An article in December 2016 issue Brain, Behavior and Immunity, investigates on whether 20-minute exercise sessions can improve someone’s anti-inflammatory response. The theory is this happens by activating the sympathetic nervous system.
More specifically, the researchers tested the hypothesis that a single 20-minute session of exercise would be enough to trigger sympathoadrenergic activation, which, in turn, would suppress the production of monocytic cytokines.
Monocytes are a type of white blood cell, or immune cell, that help to fight off bacteria and infections. Cytokines are a type of protein that help other cells to become so-called effector cells, which, in turn, kill off cancerous or infected cells.
TNF is one of these cytokines. TNF can induce cell differentiation and proliferation, but also cell death, including cancerous ones. TNF also has pro-inflammatory properties, which help the body to bring its inflammatory cells to the site of the injury, creating an immunological response.
Inflammation is a necessary part of the body’s immune response, but too much inflammation can lead to disease. Chronic inflammation may contribute to diabetes, obesity, celiac disease, arthritis, fibromyalgia, or bowel diseases such as Crohn’s disease or ulcerative colitis.
To test their hypothesis, the researchers asked 47 participants to walk on a treadmill for 20 minutes at an intensity rate adjusted to suit each individual’s fitness level. Hong and team took blood samples from the participants both before and immediately after the exercise sessions.
As little as 20 minutes of exercise reduces inflammation
The results revealed that a 20-minute session of moderate exercise can have anti-inflammatory effects.The study confirmed the researchers’ hypothesis. Exercise did seem to produce an anti-inflammatory cellular response, which could be seen in the reduction of the cytokine TNF.
“Our study found one session of about 20 minutes of moderate treadmill exercise resulted in a 5 percent decrease in the number of stimulated immune cells producing TNF,” says Hong.
Although the anti-inflammatory benefits of physical activity are already known to researchers, Hong explains, this study explains the process in more detail.
“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,” Hong adds.
The lead author also highlights the importance of this study for people with reduced strength or mobility who are under the impression that physical exercise needs to be extremely intense in order to be effective.
“Our study shows a workout session does not 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. 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.”
Suzi Hong
investigated sympathoadrenergic activation effects on monocytic TNF production.
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Acute exercise suppresses monocytic TNF production via β2-ARs.
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Physiological epinephrine levels observed during exercise inhibit TNF in vitro.
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Exercise-induced catecholamine release may have an anti-inflammatory effect.
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Exercise effects on stimulated monocytic intracellular TNF vs. plasma TNF differed.
The authors of the study
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. [They] 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.
investigated sympathoadrenergic activation effects on monocytic TNF production.•Acute exercise suppresses monocytic TNF production via β2-ARs.•Physiological epinephrine levels observed during exercise inhibit TNF in vitro.•Exercise-induced catecholamine release may have an anti-inflammatory effect.•Exercise effects on stimulated monocytic intracellular TNF vs. plasma TNF differed.AbstractRegular 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.