bubbafrombama
06-30-2009, 11:18 PM
FWIW, all the articles I'm posting are from Muscular Development, which, as we know, is one of the most hardcore and "real" bodybuilding magazines on the shelf. Tho some may say they are biased (not IMO), they still are always fair by publishing controversal health and AAS studies, whether to their liking, or results/conclusions contrary to other reports previously or currently given. Naturally, they generally always give their opinion on the matters at hand (as in if we can trust the results or not), as you can see by reading their opinions within their articles.
I'm hoping that some may find these articles helpful in their quests of fitness. I certainly have.
PDF of article attached below.
Link to article:
http://www.musculardevelopment.com/content/view/1619/57/
New Tests Detect Early Heart Damage In AAS Users
Written by Dan Gwartney, MD
Tuesday, 16 June 2009
PQ: Just as anti-doping agencies have become capable of detecting trace amounts of AAS in an athlete’s urine, doctors are using cutting-edge technology to detect the earliest changes in organ function that might indicate possible damage associated with AAS use.
Academic journals are at the forefront of reporting new findings that have the potential of impacting our health, mortality and lifestyle decisions. Users of anabolic steroids (AAS) would be hard-pressed to read all the literature relating to this class of drugs, but even those who keep up on the topic remain unclear as to the true risks and benefits of AAS when used by healthy, adult men. Certainly, there are very obvious benefits to AAS use in regard to their potent ability to increase muscle mass and strength, improve body composition, certain psychological parameters and cognitive functions. There are also identified risks, though most are transient, related to the use of oral AAS, or use by adolescents or women. The more serious, immediate risks appear to be the neuropsychological effects of various AAS or their unsupported discontinuation. Most effects associated with AAS— good or bad— are the immediate ones. People see bulging muscles, shriveled testes or irritable gym mates; researchers can measure these changes in weeks to months. One realm of concern (often mentioned by opponents to AAS use to object to expanding access through legitimate channels) is the lack of understanding of long-term risks. Though it is a tiresome argument and typically a delay tactic to forestall any productive discourse about AAS use for cosmetic or functional enhancement, there is some support for caution. Because of the moratorium against AAS research the last 30-plus years, scientists have learned little about the effect of testosterone at supraphysiologic doses maintained for extended periods, let alone the numerous chemical analogs collectively known as AAS. Truly, it is vital that research be performed to determine the therapeutic dose range and forms of AAS that can be safely used, as the demand for life-enhancement is an integral component of American culture. Just as anti-doping agencies have become capable of detecting trace amounts of AAS in an athlete’s urine, doctors are using cutting-edge technology to detect the earliest changes in organ function that might indicate possible damage associated with AAS use. A recent study published in the British Journal of Sports Medicine reports on the use of two imaging techniques to evaluate structural changes in the heart of AAS users.1 The group of authors from Naples, Italy, compared the function of the hearts of AAS-using bodybuilders (AAS+) to non-using athletes (AAS-) and sedentary controls (couch potatoes). The bodybuilders all had more than five years of power-training experience and trained for 15-20 hours per week. The AAS+ group used an average of 525mg per week AAS and was “on-cycle” for 31 weeks per year. Oddly, the “anabolic-free,” non-user group averaged 8.9 weeks per year of AAS use. Another point that will be addressed later is the comment that the AAS+ group had lower LH and FSH (pituitary hormones that are suppressed during AAS use). All subjects in the three groups were of similar age and weight. The athlete groups had higher systolic blood pressure, greater body mass and lower heart rates. They probably also had better abs, but this was not recorded. All subjects performed exercise testing on stationary bicycles to determine their work capacity. As expected, both groups of athletes outperformed the sedentary controls, demonstrating better functional capacity, reaching higher maximal workloads with lower heart rate and systolic blood pressure. The AAS- athletes achieved a greater maximal workload and did not elevate their blood pressure as highly as the AAS+ group. Contrarily, the AAS+ group reported greater strength, lifting 80 pounds more on average in the 1-rep max for the squat than the AAS- group. These differences may reflect training effects as much as drug effects, as the training routines were not standardized. Using standard Doppler imaging (similar to the ultrasound techniques used to look at a fetus in a pregnant woman), there was no difference in function between AAS+ athletes and AAS- athletes. Both groups of athletes had larger hearts (greater left ventricular mass and wall thickness) than control subjects who did not exercise, as well as a greater stroke volume, which is a measure of how much blood is pumped with each heartbeat. Thus far, the study has shown that in comparison to people who are sedentary, those who exercise have greater functional capacity and develop larger hearts. However, when using more detailed imaging that is capable of measuring how quickly the heart contracts and relaxes as well as how uniformly the regions of the heart muscle function, differences between AAS+ and AAS- athletes became apparent. Athletes who reported using AAS in fairly moderate anabolic cycles (525mg/week) displayed a slower relaxation of the heart muscle, which is the period in which blood flows back into the “pumping” area (left ventricle) to be pushed out to the rest of the body. If the left ventricle is not refilled between each heartbeat, less blood is pushed out and thus, less oxygen is delivered to working muscle. Also, the pumping action was not synchronized as well in the hearts of AAS+ athletes as compared to AAS- athletes or the sedentary controls. While this impaired coordination in the heart muscle was not sufficient to cause any noticeable differences in the health or function of the AAS+ athletes, it is an effect that could cause noticeable problems or even clinically relevant challenges to one’s health if it persists and becomes worse. In people who have had serious heart problems, such as heart failure, the types of changes here are associated with a worse outcome if they reach a critical level.2 This level is significantly below what was seen in this study, but again, the AAS+ athletes were using fairly moderate doses. The bodybuilding world has seen a number of athletes succumb to heart-related disability or even early death in recent times. Mike Matarazzo, Don Youngblood and Mike Mentzer are names that come immediately to mind. Of course, there have also been the much-publicized deaths within the ranks of professional wrestling. Some might point out the fact that in many of the cases, other drugs of abuse are involved and sadly, they would be right. Perhaps the knowledge that recreational drug abuse is present in some cases of AAS use makes the need for understanding and screening for any adverse effects even more pressing. However, this study, despite adding to the urgency to divert AAS away from the black market and back within the field of regulated medicine, is not sufficient to suggest that AAS are dangerous. The authors noted normal heart function using standard diagnostic tools and improved workload capacity in comparison to sedentary controls in this study. Further, previous studies documenting a lack of adverse cardiac effects in AAS users are referenced within the study discussion.3-6 However, this study and others, did discover previously undetectable changes utilizing more sensitive imaging techniques.1,7 Yet, another group reported that high-intensity strength training with and without AAS induced alterations in left ventricular wall motion.8 As changes in left ventricular wall motion occur in hypertensive left ventricular hypertrophy (thickening of the heart muscle in patients with hypertension) and left ventricular hypertrophy is common in athletes due to pressure overload and the degree of left ventricular hypertrophy was greater in the AAS+ group, this change might have been anticipated.9 The authors believe the changes noted in this study are consistent with an increase in interstitial fibrosis and/or â-adrenoreceptor density.1 The fibrosis is similar to scarring within the heart muscle and may represent healing or repair of myocardial cell damage, if the authors’ hypothesis is correct. The fibrosis may also be a function of certain AAS-activating aldosterone (a structurally similar but unrelated steroid) receptors. Aldosterone and a secondary hormone called angiotensin II stimulates cardiac fibrocytes to produce collagen.10,11 It may be possible that drugs blocking these pathways (ACE inhibitors or spironolactone) may prevent or reduce the AAS-associated collagen production.12 It is difficult to ascertain the importance of this study. Though differences were noted between AAS+ and AAS- athletes using highly sensitive imaging techniques, standard testing showed no significant differences. Further, while the AAS+ group did not achieve as high an average maximal workload, the value was still significantly greater than the sedentary group and the difference from the AAS- group was not statistically significant. The AAS- group may not be a valid comparison group, as the “anabolic-free” subjects still reported an average exposure to AAS of nearly nine weeks per year.1 Also, though the authors claim the AAS+ group was tested “off-cycle” or in a washout period, the LH and FSH concentrations were still suppressed, suggesting that the post-cycle period may not have been sufficiently long to clear the AAS effects.1,13 It is also possible that the post-cycle testing may account for the lower maximal workload performed by the subjects. Most adverse effects noted with AAS use are transient. While it is interesting and important to be aware of the earliest signs of possible organ damage related to AAS, it is equally important to understand how the body responds to any damage. If the increase in interstitial collagen suggested by the authors is reparative, does the heart return to its baseline state if given sufficient time to recover?14 Would the incorporation of more aerobic training alleviate some of the changes? Is there a dose-threshold or a safe range that can be used before such changes are noted? The authors analyzed the data and stated that AAS dose and duration of use are related to the changes, but considering that many of these subjects have several years of long-term use and the changes were not clinically evident, it seems that there may be some suggestion of safety when AAS use is practiced in moderation. Certainly, excessive high-dosing practices, such as is practiced by certain elite-caliber athletes and some irresponsible youth or prolonged exposure without sufficient “off-cycle” periods to allow for repair processes may contribute to impaired cardiac function. This is a valuable study in that it provides a tool to study structural and functional changes in the heart of AAS users. However, it is premature in stating whether these changes are clinically relevant. It is vital that the same protocol be performed on former users of AAS, years after discontinuance, to see if the changes persist, progress or resolve.14 Hopefully, the authors will pursue this course of study.
References:
1. D’Andrea A, Caso P, et al. Left ventricular early myocardial dysfunction after chronic misuse of anabolic androgenic steroids: a Doppler myocardial and strain imaging analysis. Br J Sports Med, 2007;41:149-55.
2. Hashimoto I, Li X, et al. Myocardial strain rate is a superior method for evaluation of left ventricular subendocardial function compared with tissue Doppler imaging. J Am Coll Cardiol, 2003;42:1574-83.
3. Thompson PD, Sadaniantz A, et al. Left ventricular function is not impaired in weightlifters who use anabolic steroids. J Am Coll Cardiol, 1992;19:278-82.
4. Dickerman RD, Schaller F, et al. Left ventricular size and function in elite bodybuilders using anabolic steroids. Clin J Sports Med, 1997;7:90-3.
5. Hartgens F, Cheriex EC, et al. Prospective echocardiographic assessment of androgenic-anabolic steroids effects on cardiac structure and function in strength athletes. Int J Sports Med, 2003;24:344-51.
6. Salke RC, Rowland TW, et al. Left ventricular size and function in body builders using anabolic steroids. Med Sci Sports Exerc, 1985;17:701-4.
7. Di Bello V, Girogi D, et al. Effects of anabolic-androgenic steroids on weightlifters’ myocardium: an ultrasonic videodensometric study. Med Sci Sports Exerc, 1999;31:514-21.
8. Climstein M, O’Shea P, et al. The effects of anabolic-androgenic steroids upon resting and peak exercise left ventricular heart wall motion kinetics in male strength and power athletes. J Sci Med Sports, 2003;6:387-97.
9. Takeuchi M, Borden WB, et al. Reduced and delayed untwisting of the left ventricle in patients with hypertension and left ventricular hypertrophy: a study using two-dimensional speckle tracking imaging. Eur Heart J, 2007 Oct 19;[Epub ahead of print].
10. Funck RC, Wilke A, et al. Regulation and role of myocardial collagen matrix remodeling in hypertensive heart disease. Adv Exp Med Biol, 1997;432:35-44.
11. Brilla CG, Maisch B, et al. Hormonal regulation of cardiac fibroblast function. Eur Heart J, 1995;16 Suppl C:45-50.
12. Payne JR, Kotwinski PJ, et al. Cardiac effect of anabolic steroids. Heart, 90:473-5.
13. Menon DK. Successful treatment of anabolic steroid-induced azoospermia with human chorionic gonadotropin and human menopausal gonadotropin. Fertil Steril, 2003;79 Suppl 3:1659-61.
14. Urhausen A, Albers T, et al. Are the cardiac effects of anabolic steroid abuse in strength athletes reversible? Heart, 2004;90:496-501.
I'm hoping that some may find these articles helpful in their quests of fitness. I certainly have.
PDF of article attached below.
Link to article:
http://www.musculardevelopment.com/content/view/1619/57/
New Tests Detect Early Heart Damage In AAS Users
Written by Dan Gwartney, MD
Tuesday, 16 June 2009
PQ: Just as anti-doping agencies have become capable of detecting trace amounts of AAS in an athlete’s urine, doctors are using cutting-edge technology to detect the earliest changes in organ function that might indicate possible damage associated with AAS use.
Academic journals are at the forefront of reporting new findings that have the potential of impacting our health, mortality and lifestyle decisions. Users of anabolic steroids (AAS) would be hard-pressed to read all the literature relating to this class of drugs, but even those who keep up on the topic remain unclear as to the true risks and benefits of AAS when used by healthy, adult men. Certainly, there are very obvious benefits to AAS use in regard to their potent ability to increase muscle mass and strength, improve body composition, certain psychological parameters and cognitive functions. There are also identified risks, though most are transient, related to the use of oral AAS, or use by adolescents or women. The more serious, immediate risks appear to be the neuropsychological effects of various AAS or their unsupported discontinuation. Most effects associated with AAS— good or bad— are the immediate ones. People see bulging muscles, shriveled testes or irritable gym mates; researchers can measure these changes in weeks to months. One realm of concern (often mentioned by opponents to AAS use to object to expanding access through legitimate channels) is the lack of understanding of long-term risks. Though it is a tiresome argument and typically a delay tactic to forestall any productive discourse about AAS use for cosmetic or functional enhancement, there is some support for caution. Because of the moratorium against AAS research the last 30-plus years, scientists have learned little about the effect of testosterone at supraphysiologic doses maintained for extended periods, let alone the numerous chemical analogs collectively known as AAS. Truly, it is vital that research be performed to determine the therapeutic dose range and forms of AAS that can be safely used, as the demand for life-enhancement is an integral component of American culture. Just as anti-doping agencies have become capable of detecting trace amounts of AAS in an athlete’s urine, doctors are using cutting-edge technology to detect the earliest changes in organ function that might indicate possible damage associated with AAS use. A recent study published in the British Journal of Sports Medicine reports on the use of two imaging techniques to evaluate structural changes in the heart of AAS users.1 The group of authors from Naples, Italy, compared the function of the hearts of AAS-using bodybuilders (AAS+) to non-using athletes (AAS-) and sedentary controls (couch potatoes). The bodybuilders all had more than five years of power-training experience and trained for 15-20 hours per week. The AAS+ group used an average of 525mg per week AAS and was “on-cycle” for 31 weeks per year. Oddly, the “anabolic-free,” non-user group averaged 8.9 weeks per year of AAS use. Another point that will be addressed later is the comment that the AAS+ group had lower LH and FSH (pituitary hormones that are suppressed during AAS use). All subjects in the three groups were of similar age and weight. The athlete groups had higher systolic blood pressure, greater body mass and lower heart rates. They probably also had better abs, but this was not recorded. All subjects performed exercise testing on stationary bicycles to determine their work capacity. As expected, both groups of athletes outperformed the sedentary controls, demonstrating better functional capacity, reaching higher maximal workloads with lower heart rate and systolic blood pressure. The AAS- athletes achieved a greater maximal workload and did not elevate their blood pressure as highly as the AAS+ group. Contrarily, the AAS+ group reported greater strength, lifting 80 pounds more on average in the 1-rep max for the squat than the AAS- group. These differences may reflect training effects as much as drug effects, as the training routines were not standardized. Using standard Doppler imaging (similar to the ultrasound techniques used to look at a fetus in a pregnant woman), there was no difference in function between AAS+ athletes and AAS- athletes. Both groups of athletes had larger hearts (greater left ventricular mass and wall thickness) than control subjects who did not exercise, as well as a greater stroke volume, which is a measure of how much blood is pumped with each heartbeat. Thus far, the study has shown that in comparison to people who are sedentary, those who exercise have greater functional capacity and develop larger hearts. However, when using more detailed imaging that is capable of measuring how quickly the heart contracts and relaxes as well as how uniformly the regions of the heart muscle function, differences between AAS+ and AAS- athletes became apparent. Athletes who reported using AAS in fairly moderate anabolic cycles (525mg/week) displayed a slower relaxation of the heart muscle, which is the period in which blood flows back into the “pumping” area (left ventricle) to be pushed out to the rest of the body. If the left ventricle is not refilled between each heartbeat, less blood is pushed out and thus, less oxygen is delivered to working muscle. Also, the pumping action was not synchronized as well in the hearts of AAS+ athletes as compared to AAS- athletes or the sedentary controls. While this impaired coordination in the heart muscle was not sufficient to cause any noticeable differences in the health or function of the AAS+ athletes, it is an effect that could cause noticeable problems or even clinically relevant challenges to one’s health if it persists and becomes worse. In people who have had serious heart problems, such as heart failure, the types of changes here are associated with a worse outcome if they reach a critical level.2 This level is significantly below what was seen in this study, but again, the AAS+ athletes were using fairly moderate doses. The bodybuilding world has seen a number of athletes succumb to heart-related disability or even early death in recent times. Mike Matarazzo, Don Youngblood and Mike Mentzer are names that come immediately to mind. Of course, there have also been the much-publicized deaths within the ranks of professional wrestling. Some might point out the fact that in many of the cases, other drugs of abuse are involved and sadly, they would be right. Perhaps the knowledge that recreational drug abuse is present in some cases of AAS use makes the need for understanding and screening for any adverse effects even more pressing. However, this study, despite adding to the urgency to divert AAS away from the black market and back within the field of regulated medicine, is not sufficient to suggest that AAS are dangerous. The authors noted normal heart function using standard diagnostic tools and improved workload capacity in comparison to sedentary controls in this study. Further, previous studies documenting a lack of adverse cardiac effects in AAS users are referenced within the study discussion.3-6 However, this study and others, did discover previously undetectable changes utilizing more sensitive imaging techniques.1,7 Yet, another group reported that high-intensity strength training with and without AAS induced alterations in left ventricular wall motion.8 As changes in left ventricular wall motion occur in hypertensive left ventricular hypertrophy (thickening of the heart muscle in patients with hypertension) and left ventricular hypertrophy is common in athletes due to pressure overload and the degree of left ventricular hypertrophy was greater in the AAS+ group, this change might have been anticipated.9 The authors believe the changes noted in this study are consistent with an increase in interstitial fibrosis and/or â-adrenoreceptor density.1 The fibrosis is similar to scarring within the heart muscle and may represent healing or repair of myocardial cell damage, if the authors’ hypothesis is correct. The fibrosis may also be a function of certain AAS-activating aldosterone (a structurally similar but unrelated steroid) receptors. Aldosterone and a secondary hormone called angiotensin II stimulates cardiac fibrocytes to produce collagen.10,11 It may be possible that drugs blocking these pathways (ACE inhibitors or spironolactone) may prevent or reduce the AAS-associated collagen production.12 It is difficult to ascertain the importance of this study. Though differences were noted between AAS+ and AAS- athletes using highly sensitive imaging techniques, standard testing showed no significant differences. Further, while the AAS+ group did not achieve as high an average maximal workload, the value was still significantly greater than the sedentary group and the difference from the AAS- group was not statistically significant. The AAS- group may not be a valid comparison group, as the “anabolic-free” subjects still reported an average exposure to AAS of nearly nine weeks per year.1 Also, though the authors claim the AAS+ group was tested “off-cycle” or in a washout period, the LH and FSH concentrations were still suppressed, suggesting that the post-cycle period may not have been sufficiently long to clear the AAS effects.1,13 It is also possible that the post-cycle testing may account for the lower maximal workload performed by the subjects. Most adverse effects noted with AAS use are transient. While it is interesting and important to be aware of the earliest signs of possible organ damage related to AAS, it is equally important to understand how the body responds to any damage. If the increase in interstitial collagen suggested by the authors is reparative, does the heart return to its baseline state if given sufficient time to recover?14 Would the incorporation of more aerobic training alleviate some of the changes? Is there a dose-threshold or a safe range that can be used before such changes are noted? The authors analyzed the data and stated that AAS dose and duration of use are related to the changes, but considering that many of these subjects have several years of long-term use and the changes were not clinically evident, it seems that there may be some suggestion of safety when AAS use is practiced in moderation. Certainly, excessive high-dosing practices, such as is practiced by certain elite-caliber athletes and some irresponsible youth or prolonged exposure without sufficient “off-cycle” periods to allow for repair processes may contribute to impaired cardiac function. This is a valuable study in that it provides a tool to study structural and functional changes in the heart of AAS users. However, it is premature in stating whether these changes are clinically relevant. It is vital that the same protocol be performed on former users of AAS, years after discontinuance, to see if the changes persist, progress or resolve.14 Hopefully, the authors will pursue this course of study.
References:
1. D’Andrea A, Caso P, et al. Left ventricular early myocardial dysfunction after chronic misuse of anabolic androgenic steroids: a Doppler myocardial and strain imaging analysis. Br J Sports Med, 2007;41:149-55.
2. Hashimoto I, Li X, et al. Myocardial strain rate is a superior method for evaluation of left ventricular subendocardial function compared with tissue Doppler imaging. J Am Coll Cardiol, 2003;42:1574-83.
3. Thompson PD, Sadaniantz A, et al. Left ventricular function is not impaired in weightlifters who use anabolic steroids. J Am Coll Cardiol, 1992;19:278-82.
4. Dickerman RD, Schaller F, et al. Left ventricular size and function in elite bodybuilders using anabolic steroids. Clin J Sports Med, 1997;7:90-3.
5. Hartgens F, Cheriex EC, et al. Prospective echocardiographic assessment of androgenic-anabolic steroids effects on cardiac structure and function in strength athletes. Int J Sports Med, 2003;24:344-51.
6. Salke RC, Rowland TW, et al. Left ventricular size and function in body builders using anabolic steroids. Med Sci Sports Exerc, 1985;17:701-4.
7. Di Bello V, Girogi D, et al. Effects of anabolic-androgenic steroids on weightlifters’ myocardium: an ultrasonic videodensometric study. Med Sci Sports Exerc, 1999;31:514-21.
8. Climstein M, O’Shea P, et al. The effects of anabolic-androgenic steroids upon resting and peak exercise left ventricular heart wall motion kinetics in male strength and power athletes. J Sci Med Sports, 2003;6:387-97.
9. Takeuchi M, Borden WB, et al. Reduced and delayed untwisting of the left ventricle in patients with hypertension and left ventricular hypertrophy: a study using two-dimensional speckle tracking imaging. Eur Heart J, 2007 Oct 19;[Epub ahead of print].
10. Funck RC, Wilke A, et al. Regulation and role of myocardial collagen matrix remodeling in hypertensive heart disease. Adv Exp Med Biol, 1997;432:35-44.
11. Brilla CG, Maisch B, et al. Hormonal regulation of cardiac fibroblast function. Eur Heart J, 1995;16 Suppl C:45-50.
12. Payne JR, Kotwinski PJ, et al. Cardiac effect of anabolic steroids. Heart, 90:473-5.
13. Menon DK. Successful treatment of anabolic steroid-induced azoospermia with human chorionic gonadotropin and human menopausal gonadotropin. Fertil Steril, 2003;79 Suppl 3:1659-61.
14. Urhausen A, Albers T, et al. Are the cardiac effects of anabolic steroid abuse in strength athletes reversible? Heart, 2004;90:496-501.