Skeletal muscle serves fundamental functions, ranging from generating mechanical force to regulating whole-body metabolic homeostasis, all of which decline with ageing. Both age- and disease-related loss of muscle mass and function are important risk factors for disability and mortality, and over half of all persons >80 years possess insufficient muscle mass and strength to perform daily activities. A major challenge is that often full restoration of muscle mass after periods of disuse is not achieved through regular rehabilitation, especially in elderly individuals, who therefore will more rapidly fall below the threshold for independent living. At opposite ends of the exercise training spectrum, it is well-established that aerobic (endurance) exercise and resistance (strength) training can individually lead to major health benefits, but completely divergent responses are also evident, reflecting the large plasticity of skeletal muscle. The distinct metabolic and molecular signalling responses underpinning these adaptations are the subject of intense research in order to develop strategies to preserve and functional capacity and restore it when it has been lost. Key to this understanding is insight into the interplay between resident and infiltrating cells, which is tightly regulated temporally and spatially to orchestrate optimal tissue maintenance, adaptation and damage repair throughout the lifespan. The main cells involved are satellite cells, fibroblasts, vascular cells, immune cells and their relative influence on the muscle fibre cells themselves at rest and during adaptation to exercise and damage stimuli. Non-steroidal anti-inflammatory medication and Angiotensin II type I receptor blockers will also be considered as potential pharmacological interventions in the context of muscle adaptation at the cellular level.