Effects of Physical Exercise on Inflammatory Markers of Atherosclerosis
A. Pinto, D. Di Raimondo, A. Tuttolomondo, C. Butta, G. Milio and G. Licata
Affiliation: U.O.C. Medicina Vascolare, Dipartimento Biomedico di Medicina Interna e Specialistica, Universita degli Studi di Palermo, Piazza delle Cliniche n° 2, 90127 Palermo, Italy.
Keywords: Physical exercise, atherosclerosis, inflammation, C-reactive protein, interleukin-6, CVD (cardiovascular disease), diabetes, cytokines, chemokines, endothelial dysfunction
It is well established that physically fit individuals have a reduced risk of developing CVD (cardiovascular disease) and other
age-related chronic disorders. Regular exercise is an established therapeutic intervention with an enormous range of benefits. Chronic
low-grade systemic inflammation may be involved in atherosclerosis, diabetes and in pathogenesis of several chronic pathological conditions;
recent findings confirm that physical activity induces an increase in the systemic levels of a number of cytokines and chemokines
with anti-inflammatory properties. The possibility that regular physical exercise exerts anti-inflammation activity, being the interaction
between contracting muscle and the other tissues and the circulating cells mediated through signals transmitted by “myokines” produced
with muscle contractions. To date the list of myokines includes IL-6, IL-8, and IL-15. During muscle contractions are also released IL-
1receptor antagonis and sTNF-R, molecules that contribute to provide anti-inflammatory actions.
Nevertheless discrepancies, analysis of available researches seem to confirm the efficacy of regular physical training as a nonpharmacological
therapy having target chronic low-grade inflammation. Given this, physical exercise could be considerate a useful
weapon against local vascular and systemic inflammation in atherosclerosis. Several mechanisms explain the positive effect of chronic
exercise, nevertheless, these mechanisms do not fully enlighten all pathways by which exercise can decrease inflammation and endothelial
dysfunction, and hence modulate the progression of the underlying disease progress.
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