Sir—Ageing is associated with declines in physical function that lead to physical disability and loss of independence [1, 2]. Traditionally, loss of muscle mass has been thought of as the most important factor leading to loss of physical function and onset of disability. However, the number of older persons with excess fat mass is increasing , and a growing body of evidence shows obesity is an independent risk factor for ageing-related disability. Cross-sectional data show a higher prevalence of frailty, low function and disability, with higher body mass index (BMI) and fat mass, even in older persons with a normal amount of lean mass [4–7]. Longitudinal data also support a greater decline in physical function in more obese older adults [7, 8]. Since most mechanistic studies focus primarily on skeletal muscle, little is known regarding the mechanisms by which excess adipose tissue contributes to loss of physical ability in older adults.
The relationship between excess fat and loss of function in older adults is, in part, mediated by biomechanical factors [9, 10]. However, increasing knowledge about the role of adipose tissue as an endocrine organ suggests there may also be biochemical effects of adipose tissue itself on properties of skeletal muscle that lead to loss of function, i.e. the association of excess adipose tissue with physical function decline may also be due to the secretion of inflammatory proteins by adipose tissue . This premise is supported by evidence that muscle strength is lower in obese persons and in conditions characterised by chronic inflammation such as diabetes and metabolic syndrome [4, 12]. Our overall hypothesis is that adipose tissue contributes to ageing-related loss of physical function, in part, via its capacity to produce and secrete inflammatory mediators that subsequently affect skeletal muscle function. This study begins to test this hypothesis by determining whether adipose tissue gene expression of specific inflammatory adipokines, interleukin-6 (IL-6) and tumour necrosis factor-α (TNFα), is associated with clinical measures of muscle strength in overweight or obese, postmenopausal women.