AAS and cardiovascular health

[Daz69]

I'm bored, so thought I'd share a few posts of mine from another forum discussing AAS and their effects on cardiovascular health:

 

There are several conditions that are often downplayed that can lead to more serious conditions by users of AAS such as >BP, LVH etc...

LVH in itself is not necessarily an issue. It often reflects the fact that bodybuilders have developed the significantly superior heart function and strength required to shift large weights and feed powerful muscles - what would be called an 'athletic' adaptation.

The problem is when this coincides with fibrosis in cardiovascular tissues. In this instance fibrosis is the deposition of less flexible collagen not just in the heart but in arteries and veins across the body. This seems to occur directly and indirectly as a result of AAS use, and some AAS are worse than others - eg Deca is notoriously bad. 

This extra collagen makes the cardiovascular tissues a bit 'stiffer' and increases the pressure (force) required by the heart to pump blood through the body (increases the 'load').

As a result, a rather less healthy (and structurally maladaptive) deposition of new muscle (LVH) will occur in an attempt to overcome the strain of the increasing load, and once past a certain size, it begins to reduce the efficiency of the heart as a pump. 

But the fibrosis also affects things like the passage of nerve impulses across the heart (often resulting in atrial fibrillation or heart block, for example), and interferes with the essential growth of new blood vessels (angiogenesis) to the new cardiac muscle, potentially starving these tissues of oxygen, resulting in pain (angina), necrosis and scarring. 

And the scarring makes the heart even more inflexible, and is thus basically a very unwelcome positive feedback loop..

All these outcomes are incredibly unhealthy for the heart, and probably explain why some powerlifters/bodybuilders (anecdotally, and I suppose relative to their otherwise incredibly healthy looking bodies) seem to suffer disproportionately from heart attacks, afib etc etc.

 

Benefits of HIIT:

 

The kind of adaptations we want in the heart are the kind that high intensity cardio bring. It can basically 'enlarge' the capacity of the heart (the chambers) and also improve the ejection fraction. 

So the heart becomes more efficient per beat, and hence the pulse rate tends to fall - very low in very fit athletes. It does cause a very mild form of hypertrophy, but it arranges the cardiac tissue structurally slightly differently to the type that forms from heavy weight lifting.

So I would always recommend HIIT. LISS doesn't really do much good or bad for the heart. It's not intense enough to cause much positive adaptation, but if you have pre-existing heart conditions, it could aggravate those by drawing on cardiac oxygen capacity.

One of the other positives of HIIT is that it helps to stretch and (theoretically) break up the scarring/fibrotic tissue. 

We have to bear in mind that intense cardio pumps very large volumes of blood through the heart (unlike weights) which causes a nice eccentric stretch to the cardiac tissue, as opposed to more concentric-focus from weights.

 

Aspirin benefits:

 

First of all, aspirin stops platelet aggregation.. It does not thin blood..

Aspirin inhibits the enzyme cyclooxygenase. This inhibition reduces the production of a number of prostaglandins, resulting in antipyretic, anti inflammatory, antiplatelet and analgesic effects..
It is used in prehospital setting for its antiplatelet effects. A platelet exposed to aspirin has permanent cyclooxygenase inhibition for the life of that platelet.
The body has to produce more platelets (that are not exposed to aspirin) to overcome the antiplatelet effect.
Each day the body produces new platelets at a rate of approximately 10% of total..

Deleterious changes to the heart can create an environment where blood could stagnate within the ventricles, blood when not moving will clot, this can create a serious condition within the cardiovascular system, leading to blockage and subsequent risk of pulmonary oedema, stroke etc..
Aspirin, via the mechanism explained can reduce the risk of clotting.. 

Obviously its better not to create an environment within the body where clots could occur through better choice of hormones, venesection, diet, and adequate cardio.. (and time off)..

 

Study on HIIT:

 

Metabolism: Clinical and Experimental
September 2015, Volume 64, Issue 9, Pages 1068?1076

Accumulating exercise and postprandial health in adolescents

Bert Bond, Craig A. Williams, Sarah R. Jackman, Adam Woodward, Neil Armstrong, Alan R. Barker

Purpose
To examine the influence of exercise intensity on postprandial health outcomes in adolescents when exercise is accumulated throughout the day.

Methods
19 adolescents (9 male, 13.7 ? 0.4 years old) completed three 1-day trials in a randomised order: (1) rest (CON); or four bouts of (2) 2 ? 1 min cycling at 90% peak power with 75 s recovery (high-intensity interval exercise; HIIE); or (3) cycling at 90% of the gas exchange threshold (moderate-intensity exercise; MIE), which was work-matched to HIIE. Each bout was separated by 2 hours. Participants consumed a high fat milkshake for breakfast and lunch. Postprandial triacylglycerol (TAG), glucose, systolic blood pressure (SBP) and fat oxidation were assessed throughout the day.

Results
There was no effect of trial on total area under the curve (TAUC) for TAG (P = 0.87). TAUC-glucose was lower in HIIE compared to CON (P = 0.03, ES = 0.42) and MIE (P = 0.04, ES = 0.41), with no difference between MIE and CON (P = 0.89, ES = 0.04). Postprandial SBP was lower in HIIE compared to CON (P = 0.04, ES = 0.50) and MIE (P = 0.04, ES = 0.40), but not different between MIE and CON (P = 0.52, ES = 0.11). Resting fat oxidation was increased in HIIE compared to CON (P = 0.01, ES = 0.74) and MIE (P = 0.05, ES = 0.51), with no difference between MIE and CON (P = 0.37, ES = 0.24).

Conclusion
Neither exercise trial attenuated postprandial lipaemia. However, accumulating brief bouts of HIIE, but not MIE, reduced postprandial plasma glucose and SBP, and increased resting fat oxidation in adolescent boys and girls. The intensity of accumulated exercise may therefore have important implications for health outcomes in youth.

http://www.metabolismjournal.com/art...160-2/abstract