RUNNING HEAD ANABOLIC-ANDROGENIC STEROID USE IN ATHLETES1.docx

RUNNING HEAD: ANABOLIC-ANDROGENIC STEROID
USE IN ATHLETES 1
Anabolic-Androgenic Steroid Use in Athletes and the
Associated Cardiovascular and Metabolic Effects
Michael W. McClellan
Des Moines University
Abstract
Anabolic-androgenic steroid use has become a popular drug for
athletes and bodybuilders to use in order to improve their
athletic performance despite health consequences associated
with its use. The use of anabolic-androgenic steroids has been
associated with adverse outcomes in prior studies, particularly
in regards to cardiovascular and metabolic systems. In order to
further evaluate the scientific data behind this proposition many

studies reviewed were small, retrospective-prospective studies
that systemically reviewed anabolic-androgenic steroid use and
the cardiovascular effects associated such as hypertension, left
ventricular hypertrophy, and myocardial infarction.
Dyslipidemia was the only metabolic component reviewed due
to the close interaction and indication it has for cardiovascular
function. Past data collected on this topic has been very
controversial and conflicting due to ethical limitations placed
on anabolic-androgenic steroid use within the athletic
community. Findings from this review will help athletes
globally to understand the adverse effects associated with
anabolic-androgenic steroid use. Healthcare providers will be
able to identify potential steroid abuse, and educate these
patients on the adverse outcomes associated, so they can help
prevent future misuse and abuse.
The development of anabolic-androgenic steroids (AAS) were
first seen in the early 1930’s when it was isolated from
testosterone (Kanayama & Pope Jr., 2017). Soon after, there
were many synthetic androgens developed such as testosterone
propionate, stanozolol, and nandrolone, which are a few of the
most common subtypes (Gheshlaghi, Piri-Ardakani, Masoumi,
Behjati, & Paydar, 2015). As athletes and bodybuilders
discovered the enhanced anabolic effects of each of these
testosterone derivatives, it was not long until they became
popular throughout the elite athletic population (Kanayama &
Pope Jr., 2017). The improved performance seen throughout
these individuals became the primary foundation for their use

and eventually, abuse. The United States Food and Drug
Administration has approved the use of anabolic-androgenic
steroids as a form of hormone replacement therapy for men who
have low testosterone production due to hypogonadism (Safety
alerts for human medical products - testosterone and other
anabolic androgenic steroids (AAS): FDA statement - risks
associated with abuse and dependence.2016)). However, studies
have shown that it is more commonplace for these synthetic
drugs to be abused for cosmetic and personal performance
rather than for any serious medical condition.
In a study conducted by Mitchell, it was found that over 30
major league baseball players reported the abuse of anabolic-
androgenic steroids and performance enhancing drugs within the
last 4 years. These players underwent anonymous questionnaires
that allowed them to openly discuss their inappropriate use of
AAS despite the ban placed on these drugs in all major league
sports (Grossman, Kimsey, Moreen, & Owings, 2007). The
study found that professional players had been administering
AAS at much higher doses to create an offensive advantage on
the baseball field (Grossman et al., 2007). On the other
spectrum, bodybuilders have utilized these drugs to increase
overall muscle workload and decrease muscular fatigue, which
helps increase strength as well as develop a more aesthetic
physique (Kanayama & Pope Jr., 2017). Bodybuilders use AAS
to improve their overall appearance for the International
Federation of Bodybuilder competitions. Despite the use of
AAS for performance enhancing reasons in all major athletic
sports and bodybuilding competitions, these drugs have many
adverse effects at the heart, liver, brain, and endocrine system
that can potentially impair the health of those who abuse AAS
(Safety alerts for human medical products - testosterone and
other anabolic androgenic steroids (AAS): FDA statement -
risks associated with abuse and dependence.2016)).
Side effects of AAS and performance enhancing drugs are not
common when used at therapeutic levels, but bodybuilders and
athletes tend to use at levels that are nearly ten times higher

than the standard dose. When AAS is administered at such high
doses the most common effects include gynecomastia, reduced
testicular function, hepatotoxicity, and psychological
dependence (Safety alerts for human medical products -
testosterone and other anabolic androgenic steroids (AAS): FDA
statement - risks associated with abuse and dependence.2016).
Cardiovascular effects, however, remain controversial within
the literature and more recent studies. Elevated blood pressure
and peripheral vascular resistance are two of the more widely
studied effects of AAS abuse, whereas severe cardiac morbidity
and mortality from arrhythmias and myocardial infarction are
more controversial cardiovascular topics. The objective of this
study is to analyze, synthesize, and report the data pertaining to
AAS abuse in athletes and the associated cardiovascular effects.
Anabolic-Androgenic Steroids
Anabolic-androgenic steroids (AAS) represent a large number
of synthetic derivatives of testosterone that are used to
maximize anabolic effects while limiting the androgenic, sex-
linked effects (Pope et al., 2014). The anabolic properties
would primarily consist of muscle tissue building and the sexual
characteristics consist of voice changes through enlargement of
the pharynx, hair growth at the pubic, axillary, and facial
regions, along with increases in sebaceous gland activity, and
CNS involvement. Most AAS composition tries to enhance the
anabolic properties while limiting the androgenic effects. These
drugs can be administered in a variety of different routes for the
body to metabolize and utilize such as oral, parenteral and
transdermal. Access to these drugs can be done through
pharmacy’s oversea where AAS are not FDA regulated. This
allows users such as athletes and bodybuilders to purchase
online through third party vendors.
AAS Mechanism of Action and Pathophysiology
The mechanism of action of these prohormones still remains
very controversial due to limited studies within the human
population, but testosterone’s similar mechanism has been
attributed to anabolic steroid’s mechanism of action.

Testosterone is produced in the testicles under the direct
influence of the luteinizing hormone. There is a negative
feedback loop between testosterone production, the
hypothalamus, the anterior pituitary, and the testicles.
Testosterone as well as dihydrotesosterone (DHT) and estrogen
all function at the hypothalamus by exerting a negative
feedback on gonadotropin releasing hormone (GnRH). GnRH
stimulates the follicle stimulating hormone (FSH) and
luteinizing hormone (LH) in the anterior pituritary which can
also exert a negative Feedback on the hypothalamus. When
FSH and LH are not being inhibited then they function to act on
the testicles to help produce and potentiate spermatogenesis and
oogenesis.
The pathophysiology of steroids at the cellular level involves
the binding of these synthetic testosterone hormones to their
corresponding nuclear androgen receptor within the cytoplasm
of the target tissue. Different tissues have different enzymes
that convert the synthetic form into a consumable form for the
body to utilize. Following this binding, the hormone is released
into the tissue where a series of enzymes are activated that
involve protein metabolism. This protein metabolism enhances
protein synthesis while inhibiting protein degradation
simultaneously. These two mechanisms working together
allows for increased muscle to tensile strength, which generates
enhanced muscle growth. The drugs optimal situation would be
to completely isolate anabolic activity from the androgenic
activity, however, molecular biologists remain unable to
completely isolate the two properties in vitro. Recent
pharmacological manipulation of androgens has allowed for this
concept to be utilized but not refined to perfection.
Although the use of androgenic anabolic steroid use has been
shown to be beneficial for certain medical conditions like
gynecomastia and hypogonadism. It remains unknown whether
short or long-term use of these drugs have potentially harmful
or fatal side effects at low and high doses. Specifically, in
regards to the cardiovascular and metabolic systems.

Hypertension
The effects of anabolic androgenic steroid use on blood pressure
is one area of concern. There has been an associated link
between AAS and increased blood pressure readings. The
mechanism behind this link associates AAS use with sodium
retention in the kidneys (Achar, Rostamian, & Narayan, 2010).
With that being said, the proposed effect of anabolic androgenic
steroid use would cause a dose-dependent and timewise step
approach to increasing blood pressure (Achar et al., 2010; P.
Angell et al., 2014). The length of time athletes and
bodybuilders are utilizing AAS should directly affect how high
their blood pressure increases. Same concept applies with
increased dosing of AAS and increased blood pressure. Many
retrospective studies look at AAS users and measure their
systolic and diastolic blood pressure reading throughout the
course of their steroid use. This in turn can be utilized to show
the mean systemic arterial hypertension, which is compared
amongst all steroid users and non-users. This review will
address each of the studies to better understand the effects of
AAS use and the precipitating effects it has on blood pressure.
Left Ventricular Hypertrophy
Another parameter to understand when analyzing athletes who
use anabolic steroids is the effect that these synthetic forms of
testosterone have on cardiac remodeling. Specifically, in
regards to left ventricular hypertrophy (LVH), which is a
common condition that causes the muscles of the left ventricle
to become thickened (P. Angell et al., 2014). LVH is observed
through electrocardiogram (EKG) and echocardiographic
observation in studied participants (P. Angell et al., 2014). This
process is believed to be a direct response from elevated blood
pressure as well as underlying congenital heart disorders. As
LVH develops, it causes the heart to work harder and less
efficiently than a typical, normal functioning heart should.
Stress on the heart over time can eventually lead to poor
outcomes such as myocardial infarction, angina, dilated
cardiomyopathy, and heart failure (Sabzi & Faraji, 2017). This

topic seems to be the most relevant within the recent literature
in human and animal studies. Understanding the link between
AAS use and abuse in athletes will help provide more insight to
potential effects that these drugs have on cardiac remodeling.
Myocardial Infarction
The most harmful and fatal cardiovascular phenomenon deals
with myocardial infarction (MI) or heart attack from an acute
episode of cardiac ischemia due to coronary syndromes and
thrombus formation (Poorzand, Jafarzadeh Esfehani,
Hosseinzadeh, & Vojdanparast, 2015). Anabolic-androgenic
steroid use has been linked to these acute conditions that can
potentially be life threatening. The exact mechanism for which
this happens is not fully understood, however, the best
interpretation is thought to be that cardiac myocyte ischemia
develops in response to the increased oxygen demand at
maximal intensity exercise during AAS use (Poorzand et al.,
2015). This exaggerated response for oxygen demand comes
from the anabolic steroids ability to enhance cardiac tissue
growth through increased workload over many years of use
(Poorzand et al., 2015). This can also be explained from the
increased deposition of lipoprotein within the vasculature,
which is a metabolic component of concern for AAS use in
athletes (Poorzand et al., 2015). Many retrospective studies and
pathology reports post-mortem in isolated incidences have
linked these myocardial infarctions and sudden death with prior
use of anabolic steroids, and raises concern for myocardial
infarction induced by anabolic steroid use.
Dyslipidemia
The one metabolic component that this review analyzes deals
with blood plasma lipoprotein levels. The evidence based
medicine between AAS use and blood plasma lipoproteins
indicates a potential increase and decrease in low density
lipoprotein (LDL) and high density lipoprotein (HDL),
respectively (Gårevik, Skogastierna, Rane, & Ekström, 2012).
The long-term sequelae of elevated LDL and decreased HDL is
coronary artery disease (Gårevik et al., 2012). Understanding

the risks associated with AAS use through evidence can help
formulate more concrete risk factors that can be educated to the
patient.
Blood plasma lipoprotein levels are more commonly composed
of cholesterol, which is synthesized in the liver (Gårevik et al.,
2012). The rate-limiting step in cholesterol synthesis is 3-
hydroxy-3methylglutaryl coenzyme A (HMG-CoA) to
mevalonate and this process is catalyzed by the enzyme HMG-
CoA reductase. This is important because in mammals, HMG-
CoA reductase is suppressed by breaking down LDL through
LDL receptor activation, which ultimately leads to decreased
cholesterol levels in the plasma (Gårevik et al., 2012). The
same mechanism of action is used by “statin” medications,”
which are used to increase the expression of LDL receptors at
the target organ and help induce the breakdown of plasma LDL
(Gårevik et al., 2012). Determining whether or not plasma
lipoproteins are affected by AAS use can serve as precipitating
factor toward cardiovascular disease.
Anabolic steroids have been around for over 50 years, but
studies have not emerged until the last 15 to 30 years. With
more public awareness of steroid use in the athletic and
bodybuilding community, more research has become available.
The examination of potential literature review articles were
found through the PubMed search engine. Numerous searches
were utilized with terms such as “anabolic androgenic steroid”,
“athlete”, “body building”, “cardiovascular effect”, and
“metabolic effect.” Extra criteria only included the terms
“animal”, and “mice” due to a large number of recent studies
being done on animals instead of humans. Several studies
included were case reports by athletes and isolated incidents of
myocardial damage from anabolic stroids. Anabolic steroids are
illegal, which poses an ethical dilemma for acute and chronic
AAS users from openly reporting their misuse and abuse. This
eliminates the use of randomized control studies in the human
population. Also, it only allows for retrospective studies to be

reviewed.
AAS Use Induced Hypertension
A retrospective-prospective study comprised of 70 total
participants that were all male and divided equally with 35
individuals in each of the experimental and control groups
(Solakovic, Totic, Vukas, & Djedovic, 2015). All participants
in the study were under the age of 35 and involved in
recreational fitness or body-building workouts without
competitive motives (Solakovic et al., 2015). They were
followed over the course of five years from January 2010 until
January 2015 (Solakovic et al., 2015). Each participant had no
underlying cardiovascular or metabolic abnormalities
(Solakovic et al., 2015). These individuals were not placed on
any dietary restrictions and were evaluated through non-
invasive procedures such as vascular ultrasound to observe
systolic and diastolic blood pressure. The studied participants
underwent daily anaerobic exercise training for two hours, four
to six times per week to show an understanding of how AAS use
can affect blood pressure (Solakovic et al., 2015). In this study,
arterial hypertension was observed in 18 of the 35 participants
using anabolic steroids. Only 2 of the 35 individuals in the
control group were observed to have a statistically significant
increase in their blood pressure. The proposed mechanism for
this increase was due to damage induced on the surface of the
venous system at the saphenous and small saphenous vein,
which causes irreversible dilation of these vessels (Solakovic et
al., 2015). Dilation of these vessels prevents them from
properly regulating peripheral vascular resistance and pressure
when placed under steroid induced stress (Solakovic et al.,
2015). However, the data collected based on this proposal was
insignificant. Only 11 of the 35 individuals using anabolic
steroids exhibited damage to each of the saphenous veins,
whereas 6 of the 35 in the control group displayed the same
type of dilating damage to vessels. In addition, they took into
account the lipid deposition in the arterial system to help

understand the cause of increased blood pressure from anabolic
steroid use, but this will be discussed later.
In contrast to the study above, there have been other
studies that do not show a statistically significant increases in
blood pressure from anabolic steroid use. A study in 2003
conducted by Grace et al found there were no cardiovascular or
morphological changes in the vasculature. This study used a
small sample size of 32 to evaluate blood pressures taken
manually with a sphygmomanometer and a stethoscope by
means of auscultation. The same researcher throughout the
study was used to take these blood pressures to help prevent
intra-observer variability (Grace, Sculthorpe, Baker, & Davies,
2003). Throughout the duration of the study, systolic blood
pressure showed minimal change from start to finish between
the control group and experimental group. Systolic pressures
ranged from 119 – 122 mmHg in the control and 119 – 124
mmHg in the individuals using steroids (Grace et al., 2003).
Significant increases in diastolic pressure were seen during the
study in subjects undergoing anabolic steroid use opposed to
subjects not using. However, these numbers returned to
baseline levels 6 to 8 weeks following drug cessation (Grace et
al., 2003). The data therefore is inconsistent with stating that
anabolic steroid use induces hypertension long-term. Acutely,
steroid use can elevate diastolic blood pressure above normal,
but systolic has no associated effects from steroid use (Grace et
al., 2003).
A different approach was used in a study by Urhausen et al
to evaluate steroid use by comparing prior steroid users against
those who are currently using anabolic steroids (2004). Systolic
blood pressure was found to be higher in current steroid users
with a mean pressure of 140 mmHg compared to ex-users whose
mean systolic pressure was 130 mmHg (A Urhausen, T Albers,
& W Kindermann, 2004). Only 5 out of 17 current users
displayed borderline hypertension with systolic pressures
greater than 140 and diastolic pressures greater than 90,
whereas 2 out of 15 non-users displayed these same levels as

well (A Urhausen et al., 2004). Five months after discontinuing
steroid intake, systolic blood pressure remained higher by 6
mmHg in steroid users compared to the control group who did
not use anabolic steroids (A Urhausen et al., 2004). With these
results it suggests that increases in blood pressure due to
anabolic steroid use are minor and transient in nature. Blood
pressure increases from baseline were minimal and short-lived
once steroid use was discontinued.
Left Ventricular Hypertrophy due to AAS Use
Athletes who abuse anabolic androgenic steroids often
develop and display left ventricular hypertrophy. Several
studies have shown that left ventricular structure, function, and
mass increase as result of exercise and anabolic-androgenic
steroid use (Achar et al., 2010). In a retrospective study
conducted by Kreig et al, 40 total male participants comprised
of 14 anabolic-androgen steroid users, 11 nonuser athletes, and
15 age-related controls were utilized to evaluate
echocardiographic findings related to interventricular septal
wall thickness and left ventricular hypertrophy. Human
subjects self-reported oral and injectable steroid use which was
confirmed by luteinizing hormone, follicle-stimulating
hormone, and testosterone ratios (Krieg, Scharhag, Albers,
Kindermann, & Urhausen, 2007). Anabolic steroid users had
significantly increased interventricular septal wall thickness and
enlarged left ventricular muscle on echocardiograph when
compared to non-users and controls (Krieg et al., 2007). As a
result of this enlargement, there were significant differences in
diastolic function that can be explained as result of myocardium
thickening. Early diastolic filling was reduced in users
compared to non-users and controls, which can be explained by
impaired myocardium relaxation and decreased compliance
secondary to myocardium enlargement (Krieg et al., 2007).
Inefficient diastolic contractions can ultimately lead to heart
failure if left untreated and appropriate management is not
taken.
In addition, a cross-sectional study conducted by Angell et

al followed 13 strength trained athletes currently using anabolic
steroids for more than 2 years and 8 strength trained athletes
not using anabolic steroids by monitoring left ventricular mass
and ejection fraction through cardiac magnetic resonance
imaging and echocardiography. The study revealed that
anabolic steroid users had a higher absolute ventricular mass
compared to non-anabolic steroid users (P. Angell et al., 2014).
As a result of the increase in left ventricular mass, the ejection
fraction of the right ventricle was significantly less (51%) in
anabolic steroid users compared to athletes not using anabolic
steroids whose ejection fraction was 59% (P. Angell et al.,
2014). When monitoring for left ventricle mass and ejection
fractions, the study discovered that the peak left ventricular
strain during diastole was much lower in athletes undergoing
anabolic steroid use (P. Angell et al., 2014). All of these
factors: elevated left ventricle mass, reduced ejection fraction,
and increased strain placed on the myocardium during strength
training in anabolic steroid users can be associated with the
phenomenon of left ventricular hypertrophy.
Another small sample size evaluated 12 anabolic steroid
users and 7 non-users for left ventricular hypertrophy through
echocardiographic examination of left ventricular mass, tissue
velocity or ejection fraction, and strain (Baggish et al., 2010).
The study found that 6 anabolic steroid users and 5 non-users
met criteria for LV hypertrophy. This suggests that non-users
were at increased risk for left ventricular hypertrophy.
However, anabolic steroid users differed greatly from non-users
in many other interdependent systolic and diastolic functions.
Left ventricular ejection fraction was less than 55 % in 10 of
the anabolic steroid users and only one non-user had an ejection
fraction of 54% (Baggish et al., 2010). Evidence of this was
confirmed through echocardiographic imaging of diastolic
filling where it revealed reduced early diastolic filling and
increased late diastolic function, which is one hallmark sign for
impaired left ventricular relaxation and function (Baggish et al.,
2010). With an impaired diastolic filling, ventricle relaxation

and compliance is decreased, which in turn causes lower left
ventricular peak systolic strain and decreases the amount of
blood forced out of the ventricle during systole (Baggish et al.,
2010).
Increased Lipid Deposition from AAS
In this cross-sectional study conducted by Severo et al.,
they evaluated 10 athletes who were users of anabolic steroids
confirmed by urine analysis and 12 non-using athletes. Both
subject groups submitted to weekly blood draws to evaluate
complete blood count (CBC), platelets, fibrinogen, lipid profile,
C-reactive protein, follicle stimulating hormone, and
testosterone levels (Severo et al., 2013). The area of importance
to this study corresponds with the lipid profile due to the
increased risk stratification cholesterol places on other
components of the cardiovascular system such as blood pressure
and vascular health. Results showed that HDL cholesterol was
lower and LDL levels were elevated in anabolic steroid users
(Severo et al., 2013). Similar findings were gathered from a
study mentioned above that was conducted by Solakovic et al
that found 19.4% of users had increased LDL, decreased HDL,
and increased total cholesterol. This information was not
statistically significant since there were 17.1% of non-anabolic
steroid users with elevated LDL, reduced HDL, and increased
total cholesterol (Solakovic et al., 2015). Therefore, findings
within the literature are very conflicting and opposing, which
makes interpreting the data very difficult.
Cardiac Arrhythmias and Myocardial Infarction Generated by
AAS Use
Despairing evidence has linked anabolic steroid use with
adverse cardiac events including but not limited to cardiac
arrhythmias, myocardial infarction, and sudden death (Achar et
al., 2010). Basic understanding into the mechanism for
anabolic steroid use induced myocardial ischemia was evaluated
in study by Major et al through comparison of
electrocardiographic criterion before and after submaximal
exercise between anabolic steroid users and non-anabolic

steroid users. Anabolic steroid users were found to have a
prolonged QT interval at rest and a significantly increased QT
prolongation during the post-exercise period when compared to
non-users (Maior et al., 2010). The prolongation of the QT
interval is generally produced by slowed repolarization in the
cardiac membrane due to reduced influx of potassium (K+)
current into the cardiac tissue, which causes irregular
ventricular contractions (Moss & Kass, 2005). Without proper
ion channel control over ventricular contractions in cardiac
tissue places individuals at increased risk for fatal cardiac
events. One life-threatening associated arrhythmia seen from
abnormal ventricular repolarization is ventricular fibrillation
(Maior et al., 2010). This arrhythmia is often predicted by
prolonged QT intervals, and can be utilized as a risk factor and
preventive measure for limiting adverse cardiac events.
Understanding the mechanism for which anabolic steroid
use causes cardiac arrhythmias aids in the explanation of
myocardial infarction (MI) and ventricular arrhythmias in young
athletes with no cardiac risk factors. A study conducted by
McNutt et discovered that an acute MI happened to a 22-year-
old bodybuilder who openly discussed his anabolic steroid
abuse in the absence of any cardiac risk factors. The patient
above had elevated LDL and decreased HDL well out of the
therapeutic range. A similar scenario happened to a 23-year-old
wrestler who presented to the emergency department with
crushing substernal chest pain (Poorzand et al., 2015). This
patient had increased serum cardiac troponin markers in
addition to ST-segment elevation on electrocardiograph, which
classically indicates an acute myocardial infarction (Poorzand et
al., 2015). Additional findings included an abnormal lipid
profile and left ventricular enlargement. The patient did not
have traditional cardiovascular risk factors such as smoking,
diabetes, or hypertension.
Non-Human Animal Studies
With ethical and legal implications placed on anabolic
steroid use and abuse in the human population, there have been

more recent studies done on non-human subjects to evaluate
time and dose-dependent relations corresponding to anabolic
steroid use. A study conducted by Fotini Vasilaki et al looked
at male rabbits over the course of 1 year under high (10mg/kg)
and low doses (4mg/kg) of nandrolone decanoate with one
control group receiving saline fluid. Rabbits under higher
anabolic doses exhibited increased myocardial mass, reduced
diastolic function, increased troponin cardiac biomarkers and
focal fibrosis of cardiac tissue (Fotini Vasilaki et al., 2016).
Subjects placed under low dose steroid injections saw these
same changes but to a significantly less extent. During the
wash-out period troponin levels continued to rise in subjects
under high and low-dose steroids and BNP levels that were
otherwise normal during the study, began to elevate during
washout as well (Fotini Vasilaki et al., 2016).
Another dose-dependent approach to anabolic steroid
administration was done in a study conducted by Pirompol et al
which took male rats of similar weights, divided into equal
groups of 4, and injected with different doses of testosterone
propionate. One control group was used and injected with ethyl
oleate. Evaluation of the cardiac parameters included but not
limited to cardiac chamber size, septal wall thickness, and blood
pressure. The study examined acute dysfunction of the cardiac
parameters described above to determine whether steroid
administration causes pathologic or physiologic impairment in
time or dose-dependent fashion (Pirompol, Teekabut,
Weerachatyanukul, Bupha-Intr, & Wattanapermpool, 2016).
Significant findings of elevated cardiac muscle mass were found
in all testosterone dosed rats compared to control (Pirompol et
al., 2016). A time-dependent enlargement of the ventricular
chamber was a significant finding in high-dose steroid using
rats compared to low-dose steroid using rats and controls
(Pirompol et al., 2016). Ventricular enlargement was found in
the absence of increased septal and ventricular wall thickness,
which implies a physiologic, time and dose-induced cardiac
hypertrophy (Pirompol et al., …

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THE LITERATURE REVIEW: A FEW TIPS ON
CONDUCTING IT
What is a review of the literature? A literature review is an
account of what has been published on
a topic by accredited scholars and researchers. Occasionally you
will be asked to write one as a
separate assignment (sometimes in the form of an annotated
bibliography—see the bottom of the
next page), but more often it is part of the introduction to an
essay, research report, or thesis. In
writing the literature review, your purpose is to convey to your

reader what knowledge and ideas
have been established on a topic, and what their strengths and
weaknesses are. As a piece of writing,
the literature review must be defined by a guiding concept (e.g.,
your research objective, the
problem or issue you are discussing, or your argumentative
thesis). It is not just a descriptive list of
the material available, or a set of summaries.
Besides enlarging your knowledge about the topic, writing a
literature review lets you gain and
demonstrate skills in two areas:
1. information seeking: the ability to scan the literature
efficiently, using manual or computerized
methods, to identify a set of useful articles and books
2. critical appraisal: the ability to apply principles of analysis
to identify unbiased and valid
studies.
A literature review must do these things:
a) be organized around and related directly to the thesis or
research question you are developing
b) synthesize results into a summary of what is and is not
known
c) identify areas of controversy in the literature
d) formulate questions that need further research

Ask yourself questions like these:
1. What is the specific thesis, problem, or research question that
my literature review helps to
define?
2. What type of literature review am I conducting? Am I looking
at issues of theory?
methodology? policy? quantitative research (e.g. on the
effectiveness of a new procedure)?
qualitative research (e.g., studies )?
3. What is the scope of my literature review? What types of
publications am I using (e.g., journals,
books, government documents, popular media)? What discipline
am I working in (e.g., nursing
psychology, sociology, medicine)?
4. How good was my information seeking? Has my search been
wide enough to ensure I’ve
found all the relevant material? Has it been narrow enough to
exclude irrelevant material? Is the
number of sources I’ve used appropriate for the length of my
paper?
5. Have I critically analysed the literature I use? Do I follow
through a set of concepts and
questions, comparing items to each other in the ways they deal
with them? Instead of just listing
and summarizing items, do I assess them, discussing strengths
and weaknesses?
6. Have I cited and discussed studies contrary to my

perspective?
7. Will the reader find my literature review relevant,
appropriate, and useful?
Ask yourself questions like these about each book or article you
include:
1. Has the author formulated a problem/issue?
2. Is it clearly defined? Is its significance (scope, severity,
relevance) clearly established?
3. Could the problem have been approached more effectively
from another perspective?
4. What is the author’s research orientation (e.g., interpretive,
critical science, combination)?
5. What is the author’s theoretical framework (e.g.,
psychological, developmental, feminist)?
6. What is the relationship between the theoretical and research
perspectives?
7. Has the author evaluated the literature relevant to the
problem/issue? Does the author include
literature taking positions she or he does not agree with?
8. In a research study, how good are the basic components of
the study design (e.g., population,
intervention, outcome)? How accurate and valid are the
measurements? Is the analysis of the
data accurate and relevant to the research question? Are the
conclusions validly based upon the
data and analysis?
9. In material written for a popular readership, does the author
use appeals to emotion, one-sided
examples, or rhetorically-charged language and tone? Is there
an objective basis to the
reasoning, or it the author merely [email protected] what he or

she already believes?
10. How does the author structure the argument? Can you
“deconstruct” the flow of the argument to
see whether or where it breaks down logically (e.g., in
establishing cause-effect relationships)?
11. In what ways does this book or article contribute to our
understanding of the problem under
study, and in what ways is it useful for practice? What are the
strengths and limitations?
12. How does this book or article relate to the specific thesis or
question I am developing?
Final Notes:
• A literature review is a piece of discursive prose, not a list
describing or summarizing one piece
of literature after another. It’s usually a bad sign to see every
paragraph beginning with the name
of a researcher. Instead, organize the literature review into
sections that present themes or
identify trends, including relevant theory. You are not trying to
list all the material published, but
to synthesize and evaluate it according to the guiding concept of
your thesis or research question.
• If you are writing an annotated bibliography, you may need to
summarize each item briefly,
but should still follow through themes and concepts and do
some critical assessment of material.
Use an overall introduction and conclusion to state the scope of

your coverage and to formulate
the question, problem, or concept your chosen material
illuminates. Usually you will have the
option of grouping items into sections—this helps you indicate
comparisons and relationships.
You may be able to write a paragraph or so to introduce the
focus of each section.
Prepared by Dena Taylor, Health Sciences Writing Centre, and
Margaret Procter, Writing Support
Over 50 other files giving advice on university writing are
available at www.writing.utoronto.ca
http://www.writing.utoronto.ca/advice
CRITERIA SCALES
0.00
Information is not organized, and
paragraphs are not well-
constructed.
4.00
Information is organized with well-
constructed paragraphs but lacks
clearly indicated subheadings.
8.00

Information is very organized with
well-constructed paragraphs and
subheadings.
0.00
length and does not contain
substantive or relevant content.
4.00
length but contains substantive and
relevant content.
8.00
Paper is 18-22 pages and not more
than 30 pages in length and
contains substantive and relevant
content.
0.00
Many grammatical, spelling, or
punctuation errors.
4.00
Almost no grammatical, spelling or
punctuation errors
8.00
No grammatical, spelling or
punctuation errors.
0.00
Percentage of matches are greater
than or equal to 40% and is not
acceptable.

4.00
Percentage of matches are less
than 40% but greater than 20% and
is tolerable.
8.00
Percentage of matches are less
than or equal to 20% and is
acceptable.
0.00
The purpose and theme of the
research project is somewhat
4.00
The research project has a clearly
stated purpose and theme, but may
8.00
The research project has a well-
stated clear purpose and theme
Organization
How well information is
organized with attention to
well-constructed paragraphs
and subheadings.
Length
Length of paper is
considered here based on

syllabus requirement but
also considered here is
l d
Grammar
Grammatical, spelling or
punctuation errors are
considered.
Originality
This is based on the
Turnitin Originality report
with "Quoted or
Bibliographic Material
Content
Whether the research project
has a well-stated clear purpose
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