Cardio to die for!

gotgame said:

This is something I care a lot about. In fact its probably what I want to be remembered most for in this area when im long gone.

I have certs in both cardiac ct of advanced proficiency ( CoAP) and cardiology cert. Also have publications as they relate to triglycerides, plaque formation and populations using ct and mri.


Bodybuilders are retarded sometimes. Those who compete do what they have to do but most people do not compete or at least dont make a living out of it. Yet they still do so many things only living in the superficial present and not caring about their health years from now.

Let me be clear... AAS are not as harmful as they are deemed to be however there is use, abuse and really fucking smart use. People on this thread are talking about reversal... ok thats great but more importantly we should be talking about prevention.

I have posted so much on this over the years on different boards and i really dont feel like copy pasting it and looking for it but ill make this short and sweet.

1. Stop with the orals. No reason to crush your HDL. Think long term. Also no need to be using such strong androgens for long periods of time. I have nothing to say to those use tren at high doses for months on end.

2. Diet: See previous posts from people on this thread. Yes it plays a sigificant role but you can have the best diet in the world but if your HDL is 8 from winny and tren it wont matter.

3. Cardio. RUN! Do legit cardio. And not just once a week or just during the summer. Dont give me that crap " ohh but gotgame im bulking so i cant run" . Dont be retarded, be health7 so you are on here posting for years to come.

4. Dont going to post everything that i have over the years but consider using low dose ARBs or ACEi when on gear to prevent cardiac remodeling. I would suggest 25mg daily of losartan or equivalent .

5. Take aspirin low dose unless contraindicated for numerous benefits.

6. steroids can DIRECTLY cause cardiac remodeling. Dont bother sending me links to athletes and having bigger hearts... that is a different type of hypertrophy that is not the kind i am referring to as AAS induced. Some of it can probably be reversed after a long time off but not all of it. So keep your doses low, cycle, and use an ARB

7. I have yet to see anyone with a calcium score over 400 make any signficant improvements on direct CT, ever. They have made cath improvements. Someone mentioned nucs stress test earlier..... that wont show you a darn thing. Had a patient who had rock solid normal nucs test on friday and came back on wednesday with a stemi and had 80% occlusion of one of the LAD diags. Its a crap test for prognostic value, it has physiologic value.

8. Keep your blood pressure in check. It is NOT ok for it to ever be elevated. I cant stress this enough. Dont give me this genetic nonsense. Sure for SOME people its genetic but most people can control it with diet/lifestyle modifications so stop being lazy. The arbs should help that too.

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gotgame said:

Angiotensin receptor blockers and angiotensin convert enzyme inhibitors. Used in patients with MI's but studies have been done showing it can prevent AAS induced remodeling. Granted they werent huge studies but they pass my face validity test as to their MOA and how AAS induced cardiac hypertrophy and at times hyperplasia.

I dont mean "run" as in only running but you understood what i was saying. HIT is fine. What i dont want is something like riding a bike at a relaxed pace while watching a movie or just walking etc. It needs to be something that you are hating your life and when 10 minutes feels like an hour and your constantly trying to convince yourself as to the reasons you should stop such has " I need to spend time with the gf, or i should probably stop doing cardio and go clean my house or cut my back lawn etc lol" It needs to be intense enough to induce VEGF levels to help with cardiac collateral flow. Running can be tough on the knees but i just mean some form of cardio that will keep your heart rate up, make you sweat bad and hate your life while your doing it.

You probably had a cardiac ct calcium score. That is the best test that is commonly available. Having a score of 0 doesnt mean you dont have any plaque it just means its not calcified and that your test was good. If there is a ton of calcium there is blooming type artifact on ct which limits its evaluation. I dont read them if its over a 1000 as its so limited and they will go right to cath. If you had a completely normal cardiac CTA you are safe for 5 years when it comes to coronary induced chest pain. But becareful having it done...having a positive test can fuck you when it comes to insurance and certain jobs

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gotgame said:

I would not take minox orally especially not for this purpose. Not going to mess around with my K+ channels sysytemically.

Nebivolol, while it might be good at a reducing BP any remodeling agent needs to work on the angiotensin system as that is what the studies looked at showing AAS induced changes. While beta blocks are sometimes still used in MI patients its to reduce the O2 demand after an MI not to directly reduced remodeling. Maybe you were thinking nebi because you NO levels...remember we arent trying to just dilate vessels we are trying to create new ones. I just used VEGF as one example of what you want to achieve. Will having slightly increase NO levels in the heart over a period of time increase local angiogenesis...maybe..probably but lets work on trying to prevent remodeling and use natural vegf production at this time until there are more studies done. Also keep in mind that when you look at studies and NO and angiogensis..is it natural NO production or artificial, the difference is the setting by which it is produced. Any setting that requires increased O2 demand ( cardio) will cause an increase i NO BUt it will also cause VEGF locally to increase for a short period of time, so its not neccessarily the NO that is beneficial its the state that caused the NO increase.

In the next 10 years there will be new drugs to combat this. Spoke with an MD PHD out of philly last week and she had just demonstrated last month the use of microRNAs to complete reverse/prevent cardiac remodeling in the acute seting. Granted her work is catheter direct but give it time.


You want to increase LOCAL vegf levels. That is what is important. It takes years and years of hard work to do this but it can save your life to have some decent collaterals if you have an MI. Granted if your 3 vessels are all crap from years of steroid abuse and "bulking" then theres not much to be done anyway

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SURGE said:

Cardio is great for health. Similar to most things being extreme with it can be bad for you. I try to get a few sessions in every week but most are fairly intense but for short periods. Besides that I walk a lot and I think everything combined definitely helps with my blood work and overall health.

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There has been re-emerging interest and significant work dedicated to investigating the metabolic effects of high intensity interval training (HIIT) in recent years. HIIT is considered to be a time efficient alternative to classic endurance training (ET) that elicits similar metabolic responses in skeletal muscle. However, there is a lack of information on the impact of HIIT on cardiac muscle in disease. Therefore, we determined the efficacy of ET and HIIT to alter cardiac muscle characteristics involved in the development of diastolic dysfunction, such as ventricular hypertrophy, fibrosis and angiogenesis, in a well-established rodent model of hypertension-induced heart failure before the development of overt heart failure. ET decreased left ventricle fibrosis by ~40% (P < 0.05), and promoted a 20% (P<0.05) increase in the left ventricular capillary/fibre ratio, an increase in endothelial nitric oxide synthase protein (P<0.05), and a decrease in hypoxia inducible factor 1 alpha protein content (P<0.05). In contrast, HIIT did not decrease existing fibrosis, and HIIT animals displayed a 20% increase in left ventricular mass (P<0.05) and a 20% decrease in cross sectional area (P<0.05). HIIT also increased brain natriuretic peptide by 50% (P<0.05), in the absence of concomitant angiogenesis, strongly suggesting pathological cardiac remodeling. The current data support the longstanding belief in the effectiveness of ET in hypertension. However, HIIT promoted a pathological adaptation in the left ventricle in the presence of hypertension, highlighting the need for further research on the widespread effects of HIIT in the presence of disease.

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