Left Ventricle Hypertrophy?

[chave2k89]

hey guys, so i was wondering, in regards to left ventricle hypertrophy ... is that indirectly related to AAS use? i know it can be caused by having high bp for an extended period of time which can be caused by AAS usage however am wondering if there's any properties of AAS themselves that would cause such w/o high bp etc?

[Turkish Juicer]

There are no known properties of AAS themselves that would cause such process without bringing in the BP into the picture as a side effect. Some studies even question whether high BP is alone the cause of LV hypertrophy, if a visible cause at all.

Check out the info below, you will be more than satisfied with this:

Left ventricular wall thickening does occur in elite power athletes with or without anabolic steroid Use.
Dickerman RD, Schaller F, McConathy WJ.

Department of Biomedical Sciences, University of North Texas Health Science Center, Fort Worth, Tex., USA.

Abstract

Reports on the occurrence of left ventricular wall thickening in resistance-trained athletes have rejected the possibility for this physiological adaptation to occur without concomitant anabolic steroid abuse. Others have concluded short bursts of arterial hypertension that occur with maximal weight lifting are not sufficient to induce left ventricular wall thickening, and left ventricular wall thickness >/=13 mm should not be found in pure resistance-trained athletes. Therefore, we examined 4 elite resistance-trained athletes by two-dimensional echocardiography. In addition, we retrospectively examined the individual left ventricular dimensions of 13 bodybuilders from our previous echocardiographic studies. All 4 elite resistance-trained athletes had left ventricular wall thicknesses beyond 13 mm. One of the elite bodybuilders has the largest left ventricular wall thickness (16 mm) ever reported in a power athlete. Retrospectively, 43% of the drug-free bodybuilders and 100% of the steroid users had left ventricular wall thickness beyond the normal range of 11 mm. In addition, 1 drug-free subject and 3 steroid users were beyond the critical mark of 13 mm. No subjects demonstrated diastolic dysfunction. In contrast to previous reports, we have demonstrated that left ventricular wall thicknesses >/=13 mm can be found routinely in elite resistance-trained athletes. The use of anabolic steroids concomitant with intensive resistance exercise does appear to augment left ventricular size without dysfunction. Anabolic steroids may accelerate left ventricular wall thickening indirectly by increasing strength, thus augmenting the pressor response.

PMID:9778553 [PubMed - indexed for MEDLINE]

[binsser]

^^^^^^^^^^^^ as above if youve been training for a while you can have it think they say its mainly cause by high impact training etc etc

[Sgt. Hartman]

There are no known properties of AAS themselves that would cause such process without bringing in the BP into the picture as a side effect.

That's not true, I wish it were but it's not.

Cardiac myocytes have androgen receptors that through upregulation from AAS use can directly cause thickening of the left ventricle wall.

It's not fully understood how hypertrophy can occur without the necessary resistance (high BP) but it is documented.




Androgen Receptors Mediate Hypertrophy in Cardiac Myocytes
James D. Marsh, MD; Michael H. Lehmann, MD; Rebecca H. Ritchie, PhD; Judith K. Gwathmey, VMD, PhD; Glenn E. Green, MD; ; Rick J. Schiebinger, MD
From the Program in Molecular and Cellular Cardiology, Departments of Medicine and Otolaryngology, Harper Hospital, Detroit, Mich; the VA Medical Center, Boston University Medical Center, Boston, Mass (J.K.G.); and the Arrhythmia Center/Sinai Hospital (M.H.L.) and Wayne State University School of Medicine, Detroit, Mich (J.D.M.).
Correspondence to James D. Marsh, MD, Wayne State University School of Medicine, 421 E Canfield Ave, Detroit, MI 48201. E-mail [email protected]


Abstract
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.

Here's the full report. http://circ.ahajournals.org/content/98/3/256.full

And again here. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1768197/

[Turkish Juicer]

I did not know about the ''... context that permits androgens to modulate the cardiac phenotype and produce hypertrophy by direct, receptor-specific mechanisms.''

All the papers I came across with so far pretty much indicated that LV hypertrophy was indirectly related to AAS use since AAS drastically increases strength which leads the user to perform sets with heavier weights thus leading to greater LV hypertrophy.

Good to know.