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Anabolic steroids and cardiac muscle

Maldorf, a couple of questions for you..

You talk about how AAS users have a lower-than-normal ejection fraction which is a measure of how much oxygenated blood delivers to the arteries with each contraction. So my first question.. every time I go to have my blood checked or have a doc appointment in general, they put this little doohicky on your index finger which is supposed to measure the oxygen in your blood. If you are indeed suffering from a low ejection fraction, would this show on or affect the reading this little machine gives? Would they see anything there that could indicate a problem or is it not enough? My readings are always 96-97 which they see as completely normal. If a problem came up would that reading start to change?

Another member that I remember died early from a heart attack here was called Queefer, really BIG guy, made Mark Dugdale look tiny in a photo I saw. Do we know much about his heart issues? I've had a hard time finding anything on him except some posts that refer to him, but I know he was a regular member here. I seem to remember from the original post that his wife Miss Q found him slumped over his computer.

Heart disease runs in my dad's side of the family, but I recently discovered it may be due to the fact that they carried a bad hemochromatosis gene. The gene is called HFE, and there are two mutations docs regularly test for, C282Y and H63D. We have the H63D mutation on his side. Even carriers can exhibit some symptoms though most don't see anything, but it often results in an early death from a heart-related event, often as early as late 50s to mid 60s. My own problem is that we also found out recently via genetic tests that my mom has the gene for the juvenile form of hemochromatosis, HJV, one they don't regularly test for. One of my sisters and I inherited both genes from our parents. For anyone who doesn't know what hemochromatosis is, it is a disorder that causes the body to accumulate iron in the body and organs. Once you get enough iron in an organ, it can start to act haywire or start to shut down in some fashion. For some it can be extremely severe, and for others not too bad. I'm lucky for it to be not too bad. However, for me it resulted in hypogonadism first at 30 years old so I've been on TRT since then, just over 20 years. I also have various problems with my thyroid, pancreas, adrenals, digestive tract, liver, gallbladder (which was removed), and pituitary (I have low growth hormone, but no doc where I live will prescribe to me because of how I look). So how do you balance having to be on TRT at a certain level to feel normal/good and factors that can cause heart disease?

There are just so many factors, and AAS can definitely exacerbate them. I keep seeing more articles about guys running into heart problems while on AAS, and it's really giving me some thought. I've been on some cycles though I'd be sure that they're pretty mild compared to what some guys here do. As in the thread that talks about your identity being connected to your physique, I feel that I my physique does contribute a lot to "who I am" as a person. I'd absolutely hate to lose what physique I have but feel torn because at my age, 50, I don't want to die early, but I'd also like to keep looking pretty good for my age. I suppose I'm rambling on now, but I'm sure there's a lot of peeps out there who know what I'm talking about.
 
Maldorf, a couple of questions for you..

You talk about how AAS users have a lower-than-normal ejection fraction which is a measure of how much oxygenated blood delivers to the arteries with each contraction. So my first question.. every time I go to have my blood checked or have a doc appointment in general, they put this little doohicky on your index finger which is supposed to measure the oxygen in your blood. If you are indeed suffering from a low ejection fraction, would this show on or affect the reading this little machine gives? Would they see anything there that could indicate a problem or is it not enough? My readings are always 96-97 which they see as completely normal. If a problem came up would that reading start to change?

Ejection fraction is the percentage of blood ejected from the left ventricle during systole.

People with hypertrophic cardiomyopathy (excessively thickened left ventricles) commonly have a high ejection fraction.

You are referring to a pulse oximeter, which measures oxygen saturation. It is possible to have a low ejection fraction and normal oxygen saturation.
 
Maldorf, a couple of questions for you..

You talk about how AAS users have a lower-than-normal ejection fraction which is a measure of how much oxygenated blood delivers to the arteries with each contraction. So my first question.. every time I go to have my blood checked or have a doc appointment in general, they put this little doohicky on your index finger which is supposed to measure the oxygen in your blood. If you are indeed suffering from a low ejection fraction, would this show on or affect the reading this little machine gives? Would they see anything there that could indicate a problem or is it not enough? My readings are always 96-97 which they see as completely normal. If a problem came up would that reading start to change?

Another member that I remember died early from a heart attack here was called Queefer, really BIG guy, made Mark Dugdale look tiny in a photo I saw. Do we know much about his heart issues? I've had a hard time finding anything on him except some posts that refer to him, but I know he was a regular member here. I seem to remember from the original post that his wife Miss Q found him slumped over his computer.

Heart disease runs in my dad's side of the family, but I recently discovered it may be due to the fact that they carried a bad hemochromatosis gene. The gene is called HFE, and there are two mutations docs regularly test for, C282Y and H63D. We have the H63D mutation on his side. Even carriers can exhibit some symptoms though most don't see anything, but it often results in an early death from a heart-related event, often as early as late 50s to mid 60s. My own problem is that we also found out recently via genetic tests that my mom has the gene for the juvenile form of hemochromatosis, HJV, one they don't regularly test for. One of my sisters and I inherited both genes from our parents. For anyone who doesn't know what hemochromatosis is, it is a disorder that causes the body to accumulate iron in the body and organs. Once you get enough iron in an organ, it can start to act haywire or start to shut down in some fashion. For some it can be extremely severe, and for others not too bad. I'm lucky for it to be not too bad. However, for me it resulted in hypogonadism first at 30 years old so I've been on TRT since then, just over 20 years. I also have various problems with my thyroid, pancreas, adrenals, digestive tract, liver, gallbladder (which was removed), and pituitary (I have low growth hormone, but no doc where I live will prescribe to me because of how I look). So how do you balance having to be on TRT at a certain level to feel normal/good and factors that can cause heart disease?

There are just so many factors, and AAS can definitely exacerbate them. I keep seeing more articles about guys running into heart problems while on AAS, and it's really giving me some thought. I've been on some cycles though I'd be sure that they're pretty mild compared to what some guys here do. As in the thread that talks about your identity being connected to your physique, I feel that I my physique does contribute a lot to "who I am" as a person. I'd absolutely hate to lose what physique I have but feel torn because at my age, 50, I don't want to die early, but I'd also like to keep looking pretty good for my age. I suppose I'm rambling on now, but I'm sure there's a lot of peeps out there who know what I'm talking about.

That finger measurement is for the 02 concentration in your blood I believe, saturation.

It should be normal unless there is something really wrong. Even with my heart failure now, 20 to 25% EF, it is normal. Im not quite sure how that occurs, maybe someone else can chime in. I think the only way that the 02 will be low is if you have bad lung disease. Not sure.

One thing a heart will do if it has a low ejection fraction is increase the heart rate to compensate. I don't run into any problems with that unless I try to push myself too hard physically or if I get really stressed out/pissed off. I also take a betablocker to keep heart rate down. So even with my heart being in really bad shape my 02 readings are normal.

So you cant rely on that measurement to tell you that your heart is healthy.


Just thought of this, I think if you are anemic that your 02 level might be a bit low.
 
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It should be normal unless there is something really wrong. Even with my heart failure now, 20 to 25% EF, it is normal. Im not quite sure how that occurs, maybe someone else can chime in. I think the only way that the 02 will be low is if you have bad lung disease. Not sure.

One thing a heart will do if it has a low ejection fraction is increase the heart rate to compensate. I don't run into any problems with that unless I try to push myself too hard physically or if I get really stressed out/pissed off. I also take a betablocker to keep heart rate down. So even with my heart being in really bad shape my 02 readings are normal.

The pulse oximeter measures the oxygen saturation of blood, not the amount of circulating blood.

So you can have normal blood oxygenation, even if the blood is circulating poorly.

You can also have normal blood pressure, heart rate and no functional limitations with a 20% ejection fraction. When Chris Leben was fighting with an 18% ejection fraction, he had more stamina than most.

Chris Leben stated:

"Unfortunately, my left ventricle is oversized, misshapen and not pumping correctly. It's pumping at 18 percent, which I'm told is not a good thing.

Interviewer: Have you been feeling symptoms of this before the exam?

You know, that's the crazy thing. I've never felt better."


https://www.mmafighting.com/2016/3/...ails-of-physical-condition-basically-my-heart

Another reason why merely relying on ejection fraction, and ignoring cardiac blood markers like BNP is idiotic.
 
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One of the most dangerous things you can do to your heart is to give it forces that it cannot comply with or recover from. Kind of like getting pinned in a heavy squat. PED's could therefore be cardioprotective in situations of extreme cardiac stress (eg the Tour de France).
 
The pulse oximeter measures the oxygen saturation of blood, not the amount of circulating blood.

So you can have normal blood oxygenation, even if the blood is circulating poorly.

You can also have normal blood pressure, heart rate and no functional limitations with a 20% ejection fraction. When Chris Leben was fighting with an 18% ejection fraction, he had more stamina than most.

Chris Leben stated:

"Unfortunately, my left ventricle is oversized, misshapen and not pumping correctly. It's pumping at 18 percent, which I'm told is not a good thing.

Interviewer: Have you been feeling symptoms of this before the exam?

You know, that's the crazy thing. I've never felt better."


https://www.mmafighting.com/2016/3/...ails-of-physical-condition-basically-my-heart

Another reason why merely relying on ejection fraction, and ignoring cardiac blood markers like BNP is idiotic.

Well, an abnormally low EF isn't something to just shrug off. Just because that guy felt fine doesn't mean shit. I hope he got examined by a good cardiologist and got some help. Much of the time I feel fine too, up until my heart decides to beat 400x a minute.
 
Well, an abnormally low EF isn't something to just shrug off. Just because that guy felt fine doesn't mean shit. I hope he got examined by a good cardiologist and got some help. Much of the time I feel fine too, up until my heart decides to beat 400x a minute.

Only a fool would shrug off any legitimate risk factor, or try to lay blame on a potential risk factor without unequivocal scientific proof. I understand Leben did actually largely restore his ejection fraction thereafter.
 
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Decent thread to look over. Multiple studies here to read over. Some great posts by Stewie, methodair, and pissbrain.
 
Ejection fraction is the percentage of blood ejected from the left ventricle during systole.

People with hypertrophic cardiomyopathy (excessively thickened left ventricles) commonly have a high ejection fraction.

You are referring to a pulse oximeter, which measures oxygen saturation. It is possible to have a low ejection fraction and normal oxygen saturation.

Not to step on any toes here but for the sake of accuracy and for everyone's knowledge, the LVEF = LVEDV - LVESV. The LVEF = left ventricular ejection fraction, LVEDV = left ventricular end diastolic volume, and the LVESV = left ventricular end systolic volume. Now what does this all mean? Read below...

LVEDV = amount of blood in the LV (left ventricle) at the end of diastole i.e. when the LV is "relaxing" and filling with blood.

LVESV = amount of blood in the LV at the end of systole i.e. when the LV has fully contracted (or pumping blood to the systemic circulation).

Ergo, the LVEF is the % of blood ejected from the LV after it has filled with blood during diastole. This ratio (or LVEF) can easily be calculated using basic math.

Take the following example:

If your LV fills up with 120 ml of blood during the time of diastole (aka the LVEDV) and your LV pumps out X ml of blood to the systemic circulation with only 40 ml of blood remaining in the LV (aka the LVESV), then the LVEF can easily be calculated as follows:

LVEF = amt of blood ejected from LV / amt of blood in LV to begin with
LVEF = 80 ml / 120 ml = 66%

It's the simple.

Enjoy.

Note: You can utilize SV (stroke volume) in lieu of the amt of blood the LV pumps out during systole but the answer comes up the same. Tomato v potato.
 
Not to step on any toes here but for the sake of accuracy and for everyone's knowledge, the LVEF = LVEDV - LVESV. The LVEF = left ventricular ejection fraction, LVEDV = left ventricular end diastolic volume, and the LVESV = left ventricular end systolic volume. Now what does this all mean? Read below...

LVEDV = amount of blood in the LV (left ventricle) at the end of diastole i.e. when the LV is "relaxing" and filling with blood.

LVESV = amount of blood in the LV at the end of systole i.e. when the LV has fully contracted (or pumping blood to the systemic circulation).

Ergo, the LVEF is the % of blood ejected from the LV after it has filled with blood during diastole. This ratio (or LVEF) can easily be calculated using basic math.

Take the following example:

If your LV fills up with 120 ml of blood during the time of diastole (aka the LVEDV) and your LV pumps out X ml of blood to the systemic circulation with only 40 ml of blood remaining in the LV (aka the LVESV), then the LVEF can easily be calculated as follows:

LVEF = amt of blood ejected from LV / amt of blood in LV to begin with
LVEF = 80 ml / 120 ml = 66%

It's the simple.

Enjoy.

Note: You can utilize SV (stroke volume) in lieu of the amt of blood the LV pumps out during systole but the answer comes up the same. Tomato v potato.
Dang,interesting pissbrain .
 
Ejection fraction is the percentage of blood ejected from the left ventricle during systole.

People with hypertrophic cardiomyopathy (excessively thickened left ventricles) commonly have a high ejection fraction.

You are referring to a pulse oximeter, which measures oxygen saturation. It is possible to have a low ejection fraction and normal oxygen saturation.

Oh yeah, I nearly forgot to mention how HCM (hypertrophic cardiomyopathy) relates to all the crap mentioned in my previous post. In HCM, you have enlarged of the heart (duh) - typically the most commonly the LV b/c normal anatomy and physiology, it is primary workhorse of the heart since it has to pump blood to the high pressure systemic circulation as opposed to the RV which in contrast pumps heart to the low pressure pulmonary circulation. In HCM (and we are excluding hypertrophic obstructive cardiomyopathy aka hypertrophic subaortic stenosis), the cardiac muscle around the LV slowly undergoes concentric enlargement. This enlargement of the LV means the LV chamber becomes smaller. Therefore, less is able to fill up within the LV chamber during diastole.Then during systole, the LV contracts and ejects approximately the same amount of blood to the systemic circulation. So you may be thinking: "The system gets what it needs. So what?" Well, this may be true but overtime the LV will hypertrophy to the point where it becomes restrictive and will no longer demonstrate compliance (i.e. the ability stretch and temporarily blood during LVEDV which in turn affects the physiologic Frank-Starling mechanism for adequate LVEF). This is particular form of cardiac pathophysiology is called Diastolic Dysfunction and last I checked, there are two types: Type 1 and Type 2 Diastolic Dysfxn. It is pretty easy to catch on 2-D Cardiac Echo.

Hope you all learned something.
 
Not to step on any toes here but for the sake of accuracy and for everyone's knowledge, the LVEF = LVEDV - LVESV. LVEDV = left ventricular end diastolic volume, and the LVESV = left ventricular end systolic volume.

It's the simple.

LVEF = LVEDV - LVESV...no this incorrect, stroke volume = LVEDV - LVESV. This calculation does not generate an ejection fraction. Stroke volume is a key metric because unlike ejection fraction, it gives a literal number of how much blood is circulating.

For example, a Tour de France cyclist typically has a low ejection but a massive stroke volume. On the other hand, a patient with severe hypertrophic cardiomyopathy typically has a high ejection fraction, and a low stroke volume.
 
LVEF = LVEDV - LVESV...no this incorrect, stroke volume = LVEDV - LVESV. This calculation does not generate an ejection fraction. Stroke volume is a key metric because unlike ejection fraction, it gives a literal number of how much blood is circulating.

For example, a Tour de France cyclist typically has a low ejection but a massive stroke volume. On the other hand, a patient with severe hypertrophic cardiomyopathy typically has a high ejection fraction, and a low stroke volume.

*** For example, a Tour de France cyclist typically has a low ejection

By way of clarification, a 50% ejection fraction is not uncommon for elite cyclists, given their large LV chamber volume and stroke volumes.
 
Not to step on any toes here but for the sake of accuracy and for everyone's knowledge, the LVEF = LVEDV - LVESV. The LVEF = left ventricular ejection fraction, LVEDV = left ventricular end diastolic volume, and the LVESV = left ventricular end systolic volume. Now what does this all mean? Read below...

LVEDV = amount of blood in the LV (left ventricle) at the end of diastole i.e. when the LV is "relaxing" and filling with blood.

LVESV = amount of blood in the LV at the end of systole i.e. when the LV has fully contracted (or pumping blood to the systemic circulation).

Ergo, the LVEF is the % of blood ejected from the LV after it has filled with blood during diastole. This ratio (or LVEF) can easily be calculated using basic math.

Take the following example:

If your LV fills up with 120 ml of blood during the time of diastole (aka the LVEDV) and your LV pumps out X ml of blood to the systemic circulation with only 40 ml of blood remaining in the LV (aka the LVESV), then the LVEF can easily be calculated as follows:

LVEF = amt of blood ejected from LV / amt of blood in LV to begin with
LVEF = 80 ml / 120 ml = 66%

It's the simple.

Enjoy.

Note: You can utilize SV (stroke volume) in lieu of the amt of blood the LV pumps out during systole but the answer comes up the same. Tomato v potato.

An easier way to conceptualize it: 50% of a large volume (50% of 1000) vs 65% of a small volume (65% of 100). A physician would therefore be misguided to base heart function solely on ejection fraction, given that the patient in the second example could be in heart failure, with a low stroke volume.
 
LVEF = LVEDV - LVESV...no this incorrect, stroke volume = LVEDV - LVESV. This calculation does not generate an ejection fraction. Stroke volume is a key metric because unlike ejection fraction, it gives a literal number of how much blood is circulating.

For example, a Tour de France cyclist typically has a low ejection but a massive stroke volume. On the other hand, a patient with severe hypertrophic cardiomyopathy typically has a high ejection fraction, and a low stroke volume.

Now that I think about it, you are correct. The LVEF = Stroke volume / LVEDV

SV = LVEDV - LVESV

SV = SV / LVEDV

My mistake for any confusion I may have caused and nice catch MethodAir.
 
Well, an abnormally low EF isn't something to just shrug off. Just because that guy felt fine doesn't mean shit. I hope he got examined by a good cardiologist and got some help. Much of the time I feel fine too, up until my heart decides to beat 400x a minute.

If your HR is 400 bpm, that number is incompatible with life according to the medical textbooks.
 
Now that I think about it, you are correct. The LVEF = Stroke volume / LVEDV

SV = LVEDV - LVESV

SV = SV / LVEDV

My mistake for any confusion I may have caused and nice catch MethodAir.

Damnit! Why do I keep typing in the wrong thing?!?

SV = LVEDV - LVESV

LVEF = SV / LVEDV

Again, sorry for the confusion x 2. Kill me now.
 
If your HR is 400 bpm, that number is incompatible with life according to the medical textbooks.
LOL, yeah it is! Mine has gotten up that high before, when it was in fibrillation I guess. My defibrillator records my HR when it gets high and keep a record of it. I can send that info to the Dr. over the internet or go in for a reading. Mine has been up to about 450 bpm before, and that's when my defibrillator fires off and saves my life.
 
Now that I think about it, you are correct. The LVEF = Stroke volume / LVEDV

SV = LVEDV - LVESV

My mistake for any confusion I may have caused and nice catch MethodAir.

Right, and the ejection fraction is expressed as a percentage of the amount of blood ejected during systole, so its (Stroke volume / LVEDV)*100.
 
So what’s the worst AAS/PEDS that should be avoided in this case?

also any clue on the mechanism? It says weight lifting wasn’t the cause so possibly increased blood viscosity? Untreated hypertension? Water retention? or just the anabolic affects causing the heart to grow?

I didn’t read the studies
I was curious, did body weight of AAS users play a part in this? Maybe just their overall body size caused the heart to have to work harder?
 

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