posted June 07, 2000 05:23 AM            

Beeing that your heart is a muscle, and if u do hard cardio workouts your heart will have possibility to grow, this is proven and it's pretty much basic logic to.

I've read a little about this, and if u don't wanna risk " Bullheart " ( That's what it's called in europe - oversized heart ) and the problems this leads to, don't do any hard cardio when on the juice.

posted June 07, 2000 10:13 AM            

i would love to hear some facts on this subject !!!

BUMP

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****"What we do in life, echoes an eternity!"**** GLADIATOR

posted June 07, 2000 02:09 PM            

facts about cardio on AS, enlarging the heart muscle??????

anybody have any info ???????

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****"What we do in life, echoes an eternity!"**** GLADIATOR

posted June 07, 2000 03:58 PM            

What does cause your heart to enlarge is high blood pressure. A/S increases blood pressure. This is not a reason to avoid mild to moderate exercise, but actually a very good reason to do it because it helps keep blood pressure down. It is more likely that heart enlargement is exacerbated by events such as peak blood pressures you get coming out of the bottom of 'ass to the grass' heavy squats or other extreme weighted exercises. Of course long term high BP can also lead to heart enlargement, and may be the reason why many life-long chronic steroid abusers have enlarged hearts.

So A/S does not directly cause the heart to enlarge, but if you let the A/S send your BP up and you're doing very heavy Valsalva type lifting then you are more at risk.

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The Mad Scientist

posted June 11, 2000 03:50 PM         

Second, cardio tends not to increase left ventricular size to any degree, but resistance exercise has been shown to cause this enlargement:

: Cardiology 1998 Oct;90(2):145-8

"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.

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.

Third, anabolics have been shown to increase cardiac size without resistance exercise:

Circ Res 1995 Sep;77(3):544-55

"Some growth factors stimulate cultured adult rabbit ventricular myocyte hypertrophy in the absence of mechanical loading."

Decker RS, Cook MG, Behnke-Barclay M, Decker ML

Department of Medicine/Cardiology, Northwestern University Medical School, Chicago, Ill 60611, USA.

Cultured adult rabbit cardiac myocytes treated with recombinant growth factors display enhanced rates of protein accumulation (ie, growth) in response to insulin and insulin-like growth factors (IGFs), but epidermal growth factor, acidic or basic fibroblast growth factor, and platelet-derived growth factor failed to increase contractile protein synthesis or growth of the heart cells. Insulin and IGF-1 increased growth rates by stimulating anabolic while simultaneously inhibiting catabolic pathways, whereas IGF-2 elevated growth modestly by apparently inhibiting lysosomal proteolysis. Neutralizing antibodies directed against either IGF-1 or IGF-2 or IGF binding protein 3 blocked protein accumulation. A monoclonal antibody directed against the IGF-1 receptor also inhibited changes in protein turnover provoked by recombinant human IGF-1 but not IGF-2. Of the other growth factors tested, only transforming growth factor-beta 1 increased the fractional rate of myosin heavy chain (MHC) synthesis, with beta-MHC synthesis being elevated and alpha-MHC synthesis being suppressed. However, the other growth factors were able to modestly stimulate the rate of DNA synthesis in this preparation. Bromodeoxyuridine labeling revealed that these growth factors increased DNA synthesis in myocytes and nonmyocytes alike, but the heart cells displayed neither karyokinesis or cytokinesis. In contrast, cocultures of cardiac myocytes and nonmyocytes and nonmyocyte-conditioned culture medium failed to enhance the rate of cardiac MHC synthesis or its accumulation, implying that quiescent heart cells do not respond to "conditioning" by cardiac nonmyocytes. These findings demonstrated that insulin and the IGFs promote passively loaded cultured adult rabbit heart cells to hypertrophy but suggest that other growth factors tested may be limited in this regard.