TY - JOUR
T1 - Modulation of human sympathetic periodicity by mild, brief hypoxia and hypercapnia
AU - Trzebski, A.
AU - Smith, M. L.
AU - Beightol, L. A.
AU - Fritsch-Yelle, J. M.
AU - Rea, R. F.
AU - Eckberg, D. L.
PY - 1995
Y1 - 1995
N2 - We determined the influence of brief mild normocapnic hyperoxia, hypoxia, and hyperoxic hypercapnia on human muscle sympathetic nerve activity and R-R intervals, as quantified by both time- and frequency-domain analyses. We obtained measurements in nine healthy young adult men and women during uncontrolled and frequency (but not tidal volume) controlled breathing. Responses were evaluated with forward selection and backward elimination statistical models, with muscle sympathetic nerve activity as the dependent variable, and power spectral techniques. Hyperoxia and hypoxia did not alter arterial pressure; hypercapnia increased diastolic pressure modestly. Average R-R intervals tended to increase during hyperoxia, and decrease during hypoxia and hypercapnia. During 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 sympathetic nerve activity. Statistical modeling suggested that chemoreceptor 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 sympathetic power at respiratory frequencies and hypercapnia increased sympathetic power at both respiratory and (primarily in one subject) cardiac frequencies. Our data suggest that mild brief hypoxia and hypercapnia increase human muscle sympathetic nerve activity, but that this tendency is opposed by chemoreflex-induced increases of ventilation. Our results suggest also that chemoreceptor activity exerts important influences on the frequency content, as well as the quantity of sympathetic neural outflow.
AB - We determined the influence of brief mild normocapnic hyperoxia, hypoxia, and hyperoxic hypercapnia on human muscle sympathetic nerve activity and R-R intervals, as quantified by both time- and frequency-domain analyses. We obtained measurements in nine healthy young adult men and women during uncontrolled and frequency (but not tidal volume) controlled breathing. Responses were evaluated with forward selection and backward elimination statistical models, with muscle sympathetic nerve activity as the dependent variable, and power spectral techniques. Hyperoxia and hypoxia did not alter arterial pressure; hypercapnia increased diastolic pressure modestly. Average R-R intervals tended to increase during hyperoxia, and decrease during hypoxia and hypercapnia. During 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 sympathetic nerve activity. Statistical modeling suggested that chemoreceptor 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 sympathetic power at respiratory frequencies and hypercapnia increased sympathetic power at both respiratory and (primarily in one subject) cardiac frequencies. Our data suggest that mild brief hypoxia and hypercapnia increase human muscle sympathetic nerve activity, but that this tendency is opposed by chemoreflex-induced increases of ventilation. Our results suggest also that chemoreceptor activity exerts important influences on the frequency content, as well as the quantity of sympathetic neural outflow.
KW - hypercapnia
KW - hypoxia
KW - sinus arrhythmia
KW - sympathetic microneurography
UR - http://www.scopus.com/inward/record.url?scp=0028904240&partnerID=8YFLogxK
M3 - Article
C2 - 7599334
AN - SCOPUS:0028904240
SN - 0867-5910
VL - 46
SP - 17
EP - 35
JO - Journal of Physiology and Pharmacology
JF - Journal of Physiology and Pharmacology
IS - 1
ER -