AAS and Cardiovascular/Pulmonary Function

[idmd]

Thanks Doc for posting these journals. They should be a must read for anybody contemplating the use of AAS.... as well as, old timers like myself.

Too often the most asked questions are...
"what type of cycle should I use for my first run...???"

Instead there should be more questions like...

"What are the effects of AAS on physiology besides hypertrophy of skeletal muscles?" or, "what are the long term effects of AAS??"

Personally, I just had a complete physical and stress test, required by my life insurance company.

During the ECG the nurse responded... we have been seeing this more and more. I questioned her...about what she was referencing. She said that my left ventricle is enlarged. Called it an Athletes Heart...

While i have been an athlete all my life... and no stranger to strenuous cardiac output both aerobic and anaerobic... Your articles have made me reevaluate things. Maybe a little to late.

Let me dust off some neurons...

Cardiac Output = stroke volume x heart rate

As the demand for O2 secondary to aerobic exercise increases you get non-pathological left-ventricular hypertrophy in an attempt to increase SV, increase ejection fraction via an increase in inotropy. During times of low O2 demand the hearts increased contractility means HR needs to be less to maintain CO and bradycardia occurs. Seems normal to me.....

 

[Pericles]

P,
I would love to hear the Doc's opinion on your question. I have been contemplating that for the last few months as well.

My opinion is... the high BP range that you and I seem to be frequenting may be the cause of the "Athletes Heart". as well as the stress level that is applied during those high rates.

Maybe reversing your thought process... and training cardio at a higher level when not at Supraphysiological hormone levels. Thoughts???

In my case training with large loads for long distances at high speeds... in various conditions. Desert and jungle.

Also, Doc...could this condition possibly be caused by deep underwater dives with no breathing apparatus? Over the years i have conditioned myself to be able to descend quite deep with prebreathing exercises and a single breath.

Navy Seal? If so, thank you for your service. Oh wait, if you told me, you would have to kill me

 

[beezil]

 

[beezil]

Let me dust off some neurons...

Cardiac Output = stroke volume x heart rate

As the demand for O2 secondary to aerobic exercise increases you get non-pathological left-ventricular hypertrophy in an attempt to increase SV, increase ejection fraction via an increase in inotropy. During times of low O2 demand the hearts increased contractility means HR needs to be less to maintain CO and bradycardia occurs. Seems normal to me.....

Thank you, Sir.

Your explanation was more detailed than my IM doc has given me. At the same time saying essentially the same. Nothing to worry about at this point. However, he has set me up with a cardiologist to monitor.

I will keep this thread posted on my results and outcome.

I know for a fact up until the age of 27... the USG kept mine and the community I worked with's health as top priority. We were in fact government property... Highly valued at that. The margins for non peak performance or health anomalies were non existent. If my left ventricle were enlarged at that time I would have been washed out. Which further reinforces my belief that the loads that were applied to my heart did not cause the enlargement.

My opinion... After reading Doc's journals... that the last ten years of moderate AAS use... mostly Test and tren cycles. May have caused this condition.
Mind you I have always run conservative cycles 350mg test and 350mg tren... with great results. This is under the 500mg Test E studies that were noted in the Journal... but stacking with Tren could be the cause....

 

[Michael Scally MD]

Fineschi V. Chronic, supra-physiological doses of nandrolone decanoate and exercise induced cardio-toxicity in an animal-model study. Acta Physiol (Oxf). Chronic, supra-physiological doses of nandrolone decanoate and exercise induced cardio-toxicity in an animal-model study - Fineschi - Acta Physiologica - Wiley Online Library

The association between synthetic androgen (SA) abuse and sudden cardiac death is often cited in literature; in this respect, to date there are little data on the effects of chronic administration of supraphysiological doses of SA on tonic cardiac autonomic control. Marques Neto et al., in their interesting paper, show that chronic treatment with a high dose of nandrolone decanoate (ND) induces cardiac parasympathetic dysfunction and disturbances in ventricular depolarization in both sedentary and exercised rats (Marques Neto et al. 2013).

This study shows, unequivocally, that the blockade of the renin-angiotensin system (RAS), and particularly of angiotensin II type 1 receptor (AT1R) by losartan, prevents QT prolongation and that the administration of chronic, supra-physiological doses of ND induces parasympathetic autonomic dysfunction.

 

[beezil]

as always... Thank You, Sir.

 

[techlogik]

Abusing anything can pretty much kill you eventually....thanks for the studies though.

Just to reiterate...this stuff can be no joke to your health when abused.

 

[Dr JIM]

Agreed Millard but these are small studies, with limited control of those factors that effect cardiac function, EF in particular. Furthermore these results are not manifested clinically since those whom use AAS, DO NOT have a considerably HIGHER cardiovascular mortality, IME (or based on the literature Im aware if)

This is in spite of evidence AAS may worsen the lipid profile, increase BP, and now we hear they may reduce cardiac function?

Until someone does the definitive test, pre and post AAS cardiac biopsy, I'm not buying the implied "cause and effect relationship"!

DOC as always your efforts are greatly appreciated. They are in part responsible for the "brighter minds" on Meso compared to every other AAS forum where "bro science" is simply regurgitated.

Jim

 

[CensoredBoardsSuck]

Docs, if you wouldn't mind, I'd like to hear your thoughts on the significance of the findings in these cites, as well as the one Dr. Scally posted, with regard to the inhibition of the renin-angiotensin-aldosterone system and the effects on the heart induced by ND.
Thanks


Med Sci Sports Exerc. 2011 Oct;43(10):1836-48.
Anabolic steroid associated to physical training induces deleterious cardiac effects. Anabolic steroid associated to physical... [Med Sci Sports Exerc. 2011] - PubMed - NCBI
Do Carmo EC, Fernandes T, Koike D, Da Silva ND Jr, Mattos KC, Rosa KT, Barretti D, Melo SF, Wichi RB, Irigoyen MC, de Oliveira EM.

Abstract
PURPOSE:

Cardiac aldosterone might be involved in the deleterious effects of nandrolone decanoate (ND) on the heart. Therefore, we investigated the involvement of cardiac aldosterone, by the pharmacological block of AT1 or mineralocorticoid receptors, on cardiac hypertrophy and fibrosis.
METHODS:

Male Wistar rats were randomized into eight groups (n = 14 per group): Control (C), nandrolone decanoate (ND), trained (T), trained ND (TND), ND + losartan (ND + L), trained ND + losartan (TND + L), ND + spironolactone (ND + S), and trained ND + spironolactone (TND + S). ND (10 mg·kg(-1)·wk(-1)) was administered during 10 wk of swimming training (five times per week). Losartan (20 mg·kg(-1)·d(-1)) and spironolactone (10 mg·kg(-1)·d(-1)) were administered in drinking water.
RESULTS:

Cardiac hypertrophy was increased 10% by using ND and 17% by ND plus training (P < 0.05). In both groups, there was an increase in the collagen volumetric fraction (CVF) and cardiac collagen type III expression (P < 0.05). The ND treatment increased left ventricle-angiotensin-converting enzyme I activity, AT1 receptor expression, aldosterone synthase (CYP11B2), and 11-? hydroxysteroid dehydrogenase 2 (11?-HSD2) gene expression and inflammatory markers, TGF? and osteopontin. Both losartan and spironolactone inhibited the increase of CVF and collagen type III. In addition, both treatments inhibited the increase in left ventricle-angiotensin-converting enzyme I activity, CYP11B2, 11?-HSD2, TGF?, and osteopontin induced by the ND treatment.
CONCLUSIONS:

We believe this is the first study to show the effects of ND on cardiac aldosterone. Our results suggest that these effects may be associated to TGF? and osteopontin. Thus, we conclude that the cardiac aldosterone has an important role on the deleterious effects on the heart induced by ND.



Acta Physiol (Oxf). 2012 Dec 20. doi: 10.1111/apha.12056. [Epub ahead of print]
The blockade of angiotensin AT(1) and aldosterone receptors protects rats from synthetic androgen-induced cardiac autonomic dysfunction. The blockade of angiotensin AT(1) and ald... [Acta Physiol (Oxf). 2012] - PubMed - NCBI
Marques Neto SR, Silva AD, Santos MC, Ferraz EF, Nascimento JH.

Abstract
AIM:

This study aimed to evaluate the combined effects of exercise and antagonists of the angiotensin II and aldosterone receptors on cardiac autonomic regulation and ventricular repolarization in rats chronically treated with nandrolone decanoate (ND), a synthetic androgen.
METHODS:

Thirty male Wistar rats were divided into six groups: sedentary, trained, ND-treated, trained and ND-treated, trained and treated with both ND and spironolactone, and trained and treated with both ND and losartan. ND (10 mg kg(-1) weekly) and the antagonists (20 mg kg(-1) daily) of the angiotensin II AT(1) (losartan) and aldosterone (spironolactone) receptors were administered for 8 weeks. Exercise training was performed using a treadmill five times each week for 8 weeks. Following this 8-week training and treatment period, electrocardiogram recordings were obtained to determine the time and frequency domains of heart rate variability (HRV) and corrected QT interval (QTc).
RESULTS:

Nandrolone decanoate treatment increased the QTc interval and reduced the parasympathetic indexes of HRV (RMSSD, pNN5 and high-frequency power) in sedentary and trained rats. The ratio between low- and high-frequency power (LF/HF) was higher in ND-treated groups. Both losartan and spironolactone treatments prevented the effects of ND on the QTc interval and the HRV parameters (RMSSD, pNN5, high-frequency power, and the LF/HF ratio).
CONCLUSION:

Our results show that chronic treatment with a high dose of ND induces cardiac parasympathetic dysfunction and disturbances in ventricular repolarization in both sedentary and exercised rats. Furthermore, inhibiting the renin-angiotensin-aldosterone system using losartan, or spironolactone, prevented these deleterious effects.

 

[Michael Scally MD]

Highlights
• Anabolic treated animals showed an increased cardiac output.
• On the other hand, myocardial mass progressively reduced significantly.
• Global myocardial function deteriorated in a dose-dependent manner.
• High dose of anabolics created a hostile oxidative environment.
• Adverse effects were more pronounced in the methanabol group.


Germanakis I, Tsarouhas K, Fragkiadaki P, et al. Oxidative stress and myocardial dysfunction in young rabbits after short term anabolic steroids administration. Food Chem Toxicol. ScienceDirect.com - Food and Chemical Toxicology - Oxidative stress and myocardial dysfunction in young rabbits after short term anabolic steroids administration

The present study focuses on the short term effects of repeated low level administration of turinabol and methanabol on cardiac function in young rabbits (4 months-old). The experimental scheme consisted of two oral administration periods, lasting one month each, interrupted by one-month wash-out period. Serial echocardiographic evaluation at the end of all three experimental periods was performed in all animals. Oxidative stress markers have also been monitored at the end of each administration period.

Treated animals originally showed significantly increased myocardial mass and systolic cardiac output, which normalized at the end of the wash out period. Re-administration led to increased cardiac output, at the cost though of a progressive myocardial mass reduction. A dose-dependent trend towards impaired longitudinal systolic, diastolic and global myocardial function was also observed. The adverse effects were more pronounced in the methanabol group. For both anabolic steroids studied, the low dose had no significant effects on oxidative stress markers monitored, while the high dose created a hostile oxidative environment.

In conclusion, anabolic administration has been found to create a possible deleterious long term effect on the growth of the immature heart and should be strongly discouraged especially in young human subjects.

 

[beezil]

thank you, Dr. Scally.

 

[eryximachus]

My opinion... After reading Doc's journals... that the last ten years of moderate AAS use... mostly Test and tren cycles. May have caused this condition.
Mind you I have always run conservative cycles 350mg test and 350mg tren... with great results. This is under the 500mg Test E studies that were noted in the Journal... but stacking with Tren could be the cause....

More evidence tren is bad news.

 

[beezil]

More evidence tren is bad news.

roger that bro.

but the gains and pumps are very well worth the moderation…

 

[eryximachus]

roger that bro.

but the gains and pumps are very well worth the moderation…

So, no regrets after all this? Outside of this heart condition, you're ok? You think it's manageable?

 

[Michael Scally MD]

Hassan AF, Kamal MM. Effect of exercise training and anabolic androgenic steroids on hemodynamics, glycogen content, angiogenesis and apoptosis of cardiac muscle in adult male rats. Int J Health Sci (Qassim) 2013;7(1):47-60. Effect of exercise training and anabolic androgenic steroids on hemodynamics, glycogen content, angiogenesis and apoptosis of cardiac muscle in adult male rats

OBJECTIVES: To investigate the effects of exercise training and anabolic androgenic steroids (AAS) on hemodynamics, glycogen content, angiogenesis, apoptosis and histology of cardiac muscle.

METHODS: Forty rats were divided into 4 groups; control, steroid, exercise-trained and exercise-trained plus steroid groups. The exercise-trained and trained plus steroid groups, after one week of water adaptation, were exercised by jumping into water for 5 weeks. The steroid and trained plus steroid groups received nandrolone decanoate, for 5 weeks. Systolic blood pressure and heart rate (HR) were monitored weekly. Heart weight/body weight ratio (HW/BW ratio) were determined. Serum testosterone, vascular endothelial growth factor (VEGF), cardiac caspase-3 activity and glycogen content were measured.

RESULTS: Compared with control, the steroid group had significantly higher blood pressure, HR, sympathetic nerve activity, testosterone level, HW/BW and cardiac caspase-3 activity. Histological examination revealed apoptotic changes and hypertrophy of cardiomyocytes. In exercise-trained group, cardiac glycogen, VEGF and testosterone levels were significantly higher while HR was significantly lower than control. HW/BW was more than control confirmed by hypertrophy of cardiomyocytes with angiogenesis on histological examination. Trained plus steroid group, had no change in HR, with higher blood pressure and HW/BW than control, cardiac glycogen and serum VEGF were higher than control but lower than exercise-trained group. Histological examination showed hypertrophy of cardiomyoctes with mild angiogenesis rather than apoptosis.

CONCLUSION: When exercise is augmented with AAS, exercise-associated cardiac benefits may not be fully gained with potential cardiac risk from AAS if used alone or combined with exercise.

 

[Michael Scally MD]

Giagulli VA, Guastamacchia E, De Pergola G, Iacoviello M, Triggiani V. Testosterone Deficiency in Male: A Risk Factor for Heart Failure. Endocr Metab Immune Disord Drug Targets. Testosterone Deficie... [Endocr Metab Immune Disord Drug Targets. 2013] - PubMed - NCBI

Testosterone deficiency syndrome (TDS) presents several sequences that generally involve different organs such as testis, bone, skeletal muscle, and heart, inducing osteoporosis, strongly reducing muscle mass, facilitating heart insufficiency and decreasing exercise capacity and strength. Approximately 25% of patients affected by chronic heart failure (CHF) are characterized by plasma Testosterone (T) levels below normal ranges also related to disease progression. In addition, reduction of testosterone concentration may contribute to some specific features of TDS syndrome such as abnormal energy handling, weakness, dyspnoea and cachexia in particular. According to some recent evidence it has emerged that testosterone replacement therapy (TRT) may be able to improve muscle strength and functional pulmonary capacity in CHF men with TDS. This review will place emphasis either on the pathophysiologic role of testosterone deficiency in CHF men or on the effects of testosterone replacement therapy.

 

[Michael Scally MD]

Severo CtB, Ribeiro JP, Umpierre D, et al. Increased atherothrombotic markers and endothelial dysfunction in steroid users. European Journal of Preventive Cardiology 2013;20(2):195-201. Increased atherothrombotic markers and endothelial dysfunction in steroid users

Background: The use of androgenic anabolic steroids (AAS) may be associated with changes in atherothrombotic markers and endothelial function. The purpose of this study was to compare atherothrombotic markers and endothelial function of AAS users and non-users.

Design: Cross-sectional study.

Methods: Ten athletes who were users of AAS (confirmed by urine analysis) and 12 non-user athletes were evaluated. Body weight, blood pressure, exercise load (hours/week), complete blood count (CBC), platelets, fibrinogen, lipids, high-sensitivity C-reactive protein (hs-CRP), follicle-stimulating hormone, testosterone and estradiol were measured. Endothelium-dependent and independent functions were assessed by brachial artery ultrasound.

Results: AAS users had higher body mass and blood pressure (p?<?0.05). Platelet count was higher whereas HDL-cholesterol was lower in AAS users compared with non-users (p?<?0.05). Levels of hs-CRP were higher in AAS users (p?<?0.001). Follicle-stimulating hormone was suppressed in all users and not suppressed in non-users (p?<?0.001). Compared with non-users, flow-mediated dilation was significantly reduced in AAS users (p?=?0.03), whereas endothelium-independent function was similar in both groups. Additionally, flow-mediated dilation was positively associated with levels of HDL- cholesterol (r?=?0.49, p?=?0.03).

Conclusions: AAS users present important changes in blood lipids as well as in inflammatory markers, which are compatible with increased cardiovascular risk. Furthermore, this profile is accompanied by a reduction in the endothelial function.

 

[Michael Scally MD]

Re: Anabolic Steroids (AAS) & Joints/Tendons

ECG interpretation in athletes
ECG interpretation in athletes

Sudden death from intrinsic cardiac conditions remains the leading cause of mortality in athletes during sport. In this context, a resting 12-lead electrocardiogram (ECG) is utilised as a diagnostic tool in the cardiovascular evaluation of both symptomatic and asymptomatic athletes for conditions associated with sudden cardiac death (SCD). We designed this series of modules based on a series of articles in the BJSM written by an international expert panel.

The modules start by identifying benign ECG changes seen in athletes, particularly those that reflect physiological electrical and structural remodelling or autonomic nervous system adaptations that occur as a consequence of regular and sustained physical activity. The modules then explore ECG changes that can indicate a variety of cardiomyopathies or primary electrical diseases.

As well as assisting any physician in the context of ECG interpretation and the cardiovascular care of athletes, these modules also provide valuable lessons in interpreting ECGs and highlight dangerous ECG patterns that may be found in any patient.

Learning outcomes

• After completing this course you should be able to:

• Recognise ECG findings in athletes that are part of normal physiological adaptation

• Recognise ECG changes associated with cardiomyopathies, including hypertrophic cardiomyopathy (HCM), arrhythmogenic right ventricular cardiomyopathy (ARVC), dilated cardiomyopathy (DCM), and left-ventricular non-compaction (LVNC)

• Calculate the corrected QT interval using an appropriate formula

• Recognise common early repolarisation patterns in athletes and distinguish these from pathological findings

• Recognise ECG changes in accessory pathways and supraventricular tachycardias

• Describe the evaluation and secondary testing of ECG abnormalities to assess for a pathological cardiac disorder.

 

[BBC3]

Re: Steroids and heart disease

@manwhore - Well, one of the best posts I have seen in this thread.

And I am referring to the first sentence before you get into some other truth. I have intentionally kept myself ignorant in the Cardio Arena as I have enough to HYPO-CHONDRIAATE over LOL. MANY People associate HEALTH and WORK HABITS. My suspicion is that Cardio Health by exercise simply does not apply in cases of GENETICALLY INVOLVED heart problems - IMIHO..

SO what about all the folks that work their BALLS OFF in the course of a day, are not too unhealthy in lifestyle, and yet drop dead of a heart attact at the age of 35, or die in their sleep not even to be autopsied.!!!

While it is proven that exercise can help to live a longer life in a healthier condition. I think it is also proven that exercise can not change genetically intended conditions and occurences, else their would be a lot less cardio docs. Hell, for that matter, I think its pretty much proven that even the healthiest of diets can not alter these courses. Further, I am not so sure that extreme exercise (of any nature) is not damaging to hearth health in the "medium run". I don't have any heart issues diagnosed or by genetic evidence/family history and I have never had so much "heart trouble" (like palpitations at night or resting, etc) as I had in my mid-thirties during the period at which I was shifting down from a fairly "athletic" condition, to a normal "walk-around guy". It was like my heart had trouble adjusting to "life out of prison" LOL.. And to be clear, this went on from 30-35 which was a time BEFORE any of my current drug regimen and consisting of minimal normal alcohol use and no other really. None of the other drugs were even a factor as they were sporatic and limited to medical instances or a couple of BRIEF periods a year. Oddly, the anomalies stopped occurring once I was completely depleted of any physical propensity for real work (38-39 yrs old). LOL

[B]@DOC, please expound (in a nutshell) for us laymen as to how the rates of the types of cardio events relates to other populations? [/B] Simply put, I am wondering if athletes are not ATTEMPTING to GRANT themselves some kind of immunity from genetically inclined heart disorder/failure, when not so entitled.? Is there something I am unaware of as a "heart ignorant reader"? Are the proportions of TYPEs of heart incidents occurring in steroid using athletes in different proportions than other athletes? Or other folks in general?

But is there something we are missing. Are all past steroid users falling over dead sooner or later or something??!???

What about all the other people who
have/had heart problems but never used gear?

The pro bodybuilding lifestyle is not healthy, period

Eating huge amounts of food, cutting carbs to zero,
building more muscle than I am sure the human body
was ever built to carry, insulin use, PGF use, HGH use..

That's all I have right now

Not saying gear is healthy, but gear was probably
a good thing compared to what else these guys did.

Mike used speed and smoked cigarettes ..

Did I just mention cigarettes? O NO!

Yeah, cigarettes seem to be taking a beating up here
with all these commercials. ...
Your toe falls off .. Must have been the
cigarettes not the diabetes ..
Heart attack? Must be the smokes, not the 5 big macs you eat every day for 20yrs ..
House went on fire?
Do you smoke? Yes .. It was the cigarettes, for sure.
Aren't you going to investigate? Nope, don't need to.
It was the smoking.

 

[Michael Scally MD]

Neves VJ, Tanno AP, Cunha TS, et al. Effects of nandrolone and resistance training on the blood pressure, cardiac electrophysiology, and expression of atrial beta-adrenergic receptors. Life Sci. ScienceDirect.com - Life Sciences - Effects of nandrolone and resistance training on the blood pressure, cardiac electrophysiology, and expression of atrial ?-adrenergic receptors

AIMS: This study was performed to assess isolated and combined effects of nandrolone and resistance training on the blood pressure, cardiac electrophysiology, and expression of the beta1- and beta2-adrenergic receptors in the heart of rats.

MAIN METHODS: Wistar rats were randomly divided into four groups and submitted to a 6 weeks treatment with nandrolone and/or resistance training. Cardiac hypertrophy was accessed by the ratio of heart weight to the final body weight. Blood pressure was determined by a computerized tail-cuff system. Electrocardiography analyses were performed. Western blotting was used to access the protein levels of the beta1- and beta2-adrenergic receptors in the right atrium and left ventricle.

KEY FINDINGS: Both resistance training and nandrolone induced cardiac hypertrophy. Nandrolone increased systolic blood pressure depending on the treatment time. Resistance training decreased systolic, diastolic and mean arterial blood pressure, as well as induced resting bradycardia. Nandrolone prolonged the QTc interval for both trained and non-trained groups when they were compared to their respective vehicle-treated one. Nandrolone increased the expression of beta1- and beta2-adrenergic receptors in the right atrium for both trained and non-trained groups when they were compared to their respective vehicle-treated one.

SIGNIFICANCE: This study indicated that nandrolone, associated or not with resistance training increases blood pressure depending on the treatment time, induces prolongation of the QTc interval, and increases the expression of beta1- and beta2-adrenergic receptors in the cardiac right atrium, but not in the left ventricle.