Around the end of the XIX century we find the earliest studies on the heart and sports practice, when it was reported cardiac enlargement among Nordic skiers (Henschen) and university rowers (Darling), by physical examination. It was postulated that cardiac enlargement was a beneficial adaptation to the exercise, although this view was not accepted easily, and even today is sometimes contested. Some studies have tried to prove that the enlargements is a sign of overuse, and that prolonged sport participation could cause a premature cardiovascular collapse, even when there is no clear evidence to support the validity of this affirmation.

Already in the early XX century, studying the pulse rate and pattern among Boston marathon runners (White), it was firstly described bradycardia in long distance runners. Early chest radiographies confirmed the heart enlargement, while the development of the electrocardiography permitted to study the electrical properties of the heart.

Physical exercise demands oxygen from the body, in an amount directly related to the exercise intensity. During exercise the pulmonary system increases the oxygen uptake (VO2), while the cardiovascular system transport the oxygen in the blood to the muscles, in an amount called cardiac output which may increase 5-fold during maximal exercise. Cardiac output is quantified in litters per minute, and it is a product of the heart rate and the stroke volume.

A larger and stronger heart gives an increased stroke volume and lower heart rate at rest. During exercise the higher stroke volume will give a higher cardiac output, and a better ability for aerobic energy production. Heart rate may vary from 40 beats per minute at rest to nearly 200 during effort in a young athlete, and it is usually the key factor affecting cardiac output. Maximal heart rate doesn´t vary with training, although stroke volume increases with prolonged training, through cardiac chamber enlargement, that gives way to the so-called “athlete´s heart”, a beneficial remodelling involving heart enlargement and thicker ventricular walls.

In the 1970s the Morganroth´s hypothesis differentiated among strength training, characterised by concentric left ventricle hypertrophy (thicker wall), and endurance training, characterised by eccentric left ventricle hypertrophy (chamber enlargement). We could talk about specific cardiac remodelling depending on the sport, with disciplines like weightlifting, track and field events causing concentric hypertrophy, and others like long-distance running, cycling, rowing or swimming causing eccentric hypertrophy.

Morganroth´s theory is nowadays challenged, as it is extensively accepted that sports cause a balanced remodelling, independent of the discipline. This cardiac remodelling is similar in male and female athletes. Regarding ethnicity, black athletes tend to have thicker left ventricle walls than white athletes.

In the second part of our series about the athlete´s heart we will focus on the techniques used to study the differences between a healthy and pathological heart, and the importance of proper studies to prevent conditions such as the sudden cardiac death.

Morganroth´s cardiac hypertrophy hypothesis (1975)
Current cardiac hypertrophy model (from "Evidence for distinct effects of exercise in different cardiac hypertrophic disorders", Life Sci. 2015)

Leave a Reply

Your email address will not be published. Required fields are marked *