AAS and Cardiovascular/Pulmonary Function

[Stretch]

I got turned down for donating blood because I foolishly mentioned I was on Avodart. But I'm getting advice on a very simple method of doing a home phlebotomy involving a 16g pin, an empty syringe, a transparent hose, and a 500 ml water bottle. An observer or helper is necessary, of course. Easy? The hard part is that 16g pin going into a fucking vein!

I'll probably need to wash my hands too.

Solo

Is it possible that little writeup is coming??

So that the rest of us could also phlebotomize ourselves?

 

[solo47]

Is it possible that little writeup is coming??

So that the rest of us could also phlebotomize ourselves?

I'm first going to try to reason with my urologist (get tested again if necessary) and my GP to see if they'll make me an appointment at the ambulatory clinic for an IV blood drip. I'm running a bit of Masteron to keep my RBC where it is, but using no Test, so I can argue my polycythemia seems to be chronic.

It's usually older guys that get polycythemia from steroid use; some even from TRT, but if you use a lot, it could happen. Best is to take 3 months off, which is much tougher when you basically produce no testosterone of your own. You shouldn't have to worry, Stretch, unless you're running high doses and not going off cycle. (And you never do things to excess, do you?)

If I do, I may report back. But no one should consider the home procedure as "recommended".

Solo

 

[Bucky]

A major part of Doc Scally's HPTA recovery program is fairly massive doses of HCG. But I was thinking that if HCG increases the body's production of testosterone (and it does), wouldn't that exacerbate or at least continue the polycethemia symptoms?

Phlebotomy Kit, 100+ Kits

I'm getting a full CBC workup from my urologist and have a talk with him before I decide anything, but if no testosterone means I become transmogrified into Mr. Magoo then I'm not having it.

Respects,
Solo

I am interested in the kit, but from the picture, it looks more like a blood sample collecting kit. Can anyone shed some light on this? I read the specs in the description, but I'm not sure what some the terms mean. I have already tried draining blood with a 23g, but I only get a few drips then it clogs up.

 

[Juice n Goose]

Baggish AL, Weiner RB, Kanayama G, et al. Long-Term Anabolic-Androgenic Steroid Use Is Associated With Left Ventricular Dysfunction. Circ Heart Fail 2010;3(4):472-6. Long-Term Anabolic-Androgenic Steroid Use Is Associated With Left Ventricular Dysfunction -- Baggish et al. 3 (4): 472 -- Circulation: Heart Failure

Background—Although illicit anabolic-androgenic steroid (AAS) use is widespread, the cardiac effects of long-term AAS use remain inadequately characterized. We compared cardiac parameters in weightlifters reporting long-term AAS use to those in otherwise similar weightlifters without prior AAS exposure.

Methods and Results—We performed 2D tissue-Doppler and speckle-tracking echocardiography to assess left ventricular (LV) ejection fraction, LV systolic strain, and conventional indices of diastolic function in long-term AAS users (n=12) and otherwise similar AAS nonusers (n=7). AAS users (median [quartile 1, quartile 3] cumulative lifetime AAS exposure, 468 [169, 520] weeks) closely resembled nonusers in age, prior duration of weightlifting, and current intensity of weight training. LV structural parameters were similar between the two groups; however, AAS users had significantly lower LV ejection fraction (50.6% [48.4, 53.6] versus 59.1% [58.0%, 61.7%]; P=0.003 by two-tailed Wilcoxon rank sum test), longitudinal strain (16.9% [14.0%, 19.0%] versus 21.0% [20.2%, 22.9%]; P=0.004), and radial strain (38.3% [28.5%, 43.7%] versus 50.1% [44.3%, 61.8%]; P=0.02). Ten of the 12 AAS users showed LV ejection fractions below the accepted limit of normal ( 55%). AAS users also demonstrated decreased diastolic function compared to nonusers as evidenced by a markedly lower early peak tissue velocity (7.4 [6.8, 7.9] cm/s versus 9.9 [8.3, 10.5] cm/s; P=0.005) and early-to-late diastolic filling ratio (0.93 [0.88, 1.39] versus 1.80 [1.48, 2.00]; P=0.003).

Conclusions—Cardiac dysfunction in long-term AAS users appears to be more severe than previously reported and may be sufficient to increase the risk of heart failure.

A good friend of mine was a Navy diver and as such as his training progressed it became physically more demanding,thus every 3 months he and his peers were subjected to very intense medical scrutiny by Naval physicians. For the first two years of diving for the navy my friend was routinely given 2-d echocardiogram tests to "look" at all aspects of his ticker. He had a great pulse during hard work, an ejection fraction of 80 and all seemed well. He told me he got a helluva scare on a night dive when he lost his breathing apparatus and couldnt withstand the pressure without air to balance his ears. He said he was gonna try using some heavy EQ,Boldenone Undec. cause it increases oxygen uptake. Well he went pretty nuts and cycled heavy for over a year using all sorts of compounds. On his next physical the dive surgeon Did an EKG and a 2-D echo and his heart was huge! his ejection fraction had dropped 50 points to a 30 and he was diagnosed with Dilated Cardiomyopathy with elements of heart failure!! Needless to say hes NOT a Navy Diver anymore although after about two years his ejection fraction was last I talked to him 40 but hes still in n out of the hospital with cardiac and pulmonary edema. Damn shame uh? This stuff is/are medicines and I suppose like any meds can have some heavy sides if the proper precautions arent taken what with all that water retention some compounds cause.

 

[Juice n Goose]

Is it possible that little writeup is coming??

So that the rest of us could also phlebotomize ourselves?

Ive started way too many IV's on downed men(SOP) and I think in the absence of a true IV catheter,All you need is an 18G needle attached to at least a 1/4" catheter(med grade and easy to get).

Hell I once drained down a friend into an empty coke bottle so we knew to get a whole unit!

Sounds ghastly but necessity is the mother of all invention

Please use only sterile apparatus!!! and betadine the inj. site. Alcohol isnt sufficient in my and Navy Corpsmans opine!!!!

Goose

 

[solo47]

Ive started way too many IV's on downed men(SOP) and I think in the absence of a true IV catheter,All you need is an 18G needle attached to at least a 1/4" catheter(med grade and easy to get).

Hell I once drained down a friend into an empty coke bottle so we knew to get a whole unit!

Sounds ghastly but necessity is the mother of all invention

Please use only sterile apparatus!!! and betadine the inj. site. Alcohol isnt sufficient in my and Navy Corpsmans opine!!!!

Goose

You're quite sure [ame="http://en.wikipedia.org/wiki/Betadine"]betadine[/ame] is a better disinfectant than 70% isopropyl alcohol?

Solo

 

[foreveryoung]

just got my blood test results back and my rbc is a little over the high range

 

[Juice n Goose]

You're quite sure betadine is a better disinfectant than 70% isopropyl alcohol?

Solo

Absolutely Not Brother..

Just because its what I was taught and retaught ..ad infinitum does NOT mean in the real world things dont go much differently,I mean things like chlorhexadine gluconate is prob. far more efficient but I would assume in the military there are other things at work like teaching a very large number of people of varying intake potential(especially at the pace we moved at) how to help an injured/wounded comrade in a safe yet expedient manner being paramount.

I spoke with a doctor last night (as we were going to bed) and put your question to her and she told me when she was in trauma prior the "Big Move" to Psych she scrubbed with Betadine, whereas the Med-Surg. Nurses prepped the Pt. With a betadine solution of a similar, but varied composition.That was,Im afraid to say..some time ago!!

But every hospital has a formulary of sorts and philosophy and they get what they get! Bean-counters often make such calls,scary huh!!To recap: I've NO Clue if it was the "Cutting Edge"But I sincerely doubt it. However,I would be quite shocked if the Docs complained as I myself came out of surgery THOROUGHLY painted it would seem from head to toe with that crap!!!

Fact:90% of severely wounded Warfighters that are gotten to a field hosp or better w/in an hour or less.. live!! Hallelujah Dust-Off whirly-birds!!

Goose

 

[B-Irons]

When you look at Cross Fit, do you see major advantages or disadvantages to using AAS? The reason I ask is in ref. the article the Dr. Scally posted about CV Endurance. Crossfit is wide open when it comes to CV and since that is the main source of what goes on, do you think this process would be sped up when it comes to possible heart failure?

 

[solo47]

just got my blood test results back and my rbc is a little over the high range

Not bad, and since your forever young, nothing to worry about.

120 days and/or a blood donation, and you should be fine.

(My blood donation took the allowed time, 20 min, and still had only filled 411cc of the 500cc container. Means I had/have viscous [thick] blood. So I'm still thinking about a self-phlebotomy but mainly not.)

Solo

 

[weekend]

Re: Adverse Cardiovascular Effects Of Anabolic Steroids: Pathophysiology Imaging

my RBC's have been elevated on every blood test i've taken, just recently gave blood for the first time.

is the consensus here that donating blood reduces the cardiovascular repercussions of cycling AAS?

 

[solo47]

Re: Adverse Cardiovascular Effects Of Anabolic Steroids: Pathophysiology Imaging

my RBC's have been elevated on every blood test i've taken, just recently gave blood for the first time.

is the consensus here that donating blood reduces the cardiovascular repercussions of cycling AAS?

Only the cardiovascular repercussions of having a dangerously high Red Blood Cell count, which may or may not mean dangerously high iron levels. Blood doping to increase endurance for certain athletes is simply artificially increasing the blood in your body, which will increase your RBC and the flow of oxygen. However, that is temporary. If you have high RBC for too long, you have viscous blood, which can lead to a stroke. I don't think donating blood does anything to help prevent sclerosis of the heart's left ventricle, the major problem for long-term AAS users.

Solo

 

[Michael Scally MD]

Canadian Bodybuilder Greg Kovaks died today of heart failure at the age of 44. "The Strongest Bodybuilder Alive" won his procard at the Canadian Nationals in 1996.
Greg Kovacs Dies at Age 44

 

[solo47]

Canadian Bodybuilder Greg Kovaks died today of heart failure at the age of 44. "The Strongest Bodybuilder Alive" won his procard at the Canadian Nationals in 1996.
Greg Kovacs Dies at Age 44

What does this mean with regard to this thread, Dr Scally? I for one don't know all that Greg Kovacs used for dietary or pharmaceutical support, but I certainly can guess he pushed himself to the max in the gym. Is this a case of steroid-use to death, or what?

Solo

 

[weekend]

i want to point out greg kovac was excessively large in the offseason and also possessed quite a gut, perhaps diet is important here in combination with aas.

 

[Michael Scally MD]

What does this mean with regard to this thread, Dr Scally? I for one don't know all that Greg Kovacs used for dietary or pharmaceutical support, but I certainly can guess he pushed himself to the max in the gym. Is this a case of steroid-use to death, or what?

Solo

I would have to speculate. Once I read heart failure, I thought of this thread. However, I think is is safe to assume there was AAS use, right?

 

[solo47]

I would have to speculate. Once I read heart failure, I thought of this thread. However, I think is is safe to assume there was AAS use, right?

Absolutely. However, from the little I've gathered, it sounds like Mr Kovacs didn't just use the roid, but abused it, likely never coming off and running large amounts of everything. There is no doubt that steroid abuse causes cardiovascular defects (as many of the studies you've cited have indicated). In some cases, even cautious cycling can lead to cardiovascular damage, especially if there is already a genetic predisposition. Along with other "medications" he likely used, plus his size, eating habits, & workout to strength max, he was a very likely candidate for a heart attack. Surely he was warned.

The commentator from the Catholic University (in the article link) seemed to simply assume that because he used "anabolics", he was just asking for a heart attack, so all such things should be banned in bodybuilding. I'm just suggesting Greg Kovacs was a unique case of overdone everything.

Respects,
Solo

 

[Michael Scally MD]

[Rats] Le TYL, Ashton AW, Mardini M, et al. ROLE OF ANDROGENS IN SEX DIFFERENCES IN CARDIAC DAMAGE DURING MYOCARDIAL INFARCTION. Endocrinology. http://endo.endojournals.org/content/early/2013/12/09/en.2013-1755.abstract (ROLE OF ANDROGENS IN SEX DIFFERENCES IN CARDIAC DAMAGE DURING MYOCARDIAL INFARCTION)

Age-specific incidence of ischemic heart disease in men is higher than in women, although women die more frequently without previous symptoms; the molecular mechanism(s) are poorly understood. Most studies focus on protection by estrogen, with less attention on androgen receptor (AR) mediated androgen actions. Our aim was to determine the role of androgens in the sex differences in cardiac damage during myocardial infarction (MI).

Mature age-matched male and female Sprague Dawley rats - intact or surgically gonadectomized (Gx) - received testosterone (T) or estradiol (E2) via subdermal silastic implants; a subset of male rats received dihydrotestosterone (DHT). After 21 days, animals were anesthetized, hearts excised and subjected to ex vivo regional ischemia-reperfusion (I-R).

Hearts from intact males had larger infarcts than those from females following I-R; Gx produced the opposite effect, confirming a role for sex steroids. In Gx males, androgens (DHT, T) and E2 aggravated I-R induced cardiac damage, whereas in Gx females, T had no effect and E2 reduced infarct area. Increased circulating T levels upregulated AR and receptor for advanced glycation end products (RAGE), which resulted in enhanced apoptosis aggravating cardiac damage in both males and females.

In conclusion, our study demonstrates for the first time that sex steroids regulate autophagy during MI, and shows that a novel mechanism of action for androgens during I-R is downregulation of antiapoptotic protein Bcl-xL, a key controller for crosstalk between autophagy and apoptosis, shifting the balance towards apoptosis and leading to aggravated cardiac damage.

 

[Michael Scally MD]

Angell PJ, Ismail TF, Jabbour A, et al. Ventricular structure, function, and focal fibrosis in anabolic steroid users: a CMR study. Eur J Appl Physiol. Ventricular structure, function, and focal fibrosis in anabolic steroid users: a CMR study - Online First - Springer

PURPOSE: Anabolic steroid (AS) misuse is widespread amongst recreational bodybuilders; however, their effects on the cardiovascular system are uncertain. Our aim was to document the impact of AS use on cardiac structure, function and the presence of focal fibrosis using the gold standard cardiovascular magnetic resonance imaging (CMR).

METHODS: A cross-sectional cohort design was utilised with 21 strength-trained participants who underwent CMR imaging of the heart and speckle-tracking echocardiography. Thirteen participants (30 +/- 5 years) taking AS for at least 2 years and currently on a "using"-cycle were compared with age and training-matched controls (n = 8; 29 +/- 6 years) who self-reported never having taken AS (NAS).

RESULTS: AS users had higher absolute left ventricular (LV) mass (220 +/- 45 g) compared to NAS (163 +/- 27 g; p < 0.05) but this difference was removed when indexed to fat-free mass. AS had a reduced right ventricular (RV) ejection fraction (AS 51 +/- 4 % vs. NAS 59 +/- 5 %; p < 0.05) and a significantly lower left ventricular E':A' myocardial tissue velocity ratio [AS 0.99(0.54) vs. NAS 1.78(0.46) p < 0.05] predominantly due to greater tissue velocities with atrial contraction. Peak LV longitudinal strain was lower in AS users (AS -14.2 +/- 2.7 % vs. NAS -16.6 +/- 1.9 %; p < 0.05). There was no evidence of focal fibrosis in any participant.

CONCLUSIONS: AS use was associated with significant LV hypertrophy, albeit in-line with greater fat-free mass, reduced LV strain, diastolic function, and reduced RV ejection fraction in male bodybuilders. There was, however, no evidence of focal fibrosis in any AS user.

 

[Michael Scally MD]

Bocalini DS, Beutel A, Bergamaschi CT, Tucci PJ, Campos RR. Treadmill Exercise Training Prevents Myocardial Mechanical Dysfunction Induced by Androgenic-Anabolic Steroid Treatment in Rats. PLoS One 2014;9(2):e87106. PLOS ONE: Treadmill Exercise Training Prevents Myocardial Mechanical Dysfunction Induced by Androgenic-Anabolic Steroid Treatment in Rats

Elevated concentrations of testosterone and its synthetic analogs may induce changes in cardiovascular function. However, the effects of the combination of anabolic/androgenic steroid (AAS) treatment and exercise training on systolic and diastolic cardiac function are poorly understood.

In the present study, we aimed to investigate the effects of low-dose steroid treatment (stanozolol) on cardiac contractile parameters when this steroid treatment was combined with exercise training in rats and the effects of chronic steroid treatment on the Frank-Starling (length-tension curves) relationship.

Male Wistar rats were randomly assigned to one of four groups:
U (untrained),
US (untrained and treated with stanozolol 5 mg/kg/week),
T (trained, 16 m/min/1 h) and
TS (trained and treated with stanozolol 5 mg/kg/week).

Continuous exercise training was conducted 5 days/week for 8 consecutive weeks. The speed of the treadmill was gradually increased to a final setting of 16 m/min/1 h.

Experiments were divided into two independent series:
1) central hemodynamic analysis for mean arterial blood pressure (MAP) and cardiac output (CO) measurements and
2) isolated papillary muscle preparation in Krebs solution.

Stanozolol treatment significantly increased the MAP and the heart size in untrained and trained rats (U 113+/-2; T 106+/-2; US 138+/-8 and TS 130+/-7 mmHg). Furthermore, stanozolol significantly decreased developed tension and dT/dt (maximal and minimal) in U rats. However, the developed tension was completely restored by training. The Frank/Starling relationship was impaired in rats treated with stanozolol; however, again, training completely restored diastolic function.

Taken together, the present data suggest that AAS treatment is able to decrease cardiac performance (systolic and diastolic functions). The combination of stanozolol and physical training improved cardiac performance, including diastolic and systolic functions, independent of changes in central hemodynamic parameters. Therefore, changes in ventricular myocyte calcium transients may play a cardioprotective role.