Augmented cardiopulmonary and integrative sympathetic baroreflexes but attenuated peripheral vasoconstriction with age.

Based on observations of smaller increases in limb vascular resistance during acute incremental hypovolemia in older adults, cardiopulmonary and integrative (combined cardiopulmonary and arterial) baroreflex control of sympatho-circulatory function is thought to be impaired with aging in humans. We tested this hypothesis directly by making intraneural measurements of skeletal muscle sympathetic nerve activity (MSNA; peroneal microneurography) in groups of young (23+/-1 years; n=11) and older (64+/-1 years; n=12) healthy adult men during progressive hypovolemia produced by graded (-5 to -40 mm Hg) lower body negative pressure (LBNP). Baseline levels of MSNA and arterial blood pressure were higher and heart rate was lower in the older subjects (P<0.05). Lower levels of LBNP (-5 to -20 mm Hg) did not affect arterial blood pressure or heart rate in either group; systolic and pulse pressures declined during higher levels of LBNP (-30 and -40 mm Hg) but only in the young subjects (P<0.05). Graded LBNP evoked progressive, linear reductions in peripheral venous pressure (PVP) and increases in MSNA, plasma norepinephrine concentration (PNE), and forearm vascular resistance (FVR) in both groups (all P<0.05). DeltaMSNA/ deltaPVP was approximately 150% greater in the older versus young men during both lower and higher levels of hypovolemia (P<0.01); however, deltaFVR/deltaPVP was approximately 50% smaller in the older men (P<0.05). There was no difference in the MSNA-PNE relation with age, but deltaFVR/deltaMSNA was approximately 65% to 70% smaller in the older subjects (P<0.05). Our findings indicate that cardiopulmonary and integrative baroreflex control of central sympathetic outflow during hypovolemia is augmented, not impaired, with age in healthy humans. However, the reflex-mediated increases in limb vascular resistance during hypovolemia are smaller in older adults because of attenuated vasoconstrictor responsiveness to sympathetic stimulation.