Does reduced vascular stiffening fully explain preserved cardiovagal baroreflex function in older physically active men?

BACKGROUND We measured cardiovagal baroreflex gain and its vascular mechanical and neural components during dynamic baroreflex engagement in 10 young untrained men, 6 older untrained men, and 12 older, physically active men. METHODS AND RESULTS Our newly developed assessment of beat-to-beat carotid diameters during baroreflex engagement estimates the mechanical transduction of pressure into barosensory stretch (diameter/pressure), the neural transduction of stretch into vagal outflow (R-R interval/diameter), and conventional integrated cardiovagal baroreflex gain (R-R interval/pressure). Integrated gain was lower in older untrained men than in young untrained men (6.8+/-1.2 versus 15.7+/-1.8 ms/mm Hg) due to both lower mechanical (9.1+/-1.0 versus 17.1+/-2.4 mm Hg/microm) and lower neural (0.57+/-0.10 versus 0.90+/-0.10 ms/microm) transduction. Integrated gain in older active men (13.3+/-2.7 ms/mm Hg) was comparable to that in young untrained men. This was achieved through mechanical transduction (12.1+/-1.4 mm Hg/microm) that was modestly higher than that in older untrained men and neural transduction (1.00+/-0.20 ms/microm) comparable to that in young untrained men. Across groups, both mechanical and neural components were related to integrated gain; however, the neural component carried greater predictive weight (beta=0.789 versus 0.588). CONCLUSIONS Both vascular and neural deficits contribute to age-related declines in cardiovagal baroreflex gain; however, long-term physical activity attenuates this decline by maintaining neural vagal control.