Thanks!
Seems as though bodybuilding and strength training on its own can lead to lvh or thickening of ventricular wall. So adding elevated testosterone/hgh and other compounds exacerbates this. I would think staying within normal physiological range would help to avoid this.
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How big a dose did you take?
Really nice to hear your anxiety has passed.
I have found in the past talking with the guys here really help me when I’m anxious. Getting my T protocol tuned up has pretty much stopped most of my anxiety that would be so strong i ended up having a panic attack. Now I just have days out of the blue where I get excited with no triggers that I can identify.
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I took 62.5 again. I have to say I’m not a guy who’s ever been anxious so it was a shock to me. I’m also not someone who generally talks about stuff but it was really nice to get the support from you guys and it did help. So thanks boys. Look forward to seeing where this dose puts me. If it’s too high I will drop back down.
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This happens from any hypertrophy. So if you weight train and put on size then your heart grows. This happens with runners as well.
Agreed, but it happens at an accelerated rate when high levels of testosterone are present. Same as with every other muscle in the body.
The normal progression of the heart growth with years of intense exercise without any enhancement whatsoever would result in a slightly larger heart muscle, but not so much that it could be detrimental. With test…different story.
Why is it different? And what level of test are you speaking of? Please cite studies.
For the same reason it’s different that your biceps wont grow past natural potential without aas. You can “max out” your potential naturally, but the line for that max gets pushed a lot further when testosterone is involved.
I am talking about cycle doses here. Supraphysiological levels of test, which is what we were talking about in the first place.
Do a search on the term Hypertrophic cardiomyopathy.
I understand and I am saying that the heart grows with normal hypertrophy and extended cardio sessions as well. I agree that the bigger you get, or more endurance trained, your heart will grow. If all you are stating is if you continue to grow then your heart will continue to grow then I have no problem with that. I thought you were generalizing with testosterone use. I will read your posted study, thanks.
As far as hypertrophic cardiomyopathy that is an inherited gene with no cure and no known causes. I think what you meant was ventricular hypertrophy.
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Problem solved! lol
Yes this is more or less what I’m getting at. It’s kind of a “grey research” area, due to the fact that ANYONE pushing supra levels of Test is also engaging in increased physical exercise. I don’t know of anybody that would run a cycle and sit on the couch. That being said, It’s “grey” because the two go hand in hand. Does the test cause the enlargement or does the increase of exercise intensity cause it? Basically was it the chicken or the egg? Does the tree make a sound if it falls and nobody is around to hear it? Same category of questioning really, but it’s safe to say that running massive doses for long periods of time will lead to accelerated enlargemnent. Of the heart and all other muscles too! lol
But whether it’s the test alone, or the combination of the AAS and exercise, I don’t think we would be able to find anyone willing to volunteer for that study.
I know that it happens to runners (endurance I believe) who are not using PEDs. Im not sure about other athletes.
Absolutely. I’m not sure however how many runners that don’t use PEDs have died from complications of heart enlargement. I don’t remember reading of any, but then again I haven’t specifically sought out information regarding that either.
I have heard of a few BBs that suffered this fate though.
From the wiki it states ventricular hypertrophy “athlete’s heart” is perfectly healthy and then goes on to say BUT it could lead to other complication.
" Eccentric hypertrophy is generally regarded as healthy, or physiologic hypertrophy and is often termed “athlete’s heart.” It is the normal response to healthy exercise or pregnancy,[6] which results in an increase in the heart’s muscle mass and pumping ability. It is a response to ‘volume-overload’, either as a result of increased blood return to the heart during exercise, or a response to an actual increase in absolute blood volume as in pregnancy. This increase in pumping ability is the result of the addition of sarcomeres in series, which enables the heart to contract with greater force.[7] This is explained by the Frank Starling mechanism, which describes the sarcomere’s ability to contract with greater force as more of the elements of its contractile units become engaged. This response can be dramatic; in trained athletes have hearts that have left ventricular mass up to 60% greater than untrained subjects. Rowers, cyclists, and cross-country skiers tend to have the largest hearts, with an average left ventricular wall thickness of 1.3 centimeters, compared to 1.1 centimeters in average adults. Though eccentric hypertrophy is termed ‘athlete’s heart’ it is typically only found in individuals who are aerobically conditioned. For example, weight lifters tend to undergo remodeling which more closely resembles concentric hypertrophy, as the heart does not experience a volume-overload, but instead responds to transient pressure overload as a consequence of increased vascular resistance from pressures exerted on arteries by sustained muscular contraction.
Though it is the case that eccentric hypertrophy is largely considered to be a healthy response to increased cardiac demand, it is also associated with risks. For example, in athlete’s with significantly increased left ventricular weight there is also a corresponding increased risk for conduction abnormalities and sudden cardiac death. Additionally, in pregnant individuals, a subpopulation progress to peripartum cardiomyopathy, characterized by a dilation of the left ventricle and a corresponding deficit in heart function. There are suggestions that this progression is partially determined by underlying metabolic derangement (diabetes) and hypertension which may result in a more maladaptive cardiac response to pregnancy. As such, though it is convenient to consider clear cut distinctions between pathologic and physiologic cardiac hypertrophy, there may be a broader range of phenotypes than may be accounted for by gross cardiac phenotypes alone.
The development of pathologic states in LVH is complex. Electrical abnormalities are commonly found in individuals with LVH, both ventricular and super-ventricular tachycardia. Additionally, cytoarchitecture and the extracellular environment of the myocardium are altered, specifically genes typically expressed in the fetal heart are induced, as are collagen and other fibrotic proteins. LVH may interfere with heart functionality in a number of ways. Before progression to a dilated phenotype, mechanical obstruction of the outflow tract can occur, leading to reduced cardiac output. Additionally, increased fibrosis of the ventricle can result in a failure to relax appropriately which impairs cardiac filling and may lead to diastolic dysfunction or heart failure with preserved ejection fraction."
I think we are on the same page here…I agree that normal (If this term could be applied to this discussion lol) levels of enlargement are perfectly safe. My argument is that running cycle levels of test will exaggerate that enlargement. The only real question here is whether it is beacuse of the test or the increase in intensity of exercise. I guess the same question could really be applied to the ability to grow every other muscle beyond natural limits on steroid cycles. Is it the test helping it grow, or is the test simply giving the person the ability to push harder than they naturally would, and the growth is a result of that? I’m not sure, but I think it goes without saying that the “above normal potential” growth happens on cycle, and it doesn’t without it right?
To add to that thought, I believe that normal TRT that brings a person’s Test levels to normal / high-normal range will not exaggerate heart growth, no more than it will give someone the ability to push other muscle development past natural limits.
Yes, we are bound by our genetic potential in the absence of PEDs. That being said if you have the potential to put on slabs of muscle in a year then you are going to experience growth of all systems in accordance to support your body.
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Agreed. And in that particular case I think the support systems would be warranted and would probably not cause any major complications.
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Interesting. In order to determine if its HCM or LVH they put them on a treadmill to see if they are an athlete. Ha. And only about 10% of American Football players tested positive for LVH which would argue the case that hypertrophy can cause it since football players are generally well conditioned and muscular. Also to argue what one would consider the average % of American Football players using PEDs.