# Physical Activity and Redox Balance in the Elderly: Signal Transduction Mechanisms
## 3 Physical Activity and Redox Balance in the Adult and the Elderly
In particular, decreases in blood lactate, free fatty-acid levels, and gastrocnemius-muscle lipid peroxidation were observed, as well as an increase in the activity of antioxidant enzymes such as SOD and catalase [34]. Interestingly, the upregulation of peroxisome proliferator-activated receptor gamma coactivator-1\(\alpha\) (PGC-1\(\alpha\)) mRNA was also observed [34], suggesting the involvement of mitochondrial biogenesis and function. Similar effects have been obtained with plant (Rhus Coriaria) extract in human myoblasts, where [PERSON] et al. (2017) [36] observed an increase of the antioxidant enzymes SOD2 and catalase, together with increased viability and adhesion of human myoblasts. Finally, oral ingestion of ascorbic acid increases muscle blood flow and oxygen consumption in older adults practising rhythmic handgrip exercises [37]. Antioxidant supplements have been tested for the treatments of sarcopenia which is a muscle disease known to be associated with the oxidant/antioxidant balance in the elderly. Specifically, sarcopenia is a condition characterized by the progressive loss of muscle mass and function, a decrease in number of motor units, and wasting of muscle fibres. Among the complex biological mechanisms associated with sarcopenia, there is a pronounced imbalance between oxidant and antioxidant species. As yet, it is not clear if antioxidant supplements have a protective effect against the development of this disease [38]. On the other hand, physical exercise could have a role in counteracting this disease, because at a low-moderate intensity, it stimulates antioxidant pathways [39]. Of note, resistance exercise increases satellite cell number, and reverses muscle atrophy in aging by increasing the number of fast fibres that are reduced in the elderly [40; 41]. For example, cycles of 12 weeks of resistance training, 12 weeks of de-training and 12 weeks of re-training induce amelioration of physiological and cellular parameters of muscle in aged men [42]. The training increases power and strength in knee-extension exercises, and reduces the number of both 2a and 2x fast fibres. The de-training induces a modest loss of power and strength. Finally, 12 weeks of re-training produce a significant increase in type-II fibre hypertrophy, satellite cell number and myonuclei [42]. On the other hand, 12 weeks of aerobic training in sedentary healthy subjects increase the cross-sectional area of both type-I and type-II fibres, while satellite activation and nuclei addition are found only in slow type-I fibres, suggesting that a differential regulation concerning myonuclear condition occurs [43]. Since the slow fibres have a higher oxidative content than do fast type-II fibres, resistance training could represent a better training method to counteract aging effects on muscle mass and function, but this point is still under debate. As the increase of antioxidant species was observed in many studies, and the reduction of oxidant species (malondyldehyde) was observed in type-II diabetic patients performing moderate aerobic exercise three times/week [44], with no changes in the control group, it suggests that there is a specific effect of exercise in diabetic patients on lipid peroxidation levels and on the susceptibility of DNA to oxidative damage. Although it is not directly influenced by physical activity, nervous tissue has the highest metabolic rates in the organism [45] and this elevated oxygen consumption promotes ROS generation, making the nervous tissue more susceptible to developing oxidative stress [45]. Moreover, antioxidant levels are lower in the brain than in other parts of the body, due to the low permeability of the blood-brain barrier to most endogenous antioxidant molecules [45]. It is well known that aging and neurodegenerative diseases show increased levels of ROS and reduction of BNDF and NGF: oxidative stress modulates the activity of neurotrophins that then become unable to save neurons from cell death and to promote neuroplasticity [46].