INFLUENCE OF AGE ON THE SYMPATHETIC NEURAL ADJUSTMENTS TO ALTERATIONSIN SYSTEMIC OXYGEN LEVELS IN HUMANS

We tested the hypothesis that aging influences the regulation of sympa thetic nervous system activity (SNA) and arterial blood pressure durin g alterations in systemic O-2 levels in humans. To accomplish this, ar e performed direct (intraneural) measurements of SNA to skeletal muscl e (MSNA) in 10 young and 7 older healthy normotensive men during room air breathing (normoxic control), moderate isocapnic hypoxemia [15 min of 10% fractional inspired O-2 (FIO2)], and hyperoxemia (10 min of 50 % FIO2). After hypoxemia, arterial O-2 saturation (SaO(2)) declined si milarly in the young and older men. MSNA (burst frequency and total mi nute activity) increased significantly (P < 0.05) in both groups. The magnitudes of the absolute increases in MSNA and the Delta MSNA/Delta SaO(2) were not significantly different in the young and older men; ho wever, because of higher normoxic baseline levels, the percentage incr eases in burst frequency were smaller (P = 0.02) and those for total m inute activity tended to be smaller (P = 0.11) in the older men. Arter ial blood pressure increased modestly (P < 0.05) and similarly in both groups, although the older men demonstrated a smaller increase in hea rt rate. After hypoxemia, SaO(2) increased and MSNA decreased (both P < 0.05) similarly in the young and older men. Arterial blood pressure did not change significantly from normoxic control levels in either gr oup; however, a small (P < 0.05) reduction in heart rate was observed in both groups. In conclusion, aging does not obviously influence the regulation of absolute levels of MSNA or arterial blood pressure durin g alterations in systemic O-2 levels in healthy men, although older me n demonstrate a smaller percentage increase in MSNA from their elevate d baseline levels, as well as an attenuated tachycardia in response to acute hypoxemia. As such, the present results are consistent with our previous findings on aging and sympatho-circulatory control during ot her types of acute stress in humans.