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sorerotators
Well-known member
Taken off ironforlife forum
Author; Unknown
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 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 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.
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Author; Unknown
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 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 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.
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