What is the clinical evidence from this study?

Study design: Cross-Sectional. Population: Healthy master athletes (n=51). Intervention: Long-term intensive endurance exercise training vs. Sedentary controls. Primary outcome: Cardiac extracellular volume (ECV) (p=0.408).

May 16, 2021Open Access

Absence of cardiac damage induced by long-term intensive endurance exercise training: A cardiac magnetic resonance and exercise echocardiography analysis in masters athletes

Key Result

Long-term intensive endurance exercise training in master athletes did not induce myocardial fibrosis or ventricular dysfunction, demonstrating normal cardiac extracellular volume (21.5%) and no late gadolinium enhancement compared to sedentary controls.

Study Design

Type

Cross-Sectional (n=51)

Blinding

Blinded outcome assessment

Multicenter

Structured PICO

Does long-term intensive endurance exercise training induce myocardial damage or fibrosis in master athletes?

Population

51 asymptomatic adults (mean age 48, 6% female), including 33 master endurance athletes training >8 hours/week for at least 15 years and 18 sedentary controls, evaluated cross-sectionally for cardiac damage.

Exposure

Long-term intensive endurance exercise training (mean 9.6 h/week for 26 years).

Comparator

Sedentary lifestyle (no history of sport activity at any level).

Outcome

Myocardial damage evaluated by CMR (LGE, T1 mapping, ECV), exercise echocardiography (LGS), and cardiac biomarkers of fibrosis.surrogate

Long-term intensive endurance exercise in master athletes induces physiological cardiac remodeling without evidence of myocardial fibrosis or ventricular dysfunction.

Main Result

Absolute Event Rate: 21.5% vs 22%

p-value: p=0.408

Limitations

Small sample size (33 athletes) may be insufficient to detect myocardial fibrosis
Low number of female athletes prevented analysis of sex differences
No histological confirmation of the absence of fibrosis with endomyocardial biopsy
Cross-sectional design limits causal inference

Abstract

OBJECTIVES: It is under debate whether the long-term practice of intensive endurance exercise induces chronic cardiac damage such as myocardial fibrosis and ventricle contractile dysfunction. Multimodality analysis was performed to evaluate myocardial damage induced by long term intensive endurance training in master athletes. METHODS: Thirty-three asymptomatic endurance master athletes (47 ± 6 year-old, 9,6 ± 1,7 h training/week for 26 ± 6 years), were compared to 18 sedentary controls (49 ± 7 year-old). They underwent a CMR protocol including 4 chambers morphological and late gadolinium-enhancement (LGE) analysis, left (LV) and right ventricular (RV) T1 mapping and calculation of cardiac extracellular volume (ECV). A maximal exercise echocardiography with left and right ventricular longitudinal global strain (LGS) analysis was performed. Cardiac biomarkers of fibrosis (high sensitive cardiac Troponin T, N-Terminal pro brain natriuretic peptide, N-terminal propeptide of procollagen type I and N-terminal propeptide of procollagen type III) were analysed. RESULTS: Athletes had larger left and right atrial volume, LV and RV end diastolic volume and increased LV and RV mass compared to controls. LGE was not found in athletes. Native T1 values of LV and RV were not significantly different in athletes compared with controls. ECV was normal in both groups (21,5%± 1,6% 18.3 - 23% in athletes, 22%± 2,2% 18.5 - 27% in controls). LV and RV peak exercise LGS values were higher in athletes. Cardiac biomarkers levels were normal. CONCLUSION: Despite significant physiological cardiac remodelling, consistent with previous descriptions of athlete's heart, there was no evidence of myocardial fibrosis or exercise left or right ventricular dysfunction or cardiac fibrosis in endurance athletes. Our results are not supporting the hypothesis of deleterious cardiac effects induced by long term and intensive endurance exercise training.

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