The heterogeneity in force and power of skeletal muscle and its capacity to adapt to changes in functinal requirements (i.e. plasticity) is though to be mainly based (i) on muscle fiber hypertrophy and atrophy (quantitative mechanism) and (ii) on the differential distribution in muscles of fiber types (type 1, 2A and 2X (pure) and type 1-2A and 2AX (hybrid)) containing specific myosin heavy chain isoforms (MHC) and having distinctive functional properties (qualitative mechanism).

Even short periods of disuse determine a significant loss of muscle mass and muscle weakness. The link between a decrease in neuromuscular activity and the development of muscle atrophy has been intensively studied and an unbalance between the pro-oxidant/anti-oxidant capacity of the muscle has been emerging as a major candidate.

The loss of force has been shown to be larger than the loss of mass both at whole muscle and single muscle fibre level indicating that the quantitative mechanism is not the only determinant of disuse induced muscle weakness. Moreover, an atrophic muscle becomes faster due to a MHC isoform shift in the direction MHC-1 > MHC-2A > MHC-2B and more fatiguable due to a shift towards a less oxidative phenotype. Interestingly, atrophic single muscle fibres are faster than control fibres containing the same myosin isoform suggesting that the faster phenotype of an atrophic muscle does not only depend on a shift in myosin isoform content, i.e. to a qualitative mechanism.

The talk will consider the mechanisms underling the development of muscle atrophy, the shift in MHC isoform expression and the change in contractile properties of individual muscle fibres which are fundamental in preventing and counteracting disuse induced deterioration of muscle function.