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Potential Cardiac Damage Induced by Strenuous Exercise

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Textbook of Sports and Exercise Cardiology

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Abstract

Regular physical exercise generally reduces all-cause and disease-specific mortality and CVD morbidity. Physiological cardiac adaptations to regular endurance exercise are summarized as “athletes’ heart”. Recent reports provided evidence for the hypothesis that extensive endurance exercise itself may also induce or accelerate non-physiologic cardiac damage. Several studies have demonstrated an unexpected degree of calcified coronary artery atherosclerosis. In one study, coronary event rates including revascularization were similar in athletes compared to non-athletic cohorts for every degree of atherosclerosis, even though coronary mortality risk was low. The presence of coronary artery calcification (CAC) may hence not just reflect “healthy hardening” of the coronary arteries, but imply an elevated risk as in non-athletic cohorts. Moreover, an unexpectedly high prevalence of myocardial fibrosis has been shown in endurance athletes. A significant association of myocardial fibrosis with years of training and numbers of completed competitions suggests that this is not just a consequence of diseases unrelated to exercise such as myocarditis or coronary artery disease but may be caused by repetitive bouts of strenuous exercise. The areas of right ventricular insertion to the septum (“hinge points”) may be particularly prone to development of myocardial fibrosis. Its presence has also been linked with higher troponin elevations during athletic competitions and with future coronary event rates, but further studies are warranted.

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Author information

Authors and Affiliations

  1. Clinic of Cardiology and Intensive Care Medicine, Bethanien Hospital Moers, Moers, Germany

    Stefan Möhlenkamp

  2. Private Center of Sports & Exercise Cardiology, Munich, Germany

    Axel Pressler

Authors
  1. Stefan Möhlenkamp
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  2. Axel Pressler
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Corresponding author

Correspondence to Stefan Möhlenkamp .

Editor information

Editors and Affiliations

  1. Private Center for Sports and Exercise Cardiology, München, Bayern, Germany

    Axel Pressler

  2. University Institute of Sports Medicine Prevention and Rehabilitation, Paracelsus Medical University Salzburg, Salzburg, Austria

    Josef Niebauer

Review

Review

1.1 Questions

  1. 1.

    An asymptomatic 65-year-old marathon runner presents for general cardiovascular check-up. He has already undergone coronary artery calcium (CAC) scoring because of a positive family history and a high-normal resting blood pressure. His Agatston Score is 529 (=high). What are the clinical implications?

    1. (a)

      A CAC score of 529 in an asymptomatic marathon runner has no clinical relevance. As he is asymptomatic, he can continue running without restriction.

    2. (b)

      The risk of a significant coronary artery stenosis is high. He should therefore directly undergo invasive coronary angiography and probably coronary artery stenting.

    3. (c)

      The Agatston score indicates calcified atherosclerosis. He may have an elevated risk of future coronary events. Additional testing for (subclinical) ischemia and risk factor modification should be considered.

    4. (d)

      The marathon runner is at elevated risk of a coronary event. He must be advised to stop running and rather pursue physical activity that is less strenuous at heart rates below 80% of maximum heart rate for age and sex.

    5. (e)

      The higher the Agatston score, the less likely it is for plaque to rupture. Therefore, he has “healthy hardening” and can be advised to continue running.

  2. 2.

    (I) Late gadolinium enhancement (LGE) in an endurance athlete is likely of no prognostic relevance

    Because

    (II) LGE in athletes often occurs at the hinge points where the right ventricular wall inserts into the interventricular septum.

    Which of the following combinations is true?

    1. (a)

      Statement (I) is correct, statement (II) is correct, the link is correct.

    2. (b)

      Statement (I) is incorrect, statement (II) is correct.

    3. (c)

      Statement (I) is correct, statement (II) is correct, the link is incorrect.

    4. (d)

      Statement (I) is correct, statement (II) is incorrect.

    5. (e)

      Both Statements are incorrect.

1.2 Answers

  1. 1.

    Correct Answer: “C”

    Explanation:

    1. (a)

      This statement is false because a very high Agatston score, i.e. >400, is associated with a higher risk of coronary events. Therefore, a thorough risk factor assessment is warranted, and risk factors should be modified according to guidelines.

    2. (b)

      Even though the risk of luminal narrowing >50% somewhere in the coronary tree is high, there is no need for invasive angiography or stenting unless there is a relevant ischemic area at risk, i.e. >10% of myocardium.

    3. (c)

      This statement is correct. There is calcified plaque (most likely accompanied by non-calcified plaque) in the coronary arteries and a considerable risk of stenosis relevant for ischemia during strenuous exercise. Additional ischemia testing should hence be considered, and risk factors should be modified according to guidelines.

    4. (d)

      This statement is not true. There is currently no evidence that ceasing endurance exercise improves prognosis in asymptomatic cohorts even in the presence of advanced subclinical atherosclerosis. Quite the opposite: regular exercise at moderate intensity and duration prevents events also in persons with CAD.

    5. (e)

      This statement is false. A high plaque density has been suggested to be somewhat protective of plaque rupture, but this cannot be concluded from the Agatston score, which is an index derived from calcified plaque area and density.

  2. 2.

    Correct Answer: “B”

    Explanation:

    Even though evidence is still limited, the presence of LGE has been shown to increase cardiac event risk in many clinical entities, including CAD, cardiomyopathy, myocarditis, sarcoidosis, etc. Initial evidence suggests that this also holds in master athletes without a history of CAD. It is likely that this elevated risk associated with LGE is generally true. Evidence accumulates that LGE in athletes often occurs at the insertion points of the RV wall into the interventricular septum, but this depends on the age and history of the cohort studied. Other patterns and locations have been published.

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Möhlenkamp, S., Pressler, A. (2020). Potential Cardiac Damage Induced by Strenuous Exercise. In: Pressler, A., Niebauer, J. (eds) Textbook of Sports and Exercise Cardiology. Springer, Cham. https://doi.org/10.1007/978-3-030-35374-2_31

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  • DOI: https://doi.org/10.1007/978-3-030-35374-2_31

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  • Online ISBN: 978-3-030-35374-2

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