T Nation

Cardio on Gear

I’ve always been a huge fan of cardio and conditioning in general. While on gear I always tried to keep doing cardio, but am starting to wonder whether it’s a good idea in the long run?

Right now I’m running Test Cyp 600mg/wk and EQ 500mg/wk, on a 12 week cycle, currently on week 3, and lifting 5 times a week and doing cardio 2-3 mornings/wk (not same session as the lifting, I lift afternoons). I’ve been competing at a high level (brown belt) in grappling for years so I’m used to grueling schedules, but I’m starting to get concerned about cardiac hypertrophy from a lot of cardio and conditioning while on gear.

Are my worries reasonable given my training or am I worrying too much about it?

Thanks all,

LB

If you are doing so much cardio that you are losing muscle mass while on gear, you are doing something very wrong my friend

This sounds dickish but that’s not his question VT.

As far as the cardiac hypertophy, from what I understand of AAS (I’m no chemist) is that it will not enlarge your organs (at least to the point that you believe). Now HGH is completely different (again, from what I understand). HGH will increase the size of all the organs in the body, hence the “HGH gut” of today’s pro bb’s.

I think you may be reading a bit too far into this lbraga. If you are that concerned about your health, why not just get off AAS? Because that is really what this boils down to. You have legitimate health concerns that are worrying you, yet you’re pumping drugs into your system. Even if your risk is unwarranted, the guilt that is eating at you is putting extra stress on your mind and body which in turn could develop in to psychosomatic illnesses.

Personally I think you’re blowing this out of proportion but then again I am not a doctor. If you are that concerned start doing research on AAS and cardiac hypertrophy. Google is your friend. Research can be cold and boring but it provides facts compared to “bro science” which is what you seem to be looking for here. That false sense of security from “one bro to another” that “I did XYZ and nothing ever happened to me”. That is the kind of mentality where people end up seriously hurt or dead (kind of like, “Hold my beer, watch this”).

Might sound a bit overdramatic but that’s what I have. So in recap…

1 Research AAS and Cardiac Hypertrophy
2 If you don’t understand, go to your doctor and spill your guts that you’ve been jagging 23 gauge needles into your body with 1100 mg’s of AAS every week and you are concerned that you’re heart is going to get too large. Run tests, ekg, c-scan, mri’s the works. Hope you have good insurance.
3 Keep jagging that shit because if you ever watched How the Grinch Stole Christmas you’d see that there is NOTHING wrong when your heart grows 3 sizes to large! Christmas is just around the corner, don’t be a Grinch.

Here is a sample of 3 seconds spent research AAS and Cardiac Hypertrophy on Bing:

3.2. Effects of AAS use on heart mass
3.2.1. The impact of AAS use
Eleven (12%) of the AAS users and 13 (7%) of the controls had heart weights greater than 500 g. Analysis of the logarithm of heart mass by multivariate statistics showed strong correlations between body mass and heart mass [F([1,261)=142.1, P<.00001], height and heart mass [F(1,261)=5.24, P<.02], and age and heart mass [F(1,261)=20.4, P<.00001]. A significantly greater heart mass [F(1, 261)=16.4, P=.0001] was also identified among AAS users (Fig. 1).

4.1. Comments on the findings
The major finding presented here was a significantly greater cardiac mass among deceased users of AAS compared to individuals with no suspected use of AAS. Multivariate analysis indicated that the increased heart size in the AAS users was explained not only by a physiological adaptation to an increased body mass, but also by some other factor related to use of AAS.

This finding correlates with earlier echocardiography-based studies that have demonstrated an elevated risk of developing concentric LVH among AAS users [14], [15], [16] and [25]. Other studies have failed to detect such a relationship [12], [17], [18] and [19]. It has been argued that the negative studies usually involved the use of moderate doses of AAS compared to the positive studies that involved a history of long-term AAS use [26]. Our sample consisted of deceased persons who were subjected to medicolegal death investigations. AAS analysis was performed only at the request of the forensic pathologist in such investigations. During the most recent 10-year period, approximately 20% of the deceased individuals subjected to postmortem medicolegal examinations were screened for illicit drugs, but less than 1% for AAS. We believe that most forensic pathologists only decide to include AAS in the toxicology screen when increased muscle mass is observed, which implies that our sample mostly consisted of long-term AAS users. If this assumption holds, AAS-related cardiac hypertrophy could be connected to long-term use of AAS.

Although our cases originated from medicolegal investigations with an expected high number of deaths from unnatural causes, it is surprising that only one of these deaths was considered to be related primarily to cardiac hypertrophy. One interpretation could be that the risk of death from cardiac hypertrophy in AAS users is not very great. However, it is also possible that cardiac death related to AAS use occurs later, perhaps with the cessation of weight training. If this is the case, the possible connections between AAS use and cardiac pathology might be overlooked. Accumulating evidence strongly indicates that the use of AAS spread outside the communities of elite athletes in the early 1980s; therefore, adverse effects that may require years or even decades to develop, such as cardiac hypertrophy, could markedly increase in the near future [26].

Yeah i was drunk posting last night and read that as “cardiac atrophy”. My bad.

[quote]SIM37 wrote:
Here is a sample of 3 seconds spent research AAS and Cardiac Hypertrophy on Bing:

3.2. Effects of AAS use on heart mass
3.2.1. The impact of AAS use
Eleven (12%) of the AAS users and 13 (7%) of the controls had heart weights greater than 500 g. Analysis of the logarithm of heart mass by multivariate statistics showed strong correlations between body mass and heart mass [F([1,261)=142.1, P<.00001], height and heart mass [F(1,261)=5.24, P<.02], and age and heart mass [F(1,261)=20.4, P<.00001]. A significantly greater heart mass [F(1, 261)=16.4, P=.0001] was also identified among AAS users (Fig. 1).

4.1. Comments on the findings
The major finding presented here was a significantly greater cardiac mass among deceased users of AAS compared to individuals with no suspected use of AAS. Multivariate analysis indicated that the increased heart size in the AAS users was explained not only by a physiological adaptation to an increased body mass, but also by some other factor related to use of AAS.

This finding correlates with earlier echocardiography-based studies that have demonstrated an elevated risk of developing concentric LVH among AAS users [14], [15], [16] and [25]. Other studies have failed to detect such a relationship [12], [17], [18] and [19]. It has been argued that the negative studies usually involved the use of moderate doses of AAS compared to the positive studies that involved a history of long-term AAS use [26]. Our sample consisted of deceased persons who were subjected to medicolegal death investigations. AAS analysis was performed only at the request of the forensic pathologist in such investigations. During the most recent 10-year period, approximately 20% of the deceased individuals subjected to postmortem medicolegal examinations were screened for illicit drugs, but less than 1% for AAS. We believe that most forensic pathologists only decide to include AAS in the toxicology screen when increased muscle mass is observed, which implies that our sample mostly consisted of long-term AAS users. If this assumption holds, AAS-related cardiac hypertrophy could be connected to long-term use of AAS.

Although our cases originated from medicolegal investigations with an expected high number of deaths from unnatural causes, it is surprising that only one of these deaths was considered to be related primarily to cardiac hypertrophy. One interpretation could be that the risk of death from cardiac hypertrophy in AAS users is not very great. However, it is also possible that cardiac death related to AAS use occurs later, perhaps with the cessation of weight training. If this is the case, the possible connections between AAS use and cardiac pathology might be overlooked. Accumulating evidence strongly indicates that the use of AAS spread outside the communities of elite athletes in the early 1980s; therefore, adverse effects that may require years or even decades to develop, such as cardiac hypertrophy, could markedly increase in the near future [26].

[/quote]

Thanks for pulling this. This is exactly the kind of thing I had been looking for. I learned about GH and all the side effects of AAS on the endocrine and GI pathways my first year of med school but I haven’t seen cardiac pathology yet. With the amount of nosing around people around and the competitive atmosphere here I couldn’t exactly ask one of the M3/M4s or one of the lecturing MDs.
Thanks again for the help

health schmealth. Live fast, die young and leave a huge, muscular corpse

[quote]rds63799 wrote:
health schmealth. Live fast, die young and leave a huge, muscular corpse[/quote]

LOLL

Heart size is correlated with overall body mass in trained and untrained subjects, so to ‘pin’ the blame on AAS solely would be mistaken.

Heart valve elasticity (forget proper medical term) can be negatively affected by adrenals (ie: Clen et al). This is unfortunately the root of the AAS - cardiac health fallacy.

-PTD