[skullsmasher]

I would just like to get feedback from members on these few studies that contain findings I was at least somewhat unaware of.

1.aboratory of Biochemistry, School of Physical Education and Sport, Avenida Prof. Mello Moraes 65, Butantã, Cidade Universitária, CEP 05508-9000 São Paulo, Brazil.

We evaluated the effects of swimming and anabolic steroids (AS) on ventricular function, collagen synthesis, and the local renin-angiotensin system in rats. Male Wistar rats were randomized into control ©, steroid (S; nandrolone decanoate; 5 mg/kg sc, 2x/wk), steroid + losartan (SL; 20 mg.kg(-1).day(-1)), trained (T), trained + steroid (T+S), and trained + steroid + losartan (T+SL; n = 14/group) groups. Swimming was performed 5 times/wk for 10 wk. Serum testosterone increased in S and T+S. Resting heart rate was lower in T and T+S. Percent change in left ventricular (LV) weight-to-body weight ratio increased in S, T, and T+S. LV systolic pressure declined in S and T+S. LV contractility increased in T (P < 0.05). LV relaxation increased in T (P < 0.05). It was significantly lower in T+S compared with C. Collagen volumetric fraction (CVF) and hydroxyproline were higher in S and T+S than in C and T (P < 0.05), and the CVF and LV hypertrophy were prevented by losartan treatment. LV-ANG I-converting enzyme activity increased (28%) in the S group (33%), and type III collagen synthesis increased (56%) in T+S but not in T group. A positive correlation existed between LV-ANG I-converting enzyme activity and collagen type III expression (r(2) = 0.88; P < 0.05, for all groups). The ANG II and angiotensin type 1a receptor expression increased in the S and T+S groups but not in T group. Supraphysiological doses of AS exacerbated the cardiac hypertrophy in exercise-trained rats. Exercise training associated with AS induces maladaptive remodeling and further deterioration in cardiac performance. Exercise training associated with AS causes loss of the beneficial effects in LV function induced by exercising. These results suggest that aerobic exercise plus AS increases cardiac collagen content associated with activation of the local renin-angiotensin system.

PMID: 17906098 [PubMed - in process]

How much do you think this relates to when humans train and use steroids? I mean, this implies that aerobic performance will diminish with the use of steroids basically correct? Do yo uagree with this?

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Department of Clinical and Experimental Pharmacology, University of Adelaide, Adelaide, SA, Australia.

Anabolic steroid abuse has been associated with thrombosis and arteriosclerosis, both of which predispose to myocardial ischemia and infarction. However, there are reports of sudden cardiac death in the absence of thrombus and atheroma following anabolic steroid use. Although treatment with the commonly abused steroid, nandrolone, has been shown to decrease recovery of systolic function following ischemia in isolated rat hearts, it is unknown whether anabolic steroids can increase the incidence of fatal arrhythmia associated with cardiac ischemia. Anesthetized male Sprague-Dawley rats were administered vehicle or nandrolone (10-160 microg/kg/min iv) 10 min prior to 15-min occlusion of the left anterior descending coronary artery followed by 10-min reperfusion. Nandrolone, in this dose range, did not significantly change heart rate, blood pressure, or cardiac rhythm in the absence of ischemia. However, the fraction of rats surviving ischemia was significantly (p < 0.05) decreased by nandrolone at both 40 and 160 microg/kg/min, while survival time during ischemia was decreased significantly (p < 0.001) by nandrolone 160 microg/kg/min. An increase (p < 0.05) in the duration of ventricular fibrillation was noted at the highest compared to the lowest dose of nandrolone, corresponding to a significant increase in the fraction of rats experiencing ventricular fibrillation (p < 0.01). Nandrolone had no effect on the frequency or duration of ventricular fibrillation or survival time during reperfusion. Although the mechanisms underlying these effects are currently unclear, they indicate that exposure to anabolic steroids in combination with transient reductions in coronary blood flow may explain some reports of sudden cardiac death in anabolic steroid users.

PMID: 17652335 [PubMed - indexed for MEDLINE]

What specifically is a "transient reduction in coronary blood flow" ?


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[Benson]

You have to be cautious using rat studies to infer too much. For whatever reason, much of the observed cardiac toxicity seen in rats given AAS are not seen in humans.

Sports Med. 2004;34(8):513-54.
Effects of androgenic-anabolic steroids in athletes.
Hartgens F, Kuipers H.

Department of Surgery, Outpatient Clinic Sports Medicine, University Hospital Maastricht, and Sports Medicine Center Maastricht, Maastricht, The Netherlands. fhartgens@home.nl

Androgenic-anabolic steroids (AAS) are synthetic derivatives of the male hormone testosterone. They can exert strong effects on the human body that may be beneficial for athletic performance. A review of the literature revealed that most laboratory studies did not investigate the actual doses of AAS currently abused in the field. Therefore, those studies may not reflect the actual (adverse) effects of steroids. The available scientific literature describes that short-term administration of these drugs by athletes can increase strength and bodyweight. Strength gains of about 5-20% of the initial strength and increments of 2-5 kg bodyweight, that may be attributed to an increase of the lean body mass, have been observed. A reduction of fat mass does not seem to occur. Although AAS administration may affect erythropoiesis and blood haemoglobin concentrations, no effect on endurance performance was observed. Little data about the effects of AAS on metabolic responses during exercise training and recovery are available and, therefore, do not allow firm conclusions. The main untoward effects of short- and long-term AAS abuse that male athletes most often self-report are an increase in sexual drive, the occurrence of acne vulgaris, increased body hair and increment of aggressive behaviour. AAS administration will disturb the regular endogenous production of testosterone and gonadotrophins that may persist for months after drug withdrawal. Cardiovascular risk factors may undergo deleterious alterations, including elevation of blood pressure and depression of serum high-density lipoprotein (HDL)-, HDL2- and HDL3-cholesterol levels. In echocardiographic studies in male athletes, AAS did not seem to affect cardiac structure and function, although in animal studies these drugs have been observed to exert hazardous effects on heart structure and function. In studies of athletes, AAS were not found to damage the liver. Psyche and behaviour seem to be strongly affected by AAS. Generally, AAS seem to induce increments of aggression and hostility. Mood disturbances (e.g. depression, [hypo-]mania, psychotic features) are likely to be dose and drug dependent. AAS dependence or withdrawal effects (such as depression) seem to occur only in a small number of AAS users. Dissatisfaction with the body and low self-esteem may lead to the so-called 'reverse anorexia syndrome' that predisposes to the start of AAS use. Many other adverse effects have been associated with AAS misuse, including disturbance of endocrine and immune function, alterations of sebaceous system and skin, changes of haemostatic system and urogenital tract. One has to keep in mind that the scientific data may underestimate the actual untoward effects because of the relatively low doses administered in those studies, since they do not approximate doses used by illicit steroid users. The mechanism of action of AAS may differ between compounds because of variations in the steroid molecule and affinity to androgen receptors. Several pathways of action have been recognised. The enzyme 5-alpha-reductase seems to play an important role by converting AAS into dihydrotestosterone (androstanolone) that acts in the cell nucleus of target organs, such as male accessory glands, skin and prostate. Other mechanisms comprises mediation by the enzyme aromatase that converts AAS in female sex hormones (estradiol and estrone), antagonistic action to estrogens and a competitive antagonism to the glucocorticoid receptors. Furthermore, AAS stimulate erythropoietin synthesis and red cell production as well as bone formation but counteract bone breakdown. The effects on the cardiovascular system are proposed to be mediated by the occurrence of AAS-induced atherosclerosis (due to unfavourable influence on serum lipids and lipoproteins), thrombosis, vasospasm or direct injury to vessel walls, or may be ascribed to a combination of the different mechanisms. AAS-induced increment of muscle tissue can be attributed to hypertrophy and the formation of new muscle fibres, in which key roles are played by satellite cell number and ultrastructure, androgen receptors and myonuclei. Copyright 2004 Adis Data Information BV

PMID: 15248788

Int J Sports Med. 2003 Jul;24(5):344-51.
Prospective echocardiographic assessment of androgenic-anabolic steroids effects on cardiac structure and function in strength athletes.
Hartgens F, Cheriex EC, Kuipers H.

Netherlands Centre for Doping Affairs, Capelle aan den IJssel, The Netherlands. fhartgens@wxs.nl

Since the abuse of androgenic-anabolic steroids (AAS) has been associated with the occurrence of serious cardiovascular disease in young athletes, we performed two studies to investigate the effects of short-term AAS administration on heart structure and function in experienced male strength athletes, with special reference to dose and duration of drug abuse. In Study 1 the effects of AAS were assessed in 17 experienced male strength athletes (age 31 +/- 7 y) who self-administered AAS for 8 or 12 - 16 weeks and in 15 non-using strength athletes (age 33 +/- 5 y) in a non-blinded design. In Study 2 the effects of administration of nandrolone decanoate (200 mg/wk i. m.) for eight weeks were investigated in 16 bodybuilders in a randomised double blind, placebo controlled design. In all subjects M-mode and two-dimensional Doppler-echocardiography were performed at baseline and after 8 weeks AAS administration. In the athletes of Study 1 who used AAS for 12 - 16 weeks a third echocardiogram was also made at the end of the AAS administration period. Echocardiographic examinations included the determination of the aortic diameter (AD), left atrium diameter (LA), left ventricular end diastolic diameter (LVEDD), interventricular septum thickness (IVS), posterior wall end diastolic wall thickness (PWEDWT), left ventricular mass (LVM), left ventricular mass index (LVMI), ejection fraction (EF) and right ventricular diameter (RVD). For assessment of the diastolic function measurements of E and A peak velocities and calculation of E/A ratio were used. In addition, acceleration and deceleration times of the E-top (ATM and DT, respectively) were determined. For evaluation of factors associated with stroke volume the aorta peak flow (AV) and left ventricular ejection times (LVET) were determined. In Study 1 eight weeks AAS self-administration did not result in changes of blood pressure or cardiac size and function. Additionally, duration of AAS self-administration did not have any impact on these parameters. Study 2 revealed that eight weeks administration of nandrolone decanoate did not induce significant alterations in blood pressure and heart morphology and function. Short-term administration of AAS for periods up to 16 weeks did not lead to detectable echocardiographic alterations of heart morphology and systolic and diastolic function in experienced strength athletes. The administration regimen used nor the length of AAS abuse did influence the results. Moreover, it is concluded that echocardiographic evaluation may provide incomplete assessment of the actual cardiac condition in AAS users since it is not sensitive enough to detect alterations at the cellular level. Nevertheless, from the present study no conclusions can be drawn of the cardiotoxic effects of long term AAS abuse.

PMID: 12868045

Probably also dependent on what steroid is used and how much.

[skullsmasher]

Yes, I see, thanks.

See thats it...there is so much conflicting info out there I am very frustrated. I know the one way to eliminate the need for all this research in a way is to get fulll blood work etc but, honestly....hjow many people actually do that or can afford to I should say?

I am basically trying to stay as healthy as possible while using anabolics but, I guess I am becoming discouraged at the likeliness of my attempts when I read everything in pubmed. I mean they have studies in there stating in healthy young adult males, sudden cardiac death has been reported to just name one incident, let alone the others.

what to do what to do.........

[Benson]

Well, suffice it to say, steroids aren't good for your heart...but, on the other hand, sudden cardiac death is not unheard of in young men using no drugs so its hard to say with authority that steroids cause heart attacks...

Hawthorn and CQ10 are probably sensible ancillaries and keeping your cycles short and taking time away is good advice.

[skullsmasher]

Yea I hear ya.

I have been taking 100mg of CQ10 ED

[Jakeshorts]

keeping a steady cardio regimen could also keep cardiac health up too. Keep in mind in that first study posted losartan is used and I believe that's a hypertension medication. An ARB to be exact. Water retension probably was noted as well.