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20 Minutes of Exercise May Suppress Inflammation

Summary: A new study reports 20 minutes of moderate exercise can act as an anti-inflammatory. The findings could be beneficial for those with inflammatory diseases such as fibromyalgia and arthritis.

Source: UCSD.

One moderate exercise session has a cellular response that may help suppress inflammation in the body.

It’s well known that regular physical activity has health benefits, including weight control, strengthening the heart, bones and muscles and reducing the risk of certain diseases. Recently, researchers at 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 diseases 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 diseases and could greatly benefit from physical activity.”

Image shows a man running up steps.

The 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. NeuroscienceNews.com image is for illustrative purposes only.

Inflammation is 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.

About this neurology research article

Study co-authors include Stoyan Dimitrov, and Elaine Hulteng, UC San Diego.

Funding: Funding from American Recovery and Reinvestment Act, National Institutes of Health.

Source: Michelle Brubaker – UCSD
Image Source: NeuroscienceNews.com image is in the public domain.
Original Research: Abstract for “Inflammation and exercise: Inhibition of monocytic intracellular TNF production by acute exercise via β2-adrenergic activation” by Stoyan Dimitrov, Elaine Hulteng, and Suzi Hong in Brain, Behavior, and Immunity. Published online December 21 2016 doi:10.1016/j.bbi.2016.12.017

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Abstract

Inflammation and exercise: Inhibition of monocytic intracellular TNF production by acute exercise via β2-adrenergic activation

Regular exercise is shown to exert anti-inflammatory effects, yet the effects of acute exercise on cellular inflammatory responses and its mechanisms remain unclear. We tested the hypothesis that sympathoadrenergic activation during a single bout of exercise has a suppressive effect on monocytic cytokine production mediated by β2 adrenergic receptors (AR). We investigated the effects of 20-min moderate (65–70% VO2 peak) exercise-induced catecholamine production on LPS-stimulated TNF production by monocytes in 47 healthy volunteers and determined AR subtypes involved. We also examined the effects of β-agonist isoproterenol and endogenous β- and α-agonists epinephrine and norepinephrine, and receptor-subtype-specific β- and α-antagonists on TNF production in a series of in vitro investigations. LPS-stimulated TNF production by peripheral blood monocytes was determined intracellularly by flow cytometry, using an intracellular protein transport inhibitor. Percent TNF-producing monocytes and per-cell TNF production with and without LPS was suppressed by exercise with moderate to large effects, which was reversed by a β2-AR antagonist in spite that plasma TNF levels did not change. This inhibitory response in TNF production by exercise was mirrored by β-AR agonists in an agonist-specific and dose-dependent manner in vitro: similar isoproterenol (EC50 = 2.1–4.7 × 10−10 M) and epinephrine (EC50 = 4.4–10 × 10−10 M) potency and higher norepinephrine concentrations (EC50 = 2.6–4.3 × 10−8 M) needed for the effects. Importantly, epinephrine levels observed during acute exercise in vivo significantly inhibited TNF production in vitro. The inhibitory effect of the AR agonists was abolished by β2-, but not by β1- or α-AR blockers. We conclude that the downregulation of monocytic TNF production during acute exercise is mediated by elevated epinephrine levels through β2-ARs. Decreased inflammatory responses during acute exercise may protect against chronic conditions with low-grade inflammation.

“Inflammation and exercise: Inhibition of monocytic intracellular TNF production by acute exercise via β2-adrenergic activation” by Stoyan Dimitrov, Elaine Hulteng, and Suzi Hong in Brain, Behavior, and Immunity. Published online December 21 2016 doi:10.1016/j.bbi.2016.12.017

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