Swim Training Improves Muscle Function in Mouse Model of ALS, Study Shows

Swim training improves muscle strength and energy metabolism in a mouse model of amyotrophic lateral sclerosis (ALS).

The study, “Swim Training Modulates Mouse Skeletal Muscle Energy Metabolism and Ameliorates Reduction in Grip Strength in a Mouse Model of Amyotrophic Lateral Sclerosis,” was published in the International Journal of Molecular Sciences.

ALS is a progressive neurological disorder in which motor neurons — the nerve cells responsible for controlling voluntary muscles — gradually degenerate and die, causing muscles to shrink (atrophy) and become weaker.

Besides lack of muscle strength, ALS is associated with mitochondria dysfunction, and metabolic impairment. Mitochondria are the cellular compartments responsible for energy production.

Previous studies have shown that physical exercise, in particular swim training, “modifies mitochondria structure and function. . . which may play an important role in the protection of muscle fibers in ALS,” the scientists stated.

In this study, a team of researchers set out to evaluate the effects of swim training on mitochondria function, energy metabolism, and muscle strength in muscle fibers of a mouse model of ALS, compared with healthy (wild) animals.

To do so, scientists performed a grip strength test (time during which the animals sustain their weight while holding onto a metal rail suspended in midair) to measure muscle strength, and collected mitochondria from muscle fibers to run a battery of metabolic tests in both healthy and ALS mice, with and without swim training, starting at 10 weeks of age.

In addition, researchers measured the activity of several enzymes involved in energy metabolism, including citrate synthase, cytochrome c oxidase and malate dehydrogenase, and the levels of oxidative stress markers in muscle fibers from healthy and ALS mice. Oxidative stress refers to the cellular damage that occurs as a consequence of having high levels of oxidant molecules.

Findings revealed that ALS mice had reduced muscle strength (70% less between 11 and 15 weeks), and showed significant alterations in energy metabolism (30% less citrate synthase activity, and higher activities of cytochrome c oxidase and malate dehydrogenase), and high levels of oxidative stress markers compared with controls.

However, swim training reduced the loss of muscle strength associated with ALS (5% less between 11 and 15 weeks), and increased citrate synthase activity by 26% compared with ALS mice that did not undergo swim training.

According to previous studies, swim training prolongs the lifespan of ALS mice by 10% to 13%. However, “from a clinical point of view, not only prolongation of lifespan, but also sustained functionality and inhibition of muscle waste are critical elements of therapy,” the study said.

“In agreement with previously published data, swim training significantly decreases the reduction in muscle strength clearly visible at the symptomatic stage of ALS, . . . reduces oxidative stress, and improves muscle energy metabolism at terminal stage of the disease,” the researchers stated.

“Our findings indicate that swim training is a modulator of skeletal muscle energy metabolism with concomitant improvement of skeletal muscle function in ALS mice,” they concluded.