The evidence consistently points in one direction: regular exercise suppresses chronic low-grade inflammation, with the strongest evidence for cardiovascular disease and in people with type 2 diabetes. Multiple human studies and meta-analyses support this, but the ideal training dose has not yet been precisely determined and for rheumatic diseases the direct evidence is still scarce and contradictory. In practical terms, this means that for most people a combination of aerobic training and resistance training is the most well-supported choice for addressing chronic inflammation.
Regular exercise demonstrably suppresses so-called low-grade chronic inflammation, a smouldering inflammatory response that is measurable through blood markers such as CRP, TNF-alpha and IL-6. An important mechanism is that working muscles produce a protein, IL-6 as a myokine, which then suppresses TNF-alpha. TNF-alpha plays a key role in insulin resistance and atherosclerosis. This biological explanatory pathway is supported by both animal and human studies1,2,3, although the exact dose at which this effect occurs optimally has not yet been established.
In people with type 2 diabetes and excess weight the effect has been studied more concretely. A meta-analysis of 20 studies involving more than 1,200 participants shows that combined aerobic and resistance training measurably lowers CRP, TNF-alpha and IL-6 compared with a control group that received standard care only4. The authors of that meta-analysis themselves caution about moderate evidence quality and an uncertain risk of bias in the underlying studies, so the precise magnitude of the effect should be read with some caution. The direction, however, is consistently positive.
In older people with frailty, the anti-inflammatory effect of exercise goes hand in hand with less oxidative damage, better mitochondrial function and an increase in cellular cleaning processes (autophagy)5. Strength, endurance, balance and flexibility training each have their own benefits for older adults; a combination tailored to the individual is preferable to a single type of training. In patients with COPD, a chronic lung condition accompanied by systemic inflammation, structured exercise rehabilitation helps suppress inflammation, improves vascular function and reduces the risk of acute deterioration6. Here too, the optimal type of training per patient has not yet been precisely determined.
At the level of hard health outcomes, the evidence is strongest for cardiovascular disease and premature death. Multiple large epidemiological and exercise studies consistently show that better fitness and higher physical activity reduce the risk of these outcomes7,8. Inflammation is one of the active mechanisms in this, alongside effects on blood pressure, lipid metabolism and cardiac function. This makes the protective effect of exercise broader than the inflammation pathway alone.
There are also limits to what the evidence shows. For people with rheumatic diseases such as rheumatoid arthritis, the anti-inflammatory effect of exercise is biologically plausible, but direct evidence is scarce and contradictory3. No clear recommendations can be based on this at the present time. Furthermore, for indirect protection via inflammation against diseases such as muscle loss, dementia and bone loss, a plausible association exists, but a fully proven causal pathway from exercise to the prevention of those diseases via inflammation does not yet exist2.
Based on multiple meta-analyses and human studies (PMID 38887616, 15772055, 31181700, 32249021, 32234291, 40255692, 26139859, 26606383). The quality of evidence ranges from moderate (inflammatory markers, frailty, COPD, rheumatic conditions) to strong (cardiovascular disease and mortality). None of the sources consulted report relevant safety risks from moderate regular exercise.