Changes to Heart Muscle

The changes to heart muscle caused by anabolic steroids are attributed to their anabolic properties in muscle tissue. Left ventricular hypertrophy is characterized by thickening of the left ventricular wall secondary to cardiac fiber enlargement. Left ventricular hypertrophy (LVH) is normally caused by a chronic increase in systemic blood pressure. It may also be seen with sudden or rapid weight gain. The thickening of the ventricular wall due to increased after-load from elevated vascular resistance can be viewed as adaptive protection up to a point. Beyond minor wall thickening, pathological LVH is a strong predictor of serious cardiovascular risk.

It is important for physicians to realize that LVH can occur in strength athletes and bodybuilders even in the absence of anabolic steroids use. It was previously believed that the intermittent increase in blood pressure that is caused by heavy lifting was not sufficient to elicit concentric left ventricular hypertrophy (CLVH). Any evidence of CLVH in strength athletes or bodybuilders was seen as a sign of anabolic steroid use.

During heavy lifting, systemic blood pressure is increased from what is called the valsalva maneuver. It is simply the act of forceful expiration with the mouth and nose closed producing a "bearing down" on the abdomen. Most people do this during heavy lifts such as squats or deadlifts. Pressure also increases due to blood vessels being occluded by contracting muscles. It should be noted that the LVH seen in bodybuilders and power lifters is called "concentric left ventricular hypertrophy", meaning that it is the result of contracting against acute increased systemic pressure, and is not considered pathological (i.e. unhealthy). "Eccentric" LVH is caused by constant increases of blood pressure, not as a result of the valsalva maneuver but instead due to clinical hypertension that forces the ventricle to expand against resistance.

AAS further exacerbate the effects of lifting on the heart. AASs cause anabolism in heart muscle, at times increasing left ventricular wall thickness to 16mm (11mm is considered normal).4 However, LVH caused by resistance training either alone or in conjunction with Anabolic Androgenic Steroids (AAS) has yet to result in diastolic dysfunction, or in other words, there is yet no evidence that this thickening of the ventricular wall is pathologic.

Treatment options

Upon cessation of high intensity resistance exercise and obviously Anabolic Androgenic Steroids (AAS) use, ventricular wall thickness returns to within normal ranges as long as hypertension unrelated to lifting is not present. There are no treatment suggestions for LVH caused by resistance training with or without the use of AAS.

It has been shown that enhancing the body's CoQ-10 can:

Reduce many of the serious side effects of cholesterol and other prescription drugs such as adriamycin, beta blockers and psychiatric drugs.

Reduce the effects of aging

Aid in the recovery from a wide range of heart problems including angina pectoris, congestive heart failure and mitral valve prolapse.

Can reduce blood pressure and blood lipids at 60 mg day.

Assists chronic fatigue sufferers when administered at 100 to 300 mg per day.

Assists in weight loss by stimulating mitochrondria and thermogenic activity

Treating chronic gum disease

Building a strong immune system as a defense against all forms of disease

May normalize blood sugar levels

Help maintain a healthy brain

CoQ10 deficiency symptoms:

Congestive heart failure

High blood pressure


Mitral valve prolapse


Cardiac arrthythmias


Lack of energy


Weakened immune system
This will be my second deca 400mg only cycle. Will the enlargment of the heart be at any level of dangerous?
Didnt have much sides. Holded alot of water. ran 400mg for 8 weeks. gained 10lbs and kept it all.

This will be my second deca 400mg only cycle. Will the enlargment of the heart be at any level of dangerous?

Or is it just for those who run 8-9 hard cycles?
Like StoneColdNTO's awesome post said, you only have to be concerned about your heart if:

- you have rapid weight gain on your cycle
- your blood pressure is consistently above 120/80
DTOX said:
Like StoneColdNTO's awesome post said, you only have to be concerned about your heart if:

- you have rapid weight gain on your cycle
- your blood pressure is consistently above 120/80

I don't think you have to be too worried if you are over 120/80. I am reading a CPR book (have to get certified if I want to be a cop) and it says that under 140/90 is okay. If you are over 140/90 for a peroid of time (a couple check ups) then you should do something about it.
dragon06 said:
Didnt have much sides. Holded alot of water. ran 400mg for 8 weeks. gained 10lbs and kept it all.

This will be my second deca 400mg only cycle. Will the enlargment of the heart be at any level of dangerous?

Or is it just for those who run 8-9 hard cycles?

It could happen on your first cycle, it happened to me on my second, but ONLY because I was ignorant as to my blood pressure.

As the post about "Changes to the Heart Muscle" said............, "It is important for physicians to realize that LVH can occur in strength athletes and bodybuilders even in the absence of anabolic steroids use."
Blood Pressure; What Do Those Numbers Mean?

I have seen a few posts where there is some confusion or misunderstanding of what blood pressure numbers mean. I found this little explanation, hope this clears things up.

What Do Those Numbers Mean?
Your doctor tells you your blood pressure is 120 over 70 (written as 120/70). Should you be elated or concerned?

The first number refers to your systolic blood pressure. Systolic is your maximum pressure, taken right after your heart pumps. The second number refers to your diastolic blood pressure. Diastolic is the lowest pressure you have, measured when your heart is relaxed.

Miller says, "120/70 is an optimal blood pressure for adults. People are identified as hypertensive if their systolic number is above 140 and/or their diastolic number is greater than 90."
Resistance exercise alone can cause LVH, & addition of Anabolic Androgenic Steroids (AAS) can make it worse.

Androgens can produce cardiac hypertrophy by direct action on cardiac myocytes:

1: Circulation 1998 Jul 21;98(3):256-61 Related Articles, Links
Click here to read
Androgen receptors mediate hypertrophy in cardiac myocytes.

Marsh JD, Lehmann MH, Ritchie RH, Gwathmey JK, Green GE, Schiebinger RJ.

Department of Medicine, Harper Hospital, Detroit, Mich, USA. marsh@cardiology.harper.wayne.edu

BACKGROUND: The role of androgens in producing cardiac hypertrophy by direct action on cardiac myocytes is uncertain. Accordingly, we tested the hypothesis that cardiac myocytes in adult men and women express an androgen receptor gene and that myocytes respond to androgens by a hypertrophic response. METHODS AND RESULTS: We used reverse transcription-polymerase chain reaction methods to demonstrate androgen receptor transcripts in multiple tissues and [3H]phenylalanine incorporation and atrial natriuretic peptide secretion as markers of hypertrophy in cultured rat myocytes. Messenger RNA encoding androgen receptors was detected in myocytes of male and female adult rats, neonatal rat myocytes, rat heart, dog heart, and infant and adult human heart. Both testosterone and dihydrotestosterone produced a robust receptor-specific hypertrophic response in myocytes, determined by indices of protein synthesis and atrial natriuretic peptide secretion. CONCLUSIONS: Androgen receptors are present in cardiac myocytes from multiple species, including normal men and women, in a context that permits androgens to modulate the cardiac phenotype and produce hypertrophy by direct, receptor-specific mechanisms. There are clinical implications for therapeutic or illicit use of androgens in humans.


The cardiac toxicity of anabolic steroids.

Sullivan ML, Martinez CM, Gennis P, Gallagher EJ.

Jacobi Medical Center, Bronx, NY 10464, USA.

Anabolic steroids are synthetic derivatives of testosterone that were developed as adjunct therapy for a variety of medical conditions. Today they are most commonly used to enhance athletic performance and muscular development. Both illicit and medically indicated anabolic steroid use have been temporally associated with many subsequent defects within each of the body systems. Testosterone is the preferred ligand of the human androgen receptor in the myocardium and directly modulates transcription, translation, and enzyme function. Consequent alterations of cellular pathology and organ physiology are similar to those seen with heart failure and cardiomyopathy. Hypertension, ventricular remodeling, myocardial ischemia, and sudden cardiac death have each been temporally and causally associated with anabolic steroid use in humans. These effects persist long after use has been discontinued and have significant impact on subsequent morbidity and mortality. The mechanisms of cardiac disease as a result of anabolic steroid use are discussed in this review.
A recently published study by Dr. Torsten from CEM:

"It is the first (really!) study dealing not only with present steroid use, but also with former Anabolic Androgenic Steroids (AAS) users. I had a hard time getting enough bbs for statistical significance with steroid experience over several years, but being clean for at least one year at the point of examination.
The very difficult recruiting of such bbs is probably the reason for the lack of data on former Anabolic Androgenic Steroids (AAS) users."

Reversibility of the effects on blood cells, lipids, liver function and hormones in former anabolic-androgenic steroid abusers.

Urhausen A, Torsten A, Wilfried K.

Faculty of Clinical Medicine, Institute of Sports and Preventive Medicine, University of Saarland, 66041, Saarbruecken, Germany

In contrast to several studies about the acute complications of anabolic steroid (AS) abuse, data from former long-term abusers (ExU) are lacking. There is also a paucity of data concerning the reversibilty of many acute side effects, e.g. a concentric left ventricular hypertrophy. We therefore investigated male bodybuilders and powerlifters, i.e. 15 ExU after withdrawel of AS for at least 12 months – 43 months on average – (weekly dosage 700 mg on 26 weeks per year over 9 years, mean values) as well as 17 athletes still abusing these substances (U, weekly dosage 750 mg on 33 weeks per year over 8 years). The “AS-Score”, which estimates the dosage and duration of AS abuse by a point score, did not differ between U and ExU. Echocardiographic and ergometry data were compared to 15 weightlifters (WL) of the German national team. U had a slightly higher systolic blood pressure in comparison with ExU (U: 140 ± 10, ExU: 130 ± 5 mmHg; means±SD; p < 0,05) and a clearly higher systolic blood pressure in comparison to WL (125 ± 10 mmHg, p < 0,001). The body dimension-related total heart volumina were similar in ExU and U, but significantly lower in WL. The LV muscle mass related to the fat-free body mass (FFM) of U (3,32 ± 0,48g/kg) was not significantly higher than in ExU (3,16 ± 0,53), but lower in WL (2,43 ± 0,26; p < 0,001). Concerning the mean LV wall thickness only the absolute values differed (p < 0,05) between U (11,8 ± 1,2mm and 0,14 ± 0,01mm/FFM) and ExU (10,8 ± 0,7 and 0,15 ± 0,02), but not if related to FFM; in WL all measures were significantly lower (9,8 ± 1,0 and 0,12 ± 0,01; p < 0,05-0,001). The mean LV wall thickness of U showed a weak correlation with the AS-Score (r = 0,49, p < 0,05). The ratio between LV wall thickness and internal diameter was not significantly different between U (42,1 ± 4,4 %) and ExU (40,3 ± 3,8), but increased in comparison with WL, respectively (36,5 ± 4,0; p < 0,001 and < 0,05). No differences in (normal) systolic and (reduced compared with WL) diastolic LV function were found between U and ExU.

In blood, haemoglobin (+5%), leukocytes (+33%) and platelets (+38%) were significantly higher in U than in ExU. The transaminases were above the normal range in all but one U and significantly higher compared to ExU, cholinesterase (CHE) in U was lower than in ExU. GPT and GOT (U: 65 ± 55 and 38 ± 27; ExU: 24 ± 10 and 18 ± 11 U/l, respectively; p < 0,001) and CHE correlated significantly with the “AS-Score” (r = 0,63 and –0,62, resp.; both p < 0,01). HDL-cholesterol was clearly lower in U as in ExU (17 ± 11 mg/dl and 43 ± 11 mg/dl, resp.; p < 0,001) with a weak correlation with the “AS-Score” (r = 0,50, p < 0,05). Total testosterone and estradiol blood levels were significantly higher in U, but LH and FSH as well as the binding protein SHBG were lower as in ExU (all p < 0,001). Two ExU had total testosterone levels below the normal range.

It is concluded that the massive long term abuse of anabolic androgenic steroids leads to a slight increase of systolic blood pressure in the high normal range and an increase in left ventricular wall thickness with an impairment in left ventricular diastolic function as well to negative alterations in lipid metabolism, liver function and hormones of the hypothalamus-pituitary-testicular axis.

The alterations were reversible in most cases after stopping the medication for longer periods. In cases of some individuals the testosterone synthesis was suppressed even years after ceasing anabolic androgenic steroid abuse. Even several years after ceasing anabolic steroid abuse there can be found at least a tendencial concentric LVH with impaired diastolic function in strength athletes