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European Heart Journal Advance Access originally published online on April 13, 2007
European Heart Journal 2007 28(9):1171-1172; doi:10.1093/eurheartj/ehm055
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© The European Society of Cardiology 2007. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org

From altus to parvus: cardiac fatigue in athletes

Erdem Kasikcioglu

Department of Sports Medicine
Istanbul University
Istanbul 34840, Turkey

E-mail address: ekasikcioglu{at}yahoo.com

With great interest, I read the article ‘Persistent and reversible cardiac dysfunction among amateur marathon runners’ by Neilan et al.1 Although the mechanism of such ‘cardiac fatigue’ is unclear, it is likely related to the increased stresses imposed by exercise which affect the functions of right and left ventricles.2,3 This study has demonstrated that volume and cavity depletion may be a trigger, but are not the major factors for persistent cardiac dysfunction after prolonged exercise. That weight and left atrial diameter returned to baseline values during the follow-up period support this conclusion. It can be hypothesized that the mechanism by which this injury could arise involves a vicious cycle of heart and muscle.4 The vicious cycle would occur among relative cardiac deterioration and oxygen kinetics in the muscle. In other words, impaired skeletal muscle aerobic energy provision and work capacity during maximal aerobic exercise in healthy, trained humans are directly related to the inability of the heart to maintain output and oxygen delivery to locomotive skeletal muscle.5

Interestingly, after prolonged exercise, changes in diastolic performance are increased velocity of atrial or late diastolic inflow, and result in a decrease in the ratio of early-to-late flow velocities.2,6 In contrast, these changes were rapidly reversible, and the left ventricular filling pattern during the 28 h of recovery is not persistent.2 Although more research is needed to better understand the molecular mechanisms by which exhaust physical activity suppresses diastolic function of left ventricle along period (persistent). I could not find authors' hypothesis about this interesting result. As a general opinion, energy turnover in the normal heart in increased demand (relative ischaemia) is expected to change faster to baseline level than that in the diseased heart. In addition, it is believed that athletes' heart has a well adaptive mechanism to ischaemic conditions due to preconditioning effects of chronic exercise.

In addition, two questions related to the study also especially interest me. First of these, whether recurrent prolonged exercises in competitive athletes may lead to permanent dysfunction of ventricles or not. Another crucial question may therefore be, does persistent diastolic dysfunction affect athletic performance and contractile functions of the heart. Exhaustive exercise may affect myocardial functions stunning-like effect.7 Related to these arguments is the speculation that the persistent diastolic dysfunction does not apparently affect systolic function and exercise performance. Indeed, it might be argued that many evidences are needed to support a theory where transient and persistent cardiac deterioration after prolonged exercise may define pseudo-stunning effect.

References

  1. Neilan TG, Yoerger DM, Douglas PS, Marshall JE, Halpern EF, Lawlor D, Picard MH, Wood MJ. Persistent and reversible cardiac dysfunction among amateur marathon runners. Eur Heart J (2006) 27:1079–1084.[Abstract/Free Full Text]
  2. Douglas PS, O'Toole ML, Hiller WD, Hackney K, Reichek N. Cardiac fatigue after prolonged exercise. Circulation (1987) 76:1206–1213.[Abstract/Free Full Text]
  3. Douglas PS, O'Toole ML, Hiller WD, Reichek N. Different effects of prolonged exercise on the right and left ventricles. J Am Coll Cardiol (1990) 15:64–69.[Abstract]
  4. Kasikcioglu E, Arslan A, Topcu B, Sayli O, Akhan H, Oflaz H, Akin A, Kayserilioglu A, Meric M. Cardiac fatigue and oxygen kinetics after prolonged exercise. Int J Cardiol (2006) 108:286–288.[CrossRef][Web of Science][Medline]
  5. Gonzalez-Alonso J, Calbet JAL. Reductions in systemic and skeletal muscle blood flow and oxygen delivery limit maximal aerobic capacity in humans. Circulation (2003) 107:824–830.[Abstract/Free Full Text]
  6. Kasikcioglu E. Diastolic performance after prolonged exercise. Med Sci Sports Exerc (2005) 37:164.
  7. Kasikcioglu E. Cardiac response to prolonged strenuous exercise: a physiologic model for stunning myocardium. Am J Cardiol (2005) 95:707.[Web of Science][Medline]

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This Article
Right arrow FREE Full Text (PDF) Freely available
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28/9/1171-a    most recent
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