Effects of Resistance Exercise Training on Mitochondrial Dysfunction

In a recent WCMR Science Seminar, Dr Valeria Di Leo talked to us about the effects of resistance exercise training on mitochondrial dysfunction in mitochondrial myopathy patients. Read on to find out more.

Skeletal muscle is a highly energy demanding tissue, requiring huge amounts of energy to perform muscle contraction. The most efficient way to produce energy takes place in the mitochondria and so when mitochondria are faulty, muscular weakness can arise leading to fatigue and difficulty to perform exercise. Exercise is recognised worldwide to give beneficial physical effects to both children and adults and it can induce massive changes in skeletal muscle. Interestingly, it is known that exercise training has the potential to improve mitochondrial function in those with muscular weakness. However, we do not understand the way this happens and a treatment for these patients does not exist yet.

My project looks at the effects of resistance exercise training on the skeletal muscle of a group of patients with a deletion in their mitochondrial DNA. The study uses skeletal muscle biopsies taken before and after the exercise training from each patient who participated, so that we can compare them. After 16 weeks of resistance exercise training, some patients of the cohort show an increase both in the number of mitochondria in the skeletal muscle and in the oxygen capability while exercising, which suggests an improvement in mitochondrial function and a reduction in exercise intolerance. Importantly, all patients in the cohort display an increase of one of the structures directly linked to the production of energy in mitochondria.

Another important finding of the study is that the muscle cells of participants after exercise change the production level of important cell components: this is scientifically called “differential gene expression”. Resistance exercise training helps mitochondrial patients to have physical beneficial effects but more importantly, is driving a reprogramming from inside the muscle cells helping mitochondria to work better and muscle to contract properly. Thanks to my last experiments, we identified some of the candidate proteins that trigger this reprogramming of the skeletal muscle after resistance exercise. Our hope is that by understanding this process, we can look for a drug that mimics the benefits of resistance exercise training for mitochondrial myopathy patients.

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