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I already searched the threads, im sure this has been asked before, sorry. I am taking test cyp at 500 per week and 50 mg oral winny ed. If steroids build muscle and I am doing cardio, dont I risk building up my heart too much? How much cardio is recommended for this combo? Please no flaming.
Androgens can cause left ventricular hypertrophy. So does heavy resistance training and cardio. The effects of androgen and LVH seem to last up to two years in individuals that both train and take high doses of androgens after the sessation of androgen use. There is a medical bias that LVH is a bad thing.
It is really only significant in athletes that suffer from cardio-megaly. LVH in the medical realm is bad, in the exercise science field it is not of great concern because it is a normal training adaptation within certain bounds.
hey musclescience isnt LVH rather rare though?
it doesnt have to be permanant either, it can regress with the lowering of blood pressure
yep resistance exercise seems to enlarge the heart, but the addition of AAS makes it worse.
"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."
http://www.ncbi.nlm.nih.gov/pubmed/9...?dopt=Abstract
http://www.ncbi.nlm.nih.gov/pubmed/1...?dopt=Abstract
http://www.ncbi.nlm.nih.gov/pubmed/1...?dopt=Abstract
Androgenic anabolic steroids and arterial structure and function in male bodybuilders.
Sader MA, Griffiths KA, McCredie RJ, Handelsman DJ, Celermajer DS.
Department of Cardiology, Royal Prince Alfred Hospital, Sydney, Australia.
OBJECTIVES: The study examined arterial and cardiac structure and function in bodybuilders using androgenic anabolic steroids (AAS), compared to non-steroid-using bodybuilder controls. BACKGROUND: Adverse cardiovascular events have been reported in bodybuilders taking anabolic steroids. The cardiovascular effects of AAS, however, have not been investigated in detail. METHODS: We recruited 20 male bodybuilders (aged 35 +/- 3 years), 10 actively using AAS and 10 who denied ever using steroids. Serum lipid and hormone levels, carotid intima-media thickness (IMT), arterial reactivity, and left ventricular (LV) dimensions were measured. Vessel diameter was measured by ultrasound at rest, during reactive hyperemia (an endothelium-dependent response, leading to flow-mediated dilation, FMD), and after sublingual nitroglycerin (GTN, an endothelium-independent dilator). Arterial reactivity was also measured in 10 age-matched non-bodybuilding sedentary controls. RESULTS: Use of AAS was associated with significant decreases in high density lipoprotein cholesterol, sex hormone binding globulin, testosterone and gonadotrophin levels, and significant increases in LV mass and self-reported physical strength (p < 0.05). Carotid IMT (0.60 +/- 0.04 mm vs. 0.63 +/- 0.07 mm), arterial FMD (4.7 +/- 1.4% vs. 4.1 +/- 0.7%) and GTN responses (11.0 +/- 1.9% vs. 14.4 +/- 1.7%) were similar in both bodybuilding groups (p > 0.2). The GTN responses were significantly lower and carotid IMT significantly higher in both bodybuilding groups, however, compared with the non-bodybuilding sedentary controls (p = 0.01). CONCLUSIONS: Although high-level bodybuilding is associated with impaired vascular reactivity and increased arterial thickening, the use of AAS per se is not associated with significant abnormalities of arterial structure or function.
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1: Circulation 1998 Jul 21;98(3):256-61 Related Articles, Links
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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. [email protected]
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.
there are alot more
Wow that was detailed and appreciated. Still no answer as to how much cardio is recommended with my doses though.
just keep it to 30min EOD
i thought that making your left venterical bigger was good? because it would push blood through the body better and quiker with less effort?
Am i way of the mark here?
it will raise your blood pressure, and sustained high blood pressure can damage blood vessels
I'd say 20-30 min...ed or eod...
Not particularly, you see it with a lot of frequency in athletes, especially endurance and powerlifting athletes.Quote:
Originally Posted by auslifta
As Muliber points out, there is a general bias in the medical community about LVH. The only time they see it is with people that have congestive heart failure. Just because an exercising athlete has the same Left Ventricle enlargement seen in an sedintary adult doesnt mean that its a sign of dysfunction.