Influence of Resistance Training on Neuromuscular Function and Physical Capacity in ALS Patients.

OBJECTIVES: The present study aimed to explore the effect of resistance training in patients with amyotrophic lateral sclerosis (ALS), a disease characterized by progressive motor neuron loss and muscle weakness. MATERIALS AND METHODS: Following a 12-week "lead-in" control period, a population of ALS patients from Funen, Denmark, completed a 12-week resistance training program consisting of 2-3 sessions/week. Neuromuscular function (strength and power) and voluntary muscle activation (superimposed twitch technique) were evaluated before and after both control and training periods. Physical capacity tests (chair rise and timed up and go), the revised ALS functional rating scale (ALSFRS-R) scores, and muscle cross sectional area (histology) were also assessed. RESULTS: Of twelve ALS patients assessed for eligibility, six were included and five completed the study. Training did not significantly affect the ALSFRS-R score, and loss of neuromuscular function (strength and power) increased following the training period. However, an improved functionality (chair rise) and an increase in greatly hypertrophied type II fibres combined with an increase in atrophied fibres following the training period compared to the control period were observed. CONCLUSION: In this small study, the present form of resistance training was unable to attenuate progressive loss of neuromuscular function in ALS, despite some changes in physical capacity and morphology.

Skeletal Muscle Remodelling as a Function of Disease Progression in Amyotrophic Lateral Sclerosis.

Muscle weakness is considered the pivotal sign of amyotrophic lateral sclerosis (ALS). Knowledge about the skeletal muscle degeneration/regeneration process and the myogenic potential is limited in ALS patients. Therefore, we investigate these processes in a time course perspective by analysing skeletal muscle biopsies from ALS patients collected before and after a 12-week period of normal daily activities and compare these with healthy age-matched control tissue. We do this by evaluating mRNA and protein (immunohistochemical) markers of regeneration, neurodegeneration, myogenesis, cell cycle regulation, and inflammation. Our results show morphological changes indicative of active denervation and reinnervation and an increase in small atrophic fibres. We demonstrate differences between ALS and controls in pathways controlling skeletal muscle homeostasis, cytoskeletal and regenerative markers, neurodegenerative factors, myogenic factors, cell cycle determinants, and inflammatory markers. Our results on Pax7 and MyoD protein expression suggest that proliferation and differentiation of skeletal muscle stem cells are affected in ALS patients, and the myogenic processes cannot overcome the denervation-induced wasting.

Transient impairments in single muscle fibre contractile function after prolonged cycling in elite endurance athletes.

AIM: Prolonged muscle activity impairs whole-muscle performance and function. However, little is known about the effects of prolonged muscle activity on the contractile function of human single muscle fibres. The purpose of this study was to investigate the effects of prolonged exercise and subsequent recovery on the contractile function of single muscle fibres obtained from elite athletes. METHODS: Nine male triathletes (26 ± 1 years, 68 ± 1 mL O2  min(-1) kg(-1) , training volume 16 ± 1 h week(-1) ) performed 4 h of cycling exercise (at 73% of HRmax ) followed by 24 h of recovery. Biopsies from vastus lateralis were obtained before and following 4 h exercise and following 24 h recovery. Measurements comprised maximal Ca(2+) -activated specific force and Ca(2+) sensitivity of slow type I and fast type II single muscle fibres, as well as cycling peak power output. RESULTS: Following cycling exercise, specific force was reduced to a similar extent in slow and fast fibres (-15 and -18%, respectively), while Ca(2+) sensitivity decreased in fast fibres only. Single fibre-specific force was fully restored in both fibre types after 24 h recovery. Cycling peak power output was reduced by 4-9% following cycling exercise and fully restored following recovery. CONCLUSION: This is the first study to demonstrate that prolonged cycling exercise transiently impairs specific force in type I and II fibres and decreases Ca(2+) sensitivity in type II fibres only, specifically in elite endurance athletes. Further, the changes in single fibre-specific force induced by exercise and recovery coincided temporally with changes in cycling peak power output.