State of the Art Reviews: The Anti-Inflammatory Actions of Exercise Training
Open accessAbstract
The list of diseases with a known inflammatory etiology is growing. Cardiovascular disease, osteoporosis, diabetes, geriatric cachexia, and Alzheimer's disease have all been shown to be linked to or exacerbated by aberrantly regulated inflammatory processes. Nevertheless, there is mounting evidence that those who are physically active, or who become physically active, have a reduction in biomarkers associated with chronic inflammation. There was strong early consensus that exercise-induced reductions in inflammation were explained by body mass index or body fatness, but recent studies provide support for the contention that exercise has body fat-independent anti-inflammatory effects. With few exceptions, the anti-inflammatory effects of exercise appear to occur regardless of age or the presence of chronic diseases. What remains unclear are the mechanisms by which exercise training induces these anti-inflammatory effects, but there are several intriguing possibilities, including release of endogenous products, such as heat shock proteins; selective reduction of visceral adipose tissue mass or reducing infiltration of adipocytes by macrophages; shift in immune cell phenotype; cross-tolerizing effects; or exercise-induced shifts in accessory proteins of toll-like receptor signaling. However, future research endeavors are likely to uncover additional potential mechanisms, and it could be some time before functional mechanisms are made clear. In summary, the potential anti-inflammatory influences of exercise training may provide a low-cost, readily available, and effective treatment for low-grade systemic inflammation and could contribute significantly to the positive effects of exercise training on chronic disease.
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The cytokine production profile during and immediately after physical exercise is dependent on several factors, such as population, intensity or duration of exercise, glucose availability, and sample collection time.
“In addition, this cytokine production profile that occurs during and immediately after physical exercise is dependent on several factors, such as; population (sedentary, presence of diseases, etc.), the intensity or duration of the physical exercise, glucose availability and sample collection time (Flynn et al., 2007).”
From Physical Exercise-Induced Myokines and Muscle-Adipose Tissue Crosstalk: A Review of Current Knowledge and the Implications for Health and Metabolic Diseases (2018) · cites this paper as Flynn et al., 2007
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- Authors
- Flynn, M. G., McFarlin, B. K., & Markofski, M. M.
- Affiliations
- Purdue University West Lafayette (US)
- University of Houston (US)
- Venue
- American Journal of Lifestyle Medicine
- Publisher
- SAGE Publications
- Published
- 2007-05
- Volume
- 1
- Issue
- 3
- Pages
- 220-235
- ISSN
- 1559-8276 (ISSN-L)
- 1559-8284
- PMC
- PMC4243532
- OpenAlex
- W2017675047
- Cited by
- 154
- References
- 196
- Citations by year
- 2026: 13 · 2025: 21 · 2024: 9 · 2023: 16 · 2022: 18 · 2021: 10 · 2020: 12 · 2019: 11 · 2018: 5 · 2017: 2 · 2016: 6 · 2015: 3 · 2013: 3 · 2012: 6
- FWCI
- 5.08
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- American Journal of Lifestyle Medicine (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute on Aging (R03AG028110)
- Topics
- Health Sciences › Medicine › Rehabilitation › Exercise and Physiological Responses
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Physiology › Physical Activity and Health
- Keywords
- exercise training, anti-inflammatory activity, chronic inflammation, low-grade inflammation, heat shock proteins, visceral adipose tissue, macrophage infiltration, immune cell phenotypes, cross-tolerance, Toll-like receptor signaling, cardiovascular disease, diabetes mellitus, osteoporosis, Alzheimer's disease
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