Title: Nutrition and sarcopenia


Key words: sarcopenia, muscle, ageing, creatinine, muscle fibres, cytokines, protein intake, skeletal mass, energy input, elderly, age, growth hormone, resistance training, strength, nutritional, genetic, vitamins, minerals, oxidative, antioxidants, superoxide transmutase, vitamin E,  


Date: Oct 2006




Nutrimed Module:


Type: Article


Author: Morgan, G



Nutrition and sarcopenia

Nutritional deficiencies in the elderly have been well documented (Finch 1998). To what extent is sarcopenia, the age-related loss of muscle mass, strength and function in the elderly attributable to nutritional deficiency and to what extent to normal metabolic ageing processes? Review of the literature provides only an incomplete answer to this question but does help to increase our understanding of the ageing process in muscle.


Muscle ageing begins at an early age, when energy intake, nutritional adequacy and physical activity are at a high level. Markers of muscle mass and muscle function, such as creatinine excretion (Tzankoff 1977), oxidative capacity (Bunker 1987), grip (Giampaoli 1999), and leg strength (Evans 1993) show a gradual decline from the early 20’s. Anthropometric measures confirm that sarcopenia is directly correlated with age, levels of disability (Baumgartner 1998) and, in men, with osteoporosis (Baumgartner 1996). Studies have shown that the sarcopenia is characterised by a more selective loss of Type II muscle fibres (Larrson 1983, Lexell 1995), the composition of this fibre in muscle dropping from 60% to around 30% in those aged over 70 (Evans 1997). Histochemically, this has been shown to be associated with an increased turnover of this fibre type (Singh 1999). Associated metabolic changes in levels of IGF-1, cytokines such as IL-6 and growth hormone have been reported (Blumberg 1996, Ferrucci 2002, Pedersen 2003).


Both protein intake and skeletal mass decline with age (Gallagher 1997), along with energy input and basal metabolic rate (Tsankoff 1978). The appendicular skeletal mass has been reported to diminish by 1.2 Kg. per decade into old age (Starling 1999). Several surveys, however, have failed to show that prevalent protein intakes in the elderly are unable to meet demands. In free-living subjects, Munro (Munro 1987) failed to find any correlation between protein intake and sarcopenia over a range of intakes. Bunker (Bunker 1987), likewise, in healthy and disabled groups, found no correlation between their nitrogen balance and protein intake. Higher protein intakes in resistance training had no effect on muscle turnover and strength gains (Bunker 1987). These studies confirmed that the elderly’s protein requirements were covered by the WHO recommendation of 0.75 g/Kg per day (WHO 1985) and were met in all the elderly groups. More refined studies, using [13C]leucine, have subsequently shown that the metabolic demand of fat free muscle in the elderly is in fact some 30% lower than in younger individuals, and that protein requirements are somewhat lower in this age group, being only 0.66 g/Kg per day for men (Millward 1997, Fereday 1997). In the resistance training group, 0.8 g/Kg per day was found to be quite adequate, an intake exceeded in all groups, both housebound and fully mobile (Campbell 2002).


In sum, these studies have shown that muscle turnover is slowed down and that, in spite of adequate protein nutrition, muscle mass and strength slowly decline with age. Research on lifetime athletes shows that, even with regular aerobic and anaerobic training, these changes still occur, though the decline is muted (Wilmore 1999). The adaptability of muscle into old age to various training regimes has been well described (Frontera 1988, Campbell 1995). Two studies have addressed the question of whether the loss of muscle mass and function might have a nutritional as well as a genetic component. Both groups were given an additional one third of the RDA of a mixture of vitamins and minerals during the course of a programme of resistance training. Strength and muscle mass gains were augmented in one group (Singh 1999) and were unchanged in the other (Fiatarone 1994). Nevertheless there are many theoretical reasons for thinking that that the muscle ageing process may be partly modulated by nutritional, and specifically oxidative, factors.


Free radical damage to protein increases with age due to mitochondrial damage, poor regeneration of antioxidant enzymes such as superoxide dismutase, and diminishing vitamin and mineral intake (Weindruch 1995, Ji 2002). Muscle damage is augmented by an increased release of cytokines and other inflammatory markers, which is more marked in aged and poorly exercised muscle (Bales 2002, Ferrucci 2002, Pedersen 2003). Even though muscle retains remarkable recuperative power (Yarasheki 1993, McGuire 2001), the number of satellite cells that can regenerate muscle cells diminishes with age and cannot meet the challenge posed by oxidative stress on poorly conditioned muscle (Singh 1999).


The ability of antioxidants to protect elderly muscle from oxidative stress has been demonstrated in several studies of vitamin E (Reznick 1992, Meydani 1993). Given the synergistic nature of the antioxidant system, it is likely that combinations of vitamins and minerals would offer greater protection. That this is likely follows from the results of epidemiological and intervention trials carried out on other degenerative disorders, such as cardiovascular disease, Alzheimer’s disease and cancer. Prospective studies looking at the long-term effects of these factors, both dietary and in supplement form, on sarcopenia are obviously called for



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