HDL and cardiovascular risk - not for the feint of science

[PeterBond]

I'm doubtful that the non-AAS lifters in the trial by Salke et al. were actual naturals. They claimed, on average, to bench press 145 kg. Similar thicknesses also aren't seen in other studies, not even in Olympic power athletes (weight lifting/wrestling/100-200 m dash athletes): Patterns of left ventricular diastolic function in Olympic athletes - PubMed (Their whole sample of 1,145 Olympic athletes, including 111 male power athletes, only had 2 cases with a LV wall thickness beyond 13 mm.)

It's better to look of the aggregate of evidence rather than focus on a single study

Furthermore, if thickness increases in parallel with strength, shouldn't all competitive powerlifters and strongman, including naturels, have massively thick ventricular walls? Many recreational lifters would suffer from the same consequences if this were true; who hasn't increased their bench press or squat weight with at least 100 or 200% of what it was before they started lifting as a natural? That would then lead to massive increases in wall thickness too. I'm not aware of any literature that supports increases in wall thickness parallel to strength. (Mind you that the study you cited was cross-sectional in nature, not prospective.) I'm only aware of literature that shows small increases in ventricular wall thickness as a result of strength training and in strength athlete populations, without these detrimental changes in cardiac function.

The HAARLEM trial investigated AAS users prospectively, not naturals. Hence I said:

The thing is that the changes in cardiac function (e.g. decrease in E/A ratio, ejection fraction, strain rate) are not seen in strength athletes who don't use AAS, but whom are strong regardless.

They saw a decrease in E/A ratio and ejection fraction (they didn't measure strain rate, but another trial I'm citing did and found a reduction only in the AAS users). This is not seen in natural strength athletes.

 

[CooSee]

Furthermore, if thickness increases in parallel with strength, shouldn't all competitive powerlifters and strongman, including naturels, have massively thick ventricular walls?

Great point here. I wonder if there there any competitive powelifters who don’t use AAS to even be able to test that particular group. But like you said, the guy who starts lifting with a 100lbs squat and 3 years later hits 275 lbs squat with no AAS, if enough studies have looked at a lot of those folks and not seen progressive wall thickening and reduced efficiency in correlation with the strength increase, then that right there is pretty darn supportive of the idea that the AAS chemicals are the culprit rather than the strength they convey being the culprit. Still the question, why? Has the “why” been hypothesized?

 

[PeterBond]

I'm not entirely sure on what you mean by the "why"? Could you elaborate? Do you mean a mechanism of action/pathways that get activated?

 

[CooSee]

I'm not entirely sure on what you mean by the "why"? Could you elaborate? Do you mean a mechanism of action/pathways that get activated?

Yes, as in: let’s say the presence of supraphysiological levels of hormones are indeed the direct cause of these changes in the heart. The why is, why do they cause the changes in the heart? As you said, what is the method of action of the hormones to affect these changes? And how is it that both T as well as chemically altered derivatives like Deca etc. cause similar things to happen to the heart?

 

[Type-IIx]

@PeterBond is there any basis in believing that Metformin could have a protective effect on cardiac function and/or remodeling? Reading that Patterns of left ventricular diastolic function in Olympic athletes paper made me think again about some basic research on Metformin having potential efficacy in ameliorating conduction delay and perhaps preventing the LV cardiac remodeling? Metformin ameliorates cardiac conduction delay by regulating microRNA-1 in mice - PubMed (Metformin ameliorates cardiac conduction delay by regulating microRNA-1 in mice)
Metformin Improves Cardiac Metabolism and Function, and Prevents Left Ventricular Hypertrophy in Spontaneously Hypertensive Rats - PubMed (Metformin Improves Cardiac Metabolism and Function, and Prevents Left Ventricular Hypertrophy in Spontaneously Hypertensive Rats)

Research reviews of its reduction of all-cause mortality tend to mention some attribution to heart function and kidney function. I haven't thought much about this but maybe you have insight to share.

How would you assess Metformin for this purpose (protection of cardiac function and structure)?

 

[PeterBond]

@PeterBond is there any basis in believing that Metformin could have a protective effect on cardiac function and/or remodeling? Reading that Patterns of left ventricular diastolic function in Olympic athletes paper made me think again about some basic research on Metformin having potential efficacy in ameliorating conduction delay and perhaps preventing the LV cardiac remodeling? Metformin ameliorates cardiac conduction delay by regulating microRNA-1 in mice - PubMed (Metformin ameliorates cardiac conduction delay by regulating microRNA-1 in mice)
Metformin Improves Cardiac Metabolism and Function, and Prevents Left Ventricular Hypertrophy in Spontaneously Hypertensive Rats - PubMed (Metformin Improves Cardiac Metabolism and Function, and Prevents Left Ventricular Hypertrophy in Spontaneously Hypertensive Rats)

Research reviews of its reduction of all-cause mortality tend to mention some attribution to heart function and kidney function. I haven't thought much about this but maybe you have insight to share.

How would you assess Metformin for this purpose (protection of cardiac function and structure)?

Do you mean in general, or in terms of the changes that are seen as a result of AAS usage?

Yes, as in: let’s say the presence of supraphysiological levels of hormones are indeed the direct cause of these changes in the heart. The why is, why do they cause the changes in the heart? As you said, what is the method of action of the hormones to affect these changes? And how is it that both T as well as chemically altered derivatives like Deca etc. cause similar things to happen to the heart?

This is really difficult to study so there are only some guesstimates from cell culture and animal research. There's some evidence of myocyte apoptosis being induced by AAS, effect on electrolyte channels and their associated proteins of the cardiac cells, shifts in the redox balance towards more oxidative stress, changes in the ionotropic response to adrenergic activity, etc. I wouldn't dare to say to what extent, if any, these (and surely other things I'm forgetting) play a role, let alone how the hemodynamic changes that are brought about by AAS use further affect its structure over time.

It shouldn't be too surprising that this is something generally seen with AAS use, regardless of the type: most of it is likely mediated by androgen receptor activation.

 

[CooSee]

Do you mean in general, or in terms of the changes that are seen as a result of AAS usage?


This is really difficult to study so there are only some guesstimates from cell culture and animal research. There's some evidence of myocyte apoptosis being induced by AAS, effect on electrolyte channels and their associated proteins of the cardiac cells, shifts in the redox balance towards more oxidative stress, changes in the ionotropic response to adrenergic activity, etc. I wouldn't dare to say to what extent, if any, these (and surely other things I'm forgetting) play a role, let alone how the hemodynamic changes that are brought about by AAS use further affect its structure over time.

It shouldn't be too surprising that this is something generally seen with AAS use, regardless of the type: most of it is likely mediated by androgen receptor activation.

interesting. so androgen receptor activation is where we believe it all starts. well I hope we can find out the 'why' one day.

 

[Type-IIx]

Do you mean in general, or in terms of the changes that are seen as a result of AAS usage?

I was hoping that it could have a protective effect for AAS cardiac remodeling/conduction changes, but from the question I am thinking not. Do you see it being useful outside of BnCing high-dose AAS? Say, during periods of cessation or for long-term recovery after AAS abuse? Or for guys that just use peptides/GH?

 

[Ambusher]

Do you mean in general, or in terms of the changes that are seen as a result of AAS usage?


This is really difficult to study so there are only some guesstimates from cell culture and animal research. There's some evidence of myocyte apoptosis being induced by AAS, effect on electrolyte channels and their associated proteins of the cardiac cells, shifts in the redox balance towards more oxidative stress, changes in the ionotropic response to adrenergic activity, etc. I wouldn't dare to say to what extent, if any, these (and surely other things I'm forgetting) play a role, let alone how the hemodynamic changes that are brought about by AAS use further affect its structure over time.

It shouldn't be too surprising that this is something generally seen with AAS use, regardless of the type: most of it is likely mediated by androgen receptor activation.

Could you offset a greal deal of these changes to the cardiac structure by implementing cardio? That way, the portions of the heart that are strengthened and hypertrophy naturally by endurance training increase close to the same rate as the AAS induced changes?