Functional impact of high protein intake on healthy elderly people

Abstract

Decline in muscle mass, protein synthesis, and mitochondrial function occurs with age, and amino acids are reported to enhance both muscle protein synthesis and mitochondrial function. It is unclear whether increasing dietary protein intake corrects postabsorptive muscle changes in aging. We determined whether a 10-day diet of high [HP; 3.0 g protein ⅐ kg fat-free mass (FFM) Ϫ1 ⅐ day Ϫ1 ] vs. usual protein intake (UP; 1.5 g protein ⅐ kg FFM Ϫ1 ⅐ day Ϫ1 ) favorably affects mitochondrial function, protein metabolism, and nitrogen balance or adversely affects insulin sensitivity and glomerular filtration rate (GFR) in 10 healthy younger (24 Ϯ 1 yr) and 9 older (70 Ϯ 2 yr) participants in a randomized crossover study. Net daily nitrogen balance increased equally in young and older participants, but postabsorptive catabolic state also increased, as indicated by higher whole body protein turnover and leucine oxidation with no change in protein synthesis. Maximal muscle mitochondrial ATP production rate was lower in older people, with no change occurring in diet. GFR was lower in older people, and response to HP was significantly different between the two groups, with a significant increase occurring only in younger people, thus widening the differences in GFR between the young and older participants. In conclusion, a short-term high-protein diet increased net daily nitrogen balance but increased the postabsorptive use of protein as a fuel. HP did not enhance protein synthesis or muscle mitochondrial function in either young or older participants. Additionally, widening differences in GFR between young and older patients is a potential cause of concern in using HP diet in older people. dietary protein; protein metabolism; mitochondrial function; kidney function; aging AGE IS ASSOCIATED WITH A PROGRESSIVE DECLINE in body protein content, as reflected by declining fat-free mass (FFM) (33). The reduction in FFM is attributed mainly to loss of skeletal muscle, i.e., sarcopenia, and is associated with reduced muscle strength and exercise endurance as well as predisposition to many metabolic disorders (33). The disabilities related to sarcopenia and associated disorders are not fully assessed but result in substantial health care costs (25).One of the potential mechanisms contributing to sarcopenia is reduced muscle protein synthesis, which was shown to decline by 3.5% per decade (49). Aging is also associated with reductions in the skeletal muscle mitochondrial ATP production and the abundance of mitochondrial DNA and transcripts of genes that encode mitochondrial proteins (44,47). Reduced ability to produce ATP, the key chemical form of energy for cellular functions, could potentially contribute to the vitality of the aging population and may contribute to the overall reduction in many muscle functions (33). The reduced ability to maintain muscle proteins may result from decreased sensitivity of muscle to efficiently use exogenous amino acids for protein anabolism. It has been reported (56) that skeletal muscle protein s...

The role of nutrition in the prevention of sarcopenia

“…They conclude that ingesting more than 30 g protein at a single meal may be an inefficient means of stimulating muscle protein synthesis. This is in agreement with a recent study that showed no benefit of very large amounts of protein for 10 days (3.0 vs. 1.5 g/kg) in terms of muscle protein synthesis [24].…”

Effect of obesity and type 2 diabetes on protein anabolic response to insulin in elderly women

“…Moreover, a recent systematic review and meta-analysis of 20 randomized controlled trials investigating dietary approaches in the management of type 2 diabetes indicated that high-protein diets are among the few approaches that are effective in improving glycemic control (Ajala et al, 2013). Several studies have reported stimulation of muscle protein synthesis with generous protein intakes with and without exercise in elderly individuals (Cermak et al, 2012;Candow et al, 2006;Esmarck et al, 2001;Symons et al, 2007;Verdijk et al, 2009;Walrand et al, 2008). Notwithstanding, the combined metabolic abnormalities associated with old age, obesity, and type 2 diabetes pose specific therapeutic challenges.…”

Insulin resistance and the metabolism of branched-chain amino acids in humans

“…Acute exercise induces activation of BCKD complex in human skeletal muscle, but after training the activity of this enzyme is reduced, along with an increase in BCKD kinase protein (Howarth et al 2007). In a small randomized crossover study, the activity of BCAT and BCKD complex in skeletal muscle has been found similar in young and elderly healthy persons and there was no difference in the activity of these enzymes during shortterm ingestion of a high-protein diet compared with usual protein dietary content (Walrand et al 2008).…”