Jaboticaba berry (Myrciaria jaboticaba) supplementation protects against micro- and macrovascular dysfunction induced...

Physical activities that are unaccustomed and involve eccentric muscle contractions have been demonstrated to temporarily impair macrovascular and microvascular functions, which may be caused by exercise-induced oxidative stress. Jaboticaba (Myrciaria jaboticaba) is a famous Brazilian berry that has been described to exhibit high antioxidant activity. However, no human study has investigated the protective effects of jaboticaba consumption against the vascular damage induced by eccentric exercise. Therefore, the present study aimed to assess whether supplementation with jaboticaba berry juice could positively affect macro- and microvascular functions within 48 hours after eccentric exercise. This randomized, double-blind, placebo-controlled, parallel trial enrolled 24 healthy participants consuming 250 mL per day of jaboticaba berry juice (containing ∼1,300 mg of total polyphenols) or placebo for 6 days. At the baseline, pre-exercise, and 24 h and 48 h postexercise stages, blood samples were taken for analysis of reduced glutathione (GSH) levels. Also, brachial artery flow-mediated dilation (FMD), blood flow, and tissue oxygen saturation (StO₂) responses to 5-minute cuff occlusion were assessed using Doppler ultrasound and near-infrared spectroscopy, respectively. Our findings revealed significant decreases in blood GSH (P < 0.001, ES = 0.76), FMD (P = 0.005, ES = 0.48), reperfusion slope of StO₂ (P = 0.018, ES = 0.42) at 24 h and blood flow (P = 0.012, ES = 0.42) at 48 h following eccentric exercise in the control group as compared to the jaboticaba berry juice group. Our results demonstrated that jaboticaba berry juice prevented the exercise-induced increase in reactive oxygen species production and protected macro- and microvascular functions against the damage caused by eccentric exercise, suggesting that jaboticaba berry consumption could protect the vascular function under conditions of imbalance in redox homeostasis.