Arterial Stiffness and Wave Reflections in Marathon Runners

Vlachopoulos, Charalambos; Kardara, Despina; Anastasakis, Aris; Baou, Katerina; Terentes‐Printzios, Dimitrios; Tousoulis, Dimitris; Stefanadis, Christodoulos

doi:10.1038/ajh.2010.99

Cited by 113 publications

(137 citation statements)

References 42 publications

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“…A study of 47 individuals who trained extensively for and competed in marathons found that pulse wave velocity and aortic stiffness were significantly higher in the group of marathoners compared with controls. 49 It is possible that the sustained shear stress caused by protracted endurance efforts eventually may induce fibrotic changes and decreases in arterial wall elasticity. Diastolic dysfunction of both the RV and LV has also been observed in individuals doing long-term extreme ET and racing.…”

Section: Biomarker Evidence For Cardiac Damage With Extreme Endurance Etmentioning

confidence: 99%

Potential Adverse Cardiovascular Effects From Excessive Endurance Exercise

O’Keefe

Patil

Lavie

et al. 2012

Mayo Clinic Proceedings

330

279

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A routine of regular exercise is highly effective for prevention and treatment of many common chronic diseases and improves cardiovascular (CV) health and longevity. However, long-term excessive endurance exercise may induce pathologic structural remodeling of the heart and large arteries. Emerging data suggest that chronic training for and competing in extreme endurance events such as marathons, ultramarathons, ironman distance triathlons, and very long distance bicycle races, can cause transient acute volume overload of the atria and right ventricle, with transient reductions in right ventricular ejection fraction and elevations of cardiac biomarkers, all of which return to normal within 1 week. Over months to years of repetitive injury, this process, in some individuals, may lead to patchy myocardial fibrosis, particularly in the atria, interventricular septum, and right ventricle, creating a substrate for atrial and ventricular arrhythmias. Additionally, long-term excessive sustained exercise may be associated with coronary artery calcification, diastolic dysfunction, and large-artery wall stiffening. However, this concept is still hypothetical and there is some inconsistency in the reported findings. Furthermore, lifelong vigorous exercisers generally have low mortality rates and excellent functional capacity. Notwithstanding, the hypothesis that long-term excessive endurance exercise may induce adverse CV remodeling warrants further investigation to identify at-risk individuals and formulate physical fitness regimens for conferring optimal CV health and longevity.

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Section: Biomarker Evidence For Cardiac Damage With Extreme Endurance Etmentioning

confidence: 99%

Potential Adverse Cardiovascular Effects From Excessive Endurance Exercise

O’Keefe

Patil

Lavie

et al. 2012

Mayo Clinic Proceedings

330

279

View full text Add to dashboard Cite

show abstract

“…Twelve studies were identified and examined to determine whether normalizing AIx to HR influences the interpretation of the findings (Table 1). Eight studies reported significantly improved between-group/condition differences using the AIx@75 versus the AIx alone [23][24][25][26][27][28][29] , two studies reported no significant differences using the AIx but a significant difference using AIx@75 30,31) , one study reported a decrease in significance using the AIx@75 32) and one study reported a change in the direction of the effect 33) . Given these findings, careful interpretation of the physiological significance of normalization to HR is warranted.…”

Section: Validity Of the Aix And Influence Of Normalization To Hrmentioning

confidence: 98%

Should the Augmentation Index be Normalized to Heart Rate?

Stoner

Faulkner

Lowe

et al. 2014

JAT

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Pulse wave analysis (PWA) is widely used to investigate systemic arterial stiffness. The augmentation index (AIx), the primary outcome derived from PWA, is influenced by the mean arterial pressure (MAP), age, gender and heart rate (HR). Gender-and age-specific reference values have been devised, and it is recommended that the MAP be used as a statistical covariate. The AIx is also commonly statistically adjusted to a HR of 75 b·min; however, this approach may be physiologically and statistically inappropriate. First, there appears to be an important physiological chronic interaction between HR and arterial stiffness. Second, the method used to correct to HR assumes that the relationship with AIx is uniform across populations. A more appropriate practice may be to include HR as an independent predictor or covariate; this approach is particularly recommended for longitudinal studies, in which changes in HR may help to explain changes in arterial stiffness.

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“…16 Following completion of a marathon, there are large reductions in pressure from wave reflections, aortic pulse pressure, and aortic diastolic pressure. 3 This is clinically relevant, as aortic diastolic pressure is a significant determinant of coronary perfusion pressure and subendocardial viability. Reduced central pulse pressure may be due to reduced forward wave genesis owing to reduced venous return and preload due to peripheral venous pooling.…”

mentioning

confidence: 99%

“…Thus, there appears to be a U curve with respect to exercise and vascular function. 3 Inactivity is detrimental, but excessive activity may be equally detrimental.…”

mentioning

confidence: 99%

“…3 It has been suggested that exercise training-induced bradycardia results in a compensatory increase in stroke volume (commensurate with cardiac chamber enlargement) to maintain cardiac output. 3 Increased load on the vasculature over time may result in elastin fatigue and fragmentation, contributing to a loss of arterial compliance. Marathon runners may also have increased pressure from wave reflections and increased central pulse pressure.…”

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confidence: 99%

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How Healthy Were the Arteries of Phidippides?

Heffernan

2011

Clinical Cardiology

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Subacute and chronic cardiac adaptations to marathon running may increase risk for sudden death. Herein, it is proposed that cardiac arrhythmogenic remodeling resulting from prolonged strenuous exertion may also have a systemic vascular component. Marathon running reduces coronary perfusion pressure and causes acute endothelial damage, possibly via altering concentrations of circulating angiogenic growth factors with novel vasoregulatory properties. Marathon runners have increased arterial stiffness and augmented pressure from wave reflections contributing to a widening of pulse pressure. Pulsatile hemodynamics may contribute to target organ damage. Moreover, each of these vascular maladaptations (increased arterial stiffness, augmented pressure from wave reflections, and widened pulse pressure) has been associated with atrial fibrillation and may provide a substrate for lethal arrhythmogenesis in the marathon runner. Clin. Cardiol. 2012 DOI: 10.1002/clc.21009The author has no funding, financial relationships, or conflicts of interest to disclose.This article ﬁrst published online 28 November 2011. It has since changed. The term “coronary pulse pressure” has been changed to “coronary perfusion pressure.”

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Arterial Stiffness and Wave Reflections in Marathon Runners

Abstract: A significant fall in wave reflections was observed after marathon race, whereas aortic stiffness was not altered. Moreover, marathon runners have increased aortic stiffness and pressures, whereas wave reflections indexes do not differ compared to controls.

Cited by 113 publications

References 42 publications

Potential Adverse Cardiovascular Effects From Excessive Endurance Exercise

Potential Adverse Cardiovascular Effects From Excessive Endurance Exercise

Should the Augmentation Index be Normalized to Heart Rate?

How Healthy Were the Arteries of Phidippides?

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