What's be your typical idea of cycling? What do you use when cycling?
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Maintaining heart health while on AAS
- Thread starter MyNameIsJeff
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What's be your typical idea of cycling? What do you use when cycling?
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Have you researched Exforge much?
That's what they have my dad on who has HBP, Diabetes, and has had some elevated kidney values in the past.
He's cleaned his act up, keeps his BS in range, and kidneys are now back in range...but I would hate to know that he could be taking something "safer" for his HBP than what they currently have him on at the moment.
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About a 700-1200 mg/w total AAS and 2-4 iu GH a day or a combination of peptides and GH. AAS ar the usual suspects:
Test on the low end 150-300 mg/w
Primo: 300-500 mg
Masteron: 300-600 mg
Equipoise: 500-700 mg
NPP: 300-500 mg
Anavar:40-60 mg/d
Turanabol: 40-60 mg/d
Tren Ace: I use it like an oral for like an afterburners inside a cycle with test an a primary anabolic. 30-50 mg/d slin pin in the delt.
Sometimes I just do TRT 100-150 mg/w for months and months with GHRP2 in and out and get really athletic, sprints, grappling, boxing drills, biking in the mountains. Then I'mm do a cycle. A good one that works really well for me is as follows:
1-8 Test C 300 mg; NPP 300 mg; EQ 500 mg; GHRP2 200 mcg 3x/d
9-11 Test C 150 mg/w; IGF- LR3 50 mcg/d
12-20 Test E 300 mg; Masteron 300 mg: Winstrol 350 mg/w;GHRP2 200 mcg 3x/d.
Started at 195. Went up to 230 in stage 1. Leaned out to 218 in stage 2. After that I cruised on 200 test and 2x 76 mg/w Parabolan for 6 weeks. After that I went back to TRT for 5 months.
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Just for info, I used to take carvedilol but my cardiologist just had me switch over to bisoprolol. Bisoprolol is more cardioselective and doesn't affect the vascular system as much. Carvedilol is better for lowering BP though because of that but it doesn't bring down the heart rate as much. Tachycardia is my main problem so he figured the Bisoprolol will work better for that. Hopefully he is right. The change came about because my defibrillator fired off 3 times in the space of 2 days back in March and then again in June. So far so good.
If you go on the drug they will have you titrate up on it, meaning the starting dose will be low and then will go up every two weeks. If you start out too high you will feel like absolute shit. No joke. With both meds it was that way for me. So follow orders and give the starting dose 2 weeks before you step it up. Bisoprolol is really strong and I started out with just 5mg/day. Now I am taking 10 one day and 5 the next. After 2 weeks of that it is up to 10mg/day. Eventually may take up to 20mg/day, which is the largest tablet. As comparison Coreg(carvedilol) I was taking a 80 mg cap each day. If you are feeling like shit on it, give it some time because the sides will get better. Another thing you can do is lower the dose and work up on it. The sides got much better for me on both drugs and eventually I have none. I am having none right now.
So if you are trying to keep down heart rate Bisoprolol is the way to go. It acts more on the Beta 1 cells which are found mostly in the heart.
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Cardiac hypertrophy
The heart is capable of growing and shrinking in size in response to the amount of stress it is faced with. Doctors distinguished between 2 types of cardiac hypertrophy: 1) Physiological growth in response to normal stressors such as exercise, pregnancy, and increased muscle mass. 2) Pathological growth due to stressors such as neurohumoral* activation, hypertension, and myocardial injury
* Neurohumoral activation refers to increased activity of the sympathetic nervous system, renin-angiotensin system, vasopressin and atrial natriuretic peptide.
1) Physiological growth
As shown in the right panel of the figure below, a physiological adaptation to exercise (and pregnancy) consists of proportional growth in the different constituents of the heart. Specifically, the growth of the ventricle (the chamber containing blood before being pumped out) is similar to the growth in the left-ventricular wall (the muscle that pumps the blood out of the chamber).
Some more info on athlete's heart: Note that the condition mostly is present in people who do a lot of aerobic exercise (endurance sports), and only to a lesser degree in (natural) weightlifters and bodybuilders.
2) Pathological growth
MMS: Error
Let's say the pathological growth is caused by someone being overweight, bloated and hypertensive. In order to deal with the higher blood pressure and blood volume, the heart's muscle, i.e. the ventricular wall, thickens, whereas the ventricle itself (the chamber) does not change in size or even shrinks. this condition is referred to as concentric hypertrophy, and depicted in the middle panel of the figure above. Initially, this growth response is compensatory in nature, i.e. it serves to maintain the heart's function in the face of a new stressor.
As mentioned above, individual's who do resistance exercise (i.e. bodybuilders) have a somewhat different pattern of cardiac hypertrophy than endurance athletes. In fact, the adaptations in bodybuilder's hearts is more similar to the concentric hypertrophy (which is usually considered pathological):
So even though (natural) bodybuilders develop concentric hypertrophy, where only the wall increases in size while the ventricle stays the same, this has no negative effect on heart function. So what I would conclude from that is that concentric heart hypertrophy need not be considered pathological in and of itself.
The thing is, though, that 99% of patients who have concentric hypertrophy are not weightlifters, but are rather people with systemic blood pressure and/or past cardiac events. of course the medical profession is gonna focus on these people in their research and definitions. In any case, a non-athlete with concentric hypertrophy is a completely different case. First, the thickening of the ventricular wall can be much more severe in these patients, and given their typically unhealthy lifestyle and nutrition, the body cannot keep up with the required growth of the myocardium. One aspect of that is insufficient blood flow:
Such insufficient blood flow can lead to small areas of muscle to die (apoptosis), and/or lead to fibrotic changes in the structure of the muscle, impairing its function. Furthermore, we have learned before that chronic inflammation as well as activity of angiotensin II promote fibrotic changes in the myocardium, and your typical hypertension patient will have high levels of both (and compared to an in-shape weighlifter).
When such detrimental changes happen to someone with concentric hypertrophy, the ventricular wall's pumping capacity deteriorates over time, leading to wall thinning. To compensate for the lower pumping power of the heart, the ventricle increases in size, which at first is once a gain beneficial in maintaining cardiac function. This situation can be described at eccentric hypertrophy (See left panel of figure). Eventually, volume becomes too large, and you end up with dilated cardiomyopathy.
Disclaimer: This is broscience, as a layperson there's a lot of details that I don't understand, and I'm not familiar with the current definitions used for the different kinds of cardiac hypertrophy (Different papers use different definitions and classifications). That being said, I'm fairly confident that the overall story is correct, but would love to be corrected by gotgame, Stewie and others who know much more about this topic.
In any case, this post is to just serve as an overview that I can use to illustrate how AAS impact cardiac hypertrophy and to argue how certain interventions could help mitigate their detrimental effects.
The heart is capable of growing and shrinking in size in response to the amount of stress it is faced with. Doctors distinguished between 2 types of cardiac hypertrophy: 1) Physiological growth in response to normal stressors such as exercise, pregnancy, and increased muscle mass. 2) Pathological growth due to stressors such as neurohumoral* activation, hypertension, and myocardial injury
* Neurohumoral activation refers to increased activity of the sympathetic nervous system, renin-angiotensin system, vasopressin and atrial natriuretic peptide.
1) Physiological growth
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3427979/
As shown in the right panel of the figure below, a physiological adaptation to exercise (and pregnancy) consists of proportional growth in the different constituents of the heart. Specifically, the growth of the ventricle (the chamber containing blood before being pumped out) is similar to the growth in the left-ventricular wall (the muscle that pumps the blood out of the chamber).
Some more info on athlete's heart: Note that the condition mostly is present in people who do a lot of aerobic exercise (endurance sports), and only to a lesser degree in (natural) weightlifters and bodybuilders.
https://en.wikipedia.org/wiki/Athletic_heart_syndrome
2) Pathological growth
MMS: Error
Let's say the pathological growth is caused by someone being overweight, bloated and hypertensive. In order to deal with the higher blood pressure and blood volume, the heart's muscle, i.e. the ventricular wall, thickens, whereas the ventricle itself (the chamber) does not change in size or even shrinks. this condition is referred to as concentric hypertrophy, and depicted in the middle panel of the figure above. Initially, this growth response is compensatory in nature, i.e. it serves to maintain the heart's function in the face of a new stressor.
As mentioned above, individual's who do resistance exercise (i.e. bodybuilders) have a somewhat different pattern of cardiac hypertrophy than endurance athletes. In fact, the adaptations in bodybuilder's hearts is more similar to the concentric hypertrophy (which is usually considered pathological):
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1905938/
So even though (natural) bodybuilders develop concentric hypertrophy, where only the wall increases in size while the ventricle stays the same, this has no negative effect on heart function. So what I would conclude from that is that concentric heart hypertrophy need not be considered pathological in and of itself.
The thing is, though, that 99% of patients who have concentric hypertrophy are not weightlifters, but are rather people with systemic blood pressure and/or past cardiac events. of course the medical profession is gonna focus on these people in their research and definitions. In any case, a non-athlete with concentric hypertrophy is a completely different case. First, the thickening of the ventricular wall can be much more severe in these patients, and given their typically unhealthy lifestyle and nutrition, the body cannot keep up with the required growth of the myocardium. One aspect of that is insufficient blood flow:
https://en.wikipedia.org/wiki/Ventricular_hypertrophy
Such insufficient blood flow can lead to small areas of muscle to die (apoptosis), and/or lead to fibrotic changes in the structure of the muscle, impairing its function. Furthermore, we have learned before that chronic inflammation as well as activity of angiotensin II promote fibrotic changes in the myocardium, and your typical hypertension patient will have high levels of both (and compared to an in-shape weighlifter).
MMS: Error
When such detrimental changes happen to someone with concentric hypertrophy, the ventricular wall's pumping capacity deteriorates over time, leading to wall thinning. To compensate for the lower pumping power of the heart, the ventricle increases in size, which at first is once a gain beneficial in maintaining cardiac function. This situation can be described at eccentric hypertrophy (See left panel of figure). Eventually, volume becomes too large, and you end up with dilated cardiomyopathy.
Disclaimer: This is broscience, as a layperson there's a lot of details that I don't understand, and I'm not familiar with the current definitions used for the different kinds of cardiac hypertrophy (Different papers use different definitions and classifications). That being said, I'm fairly confident that the overall story is correct, but would love to be corrected by gotgame, Stewie and others who know much more about this topic.
In any case, this post is to just serve as an overview that I can use to illustrate how AAS impact cardiac hypertrophy and to argue how certain interventions could help mitigate their detrimental effects.
Last edited:
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So Exforge is a combination drug (valsartan/amlodipine)--basically an ARB plus a calcium channel blocker. Good combo, standard protocol (ACEI or ARB, then add CCB, then add b-blocker if needed).
Here is an EXTREMELY thorough analysis of all ARBs and clinical evidence to help with choosing one (has many different scenarios). Just throwing it out there so you can see why they might have chosen valsartan over telmi or other therapies, and why you might want to switch to one of the others (you know his history and can sort through all this to figure out if he's on the "best" therapy).
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4947116/
This is a great read for anyone trying to figure out reasons to select one b-blocker over another, and what to expect as far as therapy goes (or what you should do if self-medicating). Thanks for the input bro!
Last edited:
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AAS and cardiac hypertrophy
There are 3 possible reasons for the observation that concentric hypertrophy is physiological in weightlifters but develops into decompensated (pathological) hypertrophy in most hypertensive patients.
1) The difference between the chronic stressor of hypertension and the intermittent stressor of exercise induced blood pressure spikes may be sufficient to explain why the former leads to degenerative changes in the ventricular wall, whereas the latter allows the myocardium to remain functional.
As an analogy, think of doing curls 24/7 without any weight in your hand. It may well be that the muscle damage induced by this is sufficiently low for your body to repair. But if you gradually increase the weights of a dumbell in that hand, then at some point, you are creating too much muscle damage for the body to repair properly. The micro tearing due to constant stretching and contraction will lead to excessive local inflammation and subsequent fibrosis. Even worse, the chronic inflammation may lead muscle cells to die in troves rather than be repaired. A similar situation may occur in the myocardium in response to the chronically elevated pressure due to hypertension.
2) It may be that the hypertrophy induced by hypertension is not different compared to that from resistance exercise, but the more chronic stimulus leads to more rapid and extensive growth. If the microvasculature were able to keep up with this higher growth, then the growth of the ventricular wall might be perfectly physiological. But as studies have shown, blood flow does typically not keep up with the growth of the myocardium in hypertensive patients, thereby leading to insufficient nutrient and oxygen delivery and subsequent cell death and scarring (fibrosis).
3) It may be that the body would be perfectly able to deal with the growth induced by hypertension in the sense of having sufficient nutrient delivery to the muscle cells and a high enough ability to repair the micro damage induced by constant exertion against high pressure. The problem in the typical hypertensive patient would instead be the high levels of pro-fibrotic agents such as angiotensin II, as well as overactive systemic inflammation that attacks the damaged muscle cells in the heart.
4) It may be a mix of the potential factors. That is, chronic pressure from hypertension is uniquely damaging even in the otherwise healthy individuals, neovascularization is generally insufficient if the growth of the myocardium is too fast and extensive, and pro-fibrotic and pro-inflammatory factors contribute towards pathological changes in the ventricular walls.
So how do AAS factor into this? AAS have 3 kinds of effects, they A) indirectly create/exacerbate stressors, B) indirectly promote fibrotic changes in the heart muscle, and C) directly promote growth of cardiac myocytes.
A)
i) AAS increase hypertension through various channels (see first post), leading to concentric hypertrophy
ii) The increased lean body mass from AAS use increases blood volume, leading to mostly eccentric hypertrophy
iii) increased training volume and frequency mean more frequent blood pressure spikes and thus contribute to concentric hypertrophy
B)
Via its upregulation of Angiotensin II, AAS increase the likelihood of fibrotic changes to the myocardium, especially in the presence of hypertrophy.
C)
AAS have a direct impact on myocyes and promote their growth. Thus, for a given stressor, AAS could increase the myocyte growth rate compared to a natural individual.
The indirect effect of AAS on hypertension can be controlled (See the first post), but the impact on blood volume and training intensity are not something that can or should be avoided in bodybuilders. So compared to a natural athlete, AAS users will face additional stressors that cause cardiac hypertrophy (which does not have to be pathological though).
Similarly, the effects of AAS on Angiotensin II and thereby fibrosis are something than can me ameliorated.
The direct growth stimulation of cardiomyocytes via the androgen receptor is, however, not something that we can do much about. It is reasonable to assume that for a given level of stressors, the anabolic action of AAS on myocytes will produce a greater growth response compared to natural athletes. So on average, the left (and to some extent right) ventricular wall of an AAS user will be larger than that of a natural athlete, even if blood pressure is controlled for.
Whether this increased size of the myocardium in AAS users is a problem is hard to say. If vascularization is sufficient, then in principle the increased size of the myocardium should not impair its functioning, especially since we control blood pressure so that the stressors only consists of higher blood volume and intermittent blood pressure spikes, which tend not to produce pathological adaptations.
However, we cannot expect that the blood supply will keep up with the myocyte growth, especially if the growth is sped up due to AAS.
Thus, supporting angiogenesis in the myocardium appears to be crucial in order to ensure that the AAS induced growth in the heart muscle is compensatory in nature and does not lead to pathological changes such as necrosis of areas with insufficient blood flow. In the next part, we will look at the role of VEGF in this and will see more evidence for the importance of angiogenesis in cardiac hypertrophy.
There are 3 possible reasons for the observation that concentric hypertrophy is physiological in weightlifters but develops into decompensated (pathological) hypertrophy in most hypertensive patients.
1) The difference between the chronic stressor of hypertension and the intermittent stressor of exercise induced blood pressure spikes may be sufficient to explain why the former leads to degenerative changes in the ventricular wall, whereas the latter allows the myocardium to remain functional.
As an analogy, think of doing curls 24/7 without any weight in your hand. It may well be that the muscle damage induced by this is sufficiently low for your body to repair. But if you gradually increase the weights of a dumbell in that hand, then at some point, you are creating too much muscle damage for the body to repair properly. The micro tearing due to constant stretching and contraction will lead to excessive local inflammation and subsequent fibrosis. Even worse, the chronic inflammation may lead muscle cells to die in troves rather than be repaired. A similar situation may occur in the myocardium in response to the chronically elevated pressure due to hypertension.
2) It may be that the hypertrophy induced by hypertension is not different compared to that from resistance exercise, but the more chronic stimulus leads to more rapid and extensive growth. If the microvasculature were able to keep up with this higher growth, then the growth of the ventricular wall might be perfectly physiological. But as studies have shown, blood flow does typically not keep up with the growth of the myocardium in hypertensive patients, thereby leading to insufficient nutrient and oxygen delivery and subsequent cell death and scarring (fibrosis).
3) It may be that the body would be perfectly able to deal with the growth induced by hypertension in the sense of having sufficient nutrient delivery to the muscle cells and a high enough ability to repair the micro damage induced by constant exertion against high pressure. The problem in the typical hypertensive patient would instead be the high levels of pro-fibrotic agents such as angiotensin II, as well as overactive systemic inflammation that attacks the damaged muscle cells in the heart.
4) It may be a mix of the potential factors. That is, chronic pressure from hypertension is uniquely damaging even in the otherwise healthy individuals, neovascularization is generally insufficient if the growth of the myocardium is too fast and extensive, and pro-fibrotic and pro-inflammatory factors contribute towards pathological changes in the ventricular walls.
So how do AAS factor into this? AAS have 3 kinds of effects, they A) indirectly create/exacerbate stressors, B) indirectly promote fibrotic changes in the heart muscle, and C) directly promote growth of cardiac myocytes.
A)
i) AAS increase hypertension through various channels (see first post), leading to concentric hypertrophy
ii) The increased lean body mass from AAS use increases blood volume, leading to mostly eccentric hypertrophy
iii) increased training volume and frequency mean more frequent blood pressure spikes and thus contribute to concentric hypertrophy
B)
Via its upregulation of Angiotensin II, AAS increase the likelihood of fibrotic changes to the myocardium, especially in the presence of hypertrophy.
C)
AAS have a direct impact on myocyes and promote their growth. Thus, for a given stressor, AAS could increase the myocyte growth rate compared to a natural individual.
http://cdn.intechopen.com/pdfs/21802.pdf
The indirect effect of AAS on hypertension can be controlled (See the first post), but the impact on blood volume and training intensity are not something that can or should be avoided in bodybuilders. So compared to a natural athlete, AAS users will face additional stressors that cause cardiac hypertrophy (which does not have to be pathological though).
Similarly, the effects of AAS on Angiotensin II and thereby fibrosis are something than can me ameliorated.
The direct growth stimulation of cardiomyocytes via the androgen receptor is, however, not something that we can do much about. It is reasonable to assume that for a given level of stressors, the anabolic action of AAS on myocytes will produce a greater growth response compared to natural athletes. So on average, the left (and to some extent right) ventricular wall of an AAS user will be larger than that of a natural athlete, even if blood pressure is controlled for.
Whether this increased size of the myocardium in AAS users is a problem is hard to say. If vascularization is sufficient, then in principle the increased size of the myocardium should not impair its functioning, especially since we control blood pressure so that the stressors only consists of higher blood volume and intermittent blood pressure spikes, which tend not to produce pathological adaptations.
However, we cannot expect that the blood supply will keep up with the myocyte growth, especially if the growth is sped up due to AAS.
ARTICLES | Physiology
Thus, supporting angiogenesis in the myocardium appears to be crucial in order to ensure that the AAS induced growth in the heart muscle is compensatory in nature and does not lead to pathological changes such as necrosis of areas with insufficient blood flow. In the next part, we will look at the role of VEGF in this and will see more evidence for the importance of angiogenesis in cardiac hypertrophy.
Blood Pressure Drug Losartan Lowers Post-Workout Myostatin Level in Older Subjects
Heisterberg, Mette Flindt; Andersen, Jesper L.; Schjerling, Peter; Bülow, Jacob; Lauersen, Jeppe Bo; Roeber, Heidi L.; Kjaer, Michael; Mackey, Abigail L. "Effect of Losartan on the Acute Response of Human Elderly Skeletal Muscle to Exercise." Medicine & Science in Sports & Exercise: Post Acceptance: October 16, 2017 - doi: 10.1249/MSS.0000000000001438
Heisterberg, Mette Flindt; Andersen, Jesper L.; Schjerling, Peter; Bülow, Jacob; Lauersen, Jeppe Bo; Roeber, Heidi L.; Kjaer, Michael; Mackey, Abigail L. "Effect of Losartan on the Acute Response of Human Elderly Skeletal Muscle to Exercise." Medicine & Science in Sports & Exercise: Post Acceptance: October 16, 2017 - doi: 10.1249/MSS.0000000000001438
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Heart Hypertrophy
Ive been taking Bystolic for a few years. It works very well at lowering heart rate and I can confirm that there are no sexual sides. I Have not had any side effects worth noting. Over all great drug.
Also with all the talk of heart hypertrophy: My echo came back that I have a LA which is 48 and the range is 19-40
I have AoROOT of 41 and the range is 20-37
Everything else was within range or normal.
I don't know how that correlates to the diagram above.
The Doctor didn't seem concerned and says he sees it frequently with guys my size.
I do several hours of cardio a week and im very active.
Ive been taking Bystolic for a few years. It works very well at lowering heart rate and I can confirm that there are no sexual sides. I Have not had any side effects worth noting. Over all great drug.
Also with all the talk of heart hypertrophy: My echo came back that I have a LA which is 48 and the range is 19-40
I have AoROOT of 41 and the range is 20-37
Everything else was within range or normal.
I don't know how that correlates to the diagram above.
The Doctor didn't seem concerned and says he sees it frequently with guys my size.
I do several hours of cardio a week and im very active.
How many mg of bystolic do you take? All at once too?
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5mg daily. all at once.
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I have a mildly dilated LA as well (4.2cm. Range <4.0cm) but that hasn’t changed for years. I believe it’s not a huge deal if EF is normal more or less. Looks like they used different measurements in your echo compared to mine.
5.0cm is how large the aortic root needs to be before you need surgery. You are a while away from that but keep an eye on it to make sure it doesn’t get worse.
Curcumin and Telmisartan for you
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Thanks for that info. Defenetly will do.
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Come off a few times a year, avoid nandrolone and NPP, do some HIT cardio a couple times a week, use the sauna every day (great for the heart) Strongman type stuff (tire flips, sled drags, wheelbarrow pushes up a hill) is great for the heart and lungs..... that kind of stuff will only benefit your physique by putting slabs of muscle on. Yeah the advice above is basic but How many guys here are actually doing this week in and week out? When was the last time any of you actually ran wind sprints up a hill?
To be clear I believe in certain supplements and I'm not trying to take a caveman approach here but at the end of the day very few guys are eating clean enough, doing the right things cardio wise to keep the heart healthy. I know guys that take all kinds of things for liver health but they will go hit in and out burger multiple times a week in the offseason when bulking. Junk food ruins the liver over time.
if you really value your heart, kidneys, liver, and even mental health don't use any gear period and eat a paleo diet year round. If you find yourself constantly worried about your health from what your taking don't juice it's not worth the stress. Not anti supplements, just not naive enough to think that some grapeseed extract is going to protect me against powerful pharmaceuticals, we are all playing with fire.
To be clear I believe in certain supplements and I'm not trying to take a caveman approach here but at the end of the day very few guys are eating clean enough, doing the right things cardio wise to keep the heart healthy. I know guys that take all kinds of things for liver health but they will go hit in and out burger multiple times a week in the offseason when bulking. Junk food ruins the liver over time.
if you really value your heart, kidneys, liver, and even mental health don't use any gear period and eat a paleo diet year round. If you find yourself constantly worried about your health from what your taking don't juice it's not worth the stress. Not anti supplements, just not naive enough to think that some grapeseed extract is going to protect me against powerful pharmaceuticals, we are all playing with fire.
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What kind of allergy do you have to telmisartan? If it's the cough, the incidence is much higher with lisinopril.
Cardioselective eta-blockers have proven mortality benefits. If all you're trying to do is control BP, calcium channel blockers work well (but not the best option, usually an add-on if using another BP control agent that isn't working well enough). Diuretic--preferably chlorthalidone--if you're prone to BP as a result of fluid-retention (longer half-life which leads to better mortality benefits over HCTZ, but the price is much higher as well).
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I broke out in hives/rashes all over my body. I was on superdrol at the same time but dermatologist told me that my rashes were classic bp med rashes. I'm only using it to control blood pressure on cycle. Thanks for the recommendations.
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