Aging is accompanied by a progressive decline in skeletal muscle mass and strength, known as sarcopenia, leading to the loss of functional capacity and an increased risk of developing chronic metabolic disease. Sarcopenia increases hospital and/or nursing home admissions and may reduce the quality of life of older individuals. It has been well established that protein turnover in skeletal muscle tissue is highly responsive to nutrient intake and muscle contraction. Protein ingestion stimulates muscle protein synthesis and inhibits muscle protein breakdown resulting in net muscle protein accretion. Disturbances in skeletal muscle protein turnover result in a structural imbalance between protein synthesis and breakdown, leading to sarcopenia.
The postprandial muscle protein synthetic and anti-proteolytic response to feeding is regulated on various levels, ranging from protein digestion and amino acid absorption, the postprandial rise in circulating insulin, the subsequent increase in microvascular recruitment, amino acid uptake in skeletal muscle tissue, and myofibrillar muscle protein synthesis and breakdown. All of these aspects of postprandial protein handling may play a role in the reduced sensitivity of senescent muscle to the anabolic properties of amino acids, a phenomenon that is now referred to as the ‘anabolic resistance of aging’.
Defence date: 04/11/16