Nutritional interventions that might influence sarcopenia, as indicated by literature reporting on sarcopenia per se as well as dynapenia and frailty, are reviewed in relation to potential physiological aetiological factors, i.e. inactivity, anabolic resistance, inflammation, acidosis and vitamin D deficiency. As sarcopenia occurs in physically active and presumably well-nourished populations, it is argued that a simple nutritional aetiology is unlikely and unequivocal evidence for any nutritional influence is extremely limited. Dietary protein is probably the most widely researched nutrient but only for frailty is there one study showing evidence of an aetiological influence and most intervention studies with protein or amino acids have proved ineffective with only a very few exceptions. Fish oil has been shown to attenuate anabolic resistance of muscle protein synthesis in one study. There is limited evidence for a protective influence of antioxidants and inducers of phase 2 proteins on sarcopenia, dynapenia and anabolic resistance in human and animal studies. Also fruit and vegetables may protect against acidosis-induced sarcopenia through their provision of dietary potassium. While severe vitamin D deficiency is associated with dynapenia and sarcopenia, the evidence for a beneficial influence of increasing vitamin D status above the severe deficiency level is limited and controversial, especially in men. On this basis there is insufficient evidence for any more specific nutritional advice than that contained in the general healthy lifestyle-healthy diet message: i.e. avoiding inactivity and low intakes of food energy and nutrients and maintain an active lifestyle with a diet providing a rich supply of fruit and vegetables and frequent oily fish.
Aging: Dynapenia: Inactivity: Anabolic resistance: DietIn a recent consensus paper sarcopenia (1) was defined as the age-associated loss of skeletal muscle mass and function, a complex syndrome associated with muscle mass loss alone or in conjunction with increased fat mass. It was argued that although cachexia may be a component of sarcopenia, the two conditions are not the same. What was not discussed in this paper was the difference between sarcopenia and dynapenia which is important in terms of the clinical relevance of the condition. Thus Jansonn (2) points out that the data on the functional implications of sarcopenia are inconsistent, possibly because we do not always recognise the distinction between sarcopenia, loss of muscle mass and dynapenia and loss of muscle strength. These, he argues, are physiologically different with dynapenia the main predictor of functional impairment and/or physical disability, chronic disease and mortality risk, to the extent that research and clinical emphasis should be placed more on dynapenia than on sarcopenia. In fact this argument can, to some extent be extended to include frailty, a much more general term for a collection