The abuse of androgenic-anabolic steroids (AAS) can cause a variety of cardiovascular side effects in athletes, including left ventricular hypertrophy, cardiomyopathy, arrhythmia, myocardial infarction, heart failure, hypertension, arterial thrombosis, and pulmonary embolism.
The Impact of AAS (Anabolic-Androgenic Steroids) Abuse
AAS disturbs the serum levels of high-density lipoprotein (HDL), low-density lipoprotein (LDL), lipoprotein A (Lp-A), total cholesterol (TC), triglycerides, and homocysteine.
A significant decrease in HDL and an increase in LDL and Lp-A increases the risk of atherogenesis (plaque formation), leading to atherosclerosis and coronary heart disease.
The increase in LDL is coupled with a decrease in HDL levels.
When HDL decreases, the LDL/TC ratio increases, leading to a distorted atherogenic index (> 5) and an elevated risk of acute myocardial infarction (AMI).
Studies suggest that serum LDL levels can increase through the induction of the hepatic triglyceride lipase enzyme and the catabolism of very-low-density lipoproteins.
The induction of hepatic triglyceride lipase can also catabolize HDL, thereby reducing its serum levels.
According to some estimates, these lipoprotein abnormalities increase the risk of coronary artery disease by 3 to 6 times.
Hyperhomocysteinemia causes endothelial damage and dysfunction, and increases platelet aggregation at sites of microvascular injury, leading to atherosclerosis.
The adverse effects on serum lipids and homocysteine vary depending on the type of AAS used, the route of administration, drug combinations, dosage, and duration of abuse.
However, research indicates that the recovery of serum lipids after AAS use is largely dependent on the duration of AAS abuse rather than the dosage.
It’s important to note that while homocysteine levels decrease after discontinuing AAS, the damage to the vascular endothelium is irreversible.
Steroids are also linked to arrhythmias (atrial fibrillation, ventricular fibrillation, tachycardia).
One reason for this is electrolyte imbalance and hypercalcemia, as it is well-known that AAS increases the absorption of electrolytes and minerals (sodium, calcium, phosphorus, magnesium), especially at doses exceeding physiological levels.
Furthermore, the use of AAS (Anabolic-Androgenic Steroids) appears to heighten the risk of sudden death from life-threatening arrhythmias.
Echocardiographic studies have shown that supraphysiological doses of AAS lead to morphological and functional changes in the heart.
These changes include a tendency to cause myocardial hypertrophy, a potential increase in ventricular diameter, and clinically impaired left ventricular systolic function.
These changes can lead to left ventricular hypertrophy (LVH), cardiomegaly, and increase the risk of chronic heart failure, hypertension, and arrhythmias.
It must be noted that long-term AAS abuse can have detrimental effects on heart structure and function.
Additionally, studies indicate that strength athletes who use AAS have a slight concentric left ventricular hypertrophy compared to non-using strength athletes, with signs of decreased diastolic function years after discontinuing AAS abuse.
Anabolic steroid (AAS) abuse, particularly androgens, can elevate blood pressure (BP) because they stimulate the production of the hormone aldosterone in the kidneys.
The degree of increase is related to the duration of abuse.
Some AAS also aromatize, meaning they are converted into estrogen by the aromatase enzyme.
Estrogenic activity is associated with water retention and edema.
Therefore, bodybuilders who abuse aromatizing steroids during the off-season have a higher probability of developing hypertension.
However, among non-aromatizing AAS, few drugs can raise blood pressure.
Fluoxymesterone and trenbolone are among them.
Both suppress the catabolic glucocorticosteroid cortisol.
(This is the reason for their high anabolic effect).
However, they also suppress the mineralocorticosteroid aldosterone.
This is precisely why there is no water retention.
Nevertheless, another mechanism involving the inhibition of the enzyme 11-hydroxylase will ultimately lead to an increase in blood pressure.
The kidneys have this specific enzyme to protect them from the blood pressure-raising effects of cortisol.
This enzyme converts cortisol into inactive cortisone (its synthetic form) because the problem starts when aldosterone receptors sometimes bind to cortisol.
When inhibition of 11-hydroxylase occurs, the overproduction of 11-beta-deoxycorticosterone by the adrenal cortex can be the cause of elevated blood pressure.
Anabolic steroids (AAS) affect hematopoiesis, causing erythrocytosis, which eventually leads to polycythemia.
Erythrocytosis can also be a risk factor for cardiovascular disease due to the sharp increase in blood viscosity.
AAS also affects platelet aggregation due to increased production of thromboxane A2 and decreased production of prostacyclin.
Furthermore, changes in the coagulation cascade can occur, including increased thrombin activity, which also contributes to a hypercoagulable state.
These side effects are exacerbated by dehydration and catecholaminergic stress, which often occur in connection with strenuous physical activity.
A hypercoagulable state increases the risk of cardiovascular events (myocardial infarction, thrombotic stroke, cerebrovascular hemorrhage).
While AAS prolongs bleeding time and hinders hemostasis, INR and APTT increase and enhance fibrinolysis.
This mechanism contradicts the platelet aggregation effect.
In conclusion, AAS breaks down the coagulation process, but on the other hand, it induces thrombus formation through elevated hematocrit and fibrinogen levels.
Preventing Cardiovascular Disease Risk
Since anabolic steroid (AAS) users have higher cardiovascular morbidity and mortality rates compared to non-users, cardiovascular physical activity is crucial for the following reasons:
1) Bodybuilders or powerlifters should perform slow-paced aerobic exercise for 30 minutes at 60% of their maximum oxygen uptake (VO2 max).
This type of exercise can eventually improve the shape and size of the myocardium, and as long as AAS is discontinued or at least taken moderately and wisely, LVF will decrease, and the ventricles will change to the heart model of an endurance athlete.
Even with low body fat percentage, overweight individuals have a higher oxygen demand on the myocardium, so BMI is also a factor to consider.
Therefore, the heart must work harder, which carries the risk of ischemic episodes.
2) Sustained long-term aerobic exercise can increase HDL, thereby improving the atherogenic index (HDL/LDL) and reducing the risk of atherothrombotic cardiovascular disease (CVD).
3) Slow-paced aerobic activity establishes what is known as ‘collateral circulation’.
This translates into a vast network of blood vessels that surround the myocardium and supply oxygen to the heart muscle.
Through this type of vasculature, an individual can survive a heart attack ischemic episode (AMI).
Many studies have shown that cardiac remodeling depends on the type of training (dynamic or static) and the type of sport.
It has been shown that more than 3 hours of exercise per week are necessary to observe adaptive changes such as a decrease in heart rate and an increase in left ventricular (LV) mass.
Marathon and triathlon athletes have a ‘drop heart’ shape, with enlarged ventricles and thin ventricular walls.
This helps to provide a greater ejection fraction (EF) and stroke volume (the heart muscle’s ability to pump blood and the volume of blood per beat) hemodynamically and functionally.
On the other hand, a combination of weight resistance training and chemical enhancement with performance-enhancing drugs (PEDs) brings about specific hemodynamic changes in the heart.
Specifically, heart rate increases, while stroke volume and ejection fraction (EF) decrease.
The left ventricle adapts to these hemodynamic changes by developing a smaller ventricular cavity and thicker ventricular walls.
A steroid user who smokes, avoids cardiovascular aerobic physical activity, and consumes saturated and trans fats will be in poor physical condition with inadequate collateral circulation, hypertension, and a higher likelihood of developing coronary heart disease due to atherosclerosis.
Their maximum oxygen uptake and aerobic respiration capacity are significantly diminished.
Since atherosclerotic CVD is typically caused by a combination of multiple risk factors, all current guidelines on CVD prevention in clinical practice recommend assessing the total CVD risk.
The higher the risk, the more intensive the measures should be.
Therefore, AAS abusers belong to a high-risk group and must follow specific rules for longevity and medical prevention.
1. Moderate aerobic cycling for 30 minutes daily at a rate of 60% of maximum heart rate (MHR).
2. Avoid excessive intake of saturated fats, trans fats, refined carbohydrates, and sugars.
3. A diet rich in lean white meat, fish, egg whites, vegetables, fruits, nuts, oats, and dietary fiber to prevent the oxidation of LDL and the rise of triglycerides and total cholesterol, lower insulin resistance, and contribute to a hypoglycemic effect.
4. Anticoagulants (EPA, DHA, salicylic acid) are preferable with breakfast rather than post-workout, as AAS abuse leads to elevated hematocrit (Htc) and increased blood viscosity.
5. Regularly use niacin (B3), phytosterols, and red yeast rice to improve the HDL/LDL ratio, along with Coenzyme Q10 and magnesium, which have the ability to increase aerobic energy production in the myocardium, and L-carnitine, which acts as a mild antiarrhythmic and energy enhancer.
6. Monitor blood pressure and heart rate weekly and undergo a stress test, ECG, and 24-hour Holter monitor once a year.
Elevated blood pressure is one of the most potent and modifiable risk factors for CVD.
The beneficial effects of blood pressure-lowering therapy in reducing stroke, myocardial infarction, heart failure, and death have been demonstrated in numerous meta-analyses.
7. Regular assessment of hematocrit, hemoglobin, platelets, HDL, LDL, total cholesterol, triglycerides, and fasting blood glucose. These assessments ensure there is no evidence of metabolic syndrome, hyperlipidemia, polycythemia, or type 2 diabetes.
Optimal control of LDL-C levels and blood pressure is crucial for all AAS abusers.
