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Review
Potential mechanisms linking high-volume exercise with coronary artery calcification
  1. Angelica Zambrano1,
  2. Yin Tintut2,3,
  3. Linda L Demer2,3,
  4. Jeffrey J Hsu2,3
  1. 1 Paul L Foster School of Medicine, Texas Tech University Health Sciences Center, Lubbock, Texas, USA
  2. 2 Medicine/Cardiology, University of California Los Angeles David Geffen School of Medicine, Los Angeles, California, USA
  3. 3 Medicine, Veterans Affairs Greater Los Angeles Healthcare System, Los Angeles, California, USA
  1. Correspondence to Dr Jeffrey J Hsu, Medicine/Cardiology, University of California Los Angeles David Geffen School of Medicine, Los Angeles, CA 90095, USA; jjhsu{at}mednet.ucla.edu

Abstract

Recent studies have found an association between high volumes of physical activity and increased levels of coronary artery calcification (CAC) among older male endurance athletes, yet the underlying mechanisms have remained largely elusive. Potential mechanisms include greater exposure to inflammatory cytokines, reactive oxygen species and oxidised low-density lipoproteins, as acute strenuous physical activity has been found to enhance their systemic release. Other possibilities include post-exercise elevations in circulating parathyroid hormone, which can modify the amount and morphology of calcific plaque, and long-term exposure to non-laminar blood flow within the coronary arteries during vigorous physical activity, particularly in individuals with pre-existing atherosclerosis. Further, although the association has only been identified in men, the role of testosterone in this process remains unclear. This brief review discusses the association between high-volume endurance exercise and CAC in older men, elaborates on the potential mechanisms underlying the increased calcification, and provides clinical implications and recommendations for those at risk.

  • Coronary Artery Disease
  • Computed Tomography Angiography
  • Atherosclerosis

https://doi.org/10.1136/heartjnl-2022-321986

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    Footnotes

    • Contributors All authors have contributed substantially to this manuscript and approve its submission for publication consideration. AZ—manuscript writing and figure preparation. YT—manuscript and figure editing. LLD—manuscript and figure editing. JJH—conceptual design, manuscript writing and editing, and figure preparation.

    • Funding This work was supported by the following grants from the National Institutes of Health/National Heart, Lung and Blood Institute (NIH/NHLBI): R01HL137647 and R01HL151391 (YT, LLD) and 1K08-HL151961 (JJH).

    • Competing interests None declared.

    • Provenance and peer review Not commissioned; externally peer reviewed.

    • Supplemental material This content has been supplied by the author(s). It has not been vetted by BMJ Publishing Group Limited (BMJ) and may not have been peer-reviewed. Any opinions or recommendations discussed are solely those of the author(s) and are not endorsed by BMJ. BMJ disclaims all liability and responsibility arising from any reliance placed on the content. Where the content includes any translated material, BMJ does not warrant the accuracy and reliability of the translations (including but not limited to local regulations, clinical guidelines, terminology, drug names and drug dosages), and is not responsible for any error and/or omissions arising from translation and adaptation or otherwise.