The underlying cause of sarcopenia and dynapenia (age-related strength loss) are not fully elucidated, but may be the result, or combination, of alterations in lifestyle or inflammatory and endocrine profiles. What is clear is that functional ability is limited and mortality risk is elevated. Mechanistically, muscle atrophy is the result of the prolonged periods of net negative muscle protein balance, brought about by the imbalance between muscle protein synthesis (MPS) and muscle protein breakdown (MPB). Contractile loading of skeletal muscle, through resistive-type exercise and amino acid ingestion both act as a strong stimulus for MPS and, when combined, can induce a net positive protein balance and muscle hypertrophy. Given that MPS in older muscles displays a blunted response to anabolic stimuli compared with the young, the combined effect and manipulation of contractile and nutrient interventions to optimize muscle anabolism could be extremely important for counteracting sarcopenia. Specifically, the dose, absorption kinetics, leucine content, but less-so the timing of ingestion, are important determinants of the mRNA translational signalling response regulating MPS. In addition, resistance exercise-induced rates of MPS and hypertrophy appear to be dependent on exercise volume (to achieve maximal muscle fibre recruitment), as opposed to the absolute load that is lifted. A number of recent studies in young adults lend weight to this notion by showing that contraction can be manipulated; allowing low load weight lifting to effectively stimulate rates of MPS to a level comparable with traditional high loads, a finding with important implications for older adults interested in undertaking resistance exercise.