Left ventricular hypertrophy

[jimmybro1]

Daz’s post on NNP influence of cardiovascular health sparked my interest. I did a little bit if research on the effects of anabolics and resistance training on cardiovascular health. This is focused on the left ventricle hypertrophy of the heart (LVH). This is thickening of the muscle of the left ventricle of the heart. Hypertophy of the ventricular occurs naturally with the stress of aerobic or anaerobic and most frequently referred to as a pathological reaction to cardiovascular disease or hypertension.

 

LHV is typically used as a health marker of the heart and can be detected by irregularly in ECG monitoring using a Holter monitor. I have recently had this examination (still awaiting a report).

 

While sifting through several research articles published by PubMed it appears that left ventricle hypertrophy is prevalent among those who are ex-users, users and non users of anabolics that undertake some form of resistance training (whether bodybuilding, powerlifting and variances of these) as expected. Exercise increases stress on the heart thereby temporarily increasing blood pressure putting additional resistance on the left ventricular which responses by undergoing hypertrophy to accommodate the additional stresses (pressure is force over an area N/m² so with increasing pressure and constant surface area force increases). Your heart is a muscle and will undergo hypertrophy like any other muscle in your body expect it will have significant health implications.   

 

“Such data must nonetheless be treated with caution. We know, for example, that the magnitude and pattern of hypertrophy is dependent on the nature, duration, and intensity of exercise undertaken.8,9,14 Thus, strength trained athletes (such as weightlifters, powerlifters, bodybuilders, and throwers) develop a greater increase in wall thickness, a more concentric pattern of LV growth, and a lesser increase in LV chamber internal dimensions8 in comparison to those undergoing predominantly aerobic/endurance exercise. “

 

(Cardiac effects of anabolic steroids, J R Payne et al).  

 

Although the journal states the growth is more prominent in users and ex-users of anabolics. There are several factors take could influence this other than just the use of anabolics for example diet, smoker/non smoke, alcoholism  etc. However to get the best picture of the effects a study was done taking into consideration lean muscle mass, body surface area and wall thickness and cavity dimensions.

 

“What evidence is there that AAS administration enhances the LV hypertrophic response to resistance exercise?

In this issue of Heart, Urhausen and colleagues report the results of a cross sectional study of cardiac morphology in relation to AAS use.13 Male bodybuilders/powerlifters currently using AAS or ex-users who had abstained from AAS exposure for over 12 months (U and ExU, n  =  17 and 15, respectively) were compared to 15 weightlifters who denied current or past use of AAS (WL). Left ventricular wall thickness and cavity dimensions were assessed using echocardiography, and muscle mass (LVMM) calculated using the Devereux equation. Absolute LVMM measures (mean (SD)) were significantly greater for U than ExU or WL (281 (54) g v 232 (42) g v 204 (44) g for U v ExU v WL, respectively), with differences between ExU and WL only reaching significance after adjustment for body surface area or fat-free mass. These results suggest that AAS use increases the LV hypertrophic response to exercise, an effect which might last for well over a year.” “

 

(Cardiac effects of anabolic steroids, J R Payne et al).  

 

Another research article identifies three potential causes of LVH in resistance training athletes. Once again stating the occurrences is more predominate in users of anabolic steroids but also factors in the effect of duration an individual has been exposed to resistance training. I was only able to get the abstract of this particular study as it wasn’t free to view.

 

“(i) acute cardiopulmonary mechanisms that minimise the increase in transmural pressure (i.e. ventricular pressure minus intrathoracic pressure) and LV wall stress during exercise; (ii) the underlying use of anabolic steroids by the athletes; or (iii) the specific type of RT performed. We propose that when LV geometry is altered after RT, the pattern is usually concentric hypertrophy in Olympic weightlifters. However, the pattern of eccentric hypertrophy (increased LV mass secondary to an increase in diastolic internal cavity dimension and wall thickness) is not uncommon in bodybuilders. Of particular interest, nearly 40% of all RT athletes have normal LV geometry, and these athletes are typically powerlifters. RT athletes who use anabolic steroids have been shown to have significantly higher LV mass compared with drug-free sport-matched athletes.”

 

  (Resistance Training and Cardiac Hypertrophy: unravelling the training effect, MJ Haykowsky et al)

 

It has also been shown that LVH isn’t recoverable to much extent.

 

“Our results suggest that AAS-using strength athletes have a slight concentric left ventricular hypertrophy, with some indication of decreased diastolic function several years after ceasing AAS abuse, compared with steroid-free strength athletes.”

 

(http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1768225/)

 

Other studies and research articles on the subject are:

 

• http://www.ncbi.nlm.nih.gov/pubmed/1917226
• http://www.ncbi.nlm.nih.gov/pubmed/10641914 (examining the hearts of 34 dead pervious users, deaths from various causing ranging from homicide to suicide)
• http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1768197/#r15

[maccaz]

Bleak

What can be done to minimise the effect ?

[jimmybro1]

Bleak

What can be done to minimise the effect ?

 

Best things to do would be to monitor you blood pressure, have diet on point and do some aerobic exercise.

 

You can buy a digital blood pressure monitor online reasonable cheap would be a good way of keeping a check on everything. 

 

Low risk blood pressure range is 130-110/80-60 suggested by MayoClinic. 

 

If you have low bpm (i.e. <60) and high blood pressure (140+/90+) I would see a doctor promptly 

[kiwicannon]

Best things to do would be to monitor you blood pressure, have diet on point and do some aerobic exercise.

 

You can buy a digital blood pressure monitor online reasonable cheap would be a good way of keeping a check on everything. 

 

Low risk blood pressure range is 130-110/80-60 suggested by MayoClinic. 

 

If you have low bpm (i.e. <60) and high blood pressure (140+/90+) I would see a doctor promptly 

Gulp looks like I'm off to the doc!

Nice one Jimmybro good info!

[Leeroid]

Good post bro. Post of the month

[jimmybro1]

Good post bro. Post of the month

Cheers mate, if people are aware of what health makers to keep an eye on the seriousness of these conditions can be controlled. 

 

So often you hear about people having heart attacks out of the blue but the truth is if they were monitoring their health this could have been avoided and quality of life improved. 

 

Post isn't mean't to be doom and gloom but rather aware people of the serious conditions that can develop with so called "no symptoms."  

[Daz69]

The problem with lvh is not so much the LV volume gets smaller so the hr has to increase to maintain the output. That's a problem but it's the smaller problem. The bigger issue is as the ventricle gets thicker it also gets stiffer. It's called relaxation abnormality or diastolic dysfunction. So it's harder to fill. Ever blow up a balloon as a kid and it was really hard? That's what a stiff ventricle is like. That raises the pressure inside the ventricle which pushes out against the coronary arteries trying to push blood into the ventricular wall. Coronary perfusion pressure equals diastolic pressure minus the pressure inside the ventricle during diastole. This is diastolic dysfunction and won't happen overnight but as the decades get on it can be a problem in some people in their 50's. Everyone gets it to some degree as we age, there are different grades, they are measured on a standard echo.

[Daz69]

Any medication that controls blood pressure (an inotrope) and to a lesser extent pulse rate (a chronotrope) while on AAS will reduce or prevent left ventricular hypertrophy (LVH) - this includes diuretics, beta blockers, alpha blockers, calcium channel blockers, ACE inhibitors as well as ARBs. But 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. ARBs are unusual in their ability to reverse tissue fibrosis, and as a bonus can also reduce blood pressure, which is a major trigger for unhealthy LVH. N-acetylcysteine has potentially been shown to have benefits in reducing fibrosis, but these unfortunately cancel out those of the ARB!

To clarify, fibrosis can be reversed, though it's unlikely to be fully, and not in everyone. And the damage to other tissues such as heart valves (due to fibrotic stiffness and years of elevated BP and raised PCV) is unlikely to be reversed.

Prevention is logically going to be a safer course of action. Unfortunately, though some compounds are thought to be harsher, there is scant human research (for obvious reasons).

BP medication should still be in everyone's arsenal though: even beyond the fibrosis aspect, controlling elevated blood pressure and the effects of raised haematocrit (PCV) should be universally important for all AAS using bodybuilders.

This means giving blood on a regular basis would also be wise (or doing it yourself via vacuum tubes if you've the balls).

And as for pre-workout stimulants dramatically aggravating all of the effects we've just been discussing.....

Losartan is the most heavily researched of the ARBs with regards to reversing fibrosis. Angiotensin receptor blockers (ARBs) are generally suffixed with ~sartan.

However one of the most efficacious of the ~sartans, at least in research, is Olmesartan, closely followed by Irbesartan. But really, most of this will simply come down to what you can get your hands on and at what price.

In the absence of any of the ARBs, you could try any of the other blood pressure medications (ACE inhibitors are probably the next choice, though personally I'd avoid diuretics), with a fairly high dose of N-acetylcysteine (iirc it was about 2g daily). The NAC approach is not as effective but it does offer something I suppose.

FWIW both ACE-inhibitors and ARBs are slightly less effective for people of West African origin (blacks) with regards to blood pressure reduction (due to differences in the renin system); the anti-fibrotic effect should remain however.

 

[Daz69]

I thought I'd walk us through an interesting case-study from a few years ago, with potentially wider implications for all AAS-using bodybuilders and powerlifters. I know I keep bringing up these cardiovascular issues, but so few people consider them, and it really is worth having some awareness and an idea of how to ameliorate effects where possible. In particular I've translated some of what the text means for a lay person, and the discussion should be of particular value as a broad summary.

Anyway, have a read...




BMJ Case Reports 2011; doi:10.1136/bcr.12.2010.3650

Anabolic androgenic steroid-induced cardiomyopathy, stroke and peripheral vascular disease

Maged Y Z Youssef, Ahmed Alqallaf, Nabila Abdella 


Summary

Acute stroke could be the presentation of unrecognised cardiomyopathy postanabolic androgenic steroid (AAS) abuse. A 39-year-old male patient displayed signs of acute stroke, which were associated with AAS abuse over the last 3 years. Despite the absence of symptoms and signs of congestive heart failure at presentation, AAS-induced cardiomyopathy with a thrombus in the left ventricle was discovered to be the aetiology of his stroke and peripheral vascular disease. Awareness of the complications of AAS led to the prompt treatment of the initially unrecognised dilated cardiomyopathy, and stroke.


Background

Acute presentation of stroke in a young patient with prolonged anabolic steroid use should alert us to underlying cardiomyopathy with thromboembolic events and peripheral vascular disease.


Case presentation

A 39-year-old male body builder presented with dizziness and expressive aphasia for the last 6 h.

Three months earlier, the patient presented to medical emergency with a transient ischaemic attack in the form of sudden loss of vision in left eye associated with weakness and numbness in the left upper and lower limbs lasting less than 1 h. The patient had intermittent claudication in the left lower limb. Neurological examination at the time, followed by CT of the head was completely normal. The patient refused admission to the hospital and was discharged on aspirin and follow-up which he did not pursue. [A rookie mistake which too many 'indestructable' bodybuilders repeat!]

The patient had no medical issues, 3 weeks prior to admission at the hospital. However, the patient admitted to have been abusing anabolic androgenic steroids (AAS) for the last 3 years, which were administered as intramuscular injections of nandrolone twice weekly [I think we can fairly assume that's not all he took!]

On physical examination, he was alert and conscious with motor aphasia. Heart rate was 100/min, and blood pressure 140/100 mm Hg. Chest, heart and abdomen were normal. Jugular venous pressure was not elevated, and no peripheral oedema was noted. Peripheral pulsations were present on right side and absent dorsalis pedis pulsation on left side. Pupils were normal to exam. His fundi were normal with no visual field defects and no nystagmus. Right facial palsy, upper motor neuron lesion. No motor weakness was detected. Deep reflexes were normal in upper and lower limbs. Plantar reflexes were normal.


Investigations

Complete blood picture, erythrocyte sedimentation rate and C reactive protein were within normal range. Fasting blood sugar, liver function test, kidney profile and serum electrolytes were normal. Troponin, and coagulation profile were normal and his creatine kinase was 500 U/l (normal range 5–130 U/l).

Serum triglycerides 1.8 mmol/l (normal <2.20 mmol/l), total serum cholesterol 5.4 mmol/l (normal <5.2 mmol/l), high density lipoprotein-C 0.85 mmol/l (normal >0.9 mmol/l), low density lipoprotein-C (LDL-C) 4.19 mmol/l (normal < 3.37 mmol/l)[A typically poor lipid profile as regularly seen in AAS users - incidentally Deca doesn't appear to negatively affect lipids so we can assume it's whatever else he's taking], apolipoprotein B 1.29 mg/dl (normal range 0.60–1.33 mg/dl). Full thrombophilia screen, antiphospholipid antibodies, virology screen and immunology screen were negative. Urinalysis and microscopy was normal. Ankle brachial index: right side=1.2, 1eft side=0.69. Chest x-ray showed cardiomegaly [FYI: enlarged heart]. ECG showed sinus rhythm. Q waves were present in leads II, III and AVF. Poor R waves were observed in V1–V3. CT and MRI of brain showed left frontal infarction [Tissue death - due to the prior stroke]. Echocardiography showed dilated left ventricle (LV) with global hypokinaesia. Left ventricular cavity size was enlarged, end diastolic diameter was 6.9 cm and end systolic diameter was 5.7 cm. Left ventricular ejection fraction was 35% [very poor/inefficient] and there was an apical thrombus[A huge clot inside the left ventricle of the heart]. The left apical thrombus was mobile, measuring 1.6×1.5 cm. Left atrium diameter was 4.1cm. Carotid Doppler ultrasound showed no significant stenosis. Dipyridamol stress test of heart ruled out myocardial ischaemia. Magnetic resonance angiogram of left lower limb showed that there was an abrupt cut-off at the left superficial femoral artery at the beginning of the left popliteal artery, with total occlusion of left popliteal artery [piece of clot lodged in leg causing total aterial blockage].


Outcome and follow-up

Patient was managed with intravenous unfractionated heparin infusion, statins, angiotensin converting enzyme inhibitors and β-blockers. Repeat CT showed no evidence of haemorrhagic transformation with progressive improvement of motor aphasia. In addition to the previously mentioned medications, the patient was discharged on aspirin and warfarin as well.

Upon follow-up after 3 months, review echo showed resolution of thrombus with partial improvement of ejection fraction ( 40–45% ).

Upon follow-up after 6 months, ankle brachial index was improved, right side=1.20 and left side=0.82. The patient’s symptoms improved and he was able to resume work.


Discussion

Some athletes whether in competitive or non-competitive sports, abuse AAS to improve their performance or even their appearance as body builders.1

Abusers typically use 5–15 times the recommended medical doses of AAS. Athletes abusing AAS for years have high potential for arterial hypertension, cardiovascular, cerebrovascular disease and lipid metabolism disorder.2

We reported a 39-year-old man, who developed dilated cardiomyopathy, embolic stroke and peripheral vascular disease after self-administration of AAS for 3 years.

Several studies show that high doses of AAS such as nandrolone, may lead to growth-promoting effects on cardiac tissue, as seen in hypertrophic cardiomyopathy, followed by apoptotic cell death which is mediated by membrane-receptor second messenger cascades that increase intracellular Ca2+ influx [Hence the potential utility of Calcium Channel Blockers for AAS users] and mobilisation, leading to the release of apoptogenic factors.3 4

AAS abuse associated with sudden cardiac death, myocardial infarction, ventricular remodelling and cardiomyopathy is related to apoptosis.5 This relation may explain the clinical observations that AAS can lead to myocardial death without coronary thrombosis or atherosclerosis.6 7

Several studies in isolated human myocytes have shown that AAS bind to androgen receptors and may directly cause hypertrophy, via tissue upregulation of the renin-angiotensin system.8 [Hence part of the rationale for using Angiotensin Receptor Blockers EG: Losartan - other important reasons include inhibtion and reversal of AAS-induced scarring and fibrotic tissue accumulation in the heart and cardiovascular system] 

AAS abuse causes decrease in high density lipoprotein cholesterol by 20% and increase in LDL cholesterol by 20% due to lipolytic degradation of lipoproteins and their removal by receptors through modification of apolipoprotein A-I and B synthesis.9 Apolipoprotein B has been experimentally linked to the development of atherosclerosis, mediating the interaction between LDL-C and the arterial wall.1

These lipoprotein abnormalities increase the risk for coronary artery disease by three to sixfold and may occur within 9 weeks of AAS self-administration.8 10 Fortunately, lipid effects seem to be reversible after discontinuation.1

AAS enhance platelet aggregation and thrombus formation by increasing platelet production of thromboxane A2, decreasing production of prostacyclin and increasing fibrinogen levels.1

Ischaemic stroke can occur as a result of atherothrombosis or embolisation either in the carotids or the heart as AAS has been associated with changes in vascular reactivity, lipid profile, haemostasis and platelet aggregation.1 Accordingly, peripheral vascular disease can occur through the same mechanism.1

Our case is unique as our patient developed an embolic stroke and peripheral vascular disease in the absence of any risk factors for either of the diseases, but rather as a complication of dilated cardiomyopathy with LV thrombus formation. These complications were deduced to be the result of AAS abuse after ruling out other aetiological factors. 


References

Santamarina RD, Besocke AG, Romano LM, et al. Ischemic stroke related to anabolic abuse. Clin Neuropharmacol 2008;31:80–5.

Lane HA, Grace F, Smith JC, et al. Impaired vasoreactivity in bodybuilders using androgenic anabolic steroids. Eur J Clin Invest 2006;36:483–8.

D’Ascenzo S, Millimaggi D, Di Massimo C, et al. Detrimental effects of anabolic steroids on human endothelial cells. Toxicol Lett 2007;169:129–36.

Achar S, Rostamian A, Narayan SM. Cardiac and metabolic effects of anabolic-androgenic steroid abuse on lipids, blood pressure, left ventricular dimensions, and rhythm. Am J Cardiol 2010;106:893–901.

Zaugg M, Jamali NZ, Lucchinetti E, et al. Anabolic-androgenic steroids induce apoptotic cell death in adult rat ventricular myocytes. J Cell Physiol 2001;187:90–5.

Fineschi V, Baroldi G, Monciotti F, et al. Anabolic steroid abuse and cardiac sudden death: a pathologic study. Arch Pathol Lab Med 2001;125:253–5.

Wysoczanski M, Rachko M, Bergmann SR. Acute myocardial infarction in a young man using anabolic steroids. Angiology 2008;59:376–8.

Liu PY, Death AK, Handelsman DJ. Androgens and cardiovascular disease. Endocr Rev 2003;24:313–40.

Hartgens F, Rietjens G, Keizer HA, et al. Effects of androgenic-anabolic steroids on apolipoproteins and lipoprotein (a). Br J Sports Med 2004;38:253–9.

Maravelias C, Dona A, Stefanidou M, et al. Adverse effects of anabolic steroids in athletes. A constant threat. Toxicol Lett 2005;158:167–75.

[Daz69]

I think most bodybuilders are less than forthcoming about their AAS use to doctors. Generally speaking we know there's a lot of sanctimonious and/or misinformed tabloid-headline crap that bounces around, and your average hospital doctor isn't likely to know much more than some 'roid rage' horror story that he once read about. I say this from years of experience dealing with them! Knowing this, you're likely to just give a dumbed-down story of what you do in the hope they'll focus on your health and not your lifestyle choices. However in this instance, given he'd had a stroke already (!), and then had to be readmitted later with a total blood clot in the leg, honesty may have be the wiser course - although it wouldn't have affected the treatment in any way.

 

However I think the take-home message from studies like this is less about specifically lipids than how all these vectors interact to cause serious health problems. So, it's not just the lipids that caused his clot - it's the platelet aggregation as the more acute factor. But furthermore, the AAS causing inflexibility of his vascular network (poor vasoreactivity) which promotes atherosclerotic plaque formation and makes the heart pump harder = the enlargement of his heart = inefficient pumping = reduced ejection fraction = relatively stagnant eddies of blood = increased risk of clotting. And of course, not even mentioned in this study is the likely increase in PCV (red blood cell concentration), which would have been an equally important factor. It seems astonishing that they don't seem to be aware of the effect AAS have on RBCs and how that could have aggravated this man's condition, but again that's part of the general lack of knowledge I'm referring to.

[Daz69]

From a previous question which AAS are particularly damaging to the heart, it's hard to answer with any certainty given the chronic lack of controlled research into compounds aside from nandrolone, stanozolol and testosterone.

 

We can speculate that since we know nandrolone is more than 10 times more damaging to blood vessel endothelial cells than testosterone (and causes stiffening/reduced vasoreactivity/fibrosis), that testosterone-derived AAS are probably safer from that specific perspective. So boldenone may be relatively safer as a test-derivative. On the other hand winstrol, for example, seems to be no more harmful to myocytes, perhaps less so in fact, than testosterone, although its effect on lipids is worse.

 

From my own experience, Deca used alone demonstrably raises blood pressure (presumably from the stiffening effect on blood vessels) more so than testosterone at similar doses. Yet since Deca is known to have little impact on lipids, possibly because it's also an oestrogen, you might say there is some balancing in that risk equation.

 

However for me I think issues around lipids - since blood tests are cheap, easy and noticeable - have perhaps become a bit of a diversion from the less obviously visible/measurable risks. Lipids > atherosclerosis > clotting > thrombus formation (in tandem with blood thickening - raised PCV via EPO), are easily reversed post-cycle and/or relatively controllable on-cycle with a combination of venesection/donation, statins, niacin, dietary modifications, fish oils, hydration and aspirin, among others.

 

In a sense therefore the lipid/thrombus issue is more of an acute concern that diminishes once the cycle is over, and for most people will pass unremarkably assuming they lead an otherwise healthy lifestyle and don't abuse high-dose AAS for prolonged periods (I'm thinking particularly of the Blast-n-Cruise brigade whose cruise dose goes way above TRT, or the 5g of gear/wk meatheads who don't also take suitable pharmaceutical precautions).

 

However it's the effect of AAS on blood vessels and blood pressure that gets the least attention and is possibly where the really irreversible, chronic issues come in to play, since this is at the root of the deleterious cardiac remodelling we so wish to avoid (be it from fibrotic, apoptotic or hypertrophic causes).

 

From this perspective, I would speculate that highly androgenic steroids and DHT-derivatives are more harmful since they raise blood pressure directly thanks to constantly elevated CNS priming/sympathetic nervous system stimulation. Combine this with stiffer arteries (and apoptosis-fibrosis) and it raises the cardiac load still further.

 

Of course, the acute issues (thicker blood, poorer lipids, platelet aggregation) feed into this further, hence the annoying circular complexity of it all, and thus presumably the reason so few give a shit about it. But if you control the inotropic/chronotropic (BP and heart rate) effect by limiting both CNS stimulation and arterial stiffening - cut out stimulants, reduce use of highly androgenic AAS, do regular cardio, or alternatively supplement with appropriate pharmaceutical blockers - the acute effects become much less likely to be in a position to cause harm.

 

Sorry this has become a bit rambling, but the point I was trying to get to is that I would speculatively rank them in terms of presumed overall cardiovascular risk factors (best to worst):

 

Test > Bold > Winstrol > Mast > Deca > Tren

 

Tren may actually not be as directly damaging as some of the others (eg doesn't seem to be too bad on lipids for example), but it is an intense CNS stimulant, and that's a huge downside when AAS causes myocyte anabolism. However, it's also hands down one of the best all-round steroids out there for most guys. And rather than avoid it, I'd choose to lessen its side effects.

 

http://www.ncbi.nlm.nih.gov/pubmed/17267145

 

http://www.ncbi.nlm.nih.gov/pubmed/11241353

 

http://www.ncbi.nlm.nih.gov/pubmed/24783419

 

http://www.ncbi.nlm.nih.gov/pubmed/22459398

 

http://www.ncbi.nlm.nih.gov/pubmed/21873939

 

http://www.ncbi.nlm.nih.gov/pubmed/20020375

 

http://www.ncbi.nlm.nih.gov/pubmed/22047750

 

http://www.ncbi.nlm.nih.gov/pubmed/17178777

 

http://www.ncbi.nlm.nih.gov/pmc/arti...er#!po=83.3333

 

http://www.anakarder.com/sayilar/32/...04-357-358.pdf

 

http://www.ncbi.nlm.nih.gov/pmc/arti...-2377-4-22.pdf

 

http://www.ncbi.nlm.nih.gov/pubmed/8531623

[yeelang]

great post be curious to hear your recommends for tests/checks that can be done to see changes over time.

 

looks like ECG monitoring using a Holter monitor and chest x-ray every quarter?

 

also I'm sure T3 has some pretty serious effects on the heart but haven't looked at any research other than for performance

[jimmybro1]

great post be curious to hear your recommends for tests/checks that can be done to see changes over time.

looks like ECG monitoring using a Holter monitor and chest x-ray every quarter?

also I'm sure T3 has some pretty serious effects on the heart but haven't looked at any research other than for performance

An ultrasound of heart, I don't think an xray would show much

[Daz69]

great post be curious to hear your recommends for tests/checks that can be done to see changes over time.

 

looks like ECG monitoring using a Holter monitor and chest x-ray every quarter?

 

also I'm sure T3 has some pretty serious effects on the heart but haven't looked at any research other than for performance

 

You can use a 12-lead ECG (electrocardiogram), but this is limited to diagnosing conduction issues in myocardium, it can suggest LVH, but mainly its use is in emergency medicine for ischaemia or infarction, which is generally too late when tissue death is occurring..

ECG (echocardiogram) is basically an ultrasound of the heart, in real time, it can measure pumping ability and ejection fraction, systolic or diastolic failure.. Its better in its ability to measure heart wall thickness and pumping efficiency..

 

Carotid ultrasound looks for occlusion or stenosis of carotid arteries, which is a good indicator as to whether atherosclerosis is occurring..

 

There are a few more I can't remember..!!

 

Of note: 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.