Anabolic Steroid Use and AbuseOct 27, Author: The steroid ring is composed of three 6-carbon rings and one 5-carbon ring joined, of which cholesterol is the most basic form and, indeed, the precursor. Although the term steroid includes all agents derived from this ringed structure, this discussion includes only testosterone and the anabolic-androgenic steroids AASs. Testosterone is the principle hormone in humans that produces male secondary sex characteristics androgenic and is an important hormone in maintaining adequate nitrogen balance, thus aiding in tissue sign of low testosterone and the maintenance of muscle mass anabolic. Testosterone has a dual action and can be described in terms of abuse of anabolic steroids could result in androgenic and anabolic capacities. AASs are drugs derived from the modification of the testosterone molecule in order to sterpids or limit certain characteristics of testosterone.
Anabolic steroids: Use, side effects, and risks
To investigate the reversibility of adverse cardiovascular effects after chronic abuse of anabolic androgenic steroids AAS in athletes. Doppler echocardiography and cycle ergometry including measurements of blood pressure at rest and during exercise were undertaken in 32 bodybuilders or powerlifters, including 15 athletes who had not been taking AAS for at least 12 months ex-users and 17 currently abusing AAS users , as well as in 15 anabolic-free weightlifters.
Left ventricular muscle mass related to fat-free body mass and the ratio of mean left ventricular wall thickness to internal diameter were not significantly higher in users 3. Left ventricular wall thickness related to fat-free body mass was also lower in weightlifters, but did not differ between users and ex-users. In all groups, systolic left ventricular function was within the normal range.
Several years after discontinuation of anabolic steroid abuse, strength athletes still show a slight concentric left ventricular hypertrophy in comparison with AAS-free strength athletes. Anabolic androgenic steroids AAS have been used by strength athletes for almost five decades in order to improve performance by increasing muscle mass and strength.
Abuse of these drugs also involves many athletes practising leisure time sports who want to enhance their physical appearance and who act upon recommendations given by training colleagues or the underground literature when choosing the preparations and fixing the dosages. Among the numerous documented toxic and hormonal effects of AAS, attention has been focused especially on the cardiovascular effects during recent years. However, the extent to which these effects are reversible after discontinuing intake of these agents and the degree to which they leave permanent impairment are still controversial matters.
In former Finnish world class powerlifters suspected of AAS intake during their sports career, a 4. In the present study, we have examined for the first time whether cardiovascular changes are detectable one to several years after discontinuing AAS abuse in male former users. This group was compared with current AAS users and with highly trained anabolic-free strength athletes.
All subjects gave written informed consent. Anonymity was expressly guaranteed. The AAS reported to be given by intramuscular injections were boldenone, drostanolone, formebolone, metenolone, nandrolone, stanozolol, esters of testosterone, and trenbolone.
The substances taken orally included 4-dehydrochlormethyltestosterone, fluoxymesterone, mesterolone, metenolone, metandienone, oxandrolone, oxymetholone, and stanozolol. All except two ex-users used combinations of both oral and injectable substances. One ex-user took cocaine sporadically three times a months for the previous four years , two users had taken cocaine once in the past. The classification into ex-users, users, and anabolic-free weightlifters was strengthened by additional measurements of luteinising and follicle stimulating hormones, showing clearly depressed blood concentrations in all users, while all ex-users and the nine weightlifters measured had normal values.
Per year each weightlifter had approximately nine doping tests out of competition, and three to four tests during competition. To estimate the extent of AAS abuse, a point score was established. The limits were chosen in order to include 6—10 athletes in each of the categories; if other anabolic substances such as growth hormone and clenbuterol were used, an additional point was accorded. The maximum point score available was therefore 14 and the minimum 3. Ex-users had been training for In addition to the bodybuilding, six ex-users and one user had also been active in powerlifting.
Body height and mass were measured and the body surface area estimated from a nomogram. The percentage of body fat and the resulting fat-free body mass were calculated from 10 skinfold measurements using the calliper method. All subjects undertook an incremental graded exercise test on an electrically braked cycle ergometer in the sitting position, increasing by 50 W every three minutes until volitional exhaustion.
The test included 12 channel ECG recordings and blood pressure measurements according to Riva-Rocci, using a cuff specially adapted to the enlarged upper arm girth at rest at least two measurements on both arms after 10 minutes in the supine position and during exercise.
Peak oxygen uptake was calculated from the maximum power output by internal regression analysis. The echocardiographic recordings and measurements were made according to the American Society of Echocardiography in the supine left lateral position by the same experienced investigator, who was blinded to AAS use and to the results of the physical examination 2. Left ventricular muscle mass was calculated according to Devereux and colleagues, 11 along with the hypertrophic index interventricular septum plus posterior wall thickness divided by the internal diameter.
Systolic function was determined by measurements of fractional shortening end diastolic left ventricular internal diameter minus end systolic diameter divided by end diastolic diameter. Diastolic function was evaluated by Doppler echocardiography based on the maximum transmitral flow velocities during the early Emax and late Amax diastolic filling phase, measured at the tips of the mitral leaflets in the four chamber view.
Data are expressed as mean SD. Relations between selected measures were calculated by Spearman rank correlation. Ex-users were older than users and weightlifters. In relation to body mass, maximum performance of weightlifters was less than that of ex-users or users, with the maximum heart rate indicating exhaustion at a lower level in the weightlifter group. One user showed constant ST segment depressions of 0. In all other subjects the ECG at rest and during exercise showed no peculiarities.
Five users, two ex-users, and one weightlifter showed high borderline blood pressure values at rest defined as systolic values between — mm Hg and diastolic values between 95— mm Hg , which returned to normal at W during exercise, with the exception of two users with borderline diastolic blood pressure values of and mm Hg, respectively.
Left ventricular muscle mass was clearly lower in weightlifters than in ex-users and users. There were no differences between users and ex-users with regard to fat-free body mass. The end diastolic left ventricular internal diameter EDD did not show any absolute or body surface area related differences between ex-users and users; related to the fat-free body mass it is slightly higher in ex-users than in users and weightlifters.
Two ex-users, seven users, and none of the weightlifters had a left ventricular wall thickness of 13 mm or more. Hypertrophic index interventricular septum plus left ventricular posterior wall thickness divided by internal diameter. Emax was lower in ex-users than in users and weightlifters. Doppler echocardiographic data on systolic and diastolic left ventricular function and heart rate during examination. This is the first time that a relatively large number of strength athletes has undergone a cardiological examination at least one year mean 43 months after discontinuation of their previous AAS abuse and been compared with current users.
In an earlier study, 12 the AAS intake was discontinued for several months only. In our subjects, AAS usage considerably exceeded the clinical dose, and the interindividual intake methods varied substantially.
However, there was no significant difference in AAS dosage between ex-users and users. National team weight lifters were used as a control group for highly trained AAS-free strength athletes. The ergometric performance in our subjects was within the normal range for untrained persons of the same age, even when considering the moderate exhaustion of the weightlifters with a lower maximum heart rate towards the end of exercise.
The typical training in bodybuilding and weightlifting, including the moderate endurance training on a cycle ergometer done by most of the athletes, does not result in significant increases in cycle ergometry performance. Our results suggest that the increases in blood pressure with AAS use are rather small and transient. Increased blood pressure values 2, 13 or a reduced fall in blood pressure during sleep 14 have been described with AAS use, but not in all studies.
Lenders and colleagues reported that five months after discontinuing AAS intake, systolic blood pressure remained higher by 6 mm Hg at rest compared with an anabolic-free control group. Particularly in athletes it is important to consider differences of fat-free body mass when comparing echocardiographic measures. The left ventricular muscle mass and wall thicknesses values of ex-users relative to fat-free body mass were similar to those of users.
The weightlifters group, however, showed significantly lower values. This suggests not only a disproportionate increase in left ventricular muscle mass with AAS, but also residual left ventricular hypertrophy more than one year after discontinuing AAS intake. Increases in left ventricular muscle mass with AAS are well documented in strength athletes 4, 7, 12, 13, 16 with case reports of typical hypertrophic cardiomyopathy 17 as well as in animals, 15, 18 where an increased protein synthesis has been shown.
In case reports, reversibility of significantly increased left ventricular muscle mass has been described after discontinuation of AAS. Our results suggest that this effect is maintained for an even longer time.
The extent to which increased left ventricular muscle mass caused by AAS abuse represents a long term risk for cardiac complications is controversial. The correlation between left ventricular muscle mass and cardiovascular mortality that is suggested by epidemiological evidence 22 may be transferable to athletes only with caution. The higher ratio of wall thickness to internal diameter in ex-users and users underlines the assumption that there is a slight degree of concentric left ventricular hypertrophy in AAS users, even more than one year after discontinuing the intake of these agents.
Today, most investigators agree that strength training without AAS intake does not induce concentric left ventricular hypertrophy. Some investigators describe significant wall thickening compared with steroid-free strength athletes, 4, 12, 27 with regression after eight weeks off treatment 12 or no change after nine weeks. Ex-users lie between the non-users weightlifters and users with respect to left ventricular muscle mass, wall thicknesses, and hypertrophic index values.
This could suggest that the hypertrophic effect of AAS decreases over the years. An impairment of systolic left ventricular function in animals has been shown with AAS. Impairment of diastolic left ventricular function with AAS use 4— 6 is not unequivocal. Fibrosis of the myocardium, as described in the case of anabolic abuse, 30 could be responsible for this. Our study has several methodological limitations. First, it was based on cross sectional rather than longitudinal data.
It does not seem reasonable, however, to suppose that strength athletes choosing to take anabolic drugs have different initial cardiac measurement results from AAS-free athletes. Age and body dimensions were not exactly the same in the three groups, which seems inevitable as former users of AAS who have taken the same quantity of drugs as current users must be somewhat older; however, when we related the echocardiographic results to body dimensions the hypertrophic index did not differ over a 10 year age period.
A longitudinal study with human subjects would also give rise ethical problems. Second, information about the intake of steroids was self reported, but it is hardly possible to assess this in an objective way. It seems unlikely that the small differences in AAS intake AAS score was not significantly different between users and ex-users could explain our results. The AAS can only attempt to approximate the relation between dose and effect, because the drugs differ in androgenic potency and bioavailability.
Finally, training related influences are also improbable as an explanation for the differences between the AAS users and weightlifters in our study. Previous echocardiographic data 13 did not differ between bodybuilders and weightlifters. Also, training in bodybuilding is more endurance oriented, with more repetition, smaller weights, and shorter pauses than in weightlifting and powerlifting , the latter involving fewer repetitions, heavier weights, and longer breaks between training sets.
Thus the typical training of bodybuilders both users and ex-users would be expected to induce a more eccentric hypertrophy characterised by a greater increase in internal diameter than in wall thickness, in contrast to the more concentric left ventricular hypertrophy found in the present study.
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.
National Center for Biotechnology Information , U. Journal List Heart v. Accepted Sep 2. This article has been cited by other articles in PMC. Table 1 Anthropometric data. Open in a separate window.
Values are mean SD. Anthropometric measurements Body height and mass were measured and the body surface area estimated from a nomogram. Ergometry All subjects undertook an incremental graded exercise test on an electrically braked cycle ergometer in the sitting position, increasing by 50 W every three minutes until volitional exhaustion.
Doppler echocardiography The echocardiographic recordings and measurements were made according to the American Society of Echocardiography in the supine left lateral position by the same experienced investigator, who was blinded to AAS use and to the results of the physical examination 2.