The athlete’s heart is a deviation of a normal shaped myocardium.
It is a natural response, a physiological remodeling to the continuous stimulus of strenuous physical activity, such as endurance running under high intensity.
Many studies have shown that cardiac adjustment varies, depending on the type of training (dynamic or static) and the type of sport.
It appears that more than three hours of exercise is required per week, in order to observe adaptive changes; such as the reduction in heart rate and increase in mass of the left ventricle (LV).
Marathon and triathlon runners have a “drop heart” shape, with enlarged ventricles and thin ventricular walls.
This helps hemodynamically-functionally providing a greater ejection fraction (EF) and stroke volume (the ability of the heart muscle to pump blood and the volume of blood in each pulse).
On the other hand, exercising with weights-resistance training, in combination with chemical enhancement with Performance Enhancing Drugs (PED’s) leads to specific hemodynamic changes in the heart.
In particular, increase in heart rate, decrease in stroke volume and ejection fraction (EF).
The LV becomes adapted to these hemodynamic changes, resulting in thickening of the wall with smaller ventricular cavities.
Heart is a muscle that is mixed, under histological evaluation; meaning it possesses cardiac muscle fibers and skeletal-striated-contractile muscle fibers.
Obviously, this explains how heart becomes bigger, just by lifting weights.
Moreover, androgenic receptors are present in a variety of organs and tissues, such as the heart muscle.
Therefore, heart will also react positively, under anabolic-androgenic steroid (AAS) abuse.
The athletic heart differs from the heart of non-athletes, provided that the exercise has a sufficient intensity and duration.
Depending on the type of exercise and the kind of sport, we observe an increase of thickening in the LV, especially in dynamic events, such as explosive sports: shot put, sprinting, weight lifting, bodybuilding, powerlifting.
An enlarged myocardium, either by aerobic exercise (marathon) or bodybuilding using AAS-HGH/IGF1 has increased requirements for oxygen consumption.
Intensive and prolonged anaerobic exercise affects the chamber size, the muscle mass of the LV and the wall thickness of the heart, resulting in an enlarged heart with thick ventricular walls and interventricular septum.
Ventricular capacity-volume is indirectly proportional to ventricular walls thickening.
Consequently, there is less adequate amount of blood pumped, EF lowers and generally EF is lower in athletes with large BMI.
Furthermore, in prolonged strength training there is increased peripheral vascular resistance which causes transient but potentially marked systolic hypertension and LV afterload.
The hypertrophic myocardium has much greater oxygen needs than usual, so ischemia is more likely to develop, under hypoxic conditions.
On the other hand, a prolonged dynamic physical activity such as aerobic training leads to physiologic hypertrophy of the heart that affects all four chambers with normal or reduced peripheral vascular resistance and with a lower heart rate of the average individual (<60beats/min).
With a larger left ventricle, the heart rate can decrease and still maintain a level of cardiac output necessary for the body.
This is an economy of energy myocardium does, since there is no need for faster heart beating.
Therefore, heart beats slower, in order to pump the same amount of blood.
Eventually, this reflects directly into a supreme physical condition and a cardiovascular capacity too.
The heart of an endurance athlete (marathon runner, cyclist, triathlon) has a characteristic shape on a chest X-ray, “drop shaped” heart with an increased left ventricle (cardio-thoracic index enlarged).
HIIT is a mixed type of aerobic/anaerobic cardio respiratory physical activity.
It’s beneficial as it saves time; it prevents catabolism through specific hormonal signal.
It boosts testosterone and growth hormone by lactate production, while it prevents cortisol to elevate dangerously.
A steroid user, who smokes, avoids cardiovascular aerobic physical activity and consumes saturated-trans fat, develops poor physical condition, with inadequate collateral circulation, high blood pressure and is more likely to develop coronary heart disease, due to atherosclerosis.
VO2max and cardio respiratory capacity are significantly dropped.
Cardio at moderate pace of 60% of VO2max-MRH mostly establishes the collateral circulation and elevates serum levels of high density lipoprotein (HDL).
Performing cardio at 80% of VO2max-MHR improves physical condition and cardio respiratory capacity.
However, that kind of intensity will lead eventually to the development of the athlete’s heart.