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Letter to the Editor |
British Heart Foundation Glasgow Cardiovascular Research Centre (M.T., F.J.C., A.F.D.), University of Glasgow, Glasgow G11 6NT, United Kingdom; and Department of Internal Medicine (E.Z.-S., W.G.), Diabetology and Nephrology, Medical University of Silesia, 41-800 Zabrze, Poland
Address correspondence to: Dr. Maciej Tomaszewski, BHF Glasgow Cardiovascular Research Centre, Division of Cardiovascular and Medical Sciences, University of Glasgow, Western Infirmary, Glasgow G11 6NT, United Kingdom. E-mail: mt65h{at}clinmed.gla.ac.uk.
To the editor:
Margelia et al. (1) have reported a dramatic increase in serum levels of C-reactive protein (CRP) and other acute phase reactants after running 246 km in Spartathlon. The authors speculate that this sudden elevation of inflammatory factors may be detrimental for the cardiovascular system (1).
Up-regulation of CRP in response to ultrastrenuous aerobic exercise is indeed a physiologically relevant observation and represents a natural immunological reaction triggered possibly by IL-6 release from injured skeletal muscle cells (2). Given that CRP promotes a proinflammatory phenotype of endothelial cells in vitro (3), potential damage to the cardiovascular system exerted by ultrastrenuous exercise may be a physiologically justified hypothesis. However, elevation of CRP serum levels after ultramarathon is not accompanied by endothelial injury (4). In our previous study on a sample of middle-age healthy men, postexercise serum levels of endothelial injury markers (E-selectin and sICAM-1) were not increased when compared with the baseline values (4), despite a significant 6-fold elevation in CRP after 100 km of ultramarathon (4). In fact, circulating concentrations of soluble intercellular adhesion molecule-1 were lower after the race than at baseline (4). In addition, markers of endothelial injury did not correlate with either CRP or IL-6 after the ultramarathon. Thus, it is unlikely that CRP up-regulation induced by acute ultrastrenuous exercise may exert a negative influence on the cardiovascular system, at least via endothelial injury. Most importantly, the increase in levels of CRP and other inflammatory markers after ultramarathon is only transient (4) and returns to strikingly low baseline values as the tissue-repair processes progress (4). After rapid normalization, circulating concentrations of CRP in ultramarathon runners remain very low long-term, despite repeated engaging in intense aerobic activities (4). Based on serum CRP levels, regular long-distance runners are classified as subjects with significantly reduced cardiovascular risk when compared with nonexercising healthy controls (4). Interestingly, suppression of CRP serum levels by regular long-distance running is independent of parallel reduction of fat mass (4), IL-6 (4), and lipid levels (5). This implicates the importance of other, yet unrecognized metabolic pathways that regulate CRP in subjects engaging in intense aerobic exercise.
Footnotes
A response to this letter was invited, but the authors of the original article chose not to provide one.
Received May 12, 2005.
References
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