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

Abstract

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 (Δdiameter/Δpressure), the neural transduction of stretch into vagal outflow (ΔR-R interval/Δdiameter), and conventional integrated cardiovagal baroreflex gain (ΔR-R interval/Δpressure). 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/μm) and lower neural (0.57±0.10 versus 0.90±0.10 ms/μm) 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/μm) that was modestly higher than that in older untrained men and neural transduction (1.00±0.20 ms/μm) 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 (β=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.