Anabolic Androgenic Steroids Induce Reversible Left Ventricular Hypertrophy
by Benjamin Bunting BA(Hons) PGCert
Written by Ben Bunting: BA(Hons), PGCert. Sport & Exercise Nutrition. L2 Strength & Conditioning Coach.
Anabolic androgenic steroids cause progressive heart failure. This condition is typically irreversible. However, with early diagnosis, patients may recover a significant portion of their ventricular function. However, long-term prognosis is not clear, and a substantial proportion of patients will require cardiac transplantation or LVADs.
Mechanisms of action
Anabolic androgenic steroids (AAS) are used by athletes to gain muscle mass and strength. However, there is an increasing concern that these anabolic steroids can lead to cardiovascular problems. These steroids have been linked to increased blood pressure and systolic dysfunction, but the exact cause is not known. The current study provides the first large-scale controlled study on the effects of anabolic steroids on cardiovascular health.
Anabolic steroids are linked with left ventricular hypertrophy and cardiac complications, including hypertension and atrial and ventricular arrhythmias. Moreover, these steroids alter lipid metabolism, increasing low-density lipoprotein levels and reducing high-density lipoprotein levels. Additionally, they can lead to polycythemia by stimulating erythropoiesis.
In addition to stimulating the release of insulin, androgens may increase insulin resistance. This happens through an increase in S6K1 and inhibition of IRS-1. Additionally, androgens may increase the expression of other receptors in the heart, including the EGFR and SHBGR.
Anabolic androgenic steroids are widely misused and can cause cardiac problems. Worldwide, AAS use is extremely common; roughly 6% of all males use them at some point in their lives. In the US, between 15 and 25% of male gymgoers use these drugs at one time or another. They are associated with serious health consequences, including sudden death, neuropsychiatric disorders, and infertility. Moreover, the average AAS user is unlikely to inform his or her physician about his or her use and many engage in unsafe injection techniques.
Moreover, AAS use has been associated with adverse cardiovascular events such as myocardial infarction, sudden cardiac death, and ventricular fibrillation during exercise. Although the effects of AS on cardiomyopathy are unclear, there is a need for more research on the long-term effects of these drugs.
One study on AAS abuse found that the cellular changes caused by chronic AAS abuse were associated with a decrease in early diastolic peak velocity. The authors concluded that these AAS also impaired cardiomyocytes' adaptive mechanisms. These alterations are reminiscent of cardiomyopathy or heart failure, and their adverse effects are often evident even after the AAS use has been discontinued.
AAS use in amateur sports should be monitored carefully, as most participants have no idea about the cardiac risks associated with AAS use. It is important to educate coaches and gyms about the dangers associated with these performance-enhancing drugs.
Despite the negative effects of AAS, they can also have beneficial effects on cardiovascular health. Studies of amateur strength athletes showed that these drugs increased their LVEF and decreased their diastolic function. Moreover, these effects are associated with the AAS dosage.
In addition to increasing muscle size, anabolic steroids also increase testosterone levels in the blood, and these steroids can improve male sexual characteristics. However, they can also cause gynecomastia and testicular atrophy in male bodybuilders. In addition to these negative effects, AAS abuse can result in impaired contraction and relaxation of the heart.
A recent study found that anabolic steroids were widely used in Canada. This study found that approximately 83,000 Canadians aged 11 to 18 used the drugs. In Canada, steroids are not legal without a prescription. However, they are available without a prescription in Mexico, Thailand, and Argentina.
The use of anabolic steroids is associated with an increased risk of myocardial infarction, sudden cardiac death, and ventricular fibrillation with exercise. It can also cause dilated cardiomyopathy and hypertension. Anabolic steroids influence cardiac function by influencing the androgen receptors, which are found on cardiac myocytes and skeletal muscle. The effects of steroid use on the heart can be reversed by stopping the use of steroids.
Anabolic-androgenic steroids are commonly used by strength athletes, and preliminary research suggests that long-term exposure to AAS can lead to cardiomyopathy and atherosclerosis. Previous studies, however, were small and methodologically limited. This is the first large-scale, controlled study to explore the relationship between long-term AAS use and cardiovascular disease.
AAS abuse has increased significantly in recent years, and there has been an increase in the incidence of adverse cardiovascular outcomes in those who use AAS. Moreover, AAS abuse is a contraindication for heart transplantation. For that reason, patients must abstain for at least six months prior to their surgery. Another important intervention is left ventricular assist device therapy, which is often used as a destination therapy.
In addition to enhancing muscle size, anabolic androgenic steroids can also promote male sexual characteristics. As a result, half of male bodybuilders experience gynecomastia or testicular atrophy. These drugs also cause impaired contraction and relaxation of the heart.
Anabolic androgenic steroids, or AAS, increase the activity of genes that regulate anabolic pathways. They also stimulate the expression of other membrane-bound receptors, including EGFR and SHBGR. Furthermore, they can activate the PI3K/Akt signalling pathway, which leads to the proliferation and differentiation of satellite cells.
Aside from increasing intracellular calcium levels, anabolic steroids also increase the formation of diacylglycerol and inositol 1,4,5-triphosphate. Androgens are also known to increase the levels of estrogens, such as Estradiol. These compounds also increase insulin resistance.
AAS induce left ventricular hypertrophy and impaired diastolic function in strength athletes. However, when AAS are discontinued, the cardiac function returns to normal. It is not known why AAS induce left ventricular hypertrophy in some individuals.
The illicit use of anabolic androgenic steroids has been associated with arrhythmias in athletes. This has led to investigations of the pathophysiology of AAS-induced left ventricular hypertrophy in rats. In this study, male Wistar rats were treated with 10 mg/kg of nandrolone decanoate for 8 weeks. The heart was then monitored using an action potential monitor, a transient outward potassium current, and KChIP2 expression. Moreover, histological analyses were conducted using Picrosirius red staining.
Cardiovascular toxicity from AAS use was also studied. These drugs cause direct myocardial toxicity, including left ventricular hypertrophy and left ventricular remodeling. In addition, they can lead to pulmonary embolism and arteriosclerosis. These effects also affect diastolic function. Despite the harmful effects of AAS, partial ventricular recovery has been noted after the discontinuation of AAS use. This may be due to individual susceptibility to toxic effects.
During the treatment period, the patient developed an enlarged left ventricular mass with a severely decreased left ventricular ejection fraction and grade 3 diastolic dysfunction. The patient also presented with dilated cardiomyopathy and mild right ventricular hypertrophy. A repeat TTE was performed and revealed an ejection fraction of less than 25%, severe global hypokinesis, and mild bi-atrial/biventricular dilation and mild mitral valve regurgitation.
Anabolic Androgenic Steroids Induce Reversible Left Ventricular Hypertrophy Conclusion
Anabolic androgenic steroids (AAS) are used by athletes to improve performance. However, the scientific evidence supporting the link between AAS abuse and cardiovascular complications is mixed and conflicting. One review analyzed 49 studies involving 1,467 athletes. Although most studies were retrospective and small, some found associations with left ventricular hypertrophy and elevated blood pressure.
The cardiovascular effects of AAS are not well understood, particularly by amateur athletes. However, it is clear that the sex differences in cardiac phenotype may depend on the type of sex steroids used. Therefore, an effort must be made to increase awareness of these drugs among amateur athletes.
In amateur strength athletes, AAS administration results in left ventricular hypertrophy and impaired diastolic function. This is thought to be a consequence of elevated AAS levels. However, these effects are reversible when the AAS use is ceased.
The exact role of androgens in cardiac hypertrophy is unknown, but it is known that cardiac myocytes express the androgen receptor gene. As a result, androgens can mediate a significant hypertrophic response in cardiac myocytes.
In addition, a variety of cardiac events, including cardiac tamponade and myocardial infarction, have been linked to prolonged use of AASs. In addition, AAS use is linked to increased levels of oxidative stress, resulting in elevated LDL cholesterol and blood pressure.