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Endurance training helps with muscle inflammation

Endurance training can actually be helpful in dealing with muscle inflammation, according to a paper co-written by faculty at Binghamton University, State University of New York, and Karolinska Institutet and Karolinska University Hospital in Stockholm, Sweden.

Muscle inflammation, or myositis, can be caused by infection, injury and chronic disease. However, specific forms of myositis like dermatomyositis and polymyositis occur when the body's immune system turns against its own muscles, damaging the muscle tissue in the process.

While there are plenty of prescribed medications to cope with muscular diseases, Binghamton University professor of pharmaceutical sciences Kanneboyina Nagaraju states the medication utilised only does half the job.

"All the drugs people are using target one immune cell or a group of immune cells, but there are no new drugs that target muscles that are dying," said Nagaraju. "Yet, exercise takes care of the immune cells that are killing the muscles, and repairs the cell death of the muscle."

In order to discover a better treatment, Nagaraju and his former graduate student Jessica Boehler, along with an international team of researchers, set out to uncover how endurance exercise changes microRNA in skeletal muscles and associate the identified microRNAs with mRNA and protein expressions. The experiment consisted of two groups, a 12-week endurance exercise group and a non-exercise group. To see how exercise affects the patients, muscle biopsies were taken before and after undergoing exercise.

This exercise trial was done by Professor Ingrid Lundeberg's group Karolinska Institutet and Karolinska University Hospital.

Researchers found that endurance exercise altered microRNAs that target and downregulate immune processes, as well as decreasing different microRNAs that target and upregulate mitochondrial content at the protein level. That is, exercise creates microRNA that decreases the number of immune cells that attack the muscle and heals the muscle by increasing aerobic metabolism through mitochondrial biogenesis.

"The results weren't surprising," said Nagaraju, "The reason why exercise wasn't considered before is that if people have muscles that are already inflamed or weak, they believed exercise would make the muscles worse. However, what is surprising is the question of why exercise is so effective. It's because exercise takes care of the immune cells that are damaging the muscle while simultaneously targeting specific parts of dead or affected muscles."

While there are no drugs today that target all the issues of muscle inflammation, Nagaraju believes a combination of medication and endurance-based exercise can help patients live a happier and healthier life.

Abstract
Objective: To identify changes in skeletal muscle microRNA expression after endurance exercise and associate the identified microRNAs with mRNA and protein expression to disease-specific pathways in polymyositis (PM) and dermatomyositis (DM) patients.
Methods: Following a parallel clinical trial design, patients with probable PM or DM, exercising less than once a week, and on stable medication for at least one month were randomized into two groups at Karolinska University Hospital: a 12-week endurance exercise group (n = 12) or a non-exercised control group (n = 11). Using an Affymetrix microarray, microRNA expression was determined in paired muscle biopsies taken before and after the exercise intervention from 3 patients in each group. Ingenuity pathway analysis with a microRNA target filter was used to identify microRNA transcript targets. These targets were investigated at the mRNA (microarray) and protein (mass spectrometry) levels in patients.
Results: Endurance exercise altered 39 microRNAs. The microRNAs with increased expression were predicted to target transcripts involved in inflammatory processes, metabolism, and muscle atrophy. Further, these target transcripts had an associated decrease in mRNA expression in exercised patients. In particular, a decrease in the NF-κB regulator IKBKB was associated with an increase in its target microRNA (miR-196b). At the protein level, there was an increase in mitochondrial proteins (AK3, HIBADH), which were associated with a decrease in microRNAs that were predicted to regulate their expression.
Conclusion: Improvement in disease phenotype after exercise is associated with increasing microRNAs that target and downregulate immune processes at the transcript level, as well as decreasing microRNAs that target and upregulate mitochondrial content at the protein level. Therefore, microRNAs may improve disease by decreasing immune responses and increasing mitochondrial biogenesis.

Authors
Jessica F Boehler, Marshall W Hogarth, Matthew D Barberio, James S Novak, Svetlana Ghimbovschi, Kristy J Brown, Li Alemo Munters, Ingela Loell, Yi-Wen Chen, Heather Gordish-Dressman, Helene Alexanderson, Ingrid E Lundberg, Kanneboyina Nagaraju

[link url="https://www.sciencedaily.com/releases/2017/11/171108124129.htm"]Binghampton University material[/link]
[link url="http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0183292"]PLOS One abstract[/link]

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