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08-31-2016, 02:00 AM #1
PUBMED: aas doesnt cause atherosclerosis!!
Good to know.
Cardiovascular effects of androgenic anabolic steroids in male bodybuilders determined by tissue Doppler imaging.
Nottin S1, Nguyen LD, Terbah M, Obert P.
Author information
Abstract
The effects of anabolic androgenic steroids (AASs) on left ventricular (LV) diastolic function in strength-trained athletes are controversial. The main objective of this study was to evaluate the effects of regular AAS administration in bodybuilders using pulsed tissue Doppler imaging (TDI) to evaluate LV relaxation properties. Fifteen male bodybuilders with a history of intensive, long-term strength training and 16 age-matched sedentary controls were recruited. Six of the bodybuilders reported regular use of AASs, and 9 were drug free. To assess LV diastolic function, each subject underwent standard Doppler echocardiography and pulsed TDI. Drug-using bodybuilders exhibited altered LV diastolic filling characterized by a smaller contribution of passive filling to LV filling compared with their drug-free counterparts. TDI measurements indicated that drug-using bodybuilders had smaller peak E(m) than drug-free bodybuilders and sedentary controls, except at the level of the anterior wall, at which peak E(m) was significantly smaller than in drug-free bodybuilders only. The E/E(m) ratio, an index of LV filling pressures, was not affected by strength training or by AAS use. Drug-using bodybuilders exhibited larger LV end-diastolic diameters, volumes, and masses than their drug-free counterparts. However, no difference was found in LV wall thickness between the groups. In conclusion, drug-using bodybuilders showed a decrease in the contribution in LV passive filling to LV filling associated with a decrease in LV relaxation properties. Because no wall thickening was obtained in drug-using bodybuilders, the decrease in LV relaxation properties might have been be due to an alteration in the active properties of the myocardium, but that has yet to be confirmed.
Comment in
A Troia horse into cardiovascular system: anabolic steroid (s). [Am J Cardiol. 2006]
PMID:
16516601
DOI:
10.1016/j.amjcard.2005.10.026
Androgenic anabolic steroids and arterial structure and function in male bodybuilders.
Sader MA1, Griffiths KA, McCredie RJ, Handelsman DJ, Celermajer DS.
Author information
Abstract
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.
PMID:
11153743
So guess its all about the diett. Bad cholestrol from diett may thicken the arterie walls, not ass. So stick to brown rice and inject tren all day!
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08-31-2016, 02:21 AM #2
Hmm, small sturdy group, HDL was lowered, no mention of LDL or VLDL. Need more data to feel.comfortable with saying it doesn't contribute to atherosclerosis ( the build-up of fats, cholesterol, and other substances in and on the artery walls).
Interesting topic for discussion, though.
No mention of doses or types of AAS used, either.There are 3 loves in my life: my wife, my English mastiffs, and my weightlifting....Man, my wife gets really pissed when I get the 3 confused...
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08-31-2016, 02:48 AM #3Anabolic Member
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topic is indeed interesting, although study is too small and inaccurate to be relied on.
I just watch the space how Sillyboy jumps on every topic with cherry-picking tactics, if he will find one sarm pill in a hay-stack, he will recommend eating hay-stacks for everyone. Lack of deep thinking... although it makes fun to watch
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08-31-2016, 03:00 AM #4
Last edited by AR's King Silabolin; 08-31-2016 at 03:04 AM.
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08-31-2016, 03:16 AM #5Anabolic Member
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You had never had respect from me sillyboy, not that you lost it, you never had it, I thought you will earn it, but you failed it, so screw you sillyboy.
Of course Im not fat-ass as you are, Im good with what I am at, you're literally threaten to spam the board shaming me of something Im not ashamed of? How low is that sillyboy?
And I am staying on topic, did you missed the first line? Cherry-picker sillyboy
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08-31-2016, 03:17 AM #6Anabolic Member
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Ah, grammar this: https://en.wikipedia.org/wiki/Cherry_picking
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08-31-2016, 10:02 AM #8Anabolic Member
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he just wants everyone to eat the hay-stacks cause he found a sarm pill in one
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08-31-2016, 10:28 AM #9
Tryin hard to get that color lol
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08-31-2016, 11:13 AM #10
Agree they should have specified for different steroids .
But really, AAS not contributing to atherosclerosis sounds pretty logical to me. The interesting part of the study, although should have been more detailed, is the decrease in LV relaxation properties. High performance athletes ussually have this LV hypertrophy, but 1st time I read about different relaxation properties.
If I understand correctly the LV doesnt fill as much as it could due to myocardio not relaxing enough, right?
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For a human study, this actually isn't to bad a size. It's large enough to do statistically analysis. When using human subjects you have to remember, it's very hard to control behaviors that would exclude them from the study. So a typical number in exercise science studies is in the n=20 range.
I would think they could have easily measured ejection fraction and stroke volume with Doppler since they were doing it anyway. Maybe they did, I didn't read the whole paper.
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08-31-2016, 12:45 PM #12
So in not so much scientific terms....? What is this actually saying
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08-31-2016, 12:49 PM #13
Should be red in no time at all with gems like this ...
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08-31-2016, 03:04 PM #14
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08-31-2016, 03:06 PM #15
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08-31-2016, 08:50 PM #16
That part threw me as well as I'm more familiar with studies that talk about the LV becoming enlarged and then past a certain point, "floppy" which lowers EF℅.
Edit: By floppy, I mean LV becomes enlarged to the point that it can't respond quickly enough to the electrical impulses that are signaling for the contraction.Last edited by almostgone; 08-31-2016 at 09:01 PM.
There are 3 loves in my life: my wife, my English mastiffs, and my weightlifting....Man, my wife gets really pissed when I get the 3 confused...
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08-31-2016, 09:14 PM #17
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