Muscle Proteome Analysis of Facioscapulohumeral Dystrophy Patients Reveals a Metabolic Rewiring Promoting Oxidative/Reductive Stress Contributing to the Loss of Muscle Function.

Facioscapulohumeral muscular dystrophy (FSHD) is caused by the epigenetic de-repression of the double homeobox 4 (DUX4) gene, leading to asymmetric muscle weakness and atrophy that begins in the facial and scapular muscles and progresses to the lower limbs. This incurable condition can severely impair muscle function, ultimately resulting in a loss of ambulation. A thorough analysis of molecular factors associated with the varying degrees of muscle impairment in FSHD is still lacking.

Neuromuscular mechanisms for the fast decline in rate of force development with muscle disuse - a narrative review.

The removal of skeletal muscle tension (unloading or disuse) is followed by many changes in the neuromuscular system, including muscle atrophy and loss of isometric maximal strength (measured by maximal force, F). Explosive strength, i.e.

Move less, spend more: the metabolic demands of short walking bouts.

The metabolic cost of steady-state walking is well known; however, across legged animals, most walking bouts are too short to reach steady state. Here, we investigate how bout duration affects the metabolic cost of human walking with varying mechanical power, metabolic intensity and duration. Ten participants walked for 10- to 240-s bouts on a stair climber at 0.