AAS and Cardiovascular/Pulmonary Function

[Dr JIM]

1) Evolution? I'm referring to the age related decline in TT levels as a protective mechanism rather than an evolutionary response that often requires hundred if not thousands of years.

The fact is as, I eluded to earlier, MANY of those now on TRT don't NEED it, but rather are following the media and big blog hype correcting a "low TT" level can cure mankind ills from A-Z. And the risks, although small and difficult to quantify, are probably the equivalent of youthful maleness, IMO

2) I suspect Nandrolone has been studied more than any other AAS except one Testosterone, and the differences are indeed striking in many respects

Moreover Nandrolone poses some distinct differences in part bc of its relatively high lipid solubility, generation of at least three active metabolites, hepatic conjugation,
and high A;A ratio. And like many drug specific metabolites, how and where they are processed physiologically is often responsible for the toxicities observed.

And bc of these and other metabolic differences, much like antibiotics have variable therapeutic and "toxic" ranges, I believe it's important to avoid charicterizing AAS as being more of the same until such data avails itself.

JIM

 

[hurricane]

The level of PA was ascertained by interviewer assisted questioner. The info obtained was further quantified as METs.

This is not the first study which has exposed the risk, or lack of benefit to VIGOROUS exercise.

Once again moderation is of paramount importance

Here's a short and relatively easy to follow synopsis of a study on CAC and it's utility in diagnosing ASYMPTOMATIC heart disease.

And since MANY of those cycling AAS experience a diminished aerobic capacity basing relative risk on the presence or absence of symptoms poses another problem ---which form of risk stratification (or "cardiac test") is most suitable for this subset of patients, as a means to an ends, preventing Sudden Cardiac Death.

To that end the use of AAS as PEDs should be included as a separate cardiac risk factor, IMO

Jim

Doc just how important is cardio in your opinion? I ask because I really regret stopping cardio once I left the service. Didn't do any for 5 years. Maybe 10 minutes here and there on the elliptical. One other thing. I've decided to drastically reduce my red meat consumption. I'll have it maybe once every 10 days now. Is it worth it?? Do you think it will benefit me or no?? Thanks Doc.

 

[hurricane]

1) Evolution? I'm referring to the age related decline in TT levels as a protective mechanism rather than an evolutionary response that often requires hundred if not thousands of years. The fact is as, I eluded to earlier, MANY of those now on TRT don't NEED it, but rather are following the media and big blog hype correcting a "low TT" level
can cure mankind ills from A-Z. And the risks, are probably the equivalent of youthful maleness.

2) I suspect Nandrolone has been studied more than any other AAS except one Testosterone, and the differences are indeed striking in many respects

Moreover Nandrolone poses some distinct differences in part bc of its relatively high lipid solubility, generation of at least three active metabolites, hepatic conjugation,
and high A;A ratio. And like many drug specific metabolites, how and where they are processed physiologically is often responsible for the toxicities observed.

And bc of these and other metabolic differences, much like antibiotics have variable therapeutic and "toxic" ranges, I believe it's important to avoid charicterizing AAS as being more of the same until such data avails itself.

JIM

Agree 100%. Men were just fine before a trt clinic opened on every corner(exaggerating). While trt may be beneficial, someone with a TT level of 400 doesn't have low T. Can't tell you how many times I've heard that one. Last check I was 584. Sure I'd like to be 900. But it's called getting older. At least that's my 2 cents.

 

[Dr JIM]

Does this apply to weight training or cardiovascular exercise?

 

[Dr JIM]

Agree 100%. Men were just fine before a trt clinic opened on every corner(exaggerating). While trt may be beneficial, someone with a TT level of 400 doesn't have low T. Can't tell you how many times I've heard that one. Last check I was 584. Sure I'd like to be 900. But it's called getting older. At least that's my 2 cents.

Many of these “low TT” folk are requesting or are interested in reaching levels two to three times their age related limits and THATS where I suspect the “risk” of TRT, however small it is, encroaches upon “benefit”, esp for those older folk with a lifelong history of csrdiac risk factors.

Jim

 

[Millard]

The study didn't mention what type of exercise the participants were doing. Does that even matter?

Does this apply to weight training or cardiovascular exercise?

Here is the CARDIA Physical Activity History Questionnaire I think they used:

https://www.cardia.dopm.uab.edu/images/more/pdf/Year25/CARDIA/Form18.pdf

At each of the 8 examinations, self-reported leisure-time PA was ascertained by the interviewer-administered CARDIA Physical Activity History Questionnaire.17 Participants were asked about the frequency of participation in 13 specific categories (8 vigorous intensity and 5 moderate intensity) of recreational sports, exercise, home maintenance, and occupational activities during the previous 12 months. Intensity for each activity was expressed as metabolic equivalents (METs), in which 1 MET is defined as the energy expended at rest, which is approximately equivalent to an oxygen consumption of 3.5 mL per 1 kg of body weight per minute.18 Vigorous activities (≥6 METs) included running or jogging; racquet sports; biking; swimming; exercise or dance class; job lifting, carrying, or digging; shoveling or lifting during leisure; and strenuous sports. Moderate-intensity activities (3-5 METs) included nonstrenuous sports, walking and hiking, golfing and bowling, home exercises or calisthenics, and home maintenance or gardening.19 Each activity was scored according to whether it was performed for 1 hour or longer during any 1 month during the past year, the number of months it was performed at that level, and the number of months the activity was performed frequently. Each activity was then assigned an intensity score, ranging from 3 to 8 METs, and a duration threshold (ranging from 2-5 hours per week), above which participation was considered to be frequent.20

A total PA score was computed using a computer-based algorithm by multiplying the frequency (number of months) by the intensity score of the activity with a weighting factor to represent duration of participation.

 

[Michael Scally MD]

[Rats] Effects of Testosterone Enanthate and Resistance Training on Myocardium

This study was performed to determine the effects of 8 weeks testosterone enanthate (TE) injection and resistance training (RT) on cardiac muscle in male Wistar rats.

A total of 28 male adult Wistar rats were randomly divided into 4 groups;
control + placebo,
RT + placebo,
TE and
TE + RT.

Testosterone enanthate (20 mg/kg BW, IM) and placebo (olive oil; 0.2 ml, IM) were injected twice a week for 2 months. The RT consisted of climbing (5 reps/3 sets) a ladder carrying a load suspended from the tail. The serum activities of aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH) and creatine kinase MB (CK-MB) and serum level of creatinine, urea and cardiac troponin I (CTnI) were evaluated. After sacrifice, samples from myocardial muscle were collected for histopathology evaluation.

The serum concentration of CTnI and CK-MB activity significantly increased in group RT compared with control (p < .05). In group RT + TE, all biomarkers of muscle damage (CTnI, CK-MB, AST, LDH) were significantly more than those in control (p < .05). Also, mild myocardial hypertrophy was observed in RT and RT + TE groups.

The higher level of all heart damage biomarkers in the RT + TE group rather than control may indicate the synergistic effects of medication and exercise.

Karbasi S, Zaeemi M, Mohri M, Rashidlamir A, Moosavi Z. Effects of testosterone enanthate and resistance training on myocardium in Wistar rats; clinical and anatomical pathology. Andrologia. Effects of testosterone enanthate and resistance training on myocardium in Wistar rats; clinical and anatomical pathology - Karbasi - 2017 - Andrologia - Wiley Online Library

 

[Millard]

It's bad enough with all the Negative AAS reports. Now too much exercise is a problem?

Not only that but AAS + resistance training is synergistically bad -- at least in rats

The higher level of all heart damage biomarkers in the RT + TE group rather than control may indicate the synergistic effects of medication and exercise.

 

[ErikR]

Not only that but AAS + resistance training is synergistically bad -- at least in rats

The amount of testosterone that the rats were given would equal about 3,000 mg for a 200lb man. Is this correct?

 

[hurricane]

Not only that but AAS + resistance training is synergistically bad -- at least in rats

Poor rats! LOL

 

[Dr JIM]

The amount of testosterone that the rats were given would equal about 3,000 mg for a 200lb man. Is this correct?

[Rats] Effects of Testosterone Enanthate and Resistance Training on Myocardium

Testosterone enanthate (20 mg/kg BW, IM) and placebo (olive oil; 0.2 ml, IM) were injected twice a week for 2 months.

That's 40mg/kg/week or FOUR Grams/ week for a 200 lb fella. (I'll review and post the study to be sure)

Not excessive by many BB standards IME, esp if ALL AAS being cycled were included.

Are these results surprising considering the dose used NIMO ------- yet these RATs were "studied" for only TWO MONTHS ---- imagine how years of use might effect cardiac enzymes such as Troponin

And for those whom are unaware how "Troponin" is used in contemporary medicine ------- its a specific marker of cardiac INJURY ---- and is the laboratory gold standard for a HEART ATTACK!

Jim

 

[Xlgx]

Justin Harris from troponin nutrition

 

[Dr JIM]

Here is the study the dose used was 40mg/kg/wk.

The Troponin level increased more three fold from baseline which is very worrisome if these results were to be reproduced in humans as such changes are consistent with a "heart attack".

More info on Troponin levels second citation

 

[Dr JIM]

If reproduced in humans these results may help explain many of the cardiac effects of AAS especially the reduced aerobic capacity many have experienced.


The Trop assay I posted above deleted the second and most important page, which contained the NORMAL values in HUMANS.

 

[Millard]

The amount of testosterone that the rats were given would equal about 3,000 mg for a 200lb man. Is this correct?

Not exactly human equivalent dose:



Source: A simple practice guide for dose conversion between animals and human



Source: https://www.fda.gov/downloads/drugs/guidances/ucm078932.pdf

 

[Dr JIM]

While I agree Millard lets remember BB are not running TT at human equivalent dosages either and for that reason the results maybe reflective of the HIGH dosages MANY competitive BB are using today, and suggest a potential MOA for many of the cardiac effects of AAS reported in the literature from cardiomyopathy to reduced exercise tolerance.

To that end Trop may be a worthwhile screening assay for those running AAS, esp in high dosages IMO

One can only hope similar studies are conducted using LOWER TT dosages,

 

[hurricane]

While I agree Millard lets remember BB are not running TT at human equivalent dosages either and for that reason the results maybe reflective of the HIGH dosages MANY competitive BB are using today, and suggest a potential MOA for many of the cardiac effects of AAS reported in the literature from cardiomyopathy to reduced exercise tolerance.

To that end Trop may be a worthwhile screening assay for those running AAS, esp in high dosages IMO

One can only hope similar studies are conducted using LOWER TT dosages,

Did the rats actually have MI's?? Just wondering out loud. That is a very good study if it can directly correlate to humans.

 

[Dr JIM]

Did the rats actually have MI's?? Just wondering out loud. That is a very good study if it can directly correlate to humans.

Good question and one I’ll defer
to a vet.

I do know rats have some of the highest collateral flow which I suspect is one reason they rarely die of an MI, in spite of eating hordes of “junk food”, perhaps
their average life span of roughly one year explains why.

Most rodents die of CA based upon the data I’ve seen.

In humans there are varying degrees of a “heart attack”

At one end of the spectrum is what many refer to as “coronary leak syndrome” in which the ECG is less than diagnostic but the tropinin is elevated while at the other end is a “transmural MI” in which the ECG is diagnostic of a heart attack and the troponin is quite high.

I just don’t know how to apply THIS data to rats but a three fold
Tropinin elevation in a human is VERY worrisome indeed.

Its thought some folk w cardiomyopathy have micro-infarcts
in which obstruction of small vessels
leads to congestive failure, this MAY
be what is going on with B.B. bc there are several case reports of SCD in spite of clean coronary arteries at autopsy.

Of course another possibility could be the development of micro-infarcts which has been shown to lower the
V-T /V-F threshold based upon EPS studies.

Nonetheless this study must be repeatef at lower dosages in rats and then in humans to determine IF a HUMAN cause and effect relationship exists.

Needless to say I find it VERY interesting.

 

[hurricane]

Good question and one I’ll defer
to a vet.

I do know rats have some of the highest collateral flow which I suspect is one reason they rarely die of an MI, in spite of eating hordes of “junk food”, perhaps
their average life span of roughly one year explains why.

Most rodents die of CA based upon the data I’ve seen.

In humans there are varying degrees of a “heart attack”

At one end of the spectrum is what many refer to as “coronary leak syndrome” in which the ECG is less than diagnostic but the tropinin is elevated while at the other end is a “transmural MI” in which the ECG is diagnostic of a heart attack and the troponin is quite high.

I just don’t know how to apply THIS data to rats but a three fold
Tropinin elevation in a human is VERY worrisome indeed.

Its thought some folk w cardiomyopathy have micro-infarcts
in which obstruction of small vessels
leads to congestive failure, this MAY
be what is going on with B.B. bc there are several case reports of SCD in spite of clean coronary arteries at autopsy.

Of course another possibility could be the development of micro-infarcts which has been shown to lower the
V-T /V-F threshold based upon EPS studies.

Nonetheless this study must be repeatef at lower dosages in rats and then in humans to determine IF a HUMAN cause and effect relationship exists.

Needless to say I find it VERY interesting.

Thanks Doc. It is very interesting. And I don't know anything about a rats makeup. That's why I was intrigued.

 

[Dr JIM]

Thanks Doc. It is very interesting. And I don't know anything about a rats makeup. That's why I was intrigued.

Agreed