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The prevalence of chronic diseases including osteoporosis and sarcopenia increases as the population ages. Osteoporosis and sarcopenia are commonly associated with genetics, mechanical factors, and hormonal factors and primarily associated with aging. Many older populations, particularly those with frailty, are likely to have concurrent osteoporosis and sarcopenia, further increasing their risk of disease-related complications. Because bones and muscles are closely interconnected by anatomy, metabolic profile, and chemical components, a diagnosis should be considered for both sarcopenia and osteoporosis, which may be treated with optimal therapeutic interventions eliciting pleiotropic effects on both bones and muscles. Exercise training has been recommended as a promising therapeutic strategy to encounter the loss of bone and muscle mass due to osteosarcopenia. To stimulate the osteogenic effects for bone mass accretion, bone tissues must be exposed to mechanical load exceeding those experienced during daily living activities. Of the several exercise training programs, resistance exercise (RE) is known to be highly beneficial for the preservation of bone and muscle mass. This review summarizes the mechanisms of RE for the preservation of bone and muscle mass and supports the clinical evidences for the use of RE as a therapeutic option in osteosarcopenia.
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Skeletal muscle is the largest organ of the body in non-obese individuals and is now considered to be an endocrine organ. Hormones (myokines) secreted by skeletal muscle mediate communications between muscle and liver, adipose tissue, brain, and other organs. Myokines affect muscle mass and myofiber switching, and have profound effects on glucose and lipid metabolism and inflammation, thus contributing to energy homeostasis and the pathogenesis of obesity, diabetes, and other diseases. In this review, we summarize recent findings on the biology of myokines and provide an assessment of their potential as therapeutic targets.
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Animal models are necessary to study the mechanism underlying the effects of exercise on depression but an effective procedure for exercise treatment and exercise effects on physiological parameters in a specific depression model need to be characterized.
Physiological parameters including lactate, partial pressue of O2 (pO2) and CO2 (pCO2) saturated O2 (sO2), pH, HCO3, total CO2 (TCO2), and base excess extracellular fluid (BEecf) levels in the blood were measured after treatment with passive exercise in normal mice and a stress-induced depression model.
Normal mice or mice that were subjected to daily 2-hour restraint for 14 days (2 hours×14 days of restraint) were placed on a running wheel that was rotating at a speed of 9 m/min for 1 hour per day for 1 to 21 days. After repeated exercise in mice that were previously subjected to 2 hours×14 days restraint, plasma lactate levels decreased, the levels of pO2, sO2, and pH tended to increase, and the levels of pCO2 decreased in the absence of significant changes in HCO3, TCO2, and BEecf. However, none of these changes were additive to the stress effects or were much more severe than those induced after repeated passive exercise in normal mice.
These results suggest that passive exercise for 1 hour daily for 14 to 21 consecutive days on a running wheel rotating at a speed of 9 m/min may be used as an exercise protocol without inducing severe additive effects on physiological burdens.
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