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Background: Recent studies have highlighted the importance of cherry and cocoa extracts consumption to protect cells from oxidative stress, paying particular attention to cocoa by-products. This study aims to investigate the protective effect of cocoa husk extract (CHE) and cherry extracts (CE) against ROS-induced oxidative stress in Human Umbilical Vein Endothelial Cells (HUVECs). Methods: CE and CHE had antioxidant activity characterized by total polyphenols content (TPC). HUVECs were treated for 2 h and 24 h with increasing TPC concentrations of CE and CHE (5-10-25-50-100 µg Gallic Acid Equivalent (GAE)/mL) and then with H2O2 for 1 h. Cell viability and ROS production were evaluated. CE and CHE polyphenols permeability on excised rat intestine were also studied. Results: CE and CHE showed a similar antioxidant activity (2.5 ± 0.01 mmol Fe2+/100 g FW (fresh weight) and 2.19 ± 0.09 mmol Fe2+/100 g FW, respectively, p > 0.05) whereas CHE had a higher TPC (7105.0 ± 96.9 mg GAE/100 g FW) than CE (402.5 ± 8.4 mg GAE/100 g), p < 0.05. The in vitro viability assay showed that both extracts were non-cytotoxic. CHE resulted in protection against ROS at lower concentrations than CE. CHE showed a 2-fold higher apparent permeability compared to CE. Conclusions: CHE represents a high-value antioxidant source, which is interesting for the food and pharmaceutical industries.

The decline of skeletal muscle mass and strength that leads to sarcopenia is a pathology that might represent an emergency healthcare issue in future years. Decreased muscle mass is also a condition that mainly affects master athletes involved in endurance physical activities. Skeletal muscles respond to exercise by reshaping the biochemical, morphological, and physiological state of myofibrils. Adaptive responses involve the activation of intracellular signaling pathways and genetic reprogramming, causing alterations in contractile properties, metabolic status, and muscle mass. One of the mechanisms leading to sarcopenia is an increase in reactive oxygen and nitrogen species levels and a reduction in enzymatic antioxidant protection. The present review shows the recent experimental models of sarcopenia that explore molecular mechanisms. Furthermore, the clinical aspect of sport sarcopenia will be highlighted, and new strategies based on nutritional supplements, which may contribute to reducing indices of oxidative stress by reinforcing natural endogenous protection, will be suggested.