Intense exercise, especially involving eccentric contractions, causes muscle damage concomitant with increased reactive oxygen species (ROS), which can lead to increased fatigue and decrements in physical performance. Additionally, inflammatory cytokines and advanced glycation end-products (AGEs) are produced as a result of eccentric exercise and may further lead to decreased exercise performance. Nutritional interventions may provide an avenue to respond to and reduce the symptoms associated with muscle damage. Of recent interest, curcumin, the main constituent in the spice turmeric, has been the focus of various studies considering post-exercise recovery. Curcumin has potent anti-oxidant and anti-inflammatory properties and can reduce the accumulation of AGEs. This review considers the current evidence for curcumin to impact muscle recovery following exercise to improve performance and the potential mechanisms of action. To date, clinical studies have considered the potential role of curcumin to reduce muscular damage following treadmill running (downhill and flat), conventional walking/running, cycling (acute and chronic), single-leg jumping (downhill), and eccentric muscular fitness exercises of the upper and lower body (single- and double-leg). Studies have been conducted in sedentary to highly active men and women, both young and old, with supplementation duration lasting from a single, acute dose to daily dosages for three months. Various curcumin-based interventions have improved self-perceived measures of pain and tenderness, reduced evidence of muscle damage, ameliorated inflammatory markers, increased markers of antioxidant capacity, diminished markers of oxidative stress, reduced markers of AGEs, and attenuated loss in mean power of single-leg sprints. However, these findings have not been consistently reported.

Heart failure (HF) is associated with increased large conduit artery stiffness and afterload resulting in stiffening of the coronary arteries. Perivascular adipose tissue (PVAT) and advanced glycation end products (AGE) both promote arterial stiffness, yet the mechanisms by which coronary PVAT promotes arterial stiffness and the efficacy of exercise to prevent coronary stiffness are unknown. We hypothesized that both chronic continuous and interval exercise training would prevent coronary PVAT-mediated AGE secretion and arterial stiffness. Yucatan miniature swine were divided into four groups: control-sedentary (CON), aortic banded sedentary-heart failure (HF), aortic banded HF-continuous exercise trained (HF+CONT), and aortic banded HF-interval exercise trained (HF+IT). The left circumflex and right coronary arteries underwent ex vivo mechanical testing, and arterial AGE, elastin, and collagen were assessed. Coronary elastin elastic modulus (EEM) and elastin protein were lower and AGE was increased with HF compared with CON, which was prevented by both HF+CONT and HF+IT. Mouse aortic segments treated with swine coronary PVAT conditioned medium had lower EEM and elastin content and greater AGE secretion and arterial AGE accumulation in HF compared with CON, which was prevented by both HF+CONT and HF+IT. Aminoguanidine (AMG), an AGE inhibitor, prevented the reduction in EEM, arterial elastin content, and AGE accumulation in mouse aortic segments treated with PVAT conditioned medium in the HF group. Our data demonstrate efficacy for chronic continuous and interval exercise to prevent coronary artery stiffness via inhibition of PVAT-derived AGE secretion in a preclinical miniswine model of pressure overload-induced HF. NEW & NOTEWORTHY Our findings show that chronic continuous and interval exercise training regimens prevent coronary artery stiffness associated with inhibition of perivascular adipose tissue-derived advanced glycation end products in a translational pressure overload-induced heart failure model potentially providing an effective therapeutic option for heart failure patients.

Background: Healthy vascular aging (HVA) and cardiorespiratory fitness (CRF) are each independently associated with lower cardiovascular disease-related mortality. It is unknown, however, whether the CRF-related reductions in cardiovascular disease risk are related to HVA. We hypothesized that HVA would be associated with higher CRF in men and women from the Ball State Adult Fitness Longitudinal Lifestyle STudy (BALL ST). Methods: Apparently healthy men and women ≥50 yr of age from the BALL ST cohort (n = 101) who underwent a maximal cardiopulmonary exercise test to assess CRF (V˙O _2peak) were included in the study. Participants were divided into either HVA, defined as brachial systolic blood pressure <140/90 mm Hg without taking medications and carotid-femoral pulse wave velocity 140/90 mm Hg and/or PWV >7.6 m/sec. Results: Participants with HVA had a higher age- and sex-adjusted CRF percentile (62 ± 5 vs 47 ± 3, P < .05), with women having a greater prevalence of HVA than men (36% vs 15%, P < .05). Both carotid-femoral pulse wave velocity (r =−0.27, P < .05) and brachial systolic blood pressure (r =−0.23, P < .05) were independently and inversely associated with CRF for the entire cohort. Men and women with HVA were younger having a lower body fat percentage and higher low-density lipoprotein cholesterol (P < .05, all). Conclusions: These data demonstrate that HVA is associated with higher CRF, which may partially explain the preventative cardioprotective effects of CRF.