Resistance training is extremely important when it comes to aging, health, heart, bones and muscles and reducing the risk of certain diseases. Resistance training improves the metabolic profile in type 2 diabetes and helps with loosing weight.
Researchers at the University of California, San Diego School of Medicine found how just one session of moderate exercise can also act as an anti-inflammatory. The findings have encouraging implications for chronic disease like arthritis, fibromyalgia and for more pervasive conditions, such as obesity.
The study, recently published online in Brain, Behavior and Immunity, found one 20-minute session of moderate exercise can stimulate the immune system, producing an anti-inflammatory cellular response.
“Each time we exercise, we are truly doing something good for our body on many levels, including at the immune cell level,” said senior author Suzi Hong, PhD, in the Department of Psychiatry and the Department of Family Medicine and Public Health at UC San Diego School of Medicine. “The anti-inflammatory benefits of exercise have been known to researchers, but finding out how that process happens is the key to safely maximizing those benefits.
The brain and sympathetic nervous system (a pathway that serves to accelerate heart rate and raise blood pressure, among other things), are activated during exercise to enable the body to carry out work. Hormones, such as epinephrine and norepinephrine, are released into the blood stream and trigger adrenergic receptors, which immune cells possess.
This activation process during exercise produces immunological responses, which include the production of many cytokines, or proteins, one of which is TNF (a key regulator of local and systemic inflammation that also helps boost immune responses).
“Our study found one session of about 20 minutes of moderate treadmill exercise resulted in a five percent decrease in the number of stimulated immune cells producing TNF”, said Hong. “knowing what sets regulatory mechanisms of inflammatory proteins in motion may contribute to developing new therapies for the overwhelming number of individuals with chronic inflammatory conditions, including nearly 25 million Americans who suffer from autoimmune diseases.”
The 47 study participants walked on a treadmill at an intensity level that was adjusted based on their fitness level. Blood was collected before and immediately after the 20 minute exercise challenge.
“Our study shows a workout session doesn’t actually have to be intense to have anti-inflammatory effects. Twenty minutes to half-an-hour of moderate exercise, including fast walking, appears to be sufficient.” said Hong. “feeling like a workout needs to be at a peak exertion level for a long duration can intimidate those who suffer from chronic inflammatory disease and could greatly benefit from physical activity.”
Inflammation as a vital part of the body’s immune response. It is the body’s attempt to heal itself after an injury, defend itself against foreign invaders, such as viruses and bacteria, and repair damaged tissue. However, chronic inflammation can lead to serious health issues associated with diabetes, celiac disease, obesity and other conditions.
“Patients with chronic inflammatory diseases should always consult with their physician regarding the appropriate treatment plan, but knowing that exercise can act as an anti-inflammatory is an exciting step forward in possibilities,” said Hong.
Study co-authors include Stoyan Dimitrov, and Elaine Hulteng, UC San Diego.
The research was funded by the American Recovery and Reinvestment Act (RO1HL090975, HL090975S) and UCSD Clinical and Translational Science Awards from the National Institutes of Health (UL1RR031980).
Biomedical engineers at Duke University have demonstrated that human muscle has an innate ability to ward off the damaging effects of chronic inflammation when exercised. the discovery was made possible through the use of lab-grown engineered human muscle, demonstrating the potential power of the first-o-its-kind platform in such research endeavors.
The results appear online on January 22 in the Journal Science Advances.
“Lots of processes are taking place throughout the human body during exercise, and it is difficult to take apart which systems and cells are doing what inside an active person” said Nenad Bursac, professor of Biomedical Engineering at Duke. “Our engineered muscle platform is modular, meaning we can mix and match various types of cells and tissue components if we want to. But in this case we discovered that the muscle cells are capable of taking anti-inflammatory actions all on their own.”
Inflammation is not inherently good or bad. when the body is injured, an initial low-level inflammation response clears away debris and helps tissue rebuild. Other times, the immune system overreacts and creates an inflammatory response that causes damage, like the often deadly cytokine storms brought on by some cases of COVID-19. And then, there are diseases that lead to chronic inflammation, such as rheumatoid arthritis and sarcopenia (muscle loss), which can cause muscle to waste away and weaken its ability to contract.
Among many molecules that can cause inflammation, one pro-inflammatory molecule in particular, interferon gamma, (a cytokine critical to both innate and adaptive immunity and functions as the main activator of macrophages in addition to stimulating natural killer cells and neurtophils) have been associated with various types of muscle wasting and dysfunction. while previous research in humans and animals has shown that exercise can help mitigate the effects of inflammation in general, it has been difficult to distinguish what role the muscle cells themselves might play, let alone how they interact with specific offending molecules, such as interferon gamma.
“We know that chronic inflammatory disease induce muscle atrophy, but we wanted to see if the same thing would happen to our engineered human muscles grown in a Petri dish,” said Zhaowei Chen, a postdoctoral researcher in Bursac’s laboratory and first author the paper. “Not only did we confirm that interferon gamma primarily works thorough a specific signaling pathway, we showed that exercising muscle cells can directly counter this pro-inflammatory signaling independent of the presence of other cell types or tissues.”
To prove that muscle alone is capable of blocking interferon gamma’s destructive powers, Bursac and Chen turned to an engineered muscle platform (https://pratt.duke.edu/about/news/first-contracting-human-muscle-grown-laboratory) that has been developed for nearly a decade. They were first to grow contracting, functional human skeletal muscle in a Petri dish, and since then the lab has been improving its processes by, for example, adding immune cells (https://pratt.duke.edu/about/news/immune-cells-help-older-muscles-heal-new) and reservoirs of stem cells to the recipe.
In the current study, the researchers took these fully function lab-grown muscles and inundated them with relatively high levels of interferon gamma for seven days to mimic the effects of a long-lasting chronic inflammation. As expected the muscle got smaller and lost much of its strength.
“There are theories out there that optimal levels and regimes of exercise could fight chronic inflammation while not overstressing the cells. Maybe our engineered muscle, we can help find out if such theories are true.” said Bursac.
This research was supported by the National Institutes of Health (UH3TR002142, U01EB028901, R01AR070543).
