muscle sympathetic nerve activity; during controlled breathing, both hypoxia and hypercapnia tended to increase muscle symp athetic nerve activity. Statistical modeling suggested that chemorecep tor stimulation increased muscle sympathetic neural outflows, but that increases of sympathetic traffic were opposed by secondary increases of ventilation. Inspiratory gases modulated the frequency distribution of muscle sympathetic nerve activity strikingly: hypoxia increased sy mpathetic power at respiratory frequencies and hypercapnia increased s ympathetic power at both respiratory and (primarily in one subject) ca rdiac frequencies. Our data suggest that mild brief hypoxia and hyperc apnia increase human muscle sympathetic nerve activity, but that this tendency is opposed by chemoreflex-induced increases of ventilation. O ur results suggest also that chemoreceptor activity exerts important i nfluences on the frequency content, as well as the quantity of sympath etic neural outflow.