Potential CV Health Issues of Atherosclerosis and Compromised Heart-Pumping
Rationale
In an attempt to improve performance and/or aid recovery, various pharmaceutical products have been used, both openly (legally) and in a clandestine manner against the rules of governing bodies, by a broad array of athletes. Dr. Aaron Hermann of the University of Adelaide recently claimed that “although the use of Performance Enhancing Drugs (PED) may produce minor improvements in one aspect of athletic performance, in other areas, it may have detrimental effects, which outweigh the positive”. The research article discussed broadly the link between PEDs and performance in professional athletes but did not detail specific examples of the long-term side effects as a result of drug use.
Throughout this essay, the claim ‘the use of performance-enhancing drugs has no long-term effects on the body’ was presented to further investigate the controversial topic. Consequently, with initial research, a broad research question ‘What are the long-term effects of Performance Enhancing Drugs on the body?’ was developed based on the claim. This was further refined to specifically consider the long-term effects of PED use (doping) on cardiovascular health. A summary of this refinement and the specific research question is detailed below.
Despite all of these supposed “benefits” associated with doping, data from several studies have identified extremely dangerous and even deadly, CV health risks that significantly contradict the initial performance-enhancing effects of the drugs. Furthermore, the abundance of negative effects these drugs can have on one’s body prompted the establishment of the international independent organization of the World Anti-Doping Authority (WADA) in 1999. Therefore, this essay proposes the following research question:
‘Does the use of Anabolic-Androgenic Steroids, present long-term cardiac health problems in the form of Systolic Dysfunction and Atherosclerosis in weightlifters?’
Background
Anabolic-androgenic steroids (AAS), also simply referred to as ‘anabolic steroids’, are commonly used PEDs derived from testosterone, a hormone that is produced in the testes of males and, to a much lesser extent, in the ovaries of females. Testosterone is partially responsible for the developmental changes that occur during puberty and adolescence and is also involved in controlling the build-up and breakdown of the main biochemical components of all tissues, including muscle.
Because testosterone affects muscle growth, raising its levels in the blood can help athletes increase muscle size and strength, along with some other benefits such as improved endurance. Anabolic steroids can be taken in tablet form or injected directly into the muscle. Athletes who use anabolic steroids claim that as well as increasing muscle mass, they reduce body fat and recovery time after injury or a heavy workout. However, the abuse of steroids has been proven to significantly increase the long-term health risks of potentially fatal conditions, including abnormalities in liver function, kidney failure, and heart disease.
Systolic Dysfunction, also known as Heart failure with reduced ejection fraction (HFrEF) is a type of heart disease caused when the muscle of the heart’s left ventricle (LV) is not able to contract adequately and, therefore, expels less oxygen-rich blood into the body. Individuals with this form of the disease will have a lower-than-normal left ventricular ejection fraction (40% or less) on an echocardiogram. There are many known causes of HFrEF, including but not limited to high blood pressure, coronary artery disease, and mitral valve regurgitation.
Atherosclerosis refers to the build-up of fats, cholesterol, and other substances in and on your artery walls (plaque), which can restrict blood flow. AAS use has been known to promote the deposits of calcium, cholesterol, and other lipids in the heart’s coronary arteries and therefore, directly linked to causing atherosclerotic plaque. Though atherosclerosis may be preventable and treatable, the plaque can burst, triggering a blood clot which in some cases can be fatal.
Evidence
Dr. A. Baggish and colleagues at Massachusetts General Hospital and McLean Hospital, assessed the heart and coronary arteries in 140 male weightlifters aged 34 to 54; 58 of which we're currently using AAS; 28 had previously used AAS for at least 2 years, and 54 had never used AAS. Compared with the nonusers, the AAS users had higher mean blood pressure and a prevalence of elevated low-density lipoprotein cholesterol, which leads to coronary artery plaque and is a risk factor for atherosclerosis.
Although, about 50% of users and 62% of nonusers had no coronary artery plaque and more than 0 mm3 but less than 100 mm3 of plaque was found in about 15% of AAS users and 20% of nonusers, from 100 mm3 to less than 200 mm3 of plaque, the percentage of AAS users was more at 18% from the 10% of nonusers. Furthermore, from 200 mm3 to less than 300 mm3 of plaque was found in approximately 5% of AAS users and 4% of nonusers. From 300 mm3 to less than 400 mm3 of plaque was found in about 2% of AAS users and 0% of nonusers. From 400 mm3 to 500 mm3 of plaque was found in about 3% of AAS users and 2% of nonusers. More than 500 mm3 of plaque was found in about 11% of AAS users and 2% of nonusers.
Therefore, the graph in Figure 1, shows how among a group of weightlifters, AAS users were less likely to have no deposits of atherosclerotic plaque and more likely to have larger plaque deposits in their coronary arteries when compared to non-users. This answers the research question ‘Does the use of Anabolic-Androgenic Steroids, present long-term cardiac health problems in the form of Systolic Dysfunction and Atherosclerosis in weightlifters?’, by providing valid evidence and data that prove AAS use is a cause of atherosclerosis in weightlifters.
The histograms display the distribution of coronary artery plaque volume, degree of stenosis for most severe stenosis, number of diseased coronary artery segments, and coronary artery calcium for AAS users (N=84) and nonusers (N=53).
According to the data in Figure 2 and Table 1, AAS users showed significantly higher volumes of built-up coronary plaque as they were more prone to developing a higher number of diseased coronary artery segments, severe coronary stenosis, and coronary artery calcium than nonusers. Consequently, this provides evidence regarding the research question, proving AAS use can lead to atherosclerosis in weightlifters.
An estimated 3 to 4 million Americans have used a form of AAS (testosterone or synthetic derivatives of testosterone) to gain muscle mass for sports. According to a new study, it has been demonstrated that the use of this PED, can lead to HFrEF by narrowing the heart’s coronary arteries and impairing LV function. Therefore, these effects weaken heart pumping and reduce the supply of oxygenated blood both to the heart and from the heart to the arteries.
Through echocardiography, it was revealed that 71% of current AAS users had a lower-than-normal LV ejection fraction, a measure of how much-oxygenated blood the heart delivers to the arteries with each contraction. Half of current AAS users exhibited slower-than-normal LV expansion, indicating that reduced amounts of oxygenated blood flowed in to refill the LV during the relaxation phase of the heartbeat. These impairments were likely related to the thickening of the LV muscle wall in the AAS users. Former AAS users had a larger LV ejection fraction than current users, suggesting that their LV had recovered some pumping strength since stopping the use of the drug.
In the boxplot, black dots represent individual weightlifters’ LVEF. All LVEF values below the horizontal red line are below the normal range, suggesting compromised heart pumping capacity. The horizontal line inside the box for each group represents the median LVEF in the group. The top and bottom lines of the boxes represent the 75th and 25th percentile LVEF in each group. Dots outside of the horizontal lines above and below each box represent weightlifters with extremely high or low LVEF, based on the overall range of LVEF in that group.
Therefore, Figure 3 shows how among a group of weightlifters, AAS users’ left ventricular ejection fractions (LVEF) were lower than those of nonusers and often below the normal range, suggesting impaired heart pumping capacity. Current AAS users had lower LVEF than former users, suggesting that some recovery may occur after quitting and how AAS use is the main cause of systolic dysfunction. Consequently, this directly links to the research question by providing evidence proving that AAS use can lead to systolic dysfunction in weightlifters.
Evaluation
The evidence provided in Table 1 and Figures 1, 2, and 3, directly link to and answer the essay’s research question ‘Does the use of Anabolic-Androgenic Steroids, present long-term cardiac health problems in the form of Systolic Dysfunction and Atherosclerosis in weightlifters?’, by providing valid evidence and data that prove AAS use can lead to systolic dysfunction and atherosclerosis in weightlifters.
Nevertheless, it is worth noting that there are limitations associated with the evidence presented. Firstly, a limiting factor is that the research and data the essay is based on are derived from a second-hand source, which limits the quality and reliability of the information, as at times the information may be misleading or outdated. Furthermore, Dr. Baggish A.L., Weiner, R.B., Kanayama, et al.’s experimental research was the only source of data about the atherosclerotic plaque and systolic dysfunction in former and current AAS users, therefore, limiting data reliability through the lack of comparison with other experimentations on the topic. Also, since both AAS users and nonusers were weightlifters, the effects of AAS might have been clouded if weightlifting contributed to cardiovascular pathology. However, another source of bias could arise from measurement error, particularly in the exposure variables (e.g. misclassifying surreptitious AAS users as nonusers or inaccurately assessing the type, duration, dose, and currency of use). In particular, AAS users provided retrospective accounts, often spanning many years of time, of the use of illicit drugs of uncertain potency or authenticity. As such, estimates of participants’ lifetime duration of AAS use and total lifetime AAS dose were only approximations. Consequently, both of these sources would likely bias results toward the null, thereby yielding an underestimate of the effects of AAS use.
In order to address the limitations previously identified, the following improvements could be made.
Conclusion
This essay has attempted to describe available data and exemplar case studies detailing the potential CV health issues of atherosclerosis and compromised heart-pumping, surrounding the use of the commonly used PED of AAS detected in doping screens on weightlifters. In conclusion, the claim that ‘the use of performance-enhancing drugs has no long-term effects on the body’ is not fully supported. This is mainly due to the broadness of the question as it requires more experimentation than is possible. If the specific research question is considered, this also cannot be fully supported. Evidence provided proves that negative CV health effects do occur, but more controlled research trials are required alongside longitudinal studies of chronic drug use. The available data demonstrate enough concern in relation to CV health and AAS use that healthcare practitioners should be fully educated to help detect signs and symptoms and support athlete treatment and recovery where appropriate.
