Graduation 2015 - Thesis

The Impact of Vitamin D Supplementation On Athletic Performance
By
Tammilee Kerr, BSc, BA
A Thesis
In
Nutrition Science
Submitted to the Graduate Faculty
of Texas Tech University in
Partial Fulfillment of
the Requirements for
the Degree of
MASTER OF SCIENCES
Approved
Dr. Jamie A Cooper
Dr. Malorie Boylan
Dr. Jennifer Mitchel
Mark Sheridan
Dean of the Graduate School
May, 2015
Copyright 2012, Tammilee Kerr
Texas Tech University, Tammilee Kerr, May 2015
ACKNOWLEDGMENTS
Foremost, I would like to thank my advisor Dr. Cooper for allowing me to do this
study. It was an immense learning experience and I will utilize the knowledge and
experiences as I move forward in my future studies and career.
I would also like to thank the rest of my thesis committee: Dr. Mallory Boylan and
Jennifer Mitchell for their encouragement and insightful comments.
My sincere thanks also goes to Dr. Matt Stock and the TTU Exercise Science
Department for the continuous accommodation and assistance with performance
testing and for the encouragement.
I thank Rebecca Compton of Everidis Health Sciences, LLC for providing us with the
Vitamin D supplements.
I thank the Covenant Hospital, medical team for providing fast and efficient testing
To the Athletics Department here at TTU, I thank you for understanding the future
implications of such a study and for allowing me to recruit the athletes. I thank the
athletes also for taking time out to participate in the study.
I thank my fellow lab mates in the HNL, especially Keely and Jada for the stimulating
discussions, encouragement and for answering my never ending questions.
I thank Avril McGhee, and Julian Munroe for supporting me and always being oncall.
Last but not the least, I would like to thank my friend my parents Ceva McPhersonKerr and Winston Kerr, for the encouragement in pursuing my MS with a research
option, for the financial support, advice, for the laughter and tears, for the upliftment
in times of doubt and for always supporting me in my endeavors.
ii
TABLE OF CONTENTS
ACKNOWLEDGEMENTS
ii
ABSTRACT
LIST OF TABLES.
vii
LIST OF FIGURES
viii
CHAPTER I INTRODUCTION.
CHAPTER II LITERATURE
3
REVIEW
Vitamin D Status in Children & Adults...
Reasons for Vitamin D Deficiency & Insufficiency..
Functions of Vitamin D.
Vitamin d on Muscle Structure, Function & Performance..
Vitamin D & Athletics Performance
4
7
9
11
17
CHAPTER III RESEARCH DESIGN & METHODS.. 20

Participants & Procedures...
Statistical Analysis
Power Analysis..
20
24
25
CHAPTER IV RESULTS..
27
Baseline Subject Characteristics
Prevalence.
Serum Vitamin D 25(OH)D & Performance Tests..
Vitamin D & Performance Tests.
Figures
27
28
32
33
37
CHAPTER V DISCUSSION.
41
CHAPTER VI CONCLUSION..
46
BIBLIOGRAPHY...
47
APPENDIX A.
53
IRB Approval.
IRB Amendment
IRB Extension
APPENDIX B.
iii
56
53
54
55

Consent Form
Vitamin D Screening Questionnaire..
56
60
APPENDIX C.
62
Supplement & Multivitamin Log..
Vitamin D Exposure Log & Key..
62
63
iv
ABSTRACT
Vitamin D (VitD) has been found to have many effects on systems in the body; these
include the immune, cardiovascular and muscular system. In the elderly vitamin D
(VitD) deficiency is implicated in reduced skeletal muscle function and physical
performance (PP); however very few studies have been done to look at the effects of
vitamin D deficiency on athletics performance in collegiate and recreational athletes. The
purpose of this study was to (1) Determine the prevalence of vitamin D insufficiency and
deficiency among Collegiate Athletes and athletic persons from the general public, (2)
Determine if a 12-week VitD supplementation at 28,000IU/week in VitD insufficient or
deficient athletes raises Vit D levels to a sufficient range, and (3) Determine VitD
supplementation of 28,000IU/week improves physical performance in Vit D insufficient
or deficient athletes. Methods: 93 athletes completed baseline measurements of serum
calcidiol 25(OH)D levels, height, weight, body composition, a Block calcium/VitD
questionnaire and a sun log. Athletes with serum calcidiol below 30ng/mL performed 5
PP tests (30m sprint, standing long jump, vertical jump, leg strength and flexibility) and
were randomly assigned to a placebo control or VitD supplement (28,000 IU of
VitD/week) group for 16 weeks. Post-intervention measures were the same as those
collected at baseline. Results 30.1% of the subject populations were VitD deficient or
insufficient at baseline while 69% of the populations were sufficient. Of the VitD
insufficient or deficient athletes, 75% were African-American. Serum levels of VitD
supplemented subject were raised to sufficient levels (39.35.1 ng/mL). There was no
significant difference in any performance variable from pre to post intervention; however
v

there were significant positive correlations between serum 25(OH)D and flexibility
(r=0.55, p=0.03), serum 25(OH)D and type II fiber percentage (r=0.66, p=0.005) and sun
exposure and leg strength (r=-0.51, p=0.04). Conclusion: VitD deficiency and
insufficiency is highest among African American athletes and VitD supplementation at
28,000 IU / week will raise serum levels to significant levels, but was ineffective in
increasing athletic performance.
vi
LIST OF TABLES
1
Subject Characteristics at Baseline
27
Subject Vitamin D Classification at Baseline
29
Subject Characteristics for those with All Pre vs. All Post Measures
& Placebo vs. Vit. D at Pre and at Post
Intervention...............................................................
31
Pearson Correlations between Subject Characteristics and Performance.
35
Pearson Correlation between change in Serum 25(OH)D and

change in performance tests..
36
vii
LIST OF FIGURES
1
Serum 25(OH)D Pre & Post Supplementation..
37
Standing LJ Pre & Post Supplementation.
37
Vertical Jump Pre * Post Supplementation...
37
30m Sprint Pre & Post Supplementation ..
38
Leg Strength Pre & Post supplementation.
38
Flexibility Pre & Post supplementation.
38
Type II Fiber Pre & Post supplementation. 38
Correlation between Vitamin Intake & Leg Strength Pre Supplementation.
39
Correlation between Sun Exposure & Weight Pre Supplementation.
39
10 Correlation between Sun Exposure & Leg Strength Pre Supplementation
39
11 Correlation between Sun Exposure & BMI Pre Supplementation.
39
12 Correlation between Serum 25(OH)D & Flexibility Post Supplementation..
40
13 Correlation between Serum 25(OH)D & Type II Fiber % Post Supplementation.
40
14 Correlation between Sun Exposure & Leg Strength Post Supplementation... 40
viii

CHAPTER 1 - INTRODUCTION
Vitamin D is a fat soluble nutrient that is an essential for optimal health. Humans
can synthesize vitamin D from UV sun exposure, and it is found in limited amounts in the
food supply (1); however it is estimated that 77% of the United States (U.S.) population
is vitamin D deficient (2). Vitamin D insufficiency and deficiency is not limited to the
U.S. population alone, it has reached epidemic proportions in worldwide populations (3).
Vitamin D insufficiency or deficiency encompasses all stages of life and includes infants,
adolescents, adults and the elderly. The risk for vitamin D inadequacy or deficiency
includes but is not limited to age, altitude/ latitude, skin color (melatonin content of skin),
use of sunblock, lack of sun exposure and clothing coverage (4).
Vitamin D insufficiency and deficiency is for the most part asymptomatic and
therefore is not easily recognized, with the exception of severe vitamin D deficiency
symptoms such as rickets and osteomalacia (softening and weakening of bones that may
lead to bone deformation) which occurs in children and adults respectively. As a result,
many individuals could have insufficient or deficient vitamin D levels without knowing
it. Therefore, the best means to determine vitamin D status is to assess serum
concentrations of Calcidiol 25(OH)D.
There are numerous benefits to maintaining adequate vitamin D levels due to the
fact that vitamin D has many vital roles in the body. It has been suggested that vitamin D
is a modulator of thousands of genes within the human genome which are involved in the
modulation of cell growth, boosting immune function, regulating muscle function,
reducing inflammation, neuromuscular function and protein synthesis. Apart from its role

in the maintenance of bone health and prevention of rickets, osteoporosis and
osteomalacia, vitamin Ds role has been implicated in many other diseases, such as
cardiovascular diseases, diabetes, multiple sclerosis, rheumatoid arthritis, inflammatory
bowel disease, macular degeneration, mental illness, and chronic pain (5).
The role of vitamin D on exercise performance is also an area of increasing
interest since improvements in strength and performance have been seen with higher
levels of serum vitamin D and with vitamin D supplementation(6) (7) (8) (9). Studies
have found that higher serum levels of vitamin D are positively correlated with gait
speed, handgrip strength, and increased muscle strength in women(7) (10,11) (11). A
study in athletes also found that vitamin D status may have a significant positive effect on
sprint times and vertical jump height in athletes (6). Further, athletes are thought to have
a similar prevalence of deficiency as the rest of the U.S. population (2). The purpose of
this study is to; (1) Determine the prevalence of vitamin D insufficiency and deficiency
among Collegiate Athletes and athletic persons from the general public, (2) Determine if
a 12-week vitamin D supplementation at 28,000IU/week in vitamin D insufficient or
deficient athletes raises vitamin D levels to a sufficient range, and (3) Determine if
vitamin D supplementation of 28,000IU/week improves physical performance in vitamin
D insufficient or deficient athletes. We are hypothesizing that at least 50% of the athletes
in our study will be vitamin D deficient or insufficient. We also hypothesize that vitamin
D supplementation will raise serum levels of vitamin D to sufficient ranges and will
improve physical performance outcomes in previously vitamin D deficient athletes.

CHAPTER II -LITERATURE REVIEW
Vitamin D is a fat soluble secosteroid that is either consumed through dietary
sources or synthesized endogenously by the absorption of ultraviolet rays into the skin.
The synthesis of vitamin D begins in the skin where 7-dehydrocholesterol is converted to
pre-vitamin D3 by the irradiation of Ultraviolet (UVB) rays. Pre-vitamin D3 is then
converted to cholecalciferol (Vitamin D3) in the dermal layer of the skin and transported
via vitamin D- binding protein (VDBP) to the liver where it is converted to calcidiol or
25-hydroxy vitamin D 25(OH)D. In the Kidney, calcidiol is then further hydroxylated to
calcitriol or 1,25 dihydroxyvitamin D 1,25(OH) 2D3 which is the biologically active form
of vitamin D (12). Although humans can obtain vitamin D in the diet, the principal source
of vitamin D is synthesis via sun exposure(4). For example fair skinned persons who
sunbathe in the summer produce approximately 20,000IU of vitamin D in 30 minutes
(13) which is the equivalent of taking 50 standard multivitamin pills (400IU per pill) (4).
Naturally occurring vitamin D is found in very few foods therefore most foods are
fortified with vitamin D. The two forms of vitamin D used in fortified foods are vitamin
D2 (ergocalciferol) (VD2) and vitamin D3 (cholecalciferol) (VD3). Good food sources of
vitamin D include egg yolk, fatty fish, such as salmon, tuna and mackerel, and milk
(fortified with 400IU/ qt. in the USA) which are higher VD3 and its metabolite calcidiol
(14). Other sources of vitamin D include fortified breakfast cereals, some brands of
fortified orange juice, fortified yogurt, fortified margarine and fortified soy beverages
(14). Vitamin D fortified foods must include the type of vitamin D added in its ingredient
label. Vitamin D supplements also come in the forms of VD2 and VD3 (14) and the
3

typical multivitamin usually contains VD2 or VD3. VD2 is made from the irradiation of
ergosterol, which is found in yeast, by ultra-violet (UV) light and VD3 is made from the
irradiation of 7-dehydrocholesterol from lanolin and the chemical conversion of
cholesterol (15). Although both forms of vitamin D raise 25(OH)D vitamin D levels,
VD3 may be more than three times as effective at maintaining those levels for a longer
period of time however both forms have been found to effectively raise calcidiol levels in
vitamin D deficient or insufficient persons(14). The recommended daily allowance
(RDA) for vitamin D intake, as set forth by the Institute of medicine (IOM), includes
daily doses of: 400-600 IUs (International Units) for ages 1-70 years; 800 IUs for ages
71 years and older; and 600 IUs for pregnant and lactating women.
Vitamin D Status in Adults, Children, and Athletes

The prevalence of vitamin D insufficiency and deficiency has reached epidemic
proportions in the world and more specifically in the United States. Assessing serum
concentrations of Calcidiol (25(OH)D) is the best indicator of vitamin D status (14)
which allows for diagnosis of vitamin D deficiency and its subsequent safe and adequate
treatment (4). Calcidiol, has a long circulating half-life of 15 days compared to that of
Calcitriol (half-life of only 15 hours), therefore Calcidiol is a better indicator of vitamin
D status (levels) as the Calcidiol levels are more stable and fluctuate less than that of
Calcitriol. Therefore, Calcidiol levels are assayed to determine vitamin D status in the
body (14). Although there are several different assays to determine calcidol levels, the
currently accepted Gold standard method is Liquid chromatography-tandem mass

spectrometry (LC-MS/MS) due to its efficiency, high specifity and high sensitivity (16).
Other methods such as Ligand-binding assays (radioimmunoassay, competitive proteinbinding assays) are less reliable as they lack the high specificity, found in LC-MS/MS,
which may lead to erroneous high or low results,
Currently accepted levels in assessing vitamin D status include calcidiol 25(OH)D
levels <20ng/mL (<50nmol/L) indicating deficiency; 20-30ng/mL (50nmol/L
75nmol/L) indicating insufficiency; and 30ng/mL (75nmol/L) indicating sufficient
vitamin D levels.
According to the Centers for Disease Control (CDC) NCHS Data Brief
approximately 25% of the population of the United States was found to be at risk for
vitamin D inadequacy, while 8% were found to be at risk for vitamin D Deficiency (5).
The National Health & Nutrition Examination Surveys (NHANES) III study from 1988
to 1994 indicated that 55% of participants had serum levels of less than 30ng/mL
indicating insufficiency or deficiency. These data were compared to the NHANES 20012004 study which showed vitamin D levels below 30ng/mL had increased to 77% of
participants, while levels below 10ng/mL, indicating deficiency, increased from 2% to
6% (1). More recent NHANES data, 2005 -2006, indicated that the overall prevalence
rate of vitamin D deficiency was 41.6% in the adult population (17). In addition to this
the NHANES Study 2001-2004 of a sample of children aged 1 to 21 years found that 9%
of the pediatric population, representing 7.6 million US children and adolescents, were
calcidiol 25(OH)D deficient and 61%, representing 50.8 million US children and
adolescents, were calcidiol 25(OH)D insufficient (18). Increases in vitamin D deficiency

and insufficiency can be attributed to an increase in obese children and adolescents an
increase in indoor activities such as watching television, playing video games, or using
computers, limited availability of vitamin D food sources and an increase in the use of
sun screen.
Various studies suggest that athletes are at great risk for vitamin D deficiencies
and insufficiencies. A recent study of 223 NCAA Division I athletes found that 33.6% of
the study population had abnormal levels (deficient and insufficient) of vitamin D. They
also reported that subjects of darker skin tones were at greatest risk for deficiency (19). A
previous pilot study looking at the effect of vitamin D supplementation on athletic
performance found that at least 83% of the athletes were vitamin D deficient or
insufficient. Currently at least 50% of the Texas Tech University (TTU) Collegiate
Athletes and athletic persons from the general public are vitamin D deficient or
insufficient. It was found that Hispanics athletes were at the highest risk for vitamin D
deficiency (100% had levels below <30ng/mL), while 83% of the black athletes were
deficient or insufficient, and 25% of the white athletes were insufficient or deficient (20).
Storie et al. found that 25% of male athletes who competed in outdoor sports (rugby,
football, track & field and cross country) in the USA where insufficient (2). Another
study conducted on male and female USA endurance athletes found that 11% of the
athletes were vitamin D deficient (21). In the UK Close et al. found that 62% of male
indoor and outdoor professional athletes were vitamin D deficient (6). Therefore, it
appears that vitamin D insufficiency and/or deficiency is a major problem in athletics and
needs to be addressed.

Reasons for Deficiency or Insufficiency
Vitamin D levels may be affected by a number of factors which includes dietary
intake, latitude and season of the year, time of day, air pollution, use of sunscreen, sun
exposure, color of the skin, weight, age, and extent of clothing coverage.
One of the main contributors to the increase in vitamin D deficiency and
insufficiency is the limited availability of vitamin D in food items. Vitamin D occurs
naturally in very few foods some of which include salmon, tuna, mackerel, egg yolk and
liver and is fortified in milk, orange juice and cereals.
A person must eat a large amount
and a variety of these food items to maintain vitamin D levels at acceptable ranges
(>30ng/mL), which is not the norm (3).
Although vitamin D is limited to a small number of foods most people meet at
least some of their vitamin D needs through consumption of foods that are naturally rich
in vitamin D or from fortified foods. However studies have shown that changing dietary
patterns in the United States which includes the decreasing consumption of the foods that
are rich in vitamin D such as salmon, tuna, mackerel and fortified milk; may account for
increases in vitamin D deficiency and insufficiency .
The principle source of vitamin D synthesis is through sun exposure where the
body naturally converts Pre-vitamin D to Calcidiol and Di-hydroxyvitamin D. As a result
of increasing time spent indoors for work, school, sporting activities and other activities,
there is very little exposure to the sun (UV- rays), which in turn contributes to the
increasing prevalence of vitamin D deficiency and insufficiency. Current
recommendations for sun exposure to maintain adequate vitamin D levels includes sun

exposure to the face, arms, legs or back without sunscreen, between 10am and 3pm for
15-30 minutes (22). Recommendations also suggest the moderate use of commercial
tanning beds which emit UVB radiation of 2%-6% (14).
Another important contributing factor to the increase in the prevalence of vitamin
D insufficiency and deficiency is the increasing use of sunscreens. The American
academy of Dermatology has advised that protective measures should be taken when one
is exposed to the sun, such as the use of broad spectrum sunscreen to prevent sunburn
and decrease the risk of developing skin melanomas, squamous cell carcinomas and
other cancers (23). Sunscreen works by combining ingredients such as zinc oxide or
titanium oxide with oxybenzone which in combination reflects or scatters ultraviolet
(UV) radiation. This inhibits the skins ability to absorb UV-rays and thus prevents the
activation of Pre-vitamin D which is a requirement for further vitamin D production
processes in the body.
Air pollution also contributes to the decreased absorption of UV rays by the skin
by deflecting UVB radiation away from the surface of the earth. Therefore cutaneous
vitamin D production is decreased or impaired.
Latitude also has a huge impact on the exposure to UVB rays. Locations that are
found 35 north or south of the equator are prone to longer winter months and therefore
receive less UVB rays. This again greatly limit and or impedes the amount of cutaneous
vitamin D that is made (24).The elderly, African Americans and the obese are at
increased risk of vitamin D insufficiency and deficiency. Elderly persons may make
much less vitamin D than their younger counterparts because of three reasons; as they

age they lose ability to synthesize vitamin D from sunlight; activation of vitamin D in the
Kidneys decreases with age and ; elderly persons who are homebound/ immobile are less
likely to participate in outdoor activities (25). African Americans and those with darker
skin face an increased risk for Vitamin D insufficiency or deficiency because of the
melanin content of their skin. Melanin is a pigment that acts as a natural and ever present
sunscreen that reduces cutaneous production of vitamin D (26) (17). Persons with excess
body fat or those who are obese may have lower vitamin D levels due to the fact that
body fat absorbs and stores vitamin D making unusable by the body (27). Finally those
who wear clothing that covers most of the body are at an increased risk for vitamin D
deficiency (28).
Functions of vitamin D
Vitamin D deficiency has been implicated with many diseases including;
cardiovascular diseases, diabetes, metabolic syndrome, diseases of the immune system,
cancer, rheumatoid arthritis, inflammatory bowel disease, macular degeneration, mental
illness, chronic pain (4) and bone diseases such as rickets and osteoporosis. This is likely
due to the multiple important functions of vitamin D in the body. These functions include
modulation of cell growth, boosting immune function, regulating muscle function,
reducing inflammation, neuromuscular function, and its most well-known role in
promoting calcium absorption and regulating calcium and phosphorus levels to maintain
bone and teeth (12). Calcium levels in the blood are regulated by three hormones: vitamin
D, calcitonin (produce by the thyroid gland) and parathyroid hormone (PTH) (produced

by the parathyroid glands). Normal blood calcium levels are maintained by the
stimulation of PTH which stimulates the conversion of calcidiol 25(OH)D to its active
form calcitriol or 1,25 dihydroxyvitamin D. Calcitriol acts on the epithelial cells of the
digestive tract to promote uptake of dietary calcium. When calcium levels are too low,
vitamin D and PTH act synergistically to increase the blood calcium to normal levels by
reducing calcium loss in the urine. Vitamin D also works to increase blood calcium levels
by promoting bone turnover which liberates calcium. Absorption of phosphorous also
occurs in a similar manner; PTH is released in response to low phosphorus levels and
stimulates vitamin D to act on the small intestines to promote phosphorus absorption(29)
(30). It is because of this role in calcium and phosphorus homeostasis that maintenance of
normal vitamin D serum levels is crucial as vitamin D promotes both calcium and
phosphorus absorption.
Low levels of vitamin D have been associated with increased risk of
cardiovascular diseases (CVD). Wang et al (31) confirmed that vitamin D receptor
(VDR) knockout mice developed hypertension and hypertrophy to the left ventricle due
to the up-regulation of the renin-angiotensin system (32). In addition to this vitamin D
may play a role in the suppression of the calcification of vascular tissues and may
promote the increased production of anti-inflammatory cytokines (33) which are
processes which affect the cardiovascular system.
Studies have shown that vitamin D may lower the risk for hypertension which is a
risk for CVD. Duprez et al and Scragg et al (34), (35), (36) showed significant inverse
correlation between blood pressure levels and vitamin D levels. The proposed
10

mechanism is that decreased vitamin D levels results in increased calcium levels, which
is a result of suppressed renin activity. Increases in calcium again may promote
calcification of vascular tissue.
Ongoing research has identified ways in which vitamin D levels may have
significant effects on diabetes mellitus (DM). Proposed mechanisms include the
dysfunction of pancreatic cells and insulin resistance of peripheral tissues due to low
or insufficient levels of vitamin D (37). Vitamin D supplementation has been shown to
improve markers of Type II diabetes such as insulin secretion, insulin sensitivity and
hemoglobin A1C, which suggests that vitamin D may play a role in the prevention/
improvement of Type II diabetes (38).
Metabolic Syndrome is a group of disorders that when combined with each other,
increase the risk of developing CVD and diabetes. Oosterwerff et al (39) have shown
that increasing vitamin D levels and decreasing other factors for metabolic disorders such
as smoking, obesity and stress significantly decreases the risk of metabolic disease and
thus the risk of developing CVD and diabetes .
Vitamin D on Muscle Structure, Function, and Performance

The issue of vitamin D deficiency among athletes is of great concern in the
sporting field especially as it relates to the athletic performance and injuries. Although
the majority of current literatures on vitamin D deficiency and its impacts on health are
focused on other populations such as the elderly, data suggests that vitamin D levels have
11

significant impacts on muscle function, bone turnover and strength, immunity, fatigue
and inflammation, all of which are applicable and relevant issues in athletics.
The impacts of vitamin D on muscle function were first identified from clinical
observations of osteomalacic myopathy, which is characterized by proximal muscle
weakness in adults (40) and muscle weakness and hypotonia in infants (41) (40). Glerup
et al (42) found that subjects with biopsy-proven osteomalacia that were treated with
alfacaciol, ergocalciferol and calcium showed vitamin D significant improvements in
muscle power (42).
Confirmation that muscle tissue is a target for vitamin D was discovered in 1985,
when vitamin D receptors (VDR) were found within cultured rat myoblast cells. The
VDR knockout mouse model (deleted VDR gene) provided substantial evidence for a
direct effect of vitamin D and VDR on skeletal muscle tissue. Characteristics of VDR
null mutant mice included alopecia, a reduction in body size and weight, impaired motor
coordination (43) and poor swimming ability (44). It was found that mice with missing
VDR genes had a 20% reduction in fiber size of the quadriceps and other muscle groups.
These mice also had an increase in the expression of myf5 (a protein with a key role in
regulating muscle differention), when compared to normal mice (45). This supported the
theory of a direct role for Vitamin D and the VDR in the metabolic processes and
transcription regulation of skeletal muscle fiber development and maturation (40) (41).
Muscle fibers are categorized into two main types: Type I (slow twitch) and Type
II (fast twitch) muscle fibers. Type II fibers are extremely important in generating short
burst of strength or speed and are necessary for peak athletic performance in athletes.
12

Biopsies of human skeletal muscle in vitamin D deficient adults have shown atrophy of
type II muscle fibers, thus researchers believe that vitamin D supplementation may have
an impact on muscle fiber composition, and may be especially important for type II
muscle fibers (46). For athletes, this could mean that adequate vitamin D levels are
especially important for strength and power or anaerobic sport athletes.
Sorenson et al (47) supplemented vitamin D3 and calcium for 6 months in elderly
women and found an overall increase in fiber composition (muscle mass) and an increase
in type II muscle fibers as a result of supplementation. In another study it was shown that
daily treatment with 1,000IU of vitamin D2 (ergocalciferol), over a period of two years in
forty-eight (n=48) vitamin D deficient stroke survivors produced a significant increase in
type II muscle fiber diameter and an increase in type II muscle fiber percentage (48).
Potential mechanisms for how vitamin D affects type II fibers and muscle
function and growth have not been clearly defined, but an hypothesized mechanism in the
interaction between insulin growth factor 1(IGF-1) and insulin growth factor binding
protein 3 (IGF-BP3) with vitamin D has been made. IGF is a polypeptide of three
isoforms (IGF-1Ea, IGF-1Eb & IGF-1Ec) which is one of many molecules that regulates
growth. Several research studies have suggested that vitamin D 3 influences IGF-1
expression during the growth of children. The circulating form of IGF-1 (IGF-1Ea)
stimulates muscle cell differentiation into myotubes and promotes and promotes stemcell-mediated muscle generation. The tissue form of IGF-1 (IGF-1Ec or mechano-growth
factor (MGF)) is expressed by skeletal muscle cells and regulates autocrine/paracrine
actions that regulates tissue damage, local tissue repair and induces muscle hypertrophy.
13

Vitamin D3 seems to be a regulator of IGFBP-3 which is the carrier protein that is bound
to circulation IGF-1. Another hypothesized mechanism is that a decrease in active
vitamin D, which results in decreased calcium absorption in muscle, will affect calcium
associated protein transcription in muscle that is necessary for producing type II fibers
(49) (50).
Vitamin Ds implication in muscle performance, function, maintenance and
strength has also been validated by studies on muscle mediated falls in elderly persons.
Pfeifer et al (8) found that vitamin D supplementation improved parameters of muscle
function on fall risk in elderly community dwelling individuals. In the study, 242 healthy
seniors with calcidiol 25(OH)D levels below 75nmol received supplementations of
1000mg of calcium or 1000mg of calcium plus 800IU of vitamin D 3 per day for a period
of 12 months(8). Those receiving the vitamin D plus calcium had a significant decrease
in the percentage of falls over a 12 month and 20 month follow-up period while
quadriceps strength was found to be significantly higher in the calcium plus vitamin D
group after 12 months and at the 20 month period. Significant improvements were also
found in body sway (the small postural movements made by an individual to maintain a
balanced position, which is used an assessment of balance)(51); here both the calcium
plus vitamin D and calcium alone group had significant decrease in body sway after 12
and 20 months follow up period.
Multiple studies in older adults and a few in adolescents and younger adults have
found direct association between vitamin D status and parameters of physical
performance and exercise(10) (9) (8). In the Progetto Veneto Anziani study (Pro.V.A
14

study), Elena et al (7) detected the positive association between vitamin D status and
physical performance in 2694 community dwelling elderly women and men. Physical
performance was assessed by tandem test, timed chairs stands (TCS), gait speed; hand
grip strength, quadriceps strength and 6-minute walking distance (6mW). There was
linear associations of calcidiol 25(OH)D serum levels and TCS, gait speed, 6mW test and
handgrip strength. Improved performances in TCSS in women, in gait speed and
handgrip strength in men and in 6mW in both genders were seen with increasing levels of
calcidiol 25(OH)D. From this it could be concluded that lower calcidiol 25(OH)D levels
were associated with decreased coordination and strength in women, a slower walking
time and a lower upper limb strength in men, and weaker aerobic capacity (6mW) in both
genders.
More recent research suggests that the effect of vitamin D on muscle performance
and exercise is not limited to older adults. A cross sectional study conducted in the
United Kingdom reported a direct relationship between calcidiol 25(OH)D levels and
muscle power and force in 99 post menarchal girls (9). It was noted that girls with lower
serum calcidiol 25(OH)D concentrations (mean of 21.3nmol/l) had lower jump height
and velocity as a result of generating less power this was significantly lower than those
with higher concentrations of calcidiol 25(OH)D (9). A similar positive relationship
between calcidiol 25(OH)D levels and muscle strength was also found in a study by Foo
et al, (11) where handgrip strength was found to positively correlate with higher calcidiol
25(OH)D levels.
15

Historically, most studies on vitamin D and school children have been geared
towards bone development and health and the prevention of rickets. However Fuleihan et
al (52) examined the impact of vitamin D deficiency on skeletal health in children and
sought to bring to the forefront the need for a focus on vitamin D and musculoskeletal
health. They studied 179 girls (aged 10-17yrs) who were randomly assigned to receive
weekly oral vitamin D3 doses of 1,400 IU, 14,000IU or a placebo for a period of 1yr.
Serum concentration of calcidiol 25(OH)D increased to a mean of 3831ng/mL in the
high dose group and to a mean of 176ng/mL and 168ng/mL in the low dose group and
placebo group, respectively versus baseline serum levels of 148ng/ mL. There was an
overall greater increase in whole body lean mass in supplemented groups compared to
placebo (9.0%8.3% in higher dose, 8.7%80% in the low dose group and 5.7%6.6% in
placebo); however, this did not reach statistical significance (52).
Muscular pain and fatigue are common with regular exercise; however, they may
also be indicators of vitamin D deficiency (4). This would obviously impact the potential
for optimal performance in athletes as well as in the general population. Knutsen et al
(53) found a positive association between inadequate vitamin D levels and non-specific
mucoskeletal pain, headaches and fatigue. In another study of primary care patients with
serum vitamin D levels of <75nmol/l (<28.0ng/ml) in 88.9%, <50 nmol/l (<20ng/mL) in
45.1%, <30 nmol/l (<12ng/mL) in 9.8%, there was a significant correlation between
muscle weakness and degree of vitamin D deficiency (p=0.04) (54). Finally, Prakash et
al (55), (56) also reported a significant correlation between vitamin D deficiency and
16

chronic tension-type headaches. Improvements were seen with vitamin D and calcium
supplementation (55).
In elite athletes lean body mass is of optimal performance in sporting events.
Collegiate Athletes and athletic persons from the general public typically have body fat
mass below the average values of (15% in college age men)and 25% in college age
women (57). Vitamin D concentrations have been shown to be associated with body fat
percentage. In a cross sectional study involving a CT scan of various muscles of 90 postpubertal females (16-20y), those with vitamin D levels below 30ng/mL were found to
have a higher body fat percentage, which was in contrast to those of vitamin D levels
greater than 30ng/mL that had lower body fat percentages. In another study of 198
adolescents between 12-17yrs, Mascarenhas et. al (58) it was also found that those with
severe vitamin D-deficiency (<10 ng/ml) had a significantly higher body fat percentage
(40.8214.59) compared to those of sufficient levels (>30ng/dl) which had a lower body
fat percentage (23.439.47).
Vitamin D and Athletic Performance

There are limited studies directly implicating vitamin D supplementation on the
improvement in athletic performances, which indicates the need for an increase in such
studies to be conducted. However, based on the numerous studies highlighting the
importance of adequate vitamin D status on muscle function, strength, muscle fiber
composition, gait speed, and body composition, it is logical to hypothesize that vitamin
D supplementation could improve athletic performance in insufficient or deficient
17

persons. A previous pilot study looked at the effect of vitamin D supplementation on
athletic performance. TTU male collegiate basketball players (n=17; n=8 placebo, and
n=9 supplement) were supplemented with either 4,000 IU/day of vitamin D3 or placebo
for 8 weeks. Baseline Calcidiol (25(OH)D) levels 21.19.27ng/mL in the supplement
group and 18.25 10.30ng/mL in the placebo group (83% of the athletes in the study
were vitamin D deficient or insufficient). To assess performance a vertical jump, 20Meter Sprint, 5-10-5 Agility Drill and body fat percentage pre and post supplementation
were measured. Supplementing with 4,000IU/day significantly increase serum
concentration of Calcidiol (25(OH)D) to (41.1 11.49 ng/ml while there was no
significant change in the placebo group (post measures: 27.88 7.77ng/mL). For
performance measures in the supplement group, there was no significant improvement in
vertical jump (pre: 27.672.61 inches versus post: 28.00 3.74 inches) (pre: 3.140.23s
versus post: 3.050.11s) or agility drill time (pre: 5.070.44s versus post: 4.950.24s).
However, it is important to note that this pilot study was greatly underpowered due to the
low subject number. Finally TTU collected data over the past 3 years on vitamin D status
and found that approximately 50% of the TTU NCAA athletes were vitamin D deficient
or insufficient in the sports of basketball, cross country, and track and field (20).
There are very few studies that have looked at the direct association of vitamin D levels
on physical performance measures in athletes. One study has shown that athletes who
have insufficient or deficient levels of vitamin D perform less in performance type tests
when compared to athletes with normal vitamin D levels (2) (2,6). In a 8 week placebo
controlled trial where 14 vitamin D insufficient or deficient male UK soccer players were
18

supplemented with 5,000IU of vitamin D3 per day, there was a significant increase in
sprint times of 10m (p=0.008) and vertical jump height (p=0.008) when compared to
athletes supplemented with a placebo, who showed no improvements in sprint times
(p=0.587) or vertical jump height (p=0.204) (2). Another unpublished study has shown
that higher 25(OH)D levels where associated with increased VO 2 max in athletics college
males when, compared to those with lower vitamin D levels (p < 0.01)(2).
However not all studies show improvements in performance with vitamin D
supplementation. In a randomized dose response study of 30 UK club level athletes who
performed three performance tests (a 1-RM bench press, leg press and vertical jump), it
was found that vitamin deficient or insufficient athletes improved their vitamin D levels
above 50 nmol/l when supplemented for 6 and 12 weeks with 20,000 IUs (7914 and
8510 nmol/l, respectively) or 40,000 IUs (9814 and 9124 nmol/l, respectively) of
vitamin D3. This was in contrast to the placebo group who had decreases in serum
vitamin D levels at 6 weeks (3718 nmol/l) and 12 weeks (4122 nmol/l). However they
found no significant between increasing serum levels and improvements in performance
parameters (P>0.05) (2,59), suggesting the need for further studies in regards to vitamin
D supplementation and athletic performance outcomes.
19

CHAPTER III RESEARCH DESIGN & METHODS
The study was a double blinded, placebo controlled study. All subjects completed a
baseline/screening visit. They were placed randomly into a placebo or vitamin D
supplementation group for a 16-week period. Following the intervention, post
measurements were taken on all subjects.
Participants
200 (n=200) collegiate athletes and athletic persons from the general public were
recruited to participate in this research study. Participants were between the ages of 18-65
years, recruited from the West Texas area. All subjects exercised five hours or more per
week. The following were used as exclusion criteria: athletes who were injured and
unable to perform exercise; any athlete who was undergoing treatment for vitamin D
deficiency or insufficiency, athletes taking medications that might have interfered with
vitamin D absorption and athletes who were using tanning beds. Multivitamin/mineral
pill use was not excluded but this information was recorded at the baseline visit. Written
informed consent was obtained from each athlete and The Institutional Review Board
(IRB) at Texas Tech University (TTU) reviewed and approved that portion of the study.
Procedures
Visit 1 Measurements at Baseline Screening Visit
Within 2 weeks prior to starting the intervention, 135 (n=135) collegiate athletes and
athletic persons from the general public were baseline tested. Participants reported to the
20

Student Health building, Human Nutrition Lab HNL at the TTU campus or Covenant
Hospital for blood draws. Assessment of Calcidiol (25(OH)D) levels were conducted at
the Covenant Hospital laboratory. A 5mL silicone coated Red Top BD vacutainer blood
collection tube containing clot activator was used to collect blood. After blood collection
the tube was inverted approximately five times to ensure mixing of clot activator with
blood. Within 30-60minutes of the blood draw the tube was spun in a Beckman Coulter
centrifuge for 7 minutes to separate blood serum. Analysis of Calcidiol (25(OH)D) was
conducted using the Architect i2000SR by Abbott Diagnostics. Automated immunoassay
was used to measure Calcidiol (25(OD)D) levels.
Also at the HNL, anthropometric measurements were taken which included height, body
weight, and body fat percentage using bioelectrical impedance analysis (RJL Systems,
located at 33939 Harper Ave. Clinton Township, Michigan).
Visit 2 Pre-Intervention
135 collegiate athletes and athletic persons from the general public were tested at the
baseline screening visit. Those athletes with sufficient Calcidiol (25(OH)D) levels above
30ng/mL did not partake in the intervention trial. Those athletes falling below 30ng/mL
of Calcidiol 25(OH)D, which indicated insufficient or deficient levels, were randomly
assigned to either the control group or the supplementation group. Within that random
assignment, subjects were matched for ethnicity. These Calcidiol (25(OH)D) insufficient
or deficient subjects reported to the Exercise Science Laboratory at TTU within 2 weeks
after their baseline screening visit for the physical performance tests. Performance tests
21

included vertical jumps performed without a countermovement (a vertical jump using the
arms only), a 30-meter sprint, standing long jump test (a test of explosive leg power), a
test of flexibility (sit and reach test) and a test of leg strength. The vertical jump was
assessed using the Vertec vertical jump measurement system (JUMPUSA.com
Sunnyvale, CA) because of its correlation to explosive power. Three vertical jumps were
completed without counter movement (from a squat and using the arms in an upward
swinging motion), the best of the three was recorded. Quick acceleration is essential in
most sports; therefore the 30m sprint was used to assess this measure of performance.
Two cones were placed 30 meters apart and participants had three attempts to accelerate
as fast as possible from one cone to the other. This was timed using a hand timer. The
Standing long jump (Broad Jump) is commonly used as a test of explosive leg power.
Using a standing long jump testing mat, participants used a two footed takeoff to jump as
far as possible and used the same two footed method to land without movement. The
distance between the takeoff line and landing was measured. Three attempts were
allowed and the highest of the three was recorded. The sit and reach test is a test of
flexibility that measures the flexibility of the hamstring and back. Using an archaic sit &
reach box, participants will sat with the soles of the feet flat against the box and were
asked to reach their fingers as far forward as possible along the top of the box and the
distance was recorded. Three attempts were allowed and the highest of the three marks
was recorded. Leg strength and estimation of type II fiber percentage was assessed using
the Isokinetic dynamometer. Participants extended their left leg for 50 repetitions and the
force exerted on each repetition was directly recorded into isokinetic dynamometers
22

computer. Values were then used to estimate Type II fiber percentage using formula from
Thorstensson et al (60). Type II fiber type percent estimation has been positively
correlated with a higher percent decline in force during isokinetic contraction of the
quadriceps. Subjects with a higher percent decline are estimated to have a higher type II
fiber type percentage.
Subjects also complete two questionnaires. A block calcium/ vitamin D screener
from NutriQuest (developed from the NHANES 1999-2001 dietary recall data) was
administered to look at usual dietary intake, and more specifically, intake of dietary
vitamin D and a sun exposure questionnaire was used to correlate vitamin D levels to the
amount of sun exposure (61). Following the performance tests, subjects received an
initial 2-week supply of pills that contained either the placebo or vitamin D supplement.
16-week Intervention Period

Participants in the control group were supplemented with placebo pills. The vitamin D
intervention group was supplemented with 14,000 IU of cholecalciferol (VD 3) (Replesta
NX Wafers) to be taken twice weekly. This level did not exceed the tolerable upper
intake levels for vitamin D of 4,000IU/day. Subjects consumed the pills with a meal that
contained dietary fat for optimal absorption. Participants were advised not to change their
daily meal intake or to intentionally change their daily sun exposure throughout the
intervention period. Participants were asked to avoid tanning beds or UV-light exposure
(other than sun exposure). Subjects returned to the NHL every two weeks to receive their
next supply of pills. Subjects kept a log of their pill use to track compliance, and turned
23

that in every two weeks when they received their next supply of pills. Athletes had to
consume at least 80% of the pills to remain in the study. If athletes regularly took a
multivitamin/mineral pill, they were allowed to continue that during the intervention.
However, any athlete not taking a multivitamin/mineral pill at baseline was asked to
refrain from taking one during the 16-week intervention. Those athletes that were taking
the multivitamin/mineral pills regularly at baseline were instructed to keep a log of
multivitamin/mineral pill usage.
Aims 2 & 3 Visit 3 Post Intervention measurements

All participants returned to the various building at the TTU campus (HNL, Covenant and
Exercise Science Lab) within 1 week of completing the intervention period for postintervention testing. Measurements taken at visit one (serum concentrations of Calcidiol
(25(OH)D), height, body weight, and body fat percentage were repeated for each person
using the same procedures and equipment. Additionally, the questionnaires and physical
performance tests described above (visit 1 and visit 2 respectively) were again performed
at the same location using the same procedures and equipment.
Statistical Analyses
Preliminary data gathered from 2010-2012 through the Department of Family Medicine
at UMC shows that approximately 50% of CA athletes tested had insufficient or deficient
Calcidiol (25(OH)D) levels. Therefore, it was anticipated that about 100 CA were needed
for the intervention phase of the study. Descriptive statistics (mean, range, and standard
24

deviation) were obtained for all outcome variables. Aim 1: A frequency distribution will
be done to assess the percentages of subjects at baseline with deficient, insufficient, or
sufficient Calcidiol (25(OH)D) levels. Pearson correlations were used to examine the
relationship between serum Calcidiol (25(OH)D) levels and sun exposure as well as
dietary vitamin D intake from the questionnaires. Aims 2 and 3: A paired t-test was used
to asses changes in serum blood concentration of Calcidiol (25(OH)D) from pre- to postintervention in both the control and intervention groups. Additionally, a multivariate
ANOVA (MANOVA) was be used to assess differences in all of the physical
performance tests between the control and intervention groups. If significance wad found,
a post hoc analysis was done using a Tukeys test. Significance was set at p<0.05.
Power Analysis
It is important to ensure that there is adequate power to detect significant differences in
the outcome variables if they do in fact exist. At the time of the beginning of this study
there were no studies that examined the effects of vitamin D supplementation on athletic
performance; therefore data from two other studies were used to calculate this. For Aim
2: A previous pilot study which involved 8-week supplementation of vitamin D
(4,000IU/d of cholecalciferol) in male basketball players showed increases in serum
calcidiol 25(OH)D from 21.19.27 to 41.111.49ng/ mL. This is the same dose of
supplementation that was used. In order to detect a significant difference between groups
with 80% power and an alpha of 0.05, a sample size of 100 for each group was needed.
For Aim 3: One study in elderly individuals looked at a number of strength measures in
25

individuals with insufficient vs. sufficient levels of vitamin D. Handgrip strength in the
insufficient vitamin D subjects was 20.05.8 vs. 23.95.6kg in the sufficient vitamin D
subjects. Another measure was gait speed which showed 0.550.2 in the insufficient
vitamin D subjects vs. 0.70.18 in the vitamin D sufficient subjects (7). In order to detect
a significant difference between groups with 80% power and an alpha of 0.05, a sample
size of 68 (based on handgrip strength) or 52 (based on gait speed) total subjects was
needed. Based on these power analyses, a sample size of 68 was necessary (35 for each
group). Similar, previous studies in nutrition lab had dropout rates of about 10-15%. To
account for a 14% dropout rate, 80 athletes with insufficient/deficient vitamin D levels
(40 in control group and 40 in intervention group) were needed. Since the pilot data
indicated that only about 40-50% of athletes had insufficient or deficient vitamin D
levels, we recruited 200 CA at the beginning of the study so we would end up with
approximately 80 CA for the supplementation portion of the study. Unfortunately, we
were unable to meet these recruitment numbers and the results presented herein are
therefore preliminary.
26

CHATPER IV - RESULTS
Baseline Subject Characteristics
Baseline characteristics of all 93 subjects that were recruited for the study are
shown in Table 1. There were no significant differences in age (p=0.48), 25(OH)D
(p=0.13) or BMI (p= 0.07) between male and female subjects. However, males had
significantly higher body weight (p<0.01) and height (p<0.01) and a lower body fat
percentage (p<0.01) compared to females.
Table 1. Subject Characteristics at Baseline (n=93)

Mean
Range
21.466.3
17 - 61
Age (yrs) All
Male
21.55.2
18-41
Female
21.37.2
17-61
13-75.7
25(OH)D (ug/mL) All 36.916.0
Male
36.415.9
13-73.6
Female
37.316.3
13-75.7
66.011.3
42.5-106.4
Weight (Kg) All
Male
72.012.5*
42.5-106.4
Female
60.56.5
49.1-76.5
171.99.5
152.0-193.5
Height (cm) All
Male
177.19.1*
157-193.5
Female
165.55.6
152-179
22.42.6
16.4-34.0
BMI (kg/m2) All
Male
22.83.1
16.4-34.0
Female
22.11.9
19.1-28.3
19.16.3
8.9-31.2
Body Fat (%) All
Male
13.63.9*
8.9-31.2
Female
24.03.4
11.3-30.6
Data is presented as Mean Standard Deviation
% = Percent
BMI = Body mass index
25(OH)D = Vitamin D
* = significant difference between males and females at p<0.05
27

Prevalence
Prevalence of vitamin D deficiency, sufficiency and insufficiency in all subjects at
baseline (n=93) are compared in Table 2. Sixty-nine percent (n=65) of the population was
found to be sufficient, while 9.7% (n=9) and 20.4% (n=19) of the population were found
to be deficient and insufficient, respectively. In terms of prevalence among racial groups,
it was found that 88.7% (n=47) of the white population was sufficient while 1.9% (n=1)
and 9.4% (n=5) were vitamin D deficient and insufficient, respectively. Thirty percent
(n=9) of the black population was vitamin D sufficient while 26.7% (n=8) and 43.3%
(n=13) were vitamin D deficient and insufficient, respectively. Finally, 90.0% (n=9) and
10.0% (n=1) of Hispanics were sufficient and insufficient, respectively. None were found
to be vitamin D deficient.
Based on gender, 69.5% (n=34) of females were vitamin D sufficient, of which
57.1% (n=28), 6.1% (n=3) and 6.1% (n=3) were Whites, Blacks and Hispanics,
respectively. Twelve point two percent (n=6) were vitamin D deficient, of which 2.0%
(n=1), 10.2% (n=5) and 0% (n=0) were Whites, Blacks and Hispanics, respectively.
Eighteen point four percent (n=9) were vitamin D insufficient, of which 4.1% (n=2),
14.3% (n=7) and 0% (n=0) were Whites, Blacks and Hispanics, respectively. Seventy
point five percent (n=31) of males were vitamin D sufficient, of which 43.2% (n=19),
13.6% (n=6) and 13.6% (n=6) were Whites, Blacks and Hispanics, respectively. Six point
eight percent (n=3) were vitamin D deficient, of which 0% (n=0), 6.8% (n=3) and 0%
(n=0) were Whites, Blacks and Hispanics, respectively. Twenty two point seven percent
28

% (n=10) were vitamin D insufficient, of which 6.8% (n=3), 13.6% (n=6) and 2.3% (n=1)
were Whites, Blacks and Hispanics, respectively.
Table 2. Subject Vitamin D Classification at Baseline

PRE Intervention
Sufficient
Deficient
Insufficient
65
9
19
All (n=93)
(69.9%)
(9.7%)
(20.4%)
47
1
5
White (n=53)
(88.7%)
(1.9%)
(9.4%)
9
8
13
Black (n=30)
(30.0%)
(26.7%)
(43.3%)
9
0
1
Hispanic (n=10)
(90.0%)
(0.0%)
(10.0%)
34
6
9
Female (n=49)
(69.4%)
(12.2%)
(18.4%)
White
28
1
2
(57.1%)
(2.0%)
(4.1%)
Black
3
5
7
(6.1%)
(10.2%)
(14.3%)
Hispanic
3
0
0
(6.1%)
(0.0%)
(0.0%)
31
3
10
Male (n=44)
(70.5%)
(6.8%)
(22.7%)
White
19
0
3
(43.2%)
(0%)
(6.8%)
Black
6
3
6
(13.6%)
(6.8%)
(13.6%)
Hispanic
6
0
1
(13.6%)
(0.0%)
(2.3%)
Data are presented as the n (subject number) with the prevalence as a percentage in
parentheses.
Of the 93 subjects tested at baseline, 28 subjects had insufficient or deficient

vitamin D levels, and therefore, qualified for the intervention portion of the study. From
those 28 individuals, 16 subjects completed the intervention (n=8 for placebo; n=8 for
vitamin D group). Twelve subjects dropped out of the study due to injury not related to
29

the study, time commitment issues, and lack of response. The baseline and postintervention subject characteristics for those 16 athletes can be found in Table 3. There
was no significant difference in age, weight, height, BMI, body fat %, dietary vitamin D
intake, dietary calcium intake, or sun exposure between the placebo and vitamin D
groups at baseline (pre intervention). There was also no significant difference in age,
weight, height, BMI, body fat %, dietary vitamin D intake, dietary calcium intake, or sun
exposure between the placebo and vitamin D groups at post intervention. Finally, within
each group, there were no significant changes in weight, height, BMI, body fat %, dietary
vitamin D intake, dietary calcium intake, or sun exposure from pre to post intervention in
the vitamin D group or placebo group. There was, however, a significant decrease in sun
exposure (pre: 110.049.7minutes, post 65.134.7minutes, p=0.01 within the placebo
group but not the vitamin D group.
30

Table 3. Subject Characteristics for those with All Pre vs. All Post Measures & Placebo vs. Vit. D at Pre and at Post intervention
Time
PRE Intervention
POST Intervention
Group
All
(n= 16)
21.44.6
Placebo (n= 8)
20.12.3
Vit. D
(n=8)
22.66.1
All
(n= 16)
21.44.6
Placebo
(n= 8
20.12.3
Vitamin D
(n=8)
22.66.1
21.95.3
25.820.7
23.88.3
21.95.3
25.820.7
23.88.3
Women
25(OH)D (ug/mL)
20.63.0
22.35.3
19.82.5
23.15.8
21.53.7
31.410.8**
20.63.0
31.410.8
19.82.5
23.69.0*
21.53.7
39.35.1
Men
Women
22.67.0
22.34.1
23.38.7
23.04.6
32.08.9
29.912.6
32.08.9
29.912.6
28.710.9
20.57.2
36.95.2
41.74.2
Weight (kg)
68.312.4
64.811.6
68.812.4
68.812.4
65.911.6
71.613.2
Men
Women
Height (cm)
78.06.8
60.49.2
171.110.9
77.06.6
57.46.1
168.710.3
79.06.1
60.68.7
171.210.9
79.06.1
60.68.7
171.210.9
78.33.8
58.56.9
168.910.4
80.19.6
63.111.1
173.511.6
Men
Women
BMI (kg/m2)
180.26.2
163.35.8
23.12.2
178.26.5
163.07.5
24.20.4
180.56.1
163.35.8
23.42.0
180.56.1
163.35.8
23.42.0
178.76.3
163.07.5
23.11.3
183.36.3
163.64.1
23.62.6
Men
Women
24.01.5
22.52.4
19.45.7
21.50.6
21.31.0
20.15.0
24.21.6
22.82.1
20.16.4
24.21.6
22.82.1
20.16.4
24.50.7
22.30.7
20.35.9
23.82.5
23.43.1
19.97.2
14.22.9
23.62.9
114.077.0
149.196.4
84.255.3
418.2267.0
383.7249.6.9
418.0278.4
100.164.4
87.037.1
14.42.9
23.51.3
117.588.0
141.6136.2
103.159.8
411.1211.2
302.9204.5
476.0207.6
110.049.7**
96.710.4
13.41.3
25.32.0
103.680.4
99.348.2
105.397.7
425.3328.7
505.0313.9
345.5269.6
90.178.7
72.559.2
13.41.3
25.32.0
103.680.4
99.348.2
105.397.7
407.7227.2
436.2179.4
384.4248.2
70.737.5
81.226.5
13.41.7
24.41.9
87.246.9
94.110.6
83.061.1
435.7200.5
432.799.0
437.4255.8
65.134.7
78.723.0
13.31.2
26.51.6
120.1105.1
107.281.8
133.1136.4
379.8261.9
441.4288.8
318.2258.0
76.341.7
85.037.0
113.476.5
118.063.7
107.8100.6
61.742.1
57.040.2
67.549.9
Age (years)
Men
Body Fat %
Men
Women
Dietary Vitamin D (IU)
Men
Women
Dietary Calcium (mg)
Men
Women
Sun Exposure (minutes)
Men
Women
Data is presented as Mean Standard Deviation

% = Percent
* = significant difference between placebo and vitamin D at p<0.05
BMI = Body mass index 25(OH)D = Vitamin D (Calcidiol)

**= significant difference within intervention groups (placebo or vitamin D) at p<0.05
31

Serum Vitamin D -25(OH)D
We looked at baseline values of 25(OH)D serum concentrations to test for differences
between the Vitamin D group and placebo group. There was no significant difference found in
serum 25(OH)D between the placebo and vitamin D groups at baseline (vitamin D:
21.54.9ug/mL, placebo: 23.15.8 ug/mL). There was also no significant change in 25(OH)D
(p=0.90) for the placebo group from pre to post supplementation. Not surprisingly, however,
there was a significant difference in serum 25(OH)D levels between the groups at post
intervention (vitamin D: 39.35.1 ug/mL, placebo: 23.69.0 ug/mL, p<0.01) because serum
25(OH)D levels had increased significantly from pre to post intervention in the vitamin D group
(pre: 21.54.9 ug/mL, post: 39.35.1 ug/mL, p<0.01) (Table 3 and Figure 1).
Performance tests
All data from the performance tests are shown in the Figures 1-5. A multivariate
ANOVA was done to compare differences between pre and post intervention performance test
results in both the vitamin D and placebo groups. There were no significant differences in any
performance variable (standing long jump, Flex, 30m sprint, vertical jump, LS and Type II fiber
%) at baseline between the groups, at post-intervention between the groups, or from pre to post
within each group. There was no significant changes in the standing long jump within the
vitamin D group (pre 222.748.0 cm, post: 201.173.4 cm) or placebo group (pre: 232.137.7
cm, post: 237.436.2cm) as well as no differences between treatment groups (Figure 2) from pre
to post intervention. There was no significant changes in the vertical jump within the vitamin D
group (pre 26.25.5 cm, post: 27.54.7 cm) or placebo group (pre: 24.95.7 cm, post:
27.66.5cm) as well as no differences between treatment groups (Figure 3from pre to post
intervention. For the 30m sprint, there were no differences between groups or across the
intervention within each group (vitamin D group pre: 4.40.3s, post: 4.10.3s; and placebo
32

group pre: 4.50.4s, post: 4.40.3s) (Figure 4). Similarly, there were no differences between
groups or across the intervention for either group for LS (vitamin D group pre: 97.125.9N, post:
100.420.3N; and placebo group pre: 84.032.9N, post: 88.529.1N) (Figure5). There were no
differences between groups or across the intervention for either group for flexibility (vitamin D
group pre: 30.78.3cm, post: 32.68.5cm; and placebo group pre: 23.812.2cm, post:
24.9cm10.1cm) (Figure 6). Finally there were no differences between groups or across the
intervention for either group for type II fiber percentage (vitamin D group pre: 56.019.3%, post:
64.97.4%; and placebo group pre: 47.615.9%, post: 49.815.5%) (Figure 7).
Vitamin D & Performance Tests

Pearson correlations were run to determine the relationship between serum 25(OH)D
levels vs. age, serum 25(OH)D levels vs. body fat percentage and serum 25(OH)D levels vs.
body weight at baseline for all subjects (n=93) that had been recruited for the study. There was
no correlation found between serum 25(OH)D levels and body weight, age or body fat
percentage.
Pearson correlations were also run to determine the relationship between serum 25(OH)D
levels and subject characteristics and performance tests at baseline and post intervention for
those subjects that had insufficient or deficient vitamin D status at baseline (n=16). At baseline,
there was a significant positive correlation between vitamin D intake and leg strength (r=0.55,
p=0.03) (Figure 8). However, no significant correlations were found between baseline dietary
vitamin D intake and any other subject characteristics (body weight, BMI, height, body fat%, or
sun exposure) or physical performance tests (standing long jump, vertical jump, 30m sprint, or
flexibility.) or type II fiber type percentage.
There was a significant negative correlation between sun exposure and leg strength (r=0.55, p=0.03) (Figure 9) at baseline. A significant negative correlation between sun exposure and
33

weight (r=-0.51, p=0.04) (Figure 10) and BMI (r=-0.73, p=0.001) (Figure 11) was also found at
baseline. However sun exposure was not significantly correlated with any other subject
characteristic or performance variable at baseline. Calcium intake was also not correlated with
subject characteristics or performance tests at baseline.
The same correlation analyses were run at post intervention (n=16 weeks). We found a
significant positive correlation between serum 25(OH)D and flexibility (r=0.55, p=0.03) (Figure
12) and serum 25(OH)D type II fiber percentage (r=0.66, p=0.005) (Figure 13 and Table 4)).
However, serum 25(OH)D was not significantly correlated with any other subject characteristic
or performance test after the 16 week period. There was a significant positive correlation
between sun exposure and leg strength (r=0.51, p=0.04) (Figure 14 and Table 4). Sun exposure
was not significantly correlated with any other subject characteristic or performance test after the
16 week period (Table 4). Similarly, calcium intake was also found to have no significant
correlation with any subject characteristic or performance test post intervention (Table 4).
34

Table 4. Pearson Correlations between Subject Characteristics and Performance Tests and change in Serum 25(OH)D, Dietary
Vitamin D and Calcium Intake and Sun Exposure
Measure
Weight (kg)
BMI (kg/m2)
Height (cm)
Body Fat (%)
Flexibility (cm)
Standing Long Jump (cm)
30m Sprint (s)
Vertical Jump (cm)
Leg Strength (N)
Type II Fiber (%)
Dietary Vitamin D Intake (IU)
Dietary Calcium Intake (mg)
Sun Exposure (min)
Serum
25(OH)D
(ug/mL)
0.19
0.17
0.14
0.02
0.11
-0.05
0.18
0.08
-0.03
0.03
0.35
0.22
0.10
PRE
Dietary Dietary
Vitamin Calcium
D
Intake
Intake
(mg)
(IU)
0.40
0.14
0.13
0.06
0.46
0.16
-0.34
-0.04
0.19
0.44
0.48
-0.21
-0.02
0.32
0.48
-0.35
-0.03
0.55**
0.23
-0.04
1
0.13
0.13
1
-0.16
-0.04
Data is presented as the correlation coefficient (r value)

% = Percent
min=Minutes
BMI = Body mass index
25(OH)D = Vitamin D
cm= Centimeter
s= Seconds
IU=International Units
N=Newton
* = significant negative correlation at p<0.05
**= significant positive correlation at p<0.05
35
POST
Sun
Serum
Dietary Dietary
Sun
Exposure 25(OH)D Vitamin Calcium Exposure
(min)
(ug/mL)
D
Intake
(min)
Intake
(mg)
(IU)
0.33
0.30
0.24
0.22
-0.52*
0.23
0.50
0.11
0.18
-0.73*
-0.20
0.24
0.04
0.21
0.15
0.02
-0.09
0.13
-0.09
-0.27
0.21
-0.11
0.24
-0.27
0.55**
-0.48
-0.08
0.01
0.15
-0.30
-0.00
-0.29
0.10
0.06
-0.28
-0.22
0.06
-0.08
-0.04
0.32
0.34
0.17
0.07
-0.55*
0.51**
-0.47
0.26
0.22
0.26
0.66**
-0.16
0.40
1
0.22
0.30
-0.04
-0.07
0.22
1
-0.58
1
0.22
0.30
-0.58
1

Finally, correlations were run on the change in serum 25(OH)D levels vs. change in
physical performance measurements in the vitamin D group. There was no significant correlation
between change in serum 25(OH)D levels and change in physical performance measurements
(standing long jump, vertical jump, LS, Flex., 30m sprint and type II fiber %) in the vitamin D
group (Table 5).
Table 5. Pearson Correlation between change in Serum 25(OH)D and change in performance tests
Serum 25(OH)D (ug/mL)
Performance Measure
-0.28
Flexibility (cm)
-0.50
Standing Long Jump (cm)
0.67
30m Sprint (s)
-0.05
Vertical Jump (cm)
-0.05
Leg Strength (N)
0.03
Type II Fiber (%)
Data is presented as the correlation coefficient (r value)
% = Percent
cm= Centimeter
s= Seconds
25(OH)D = Vitamin D
IU=International Units
N=Newton
36

Figures
45
40
35
30
25
20
15
10
5
Standing LJ Pre & Post Supplementation

300
**
Standing LJ (cm)
Serum 35(OH)D (ug/mL)
Serum 25(OH)D Pre & Post Supplementation
Pre Placebo
Pre Vitamin D
Post Placebo
Post Vitamin D
250
200
Pre Placebo
150
Pre Vitamin D
100
Post Placebo
50
Post Vitamin D
0
Time Point
Time Point
Figure 2: Standing Long Jump (standing long jump) for placebo and
vitamin D (vitamin D) study groups at pre and post supplementation (16
weeks). There were no significant difference between groups pre
supplementation (p=0.66) and post supplementation (p=0.51). There was
also no significant difference seen within each group from pre to post
supplementation
Figure 1: 25(OH)D for placebo and vitamin D (vit. D) study groups at pre and post
supplementation (16 weeks). There were no significant difference between
groups pre supplementation (p=0.56). There was a significant increase in the vit
D. group post intervention (p<0.01) but no change in the placebo group (p=0.90).
As a result there was a significant difference between the vitamin D group and
placebo group (p<0.01) post intervention.
* denotes significant increase from pre to post supplementation with the
vitamin D group.
** denotes significant increase from pre to post supplementation between the
vitamin D and placebo group.
Vertical Jump Pre & Post Supplementation

Vertical Jump (cm)
75
70
Pre Placebo
65
Pre Vitamin D
Post Placebo
60
Post Vitamin D
55
Time Point
Figure 3: Vertical Jump (VJ) for placebo and vitamin D (vit. D) study groups at pre
and post supplementation (16 weeks). There were no significant difference
between groups pre supplementation (p=0.65)) and post supplementation
(p=0.75). There was also no significant difference seen within each group from
pre to post supplementation.
37

Leg Strength
4.8
120
4.6
100
Leg Strength (N)
30m Sprint (s)
30m Sprint Pre & Post Supplementation
Pre Placebo
4.4
Pre Vitamin D
4.2
Post Placebo
4.0
Post Vitamin D
80
Pre Placebo
60
Pre Vitamin D
40
Post Placebo
20
Post Vitamin D
3.8
Time Point
Time Point
Figure 5: Leg strength (LS)) for placebo and Vit. D (vitamin D) study groups pre
between groups pre supplementation (p=0.39) and post supplementation
(p=0.61). There was also no significant difference seen within each group from
pre to post supplementation.
Figure 4: 30m sprint for placebo and Vit. D (Vitamin D) study groups pre
between groups pre supplementation (p=0.54) and post supplementation
(p=0.11). There was also no significant difference seen within each group
from pre to post supplementation.
Flexibility Pre & Post Supplementation
Type II Fiber Pre & Post Supplementation

80
30
Type II Fiber (%)
Flexibility (cm)
40
Pre Placebo
Pre Vitamin D
20
Post Placebo
10
Post Vitamin D
60
Pre Placebo
Pre Vitamin D
40
Post Placebo
20
Post Vitamin D
0
Time Point
Time Point
Figure 7: Type II fiber percent for placebo and Vit. D (vitamin D) study
groups at pre and post supplementation (16 weeks). There were No
significance difference between groups pre supplementation (p=0.35).
There was a significant increase in the vitamin D group post intervention
(p<0.01) but no change in the placebo group (p=0.90). As a result there
was a significant difference between the vitamin D group and placebo
group (p<0.01) post intervention.
Figure 6: Flexibility (Flex.) for placebo and vitamin D (vitamin D) study

groups pre and post supplementation (16 weeks). There were no significant
difference between groups pre supplementation (p=0.20) and post
supplementation (p=0.23). There was also no significant difference seen
within each group from pre to post supplementation.
38
Correlation between Sun Exposure & Weight Pre Supplementation
150
105.0
100
85.0
Weight (Kg)
Leg Strength(N)
Correlation between Vitamin D Intake & Leg

Strength- Pre Supplementation
50
0
10.0
110.0
210.0
310.0
45.0
25.0
10
60
Vitamin D (25(OH)D (IU)
100
25.0
BMI (Kg/m2)
30.0
50
0
110
160
210
260
Correlation between Sun Exposure & BMI Pre Supplementation
150
60
160
Figure 10: Correlation of Weight to sun exposure for placebo

and Vit. D (vitamin D) study groups at pre supplementation.
There was a significant negative correlation between sun
exposure and weight (r=-0.51, p=0.04) pre intervention.
Correlation between Sun Exposure & Leg

Strength- Pre Supplementation
10
110
Figure 8: Correlation of Leg strength to vitamin D intake for

placebo and Vit. D (vitamin D) study groups at pre
supplementation. There was a significant positive correlation
between vitamin d intake and leg strength (r=0.55, p=0.03) pre
intervention.
Leg Strength(N)
65.0
210
260
20.0
15.0
10
60
110
160
210
260
Figure 11: Correlation of BMI to sun exposure for placebo and

Vit. D (vitamin D) study groups at pre supplementation. There
was a significant negative correlation between sun exposure and
BMI (r=-0.73, p=0.001) pre intervention.
Figure 9: Correlation of Leg strength to sun exposure for placebo

and Vit. D (vitamin D) study groups at pre supplementation.
There was a significant negative correlation between sun
exposure and leg strength (r=-0.55, p=0.03) pre intervention.
39

Correlation between Serum 25(OH)D & Type II
Fiber % -Post Supplementation
50
100
40
80
Type II Fiber (%)
Flexibility (cm)
Correlation between Serum 25(OH)D &

Flexibility - Post Supplementation
30
20
10
0
10
20
30
40
50
Leg Strength(N)
0
20
30
40
50
Figure 13: Correlation of type II fiber percentage to serum 25(OH)D

for placebo and Vit. D (vitamin D) study groups at post
supplementation. There was a significant positive correlation
between serum 25(OH)D and type II fiber percentage (r=0.66,
p=0.005) post intervention.
Correlation between Sun Exposure & Leg

Strength- Post Supplementation
145
125
105
85
65
45
25
110
20
Serum (25(OH)D (ug/mL)
Figure 12: Correlation of flexibility to serum 25(OH)D for placebo

and Vit. D (vitamin D) study groups at post supplementation.
There was a significant positive correlation between serum
25(OH)D and flexibility (r=0.55, p=0.03) post intervention.
60
40
10
Serum (25(OH)D (ug/mL)
10
60
160
Figure 14: Correlation of Leg strength to sun exposure for placebo and
Vit. D (vitamin D) study groups at post supplementation. There was a
significant positive correlation between sun exposure and leg strength
(r=-0.51, p=0.04) post intervention.
40

CHPATER V - DISCUSSION
Prevalence data has shown that vitamin D deficiency is increasing in populations
worldwide (3). At greatest risk are Black and Hispanics, who have limited UVB absorption due
to melanin content of the skin (17) (26). We found that African Americans and Hispanics were at
a greater risk for vitamin D deficiency than whites which is similar to prevalence data worldwide
(17) (19). Supplementation at 28,000IUs of vitamin D over 16 weeks was shown to
significantly improve deficient or insufficient serum levels of 25(OH)D to sufficient levels in our
adult athlete population. However, there was no effect of supplementation of 28,000IUs of
vitamin D per week on any of our physical performance measures over a 16 week period. There
were also no associations between serum 25(OH)D, dietary calcium intake, sun exposure and
dietary vitamin D intake on subject characteristics or improvements in physical performance
tests over a 16 week period.
There are very few clinical studies that have examined the relationship between vitamin
D supplementation on physical performance measures in athletes (6) (59) (62). Supplementation
data in this study showed that 28,000IU of vitamin D led to no significant improvement in any
performance measures, which is in agreement with the few other studies done on physical
performance measures following vitamin D supplementation in an athletic population. Close et
al. found mixed results on the effect of vitamin D supplementation on similar performance tests.
One study of 30 club level athletes found that vitamin D supplementation had no effect on
vertical jump height in 30 club level athletes (p>0.05) (59). However in a follow up study in 30
UK soccer players they reported a significant effect of vitamin supplementation on
improvements in the 10m sprint (p=0.008) and vertical jump height (p=0.008). (6). A similar
study done by Niemen et al. (62) also found no significant effect of vitamin D supplementation
41

at 3,800 IUs per day over a 16 week period on physical performance tests in 28 NASCAR pit
crew athletes (vertical jump (p=0.29) and bench press (p=0.08). However, it should be noted that
the aforementioned studies, as well as our study, may have been underpowered which suggests
the need for a larger subject population to possibly find significant results.
Vitamin D supplementation may be useful for improving physical performance tests,
such as handgrip strength, gait speed, quadriceps strength, body sway and decreased falls in
elderly populations (7) (8) (51). However, it does not appear to have a significant effect on
physical performance tests in most young athletic populations. Differences in age may be a
significant factor in this outcome. Elderly persons are at greater risk for vitamin D deficiency due
to decreased exposure to sun and decreased metabolic activity (25), therefore supplementation
may have a stronger effect on this population. The studies on physical performance in the elderly
also tend to have much higher subject numbers. As stated previously, most studies in younger
athletic populations may have had fewer subjects and small differences may be overshadowed by
a larger variation in these outcome measures. Finally, it is possible that in highly trained athletes,
there is little room for improvements on physical performance measures whereas in elderly
individuals, there is likely much greater potential for physical performance improvements.
In our study, correlation data suggested a positive relationship between serum 25(OH)D
concentration and flexibility and serum 25(OH)D concentrations and type II fiber percentage.
We believe we are the first to report an association between serum 25(OH)D concentration and
flexibility. An increase in flexibility with increasing 25(OH)D may be explained by the fact that
vitamin D receptors are multi-potent and are found in various organs and tissues of the body,
including muscle and it is safe to assume that it may also be present in joints. An increase in
serum 25(OH)D may therefore have a positive effect on the presence of this receptor thus
42

increasing flexibility. While we may have to assume that VDR are present in joints, studies have
shown that VDR are present in muscle tissue (43) (44) (45). The VDR knockout mouse model
showed that mice without VDR showed atrophy of muscle tissue and week swimming ability.
Increased serum levels of 25(OH)D have also been inversely associated with fall risk and
positively associated with performance measures, such as gait speed, in the elderly (7). This can
be attributed to an increase in type II fibers, which are the first to be recruited in preventing falls
and when needed for short bursts of speed (46). Therefore the increase in type II fibers after an
increase in serum 25(OH)D concentration may be as a result of increased muscle fiber
differentiation into type II fibers (41) therefore increasing type II fiber percent. There were no
correlations found between serum 25(OH)D and any other physical performance tests (standing
long jump, vertical jump, 30m sprint and leg strength) or subject characteristics (body fat
percentage, BMI or weight). However previous studies have indicated a positive correlation
between serum 25(OH)D and physical performance measures; such as vertical jump, gait speed
and quadriceps strength (9) (7) (6) and an inverse relationship between serum 25(OH)D and
body composition (57) (58). We did not find any correlations between the change in serum
25(OH)D with changes in body weight, body fat% or BMI.
Thirty minutes of sun exposure can provide up to 20,000 IUs of vitamin D in fair
skinned individuals. Since we measured sun exposure, we wanted to test for associations
between sun exposure to serum 25(OH)D concentrations. Interestingly, we found that there was
a significant positive correlation between sun exposure and leg strength, which is the first such
correlation to our knowledge. Vitamin D (63) (64,65) (65)and elderly (66) (67)which was found
to improve after several weeks of supplementation(63) (66). At baseline, sun exposure was
negatively correlated with leg strength, when compared to post intervention where sun exposure
43

was positively correlated to leg strength. These results were somewhat surprising to us and are
difficult to explain. There is a possibility that other variables may have had an effect on leg
strength. At baseline the intensity of training of the subjects was lower when compared to the
intensity of training at post testing. This could have been the reason for the positive correlation
between sun exposure and leg strength in the post testing. Sun exposure was not correlated to
any other performance measure or subject characteristic after 16 weeks.
The prevalence of vitamin D deficiency and association between vitamin D and
performance in athletes has become a clinical hot topic. In our study of athletic populations
(n=93) we found that 30.1% of the subject population were below the US Endocrine Societys
defined sufficient level of serum 25(OH)D (<30ng/mL). This is consistent with previous studies
indicating that athletes have become at increased risk for vitamin D deficiency(19) (20). In those
previous studies it was noted that whites were at lower risk for vitamin D deficiency or
insufficiency when compared to blacks and Hispanics, this was reflected in our study where
whites were found to be at lower risk for insufficiency (9.4%) while the majority were sufficient
(88.7%) but blacks were at highest risk for deficiency (26.7%) and blacks and Hispanics were at
highest risk for insufficiency (43.3% and 10.0% respectively). This is likely to be related to a
number of factors, including use of tanning beds and differences in melanin content of the skin.
Our results also indicated that women were at greater risk for deficiency and insufficiency
(30.6%) when compared to men (28.8%), which is not unusual and has been reported in previous
studies (68); however, this different was not statistically significant.
There were some limitations to our study. A structured training plan or training log was
not provided to the subjects over the 16 week period and could be included in future designs. We
also did not collect any training logs or other training data from the participants. Due to
44

limitation in budget, we did not test skin reflectance which would indicate UVB absorption. Use
of this equipment would help to differentiate the amount of serum 25(OH)D produced by
supplementation versus UVB exposure. A sun exposure questionnaire was used to measure time
spent outdoors at the baseline and post testing visit. Our study was therefore unable to detect
changes in sun exposure of the 16 week period, which would be a better predictor of serum
25(OH)D over the 16 week period. Future studies could use this log more frequently during the
supplementation period and can also use this with serum 25(OH)D sufficient subjects to correlate
serum 25(OH)D with sun exposure. We also only collected dietary vitamin D and calcium
intake data and pre- and post-intervention. Future studies should use this questionnaire more
frequently to better associate dietary changes to serum levels of 25(OH)D in deficient and
insufficient subjects. Another limitation was that we did not collect sun exposure or dietary
vitamin D/Calcium intake via questionnaires from all 93 subjects that were tested at baseline due
to budget limitations. Having that data could have been beneficial for assessing the relationship
between sun exposure, dietary intake of vitamin D/ calcium and serum 24(OH)D levels. Finally,
since we did not find effects on most of our measures of physical performance following vitamin
D supplementation, higher doses, such as 50,000IU/week, or a greater number of subjects may
be necessary to see significant changes in performance.
45

CHAPTER VI - CONCLUSION
Collegiate and recreational athletes, especially those of the black and Hispanic
populations are at an increased risk for vitamin D (25(OH)D) deficiency. Supplementation at
28,000IU of vitamin D3 for 4 months was an effective therapy in raising serum 25(OH)D levels
from insufficient or deficient levels (20-30ng/mL and <20ng/mL respectively) to sufficient levels
(>30ng/mL). This revealed that supplementing with 28,000IU of vitamin D 3 for 4 months may
have a no effect on any performance variable (flexibility, vertical jump, 30m sprint, standing
long jump, LS and type II fiber percentage). Serum 25(OH)D was positively correlated with
flexibility and type II fiber percentage but not with any of the other above named variables.
Further studies with a larger subject population should reexamine these effects.
46

BIBLIOGRAPHY
1. Ginde AA, Liu MC, Camargo CA, Jr. Demographic differences and trends of vitamin D
insufficiency in the US population, 1988-2004. Arch Intern Med. 2009 Mar 23;169:62632.
2. Ogan D, Pritchett K. Vitamin D and the athlete: risks, recommendations, and benefits.
Nutrients. 2013 Jun;5:1856-68.
3. Bordelon P, Ghetu MV, Langan RC. Recognition and management of vitamin D
deficiency. Am Fam Physician. 2009 Oct 15;80:841-6.
4. Cannell JJ, Hollis BW. Use of vitamin D in clinical practice. Altern Med Rev. 2008
Mar;13:6-20.
5. Looker AC JCLDea. Vitamin D status: United States 20012006. no 59 ed. Hyattsville,
MD: National Center for Health Statistics: 2011.
6. Close GL, Russell J, Cobley JN, Owens DJ, Wilson G, Gregson W, Fraser WD, Morton
JP. Assessment of vitamin D concentration in non-supplemented professional athletes
and healthy adults during the winter months in the UK: implications for skeletal muscle
function. J Sports Sci. 2013;31:344-53.
7. Toffanello ED, Perissinotto E, Sergi G, Zambon S, Musacchio E, Maggi S, Coin A,
Sartori L, Corti MC, et al. Vitamin D and physical performance in elderly subjects: the
Pro.V.A study. PLoS One. 2012;7:e34950.
8. Pfeifer M, Begerow B, Minne HW, Suppan K, Fahrleitner-Pammer A, Dobnig H. Effects
of a long-term vitamin D and calcium supplementation on falls and parameters of muscle
function in community-dwelling older individuals. Osteoporos Int. 2009 Feb;20:315-22.
9. Ward KA, Das G, Berry JL, Roberts SA, Rawer R, Adams JE, Mughal Z. Vitamin D
status and muscle function in post-menarchal adolescent girls. J Clin Endocrinol Metab.
2009 Feb;94:559-63.
10. Bischoff-Ferrari HA, Dietrich T, Orav EJ, Hu FB, Zhang Y, Karlson EW, DawsonHughes B. Higher 25-hydroxyvitamin D concentrations are associated with better lowerextremity function in both active and inactive persons aged > or =60 y. Am J Clin Nutr.
2004 Sep;80:752-8.
11. Foo LH, Zhang Q, Zhu K, Ma G, Hu X, Greenfield H, Fraser DR. Low vitamin D status
has an adverse influence on bone mass, bone turnover, and muscle strength in Chinese
adolescent girls. J Nutr. 2009 May;139:1002-7.
12. Hamilton B. Vitamin D and human skeletal muscle. Scand J Med Sci Sports. 2010
Apr;20:182-90.
47

13. Hollis BW. Circulating 25-hydroxyvitamin D levels indicative of vitamin D sufficiency:
implications for establishing a new effective dietary intake recommendation for vitamin
D. J Nutr. 2005 Feb;135:317-22.
14. NIH Office of Dietary Suuplements. Vitamin D: Dietary Supplement Fact Sheet. 2012.
15. Allain TJ, Dhesi J. Hypovitaminosis D in older adults. Gerontology. 2003 Sep;49:273-8.
16. Singh RJ. Quantitation of 25-OH-vitamin D (25OHD) using liquid tandem mass
spectrometry (LC-MS-MS). Methods Mol Biol. 2010;603:509-17.
17. Forrest KY, Stuhldreher WL. Prevalence and correlates of vitamin D deficiency in US
adults. Nutr Res. 2011 Jan;31:48-54.
18. Kumar J, Muntner P, Kaskel FJ, Hailpern SM, Melamed ML. Prevalence and
associations of 25-hydroxyvitamin D deficiency in US children: NHANES 2001-2004.
Pediatrics. 2009 Sep;124:e362-e370.
19. Diego V, Anthony Y, Ryan J, Curtis K, Timothy C, Seth C, Russ R, James T, George R.
Prevalence of Abnormal Vitamin D Levels Among Division I NCAA Athletes. Sports
Health: A Multidisciplinary Approach; 2014.
20. Mitchell JJEDSBDCJ. Prevalence of Vitamin D Insufficiency in Division I Collegiate s.
Clin J Sports Med. PND Publication; 2013.
21. Willis KS, Smith DT, Broughton KS, Larson-Meyer DE. Vitamin D status and
biomarkers of inflammation in runners. Open Access J Sports Med. 2012;3:35-42.
22. Holick MF. Vitamin d, sunlight and cancer connection. Anticancer Agents Med Chem.
2013 Jan 1;13:70-82.
23. American Academy of Dermatology. Position statement on vitamin D. 2008.
24. Willis KS, Peterson NJ, Larson-Meyer DE. Should we be concerned about the vitamin D
status of athletes? Int J Sport Nutr Exerc Metab. 2008 Apr;18:204-24.
25. Vasquez A, Manso G, Cannell J. The clinical importance of vitamin D (cholecalciferol):
a paradigm shift with implications for all healthcare providers. Altern Ther Health Med.
2004 Sep;10:28-36.
26. Holick MF. Vitamin D: importance in the prevention of cancers, type 1 diabetes, heart
disease, and osteoporosis. Am J Clin Nutr. 2004 Mar;79:362-71.
27. Wortsman J, Matsuoka LY, Chen TC, Lu Z, Holick MF. Decreased bioavailability of
vitamin D in obesity. Am J Clin Nutr. 2000 Sep;72:690-3.
48

28. Hatun S, Islam O, Cizmecioglu F, Kara B, Babaoglu K, Berk F, Gokalp AS. Subclinical
vitamin D deficiency is increased in adolescent girls who wear concealing clothing. J
Nutr. 2005 Feb;135:218-22.
29. Yamaguchi T, Chattopadhyay N, Brown EM. G protein-coupled extracellular Ca2+
(Ca2+o)-sensing receptor (CaR): roles in cell signaling and control of diverse cellular
functions. Adv Pharmacol. 2000;47:209-53.
30. Carling T, Ridefelt P, Hellman P, Juhlin C, Lundgren E, Akerstrom G, Rastad J. Vitamin
D receptor gene polymorphism and parathyroid calcium sensor protein (CAS/gp330)
expression in primary hyperparathyroidism. World J Surg. 1998 Jul;22:700-6.
31. Wang TJ, Pencina MJ, Booth SL, Jacques PF, Ingelsson E, Lanier K, Benjamin EJ,
D'Agostino RB, Wolf M, Vasan RS. Vitamin D deficiency and risk of cardiovascular
disease. Circulation. 2008 Jan 29;117:503-11.
32. Gangula PR, Dong YL, Al-Hendy A, Richard-Davis G, Montgomery-Rice V, Haddad G,
Millis R, Nicholas SB, Moseberry D. Protective cardiovascular and renal actions of
vitamin D and estrogen. Front Biosci (Schol Ed). 2013;5:134-48.
33. Zittermann A, Schleithoff SS, Koerfer R. Putting cardiovascular disease and vitamin D
insufficiency into perspective. Br J Nutr. 2005 Oct;94:483-92.
34. Duprez D, de BM, de BT, Clement D. Relationship between vitamin D3 and the
peripheral circulation in moderate arterial primary hypertension. Blood Press. 1994
Nov;3:389-93.
35. Scragg R, Holdaway I, Singh V, Metcalf P, Baker J, Dryson E. Serum 25hydroxycholecalciferol concentration in newly detected hypertension. Am J Hypertens.
1995 Apr;8:429-32.
36. Scragg R, Sowers M, Bell C. Serum 25-hydroxyvitamin D, ethnicity, and blood pressure
in the Third National Health and Nutrition Examination Survey. Am J Hypertens. 2007
Jul;20:713-9.
37. Wang AP, Li X, Chao C, Huang G, Liu BL, Peng J, Zhou ZG. [1alpha, 25(OH)(2) D(3)
protects pancreatic beta-cell line from cytokine-induced apoptosis and impaired insulin
secretion]. Zhonghua Yi Xue Za Zhi. 2012 Mar 13;92:695-9.
38. Pittas AG, Lau J, Hu FB, Dawson-Hughes B. The role of vitamin D and calcium in type 2
diabetes. A systematic review and meta-analysis. J Clin Endocrinol Metab. 2007
Jun;92:2017-29.
39. Oosterwerff MM, Eekhoff EM, Heymans MW, Lips P, van Schoor NM. Serum 25hydroxyvitamin D levels and the metabolic syndrome in older persons: a populationbased study. Clin Endocrinol (Oxf). 2011 Nov;75:608-13.
49

40. Hamilton B. Vitamin d and athletic performance: the potential role of muscle. Asian J
Sports Med. 2011 Dec;2:211-9.
41. Ceglia L. Vitamin D and skeletal muscle tissue and function. Mol Aspects Med. 2008
Dec;29:407-14.
42. Glerup H, Mikkelsen K, Poulsen L, Hass E, Overbeck S, Andersen H, Charles P, Eriksen
EF. Hypovitaminosis D myopathy without biochemical signs of osteomalacic bone
involvement. Calcif Tissue Int. 2000 Jun;66:419-24.
43. Burne TH, McGrath JJ, Eyles DW, Mackay-Sim A. Behavioural characterization of
vitamin D receptor knockout mice. Behav Brain Res. 2005 Feb 28;157:299-308.
44. Kalueff AV, Lou YR, Laaksi I, Tuohimaa P. Impaired motor performance in mice
lacking neurosteroid vitamin D receptors. Brain Res Bull. 2004 Jul 30;64:25-9.
45. Endo I, Inoue D, Mitsui T, Umaki Y, Akaike M, Yoshizawa T, Kato S, Matsumoto T.
Deletion of vitamin D receptor gene in mice results in abnormal skeletal muscle
development with deregulated expression of myoregulatory transcription factors.
Endocrinology. 2003 Dec;144:5138-44.
46. Ceglia L. Vitamin D and its role in skeletal muscle. Curr Opin Clin Nutr Metab Care.
2009 Nov;12:628-33.
47. Sorensen OH, Lund B, Saltin B, Lund B, Andersen RB, Hjorth L, Melsen F, Mosekilde
L. Myopathy in bone loss of ageing: improvement by treatment with 1 alphahydroxycholecalciferol and calcium. Clin Sci (Lond). 1979 Feb;56:157-61.
48. Sato Y, Iwamoto J, Kanoko T, Satoh K. Low-dose vitamin D prevents muscular atrophy
and reduces falls and hip fractures in women after stroke: a randomized controlled trial.
Cerebrovasc Dis. 2005;20:187-92.
49. Gupta V. Vitamin D: Extra-skeletal effects. J Med Nutr Nutraceut. 2012;1:17-26.
50. Berchtold MW, Brinkmeier H, Muntener M. Calcium ion in skeletal muscle: its crucial
role for muscle function, plasticity, and disease. Physiol Rev. 2000 Jul;80:1215-65.
51. Wang F, Skubic M, Abbott C, Keller JM. Body sway measurement for fall risk
assessment using inexpensive webcams. Conf Proc IEEE Eng Med Biol Soc.
2010;2010:2225-9.
52. El-Hajj FG, Nabulsi M, Tamim H, Maalouf J, Salamoun M, Khalife H, Choucair M,
Arabi A, Vieth R. Effect of vitamin D replacement on musculoskeletal parameters in
school children: a randomized controlled trial. J Clin Endocrinol Metab. 2006
Feb;91:405-12.
50

53. Knutsen KV, Brekke M, Gjelstad S, Lagerlov P. Vitamin D status in patients with
musculoskeletal pain, fatigue and headache: a cross-sectional descriptive study in a multiethnic general practice in Norway. Scand J Prim Health Care. 2010 Sep;28:166-71.
54. Merlo C, Ross C, Trummler M, Zeller A. [Prevalence and symptoms of vitamin D
deficiency in general practices]. Praxis (Bern 1994 ). 2012 Oct 31;101:1417-22.
55. Prakash S, Shah ND. Chronic tension-type headache with vitamin D deficiency: casual or
causal association? Headache. 2009 Sep;49:1214-22.
56. Prakash S, Mehta NC, Dabhi AS, Lakhani O, Khilari M, Shah ND. The prevalence of
headache may be related with the latitude: a possible role of Vitamin D insufficiency? J
Headache Pain. 2010 Aug;11:301-7.
57. Fleck SJ. Body composition of elite American athletes. Am J Sports Med. 1983
Nov;11:398-403.
58. Mascarenhas LPG, Dellagrana RA, Neto AS, Campos W, Bozza R, Boguszewski MCS,
Filho JP, Borba VZC. Levels of Vitamin D and the Association with Body Composition
in Adolescents . Scientific Reports. 12 A.D.;1.
59. Close GL, Leckey J, Patterson M, Bradley W, Owens DJ, Fraser WD, Morton JP. The
effects of vitamin D3 supplementation on serum total 25[OH]D concentration and
physical performance: a randomised dose-response study. Br J Sports Med. 2013 Feb 14.
60. Thorstensson A, Karlsson J. Fatiguability and fibre composition of human skeletal
muscle. Acta Physiol Scand. 1976 Nov;98:318-22.
61. Piccolo B, Hall L, Stephensen C, Gertz E, Woodhouse L, Souza E, Keim N, Adams S,
Van Loan M. Validation of a Method to Predict Serum Vitamin D from Sun Exposure,
Skin Reflectance & Dietary Intake in Overweight and Obese Subjects. 2012.
62. Nieman DC, Gillitt ND, Shanely RA, Dew D, Meaney MP, Luo B. Vitamin D2
supplementation amplifies eccentric exercise-induced muscle damage in NASCAR pit
crew athletes. Nutrients. 2014 Jan;6:63-75.
63. Mingrone G, Greco AV, Castagneto M, Gasbarrini G. A woman who left her wheelchair.
Lancet. 1999 Mar 6;353:806.
64. Ziambaras K, Dagogo-Jack S. Reversible muscle weakness in patients with vitamin D
deficiency. West J Med. 1997 Dec;167:435-9.
65. Russell JA. Osteomalacic myopathy. Muscle Nerve. 1994 Jun;17:578-80.
66. Prabhala A, Garg R, Dandona P. Severe myopathy associated with vitamin D deficiency
in western New York. Arch Intern Med. 2000 Apr 24;160:1199-203.
51

67. Rimaniol JM, Authier FJ, Chariot P. Muscle weakness in intensive care patients: initial
manifestation of vitamin D deficiency. Intensive Care Med. 1994 Nov;20:591-2.
68. Dam TT, von MD, Barrett-Connor EL. Sex-specific association of serum vitamin D
levels with physical function in older adults. Osteoporos Int. 2009 May;20:751-60.
52
APPENDIX A
IRB APPROVAL FORM
53
IRB AMMENDMENT FORM
54
IRB EXTENSION FORM
55
APPENDIX B
CONSENT FORM
The Impact of Vitamin D Supplementation on Athletic Performance
WRITTEN CONSENT TO PARTICIPATE IN A RESEARCH STUDY
Protocol Number:
What is this project studying?
The proposed study is examining three different areas relating to vitamin D deficiency in
collegiate athletes and active individuals (exercise 5 or more hours per week). This study will
examine and determine:
(1) The number of athletes and active individuals with vitamin D deficiency or insufficiency
(2) If vitamin D supplementation will raise vitamin D levels in the blood in vitamin D
deficient or insufficient athletes and active individuals
(3) If vitamin D supplementation will improve markers of athletics performance in vitamin
D deficient or insufficient athletes and active individuals
This study will help scientists, doctors, and possibly athletes in two ways: It will help them to (1)
become aware of the percentage of vitamin D deficiency in athletics, and (2) become aware that
vitamin D supplementation in vitamin D deficient or insufficient may serve as a safe and legal
aid in sports and can be used to improve performance.
What is Vitamin D?
Vitamin D is an essential vitamin stored in fat that is required by the body for the proper
absorption of calcium for bone development.
What would I do if I participate?
1. There are a total of three (3) visits that you will be asked to complete. Each visit will take
approximately 1-2 hours and will occur between the hours of 6:00am and 6:00pm.
a. Visit1
At visit 1, we take a small sample of blood (approximately 2 teaspoons.) for the
vitamin D analysis. We will then take some body measurements including body
composition which is described below. You will also fill out 2 short
questionnaires.
Blood draws will be taken to determine your vitamin D status (i.e. if you
are vitamin D sufficient, deficient or insufficient). You will be selected to
participate in the second part of this study based on your vitamin D status.
If you are being treated for vitamin D insufficiency or deficiency you will
not be selected to participate further in the study. If you are selected to
participate in the second part of the study, you will be informed of your
vitamin D status at the end of the study. If you are not selected to
participate in the second part of the study, you will be informed of your
vitamin D status within 1 week of us receiving your results.
Body composition will tell us what percentage of your body mass is fat
and what percent is lean. This will be measured by an instrument called
bioelectrical impedance analysis (BIA). This is non-invasive and painless
and involves you standing on a scale for a few seconds.
b. Visit 2
56

If you are selected to participate in the second part of the study, you will
participate in visits 2 and 3. In visit 2 we will perform physical performance tests
similar to ones done by your strength and conditioning coaches. They include a:
A timed 30m Sprint Timed using a hand timer
A standing long jump (Broad Jump):
A Vertical jump
A test of flexibility
A test of leg strength and endurance
c. Intervention Period
At the end of the physical performance tests, you will receive a two (2)
week supply of Replesta NX which is a vitamin D3 supplement or placebo.
You will be randomly assigned to take the placebo or the Replesta NX
(you will not know which one you are assigned to).
If you are taking the Replesta NX:

o You will be consuming 28,000IU of vitamin D3 per week (which is
similar to taking 4000IU per day). This equals the recommended
highest intake per day of vitamin D (4,000IU/day).
o The supplement will be in wafer form and each wafer will contain
14,000IU of vitamin D3. Therefore, you will take 1 wafer twice
weekly in order to get 28,000IU per week.
If you are taking the Placebo:

o You will consume wafers that do not have any vitamin D. These
wafers contain a very small amount of sugar. You will take the
wafers two times each week.
When you take the wafers, you will need to eat some fat in the meal with
it to help with absorption. Some examples include 1 tablespoon of salad
dressing, peanut butter, or mayonnaise, and any amount of nuts, butter,
avocado, or oils.
o You will be instructed to keep a log of the use of the wafers.
o If you are currently taking multivitamins you will also be given a
log to complete so that we can track usage.
o At the end of the week you will receive another two (2) week
supply of the wafers. This process will continue for a 12-week
period.
d. Visit 3
At the end of the 12 weeks, you will complete visit 3 which is the same
measurements and procedures from visit 1 and visit 2.
What if I want to withdraw from the study?
You do not have to participate in this research. It is entirely voluntary. You will not lose
anything to which you are entitled by refusing to participate. Also, you can withdraw from the
57

study any time you want, even in the middle of a test. If you decide to withdraw from the study,
please contact Dr. Cooper.
How long will participation take?
This study will include three (3) different visits:
Visit 1 and 2 will take approximately 1 2 hrs.
Visit 3 will take approximately 2-4 hrs.
How are you protecting privacy?
Only Dr. Jamie Cooper and her research team will see all the data. All participants will be
assigned a code study number and will only be identified using code study number. A copy of
this consent from will be kept on file in Dr. Coopers laboratory in a locked file cabinet.
Are there risks and discomforts to me?
Exercise Protocol
o The risk of a fatal occurrence is extremely rare although there are complications
that can occur due to the nature of the exercise protocol. Some possible risks
include nausea, muscular soreness, sprains, and strains, syncope, and/or falling
during exercise. Trained, qualified staff will closely monitor participants
throughout the exercise protocol and recovery process. Although we do not think
being in this study will be harmful to you, if this research project causes injury,
Texas Tech University or the Student Health Services, may not be able to treat
your injury. You will have to pay for treatment from your own insurance. The
University does not have insurance to cover such injuries. More information about
these matters may be obtained from Dr. Alice Young, Faculty Fellow for
Research Integrity, Office of the Vice President for Research, (806) 742-3905,
Room 103 Holden Hall, Texas Tech University, Lubbock, Texas, 79409
Vitamin D Supplementation
o Most people do not commonly experience side effects with vitamin D, unless too
much is taken. Some side effects of taking too much vitamin D include weakness,
fatigue, sleepiness, headaches, loss of appetite, dry mouth, metallic taste, nausea,
and vomiting.
o Taking vitamin D for long periods of time in doses higher than 4000IU per day or
28,000IU per week is possibly unsafe and may cause excessively high levels of
calcium in the blood. For the purpose of this research you will not consume
more than 4,000IU per day or 28,000 IU per week and only for a short time
(12 weeks).
Blood Draws
o Side effects to blood draws are rare and, if they occur, are usually mild. Side
effects are similar to those experienced by some people following a blood
donation. Possible side effects include nausea, lightheadedness or dizziness from
58

watching someone draw your blood and bruising or minor swelling at the site of
the injection. Trained qualified staff will perform blood draws.
I have some questions about this study, who can I ask?
Dr. Cooper (806-742-3068) will answer any questions you have about the study.
For questions about your rights as a subject or about injuries caused by this research,
contact the Texas Tech University Institutional Review Board for the Protection of
Human Subjects, Office of the Vice President for Research, Texas Tech University,
Lubbock, Texas 79409. You can also call (806) 742-3905.
How will this study benefit me?

You will receive free testing for your vitamin D levels in the body
If you are found to be vitamin D deficient or insufficient you will be notified at the end of
the study.
You will receive free body composition (body fat and lean muscle) testing
You will gain knowledge of weight and height
You will receive free physical performance testing (speed, agility, endurance and strength
testing)
SIGNATURE OF RESEARCH SUBJECT):
I have read and understood the material in this consent form. The investigator has also
explained the research to me and has answered all of my questions and therefore I am deciding
freely to participate.
_________________________________________
Printed name of Research Subject
___________________________________________
Signature of Research Subject
This consent form is not valid after 5/31/2015
59
_______________
Date

VITMAN D SCREENING QUESTIONNAIRE
Screening Sheet
Last Name: _____________________ First Name: __________________________
Phone Number: __________________ Email: ______________________________
#
Questions
Yes
NO
1
How old are you? ______________

What is your Gender? _________________
What is your Ethnicity? __________________
What is your current Height? ________________
What is your current Weight? ________________
Calculated BMI: _________________

(Research personnel will use given height and weight to
calculate)
Are you a member of a TTU/ SPC/ LCU Varsity Athletics

Team?
Indicate which Team and University (E.g. Baseball - TTU)
___________________________________________________________
Are you a non-varsity active individual who exercises for 5 or

more hours per week?
If yes, indicate the sport or activities you participate in
____________________
If yes, how many hours do you train per week?
________________
Non-Varsity Active Individuals (Only). List the amount of

hours you participate in each activity:
Strength Training: _____________________
Aerobic Exercises (E.g. cycling, swimming, walking,
running, hiking, tennis, cardio)
_____________________
Anaerobic Exercises (E.g. Sprinting, Interval Training)
________________________________________
60
Are you currently using tanning beds?
Are you currently being treated for Vitamin D deficiency/

insufficiency?
Do you currently have a sports injury that limits your athletic

participation/ performance?
Are you currently taking a multi-vitamin?

If yes what is the name of the multi-vitamin
______________________
Are you taking any other supplements?

If yes, please list them:
______________________________________
___________________________________________________
_
Are you currently taking any of the following medications?
Antacids,
calcium
channel
blockers
(Verapamil),
cholestyramine, anticonvulsants (Dilantin), thiazides (diuretics),
mineral oil and weight loss products such as Orlistat and Olestra
If
yes,
please
list
________________________________________
them:
___________________________________________________
________
Are you currently taking any other medications?

If yes, please list them:
________________________________________
___________________________________________________
________
Do you use sunscreen?

If yes, what is the sunscreen number (SPF)? _________
61
APPENDIX C
SUPPLEMENT & MULTIVITAMIN LOG
SUPPLEMENT & MULTIVITAMIN LOG
Code Study #:_________
Week: ___________
Indicate the days on which you took the Supplement (check the box)
Day
Monday
Tuesday
Wednesday
Thursday
Friday
Saturday
Sunday
Indicate the days on which you took the multivitamins/ other drugs & list them
Days
List of Multivitamins and/or drugs
Monday
Tuesday
Wednesday
Thursday
Friday
Saturday
Sunday
62
VITAMIN D SUNEXPOSURE LOG & KEY
Code Study #:__________________
Day of the week:_______________________
Date:_______________________
SUN EXPOSURE LOG # 1

Please fill out an extra sun exposure log(s) if your sun exposure was unusually higher than days for this week.
Were you wearing sunscreen TODAY? Y / N SPF___________
Outdoor
activity
Time of day
Location (Note if outside

Lubbock)
Time spent outdoors

in minutes
Direct
sun
Shade
7am-7:59am
8am-8:59am
9am-9:59am
10a-10:59am
11a-11:59am
12p-12:59pm
1pm-1:59pm
2pm-2:59pm
3pm-3:59pm
4pm-4:59pm
5pm-5:59pm
6pm-6:59pm
Total time outdoors today: _______________
63
Yes (Y)
for neck
covered
Yes (Y)
for
gloves
Body parts exposed to

the sun (use key)
Body parts with sunscreen

(use key)
64

Graduation 2015 - Thesis

Uploaded by

Document Information

Original Description:

Original Title

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Graduation 2015 - Thesis

Uploaded by

Copyright:

Available Formats

The Impact of Vitamin D Supplementation On Athletic Performance

Dr. Jamie A Cooper

Dr. Malorie Boylan

Dr. Jennifer Mitchel

Copyright 2012, Tammilee Kerr

Texas Tech University, Tammilee Kerr, May 2015

Texas Tech University, Tammilee Kerr, May 2015

CHAPTER III RESEARCH DESIGN & METHODS.. 20

Texas Tech University, Tammilee Kerr, May 2015

Texas Tech University, Tammilee Kerr, May 2015

Texas Tech University, Tammilee Kerr, May 2015

Texas Tech University, Tammilee Kerr, May 2015

Subject Characteristics at Baseline

Subject Vitamin D Classification at Baseline

Pearson Correlations between Subject Characteristics and Performance.

Pearson Correlation between change in Serum 25(OH)D and

Texas Tech University, Tammilee Kerr, May 2015

Serum 25(OH)D Pre & Post Supplementation..

Standing LJ Pre & Post Supplementation.

Vertical Jump Pre * Post Supplementation...

30m Sprint Pre & Post Supplementation ..

Leg Strength Pre & Post supplementation.

Flexibility Pre & Post supplementation.

Type II Fiber Pre & Post supplementation. 38

Correlation between Vitamin Intake & Leg Strength Pre Supplementation.

Correlation between Sun Exposure & Weight Pre Supplementation.

10 Correlation between Sun Exposure & Leg Strength Pre Supplementation

11 Correlation between Sun Exposure & BMI Pre Supplementation.

12 Correlation between Serum 25(OH)D & Flexibility Post Supplementation..

13 Correlation between Serum 25(OH)D & Type II Fiber % Post Supplementation.

14 Correlation between Sun Exposure & Leg Strength Post Supplementation... 40

Texas Tech University, Tammilee Kerr, May 2015

Texas Tech University, Tammilee Kerr, May 2015

Texas Tech University, Tammilee Kerr, May 2015

Texas Tech University, Tammilee Kerr, May 2015

Vitamin D Status in Adults, Children, and Athletes

Texas Tech University, Tammilee Kerr, May 2015

Texas Tech University, Tammilee Kerr, May 2015

Texas Tech University, Tammilee Kerr, May 2015

A person must eat a large amount

Texas Tech University, Tammilee Kerr, May 2015

Texas Tech University, Tammilee Kerr, May 2015

Texas Tech University, Tammilee Kerr, May 2015

Texas Tech University, Tammilee Kerr, May 2015

Vitamin D on Muscle Structure, Function, and Performance

Texas Tech University, Tammilee Kerr, May 2015

Texas Tech University, Tammilee Kerr, May 2015

Texas Tech University, Tammilee Kerr, May 2015

Texas Tech University, Tammilee Kerr, May 2015

Texas Tech University, Tammilee Kerr, May 2015

Texas Tech University, Tammilee Kerr, May 2015

Vitamin D and Athletic Performance

Texas Tech University, Tammilee Kerr, May 2015

Texas Tech University, Tammilee Kerr, May 2015

Texas Tech University, Tammilee Kerr, May 2015

Texas Tech University, Tammilee Kerr, May 2015

Texas Tech University, Tammilee Kerr, May 2015

Texas Tech University, Tammilee Kerr, May 2015

16-week Intervention Period

Texas Tech University, Tammilee Kerr, May 2015

Aims 2 & 3 Visit 3 Post Intervention measurements

Texas Tech University, Tammilee Kerr, May 2015