The poorly conducted orchestra of steroid hormones, oxidative stress and inflammation in frailty needs a maestro: Regular physical exercise.

This review outlines the various factors associated with unhealthy aging which includes becoming frail and dependent. With many people not engaging in recommended exercise, facilitators and barriers to engage with exercise must be investigated to promote exercise uptake and adherence over the lifespan for different demographics, including the old, less affluent, women, and those with different cultural-ethnic backgrounds. Governmental and locally funded public health messages and environmental facilitation (gyms, parks etc.) can play an important role. Studies have shown that exercise can act as a conductor to balance oxidative stress, immune and endocrine functions together to promote healthy aging and reduce the risk for age-related morbidities, such as cardiovascular disease and atherosclerosis, and promote cognition and mood over the lifespan. Like a classic symphony orchestra, consisting of four groups of related musical instruments - the woodwinds, brass, percussion, and strings - the aging process should also perform in harmony, with compassion, avoiding the aggrandizement of any of its individual parts during the presentation. This review discusses the wide variety of molecular, cellular and endocrine mechanisms (focusing on the steroid balance) underlying this process and their interrelationships.

Melatonin improves the antioxidant capacity in cardiac tissue of Wistar rats after exhaustive exercise.

We investigated the effects of melatonin on the onset and resolution of the oxidative stress in the cardiac muscle in melatonin-treated and nontreated rats subjected to an exhaustive exercise session. Forty male rats were divided into: melatonin-treated (20 mg/kg supplemented for 10 d) and control. On the 10th day, each group was subdivided according to euthanasia moments: control or melatonin-treated not exercised (C0h and M0h); immediately after the exercise (CIA and MIA); and 2 h after exercise (C2h and M2h). The heart of animals was removed and the levels of oxidative stress index (OSI) and the formation of thiobarbituric acid reactive substances (TBARS), protein carbonyl, and the activities of aconitase, catalase (CAT), glutathione peroxidase (GPx), and superoxide dismutase (SOD) were evaluated. Total antioxidant status (TAS), total oxidant status (TOS), and the protein expression of CAT, GPx, and SOD was also measured. Our data revealed significant differences on: (i) OSI (p=.029), CAT activity (p=.016), CAT content (p<.001), GPx content (p=.014), reduced glutathione levels (p<.001), and aconitase activity (p<.001) for interaction of melatonin; (ii) GPx activity (p=.005), reduced glutathione (p=.004), protein carbonyl (p=.035), and TBARS levels (p=.028) between groups, and (iii) TBARS levels (p=.016) for significance between moments. Although the exhaustive exercise protocol imposed mild oxidative stress on the cardiac tissue of rats, melatonin induced antioxidant responses that rebalanced the redox status of the cardiac tissue, especially after exhaustive exercise.