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Patients with the condition display a significant reduction in their level of physical activity even at relatively early stages [ 2– 5], and there is evidence that physical inactivity is independently associated with dyspnoea, quality of life, lung function decline, muscle strength and endurance, the frequency of acute exacerbations and mortality in COPD [ 1, 6– 10].
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Apart from overt changes, such as declining muscle strength, extensive metabolic alterations also occur with aging, one of the most prominent being impaired glucose tolerance [2].
The pathophysiologic mechanisms and the histological and biochemical changes differ greatly between these different etiologies, however fatty infiltration and the consequent decrease of muscle cross sectional area results in declined muscle strength, elasticity and range of joint motion [ 13- 15].
As well as indicating the presence of an illness or illnesses sufficiently serious to require hospital admission, hospitalisation in older people is associated frequently with complications such as delirium, declining muscle strength and respiratory function, and is often followed by functional decline [ 30].
Although the biggest decline in muscle strength was measured in the 54 56 year old age group, the decline was most significant in participants older than 60 years.
Moreover, the decline in muscle strength caused by the loss of muscle mass contributes to the decline in physical function, as well as increasing disability, frailty and loss of independence [ 10, 11].
Muscle mass has been reported to decline 1 2% annually after age 50 years [ 14], which contributes to a decline in muscle strength [ 5, 15].
Aging is intrinsically associated with a progressive decline in muscle strength and mass, and aerobic capacity.
A natural decline of muscle strength occurs during the aging process; however, preserving muscle strength may lower the rate of many preventable diseases such as diabetes, especially in higher risk populations.
Interestingly, a recent observational study by Onder and colleagues [50] demonstrated that chronic ACE inhibitor treatment slowed the age-related decline in muscle strength in elderly, hypertensive women.
This suggests that the decline in muscle strength is not mediated by changes in gene transcription within muscle itself, but may be mediated post-transcriptionally or by neuronal and/or hormonal adaptations to immobilization.
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