Researchers explore how decades of intense training helped a 77-year-old former world record holder maintain heart function
Study: Lifelong physiology of a former marathon world-record holder: the pros and cons of extreme cardiac remodeling. Image Credit: Hlib Shabashnyi/Shutterstock.com
In a recent life study published in the Journal of Applied Physiology, researchers studied the effects of lifelong rigorous endurance exercises on cardiac physiology and illness risk by analyzing the health records of a marathoner (DC) aged 77 years who previously held the world record (2 hours, 08 minutes, and 33.6 seconds).
Background
Regular aerobic exercise is vital for maintaining a healthy cardiovascular system as we age. It enhances electrical, structural, and functional heart remodeling. These alterations enhance the age-related cardiac reserves and functional capability. Increased functional reserve lowers the risks of disabilities, heart disease, and death in older individuals. However, severe activity may raise the likelihood of adverse effects.
DC, a former marathoner, world record holder, and Olympian, broke the marathon's 2-hour and 10-minute barrier in 1967 and 1969. Since quitting competitive running in 1974, he has maintained high endurance training levels, running 150 to 300 miles weekly and logging 10 to 15 hours of exercise post-retirement. Since 1994, DC has participated in the cyclic category in the Australian Master's Games and the World Master's Games.
About the study
In the present report, researchers analyzed DC data to demonstrate the benefits and potential adverse effects of decades of intensive endurance training.
DC completed maximal cardiovascular exercise tests in 1970, 1991, and 2020 to assess maximum oxygen consumption (VO2max), a measure of functional capability. In 2020, he underwent extensive cardiac examinations. Electrically-braked cycle ergometers and the Douglas bag method measured VO2max during cardiopulmonary exercise testing. The Tanaka method computed the age-estimated maximal heart rate (HR).
The team performed cardiac-type magnetic resonance imaging (CMR) to assess heart function and structure. Speckle-tracking and Doppler echocardiography assessed resting left ventricular global strain and diastolic functions. Left ventricular end-systolic volume (LV ESV) and end-diastolic volume (EDV) determined stroke volume (SV) and ejection fraction. SV and heart rate (HR) determined the cardiac output. Dual-energy X-ray absorptiometry (DEXA) assessed body composition in 2020.
The athlete received a clinical cardiology examination and treatment for atrial fibrillation (AF), including invasive electrophysiological procedures and radiofrequency ablation. Inversion recovery imaging detected myocardial scarring or inflammation. The team compared DC's hemodynamic responses with those of a young, healthy control (YHC) and a young endurance athlete (YEA).
Results
DC's VO2 max decreased considerably from 27 to 49 years. At 77 years, his VO2max was 44 mL/kg/minute (3.3 L/minute), similar to the 50th percentile value for healthy males aged between 20 and 29 years and 2.40-fold higher than the need (18 mL/kg/minute) for sustaining functional independence. The VO2 max was 238% higher than the age-estimated values, as determined by the United States-based Fitness Registry and the Importance of Exercise National Database (FRIEND) values. The VO2max value partially resulted from significant ventricular dilation, which allows for increased cardiac output (22 L/minute) based on a high peak supine workout SV (200 mL).
DC's resting EDV indexed to the body surface area was significantly higher than the 95th percentile value for males aged 65 to 74 in the United Kingdom Biobank. DC's extensive ventricular remodeling is associated with several severe characteristics, including considerable resting bradycardia and low to normal systolic function indices derived from echocardiography. Good myocardial nulling suggested a normal myocardium with no scar.
DC developed significant biatrial dilatation and a large left atrium with minimal contractile activity. He exhibited similar or better SV enhancement than the young athlete. He had a 44 mL bigger resting SV than the control individual, owing to a higher LV EDV (273 mL versus 216 mL). He also showed increased stroke volume augmentation with activity, reaching a maximal workout SV higher than the healthy control (200 versus 128 mL). He could not equal the highest cardiac output observed in the young athlete.
However, at 78 years, DC acquired AF, which caused palpitations, exhaustion, and a decrease in exercise ability, necessitating ablation therapy. He experienced symptomatic AF recurrence after four months. Electrical cardioversions reestablished sinus rhythm, whereas radiofrequency ablation separated the fibrotic pulmonary veins and healthy atrial areas, which improved the athlete's exercise tolerance. However, four weeks later, he underwent direct current cardioversion (DCR) due to an AF recurrence. Surgeons isolated the left-sided veins from the healthy posterior left atrial wall. DC was released on 50 mg of flecainide daily.
DC's trajectory demonstrates that obtaining a high VO2 max in midlife by intensive endurance exercise results in a VO2 max in later life that is more than enough for everyday activities and promotes healthy aging. Intense ventricular remodeling allowed a high cardiac output value during physical activity despite a lower maximum HR. This remodeling with low contractile function and AF development demonstrates the cost of lifetime endurance exercise. However, these costs do not outweigh the advantages to heart health, body composition, lifespan, and quality of life.
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