The inaugural UK conference on sarcopenia was held in central London on 9th July 2013.
Delegates included clinicians, therapists, nutritionists and scientists, with representatives from Spain, Belgium, the Netherlands, Poland, the Ukraine, the United States and Japan. The meeting was organised and chaired by Professor Avan Aihie Sayer, MRC Clinical Scientist and Professor of Geriatric Medicine at the MRC Lifecourse Epidemiology Unit in Southampton, who opened the meeting with an overview of why sarcopenia is important. Sarcopenia is the loss of skeletal muscle mass and function with age. It is common in older men and women and has serious health consequences and significant healthcare costs. Professor Sayer outlined the lifecourse influences on sarcopenia that have been identified through research with the unique UK birth cohorts such as the Hertfordshire Cohort Study. This allows identification of factors associated with peak muscle mass and strength in early adulthood and those modifying decline in later life, thus informing the development of beneficial interventions across the lifecourse. For example the association of low birth weight with sarcopenia in later life is now well recognised, and recent work by Dr Harnish Patel, Clinical Lecturer in Geriatric Medicine in Southampton, on muscle biopsies from this cohort has identified changes in the morphology of muscles in those with low birth weight.
The rest of the morning programme was devoted to the underlying mechanisms of sarcopenia.Professor Malcolm Jackson, Head of the Institute of Ageing and Chronic Disease at the University of Liverpool, discussed the role of oxidative damage and denervation. He explained that the loss of muscle mass with ageing was predominantly due to a reduction in the number of muscle fibres, with atrophy and weakening of the remaining fibres. The research group in Liverpool have used the rodent model to determine the contribution of reactive oxygen species to myofibre loss. During normal contraction, muscle generates free radicals as part of the normal physiological response. This in turn activates a plethora of intracellular signaling molecules that increases the production of cytoprotective molecules such as the heat shock proteins (HSPs) and the superoxide dismutatses that neutralize free radicals and limit free radical damage. In aged animals, these normal adaptive mechanisms are attenuated or even abolished. In addition, older animals have been shown to have an increased free radical production at rest. This culminates in increased myofibre damage and loss. Transgenic mice that are deficient for the superoxide dismutase gene have decreased hind limb muscle mass. This work now needs to be translated to humans and preliminary studies are ongoing. Older rodents also demonstrate disruption at the neuromuscular junction within the motor unit, and this denervation to just a small number of fibres can further adversely influence the redox processes within skeletal muscle. Unanswered questions remain; namely, what drives denervation in older people and does denervation promote increases in oxidative species?