Changes in skeletal muscle quantity and quality lead to disability in the aging population. Physiological changes in aging skeletal muscle are associated with a decline in mass, strength, and inability to maintain balance. Glucocorticoids, which are in wide exploitation in various clinical scenarios, lead to the loss of the myofibrillar apparatus, changes in the extracellular matrix, and a decrease in muscle strength and motor activity, particularly in the elderly. Exercise therapy has shown to be a useful tool for the prevention of different diseases, including glucocorticoid myopathy and muscle unloading in the elderly. The purpose of the paper is to discuss the possibilities of using exercise therapy in the prevention of glucocorticoid caused myopathy and unloading in the elderly and to describe relationships between the muscle contractile apparatus and the extracellular matrix in different types of aging muscles. 1. Introduction Aging is a multifactorial process influenced by biological, physiological, psychological, and social changes. The biological and physiological changes are primarily associated with a decline in muscle mass, strength, endurance and the inability to maintain balance [1–3]. Physical risk factors for falling, such as muscle weakness and an inability to maintain static or dynamic balance, lead to severe injury in the elderly [3]. Changes in skeletal muscle quantity and quality lead to disability in the aging population [4]. The rate of muscle loss has been estimated to range from 1% to 2% per year past the age of 50, as a result of which 25% of people under the age of 70 and 40% over the age of 80 are sarcopenic [5, 6]. In both young and aged skeletal muscle, it has been shown that oxidative stress increases in response to unloading [7] and may have an important role in mediating muscle atrophy [8]. It has also been proposed that changes caused by aging and unloading are muscle specific [9]. Muscle unloading results in a decrease in the number of myonuclei and an increase in the number of apoptotic myonuclei in skeletal muscle [10]. Heat-shock protein (HSP) 70 inhibits caspase-dependent and caspase-independent apoptotic pathways and may function in the regulation of muscle size by inhibition of necrotic muscle fiber distribution and apoptosis in aged muscle [11, 12]. The decline of muscle mass is primarily caused by type II fiber atrophy and loss in the number of muscle fibers. Increased variability in fiber size, accumulation of nongrouping, scattered and angulated fibers, and expansion of extracellular space are characteristic
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