Reduced large elastic artery stiffness in older exercising adults is associated with suppressed nuclear factor kappa B signaling

Abstract

Large elastic artery stiffness increases with age and is a strong independent predictor of incident cardiovascular diseases (CVD) in healthy middle‐aged and older (MA/O) adults. Regular aerobic exercise attenuates this age‐associated stiffening. We hypothesized that suppression of the pro‐inflammatory transcription factor nuclear factor κB (NFκB) may be involved. Aortic pulse‐wave velocity (aPWV) was measured in young sedentary (YS, n=7, blood pressure [BP] 101±3/58±2 mmHg), MA/O sedentary (OS, n=11, 110±4/67±2 mmHg) and MA/O aerobic exercise‐trained (OT, n=12, 120±6/70±4 mmHg) healthy non‐hypertensive men and women. Baseline aPWV increased with age (602±25 [YS] vs. 852±38 [OS] cm/sec, p<0.001) but was 20% lower in OT (686±30 cm/sec) compared with OS (p<0.01). Short‐term (4 d × 2500–4500 mg) treatment with the NFκB inhibitor salsalate (randomized, cross‐over design), reduced aPWV (to 782±44 cm/sec, p<0.05) without changing BP (p=0.74) in OS, but had no effect in YS (599±23) or OT (699±30). Following salsalate treatment, aPWV no longer was significantly different in OS vs. OT (p=0.14). These results support the hypothesis that reduced NFκB signaling contributes to the lower large elastic artery stiffness in MA/O adults who regularly perform aerobic exercise. NIH AG013038, AG006537, AG03114, AG033994, RR025780