Abstract
Amyotrophic lateral sclerosis (ALS), a fatal neurodegenerative disease, involves the rapid deterioration of motor neurons resulting in severe muscle atrophy and respiratory insufficiency. It is considered a “multisystemic” disease with many potential mechanisms responsible for its pathology. Currently, there is no cure for ALS. Exercise training is suggested as a potential approach to reduce ALS pathology, but its beneficial role remains controversial. This review provides an overview of the effects of exercise training in ALS-affected mice and patients. It will compare the intensity, duration, and type of exercise on the health of SOD1G93A mice, a mouse model of familial ALS, and review clinical studies involving ALS patients undergoing both endurance and resistance training. In summary, mild-to-moderate swimming-based endurance training appears the most advantageous mode of exercise in SOD1G93A mice, improving animal survival, and delaying the onset and progression of disease. Furthermore, clinical studies show that both endurance and resistance training have an advantageous impact on the quality of life of ALS patients without extending life expectancy. However, small sample sizes, non-representative control populations, heterogeneous disease stage of patients, and the presence of confounders often exist in the exercise studies conducted with ALS patients. This raises concerns about the interpretation of these findings and, therefore, these results should be considered with caution. While promising, more pre-clinical and clinical studies with improved experimental design and fewer limitations are still necessary to confirm the impact of exercise training on the health of ALS patients.
Highlights
Amyotrophic lateral sclerosis (ALS), a subtype of fatal motor neuron disease (MND), is a progressive and degenerative neuromuscular disorder
This observation is contrary to results of Veldink et al [44], who found no significant differences in motor neuron counts between exercising and sedentary low-copy SOD1G93A mice in both male and female after moderate-intensity endurance exercise
Previous evidence suggests a potential relationship between heavily active lifestyles and an increased incidence of ALS [30, 31, 109], recent studies support that physical activity is not necessarily a risk factor for ALS [42, 43, 110]
Summary
Amyotrophic lateral sclerosis (ALS), a subtype of fatal motor neuron disease (MND), is a progressive and degenerative neuromuscular disorder. Carreras et al found that moderate intensity endurance exercise significantly delayed the onset of motor performance deficit in male SOD1G93A mice (copy number is not reported) [61] This delay correlated with a 2-fold higher motor neuron density in the ventral horn of the lumbar spinal cord. This observation is contrary to results of Veldink et al [44], who found no significant differences in motor neuron counts between exercising and sedentary low-copy SOD1G93A mice in both male and female after moderate-intensity endurance exercise. 56 Scores >15 points (3 points for each electrical shock, 1 Treadmill running at 16 m/min for 45 min, 5 days/week point after resting for 5 s)
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