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 Michigan Technological University
Digital Commons @ Michigan Tech

Dissertations, Master's Theses and Master's Reports

2018

Workplace Standing Desks and Arterial Stiffness

Ian Greenlund
Michigan Technological University, [email protected]

Copyright 2018 Ian Greenlund

Recommended Citation
Greenlund, Ian, "Workplace Standing Desks and Arterial Stiffness", Open Access Master's Thesis,
Michigan Technological University, 2018.
https://digitalcommons.mtu.edu/etdr/582

Follow this and additional works at: https://digitalcommons.mtu.edu/etdr

Part of the Cardiovascular Diseases Commons, and the Circulatory and Respiratory Physiology Commons
WORKPLACE STANDING DESKS AND ARTERIAL STIFFNESS

By
Ian M. Greenlund

A THESIS
Submitted in partial fulfillment of the requirements for the degree of
MASTER OF SCIENCE
in Biological Sciences

MICHIGAN TECHNOLOGICAL UNIVERSITY

2018

© 2018 Ian M. Greenlund

This thesis has been approved in partial fulfillment of the requirements for the
Degree of MASTER OF SCIENCE in Biological Sciences.

Department of Biological Sciences

Thesis Advisor: John J. Durocher, PhD

Committee Member: Jason R. Carter, PhD

Committee Member: Steven J. Elmer, PhD

Department Chair: Chandrashekhar P. Joshi, PhD

Table of Contents
List of figures ........................................................................................................ v

List of tables ......................................................................................................... vi

Acknowledgements ............................................................................................. vii

List of abbreviations.............................................................................................. ix

Abstract ................................................................................................................ x

1 Introduction ................................................................................................... 1
1.1 Historic Employment vs. Today ........................................................... 1
1.1.1 Shift from Active to Sedentary Work ....................................... 2
1.2 Types of Employment & Health Consequences .................................. 3
1.2.1 London Bus Drivers and Post Office Workers ......................... 3
1.2.2 Dallas Astronaut Studies ......................................................... 4
1.3 Sedentary Behavior............................................................................. 5
1.3.1 Definition and Classification of Sedentary Behavior ................ 5
1.3.2 Negative Health Outcomes ..................................................... 5
1.3.3 Physiologic Mechanisms of Sedentary Behavior .................... 6
Lipoprotein Lipase................................................................... 6
Nitric Oxide and Endothelin-1 ................................................. 7
1.3.4 Physical Activity Recommendations........................................ 8
1.3.5 Increased Physical Activity and Positive Health Outcomes..... 9
1.3.6 Light Physical Activity and Human Health ............................... 9
1.4 Arterial Stiffness ................................................................................ 10
1.4.1 Normal Arterial Function ....................................................... 10
Pulse Wave Reflection .......................................................... 11
1.4.2 Methodological Development ................................................ 12
1.4.3 Applanation Tonometry ......................................................... 13
1.4.4 Pathological Associations with Arterial Stiffness ................... 17
1.5 Factors Influencing Arterial Stiffness ................................................. 19
1.5.1 Non-Modifiable Risk Factors ................................................. 19
1.5.2 Modifiable Risk Factors ......................................................... 20
1.6 Alternative Workstations ................................................................... 20
1.6.1 Examples of Alternative Workstations ................................... 20
1.6.2 Standing Desk ....................................................................... 21
1.6.3 Standing Desks and Productivity .......................................... 21
1.6.4 Standing Desks and Health................................................... 22
1.6.5 Standing Desks and Energy Expenditure.............................. 23

iii
 1.7 Standing Desks and Arterial Stiffness ............................................... 24
1.7.1 Acute Effect of Standing Desk on Arterial Stiffness............... 24

2 Methods...................................................................................................... 25
2.1 Participant Information ...................................................................... 25
2.2 Procedures ........................................................................................ 26
2.3 Measurements .................................................................................. 27
2.3.1 Body Fat Percentage ............................................................ 27
2.3.2 Rockport Walk Test ............................................................... 28
2.3.3 Blood Pressure ..................................................................... 28
2.3.4 Pulse Wave Analysis............................................................. 29
2.3.5 Pulse Wave Velocity ............................................................. 29
2.4 Data and Statistical Analyses ............................................................ 30
2.4.1 Power Analysis ..................................................................... 31

3 Results ....................................................................................................... 32
3.1 Participant Characteristics ................................................................ 32
3.2 Carotid-Femoral Pulse Wave Velocity............................................... 33
3.3 Peripheral Pulse Wave Velocity ........................................................ 35

4 Discussion .................................................................................................. 36
4.1 Carotid-Femoral Pulse Wave Velocity............................................... 36
4.2 Carotid-Radial and Leg Pulse Wave Velocity.................................... 38
4.3 Limitations ......................................................................................... 39
4.4 Implications ....................................................................................... 40
4.5 Future Directions ............................................................................... 40
4.6 Summary........................................................................................... 41

5 Reference List ............................................................................................ 42

A Appendix A – Raw Data ............................................................................. 56

A.1 Participant Characteristics ................................................................ 56
A.2 Rockport Walk Test ........................................................................... 58
A.3 Pulse Wave Velocity Raw Data ......................................................... 60

B Appendix B - Statistical Analyses ............................................................... 62

iv
List of figures
Figure 1.1 Wave Reflection & Arterial Stiffness…………………………………….11

Figure 1.2 Applanation Tonometry…………………………………………………...14

Figure 1.3 Sample Pulse Wave Analysis……………………………………………15

Figure 1.4 Sample Pulse Wave Velocity…………………………………………….16

Figure 2.1 Study Enrollment Schematic……………………………………………..25

Figure 3.1 cfPWV Seated vs. Standing ……………………………………………...33

Figure 3.2 Differences in cfPWV with age, fitness, and fat …………………….......34

Figure 3.3 crPWV & lPWV Seated vs. Standing ……………………………………35

v
List of tables
Table 3.1 Participant Characteristics: Seated vs. Standing …………………….. 32

vi
Acknowledgements
I would first like to thank the department of Biological Sciences for their
support during the first two semesters of my degree and the opportunity to teach
Anatomy & Physiology Lab I and II. Without this opportunity, I do not think I would
have found myself as an educator and researcher within higher education.
The greatest thanks and gratitude goes to my master’s advisor and mentor,
Dr. John Durocher. You approached me with this opportunity when I was not sure
what my future would look like. You took a chance on me and I will be forever
thankful for that. It started rocky with a steep learning curve for me, but with your
guidance, I learned and excelled in my new role. Your mentoring provided me with
opportunity to practice my presentation skills, grant writing, and better my teaching
strategies. It is my hope that I will be able to translate much of this moving into my
PhD and forward into my career. I will always beat you on the SDC stairs though.
I would also like to thank both of my committee members for their help and
guidance throughout my master’s journey who were always available for help and
feedback. Dr. Jason Carter, your attention to detail and advice on any speedbump
I had through this process is greatly appreciated. I look forward our continued work
together in the coming years. I know that you will provide many more training
experiences and skills to learn. Dr. Steven Elmer, thank you for always passing
along new opportunities to get involved and to get out of my comfort zone. You
have allowed me to fine-tune my critical thinking and presentation skills, which I
will value throughout the duration of my career.
I would also like to thank fellow graduate student Travis Wakeham for help
in exposing me to new lines of research and guidance on my project. A special
thanks to Piersan Kimmes, Malina Felten, and Katie Heikkinen for your help in Dr.
Durocher’s lab during the data collection and analysis process. Without your help,
we would have not been able to recruit as many participants for this study.
To the big man upstairs, I never lost my faith throughout this journey. I know
that you have a plan for me and I have finally found it. Thank you Jesus Christ, my

vii
lord and savior, for the gifts you have and will bestow upon me past, present, and
future.
To my parents, thank you for your love and support through this journey and
telling me to never give up on my dreams. You both inspire me to keep moving
forward and provide me with an example for when I am a father someday.
To my brother, thank you for always being the confidence boost I need when
I am overwhelmed. We’ve been through lots together and will continue to be there
for each other.
To my wonderful girlfriend, I have loved you more with each passing day.
You have always been there when times seemed bleak. You kept me level headed
through it all. If we can handle six years of a long distance relationship, which was
busy with school, there is nothing we cannot do. I cannot wait to see what our
future together has in store for us.

viii
List of abbreviations
AIx Aortic Augmentation Index

ATP Adenosine Triphosphate

cfPWV Carotid-Femoral Pulse Wave Velocity

crPWV Carotid-Radial Pulse Wave Velocity

CVD Cardiovascular Disease

DAP Diastolic Arterial Pressure

ECG Electrocardiogram

HDL High Density Lipoprotein

LDL Low Density Lipoprotein

LPL Lipoprotein Lipase

lPWV Leg Pulse Wave Velocity, or Femoral-Dorsalis Pedis PWV

MET Metabolic Equivalent of a Task

NO Nitric Oxide

PP Pulse Pressure

PWA Pulse Wave Analysis

SAP Systolic Arterial Pressure

ix
Abstract
Many jobs in today’s society require sitting at a desk with little physical activity.

Individuals who engage in ten hours of sedentary behavior per day double their

CVD risk. Standing desks are thought to decrease sedentary time and improve

cardiovascular health. Acute use of standing desks is shown to lower PWV.

However, chronic effects remain unknown. Forty eight participants qualified as

seated (19 females, 5 males: age 41 ± 2 years, BMI 25 ± 1 kg/m2) or standing (21

females, 3 males: age 45 ± 2 years, BMI 25 ± 1 kg/m2) groups based on habitual

workplace use. Arterial stiffness was assessed as pulse wave velocity (PWV) by

using applanation tonometry in conjunction with electrocardiography. No

differences were detected in carotid-femoral PWV (cfPWV) between seated and

standing groups (p = 0.47). However, age (p < 0.01), aerobic fitness (p < 0.01),

and fat percentage (p = 0.02) classifications revealed significant differences

between groups. Standing for 50% of a workday does not affect cfPWV. Although,

cardiorespiratory fitness and healthy body composition are associated with less

arterial stiffness.

x
1 Introduction
To further explore the potential relation between workplace standing desks

and arterial stiffness, the introduction portion of this thesis will focus on historic vs.

current employment modalities to demonstrate how this may have contributed to

the increase in sedentary activity in the United States. The associated negative

health consequences of sedentary behavior along with recommendations of

physical activity will be discussed. Arterial stiffness, an indicator of cardiovascular

health, will be introduced along with the technique used to assess arterial health

and factors that can influence it. Finally, alternative workstations, namely standing

desks, will be introduced to examine their effect on workers who regularly use them

to potentially influence overall health and arterial stiffness.

1.1 Historic Employment vs. Today

Since the turn of the 20th century to present, employment in the United States

has changed drastically. Take for example the types of jobs that founded many of

the cities and villages of the Upper Peninsula of Michigan and the Midwest region.

Employment consisted of occupations such as farming, logging, and mining, which

were labor intensive. In the early 1900s, 38% of the labor force consisted of

farmers compared to less than 3% by 2000. In contrast, the service industry grew

dramatically throughout the 20th century, indicative of the growth of healthcare,

education, personal services, and the business community. In 1900, 31% were

employed in service compared to 78% in 1999 (Fisk, 2001). This shift of the service

industry becoming the largest portion of the United States economy changed the

1
way Americans work every day. Those who may have worked on the farm, in the

forest, or in a mine, now could find themselves at a desk sitting in front of a

computer for extended portions of the day.

1.1.1 Shift from Active to Sedentary Work

Since the 1960s, the American work place has undergone a massive

transformation, to primarily benefit productivity. However, this productivity may

come at a cost to human health. Previously, much of the American workforce

consisted of jobs in agriculture and goods producing which required significant

energy expenditure from the worker. Beginning in the 1960s, new jobs entering the

workforce required more sedentary activity like desk work. Nearly 50% of all jobs

in 1960 required moderate intensity physical activity, decreasing to 30% by 1970

compared to a dismal 20% in today’s workplace (Church et al., 2011). Additionally,

jobs where the worker is sedentary, or only required to perform light physical

activity, doubled from 20% to 40% between 1970 and 2000 (Brownson, Boehmer,

& Luke, 2005). Several physiologists noted differences in employee health

between the 1950s and 1990s (Convertino, Bloomfield, & Greenleaf, 1997; Morris,

Heady, Raffle, Roberts, & Parks, 1953; Norman, 1958). Much of the classic work

done in the United Kingdom is considered the advent of sedentary behavior

research.

2
1.2 Types of Employment & Health Consequences

1.2.1 London Bus Drivers and Post Office Workers

The very beginnings of modern inactivity physiology began in the 1950s when

physiologists examined the health status of a variety of occupations in the United

Kingdom. Specifically, a group examined the health of London bus workers and

their occupation as either the driver or the conductor. Novel observations of the

time was the lack of physical activity of the bus drivers as compared to the

conductors, who move about the vehicle throughout the day (Morris et al., 1953;

Norman, 1958). The participants were followed longitudinally for nearly ten years,

and the risk of myocardial infarction in the bus drivers was twice that of bus

conductors. It was noted that this risk was apparent independent of the individual’s

physique (i.e. measurements of chest, waist, and hip circumference) (Morris,

Kagan, Pattison, & Gardner, 1966). These findings provided some of the first

clinical evidence of physical inactivity and the relation to human health. Similar

associations of cardiovascular disease incidence was observed between

sedentary government employees and postmen. The decreased level of coronary

artery disease, when compared to seated government employees, was attributed,

in part, to the increased physical activity of the postmen (Morris et al., 1953). These

classic studies provide the first examples that simply moving more throughout the

day can significantly benefit human health.

3
1.2.2 Dallas Astronaut Studies

Other classic studies with detrimental implications for sedentary behavior

include a variety of bed rest studies. Bed rest studies began during the World War

II and space race eras where they sought to examine the effect of prolonged

hospitalization and microgravity on human physiology. The consensus on a variety

of work confirmed prolonged best rest had lasting negative effects on the

cardiovascular and musculoskeletal systems in addition to many other body

systems (Convertino et al., 1997). One of the most striking studies involved four

NASA astronauts who were enrolled in a 21-day bed rest study, where their

aerobic capacity was measured before and after the bed rest intervention. The bed

rest significantly reduced the astronauts aerobic capacity by an average of 26%,

providing insight of the effect of microgravity and the act of doing nothing has on

the body (Saltin, 1968). Another group of researchers decided to follow up on the

same group of astronauts 30 and 40 years later. The group of astronauts still had

higher VO2max values three decades later compared to the 21-day bed rest

intervention (McGuire et al., 2001). Forty years of aging produced similar

decreases in VO2max as did a mere 21 days of bed rest, 27% vs. 26% respectively

(McGavock et al., 2009). Bed rest studies continue to provide evidence of how

acute sedentary behavior alters human physiology and has potential to reveal new

mechanistic insight as to why “sitting is the new smoking” (Baddeley, Sornalingam,

& Cooper, 2016).

4
1.3 Sedentary Behavior

1.3.1 Definition and Classification of Sedentary Behavior

Sedentary behavior is an epidemic that plagues the daily lives of American

citizens, which is predicted to become worse with further advancements in

technology. However, what is the actual definition of sedentary behavior from a

physiological perspective? Given 1 metabolic equivalent of a task (MET) is 3.5

mL/kg/min or an individual’s resting basal metabolic rate, Gibbs, et al. (2015)

concluded any seated activity less than 1.5 MET is classified as sedentary

behavior (American College of Sports Medicine, 2013). There remains an open

debate as to whether standing activities are classified as sedentary behavior (B.

B. Gibbs, Hergenroeder, Katzmarzyk, Lee, & Jakicic, 2015).

1.3.2 Negative Health Outcomes

A popular buzz phrase related to sedentary behavior literature is “sitting is

the new smoking” (Baddeley et al., 2016). Some may deem this an exaggeration,

however many studies highlight that simply doing nothing can be as detrimental to

human health as smoking. For example, a recent study on older cigarette smokers

reported a hazard ratio of 2.81, or 181% more likelihood to die from a

cardiovascular disease (CVD) (Taghizadeh, Vonk, & Boezen, 2016). In

comparison, a 2012 review found individuals who reported long bouts of sedentary

activity are associated with a 147% increased risk of CVD or cardiovascular event.

Engaging in sedentary behavior also increased cardiovascular mortality by 90%

(Wilmot et al., 2012). Further examination of women with CVD like coronary artery

5
disease and cerebrovascular events revealed a 63% increased risk when average

sitting time was 10 or more hours per day (Chomistek et al., 2013). The risk of

CVD is further increased when obesity is factored into physical activity status

(Warren et al., 2010). There remains a need to outline specific mechanisms

associated with the detrimental changes of sedentary behavior (Hamilton,

Hamilton, & Zderic, 2007).

1.3.3 Physiologic Mechanisms of Sedentary Behavior

Lipoprotein Lipase

In an effort to provide mechanistic insight into the relation between

sedentary behavior and a variety of CVDs, experts in the field of inactivity

physiology suggested the role of lipoprotein lipase (LPL) and its regulation. In

healthy individuals, the LPL enzyme is located within the vasculature where

triglycerides are catabolized and shuttled into glycolytic muscle tissue for energy

production (Miles et al., 2004). Research in animal models revealed a reduction in

LPL activity led to an increase in the triglyceride level in circulation (Bey &

Hamilton, 2003), which puts the individual at increased risk of metabolic syndrome

development. This accumulation of triglycerides in the blood is also one of the

hallmarks of atherosclerotic plaque formation in the arteries (Huang, 2009).

Hamilton and colleagues determined that immobilization of a rat’s hind limb caused

decreased activity of LPL as the energy demand decreased (Zderic & Hamilton,

2006). In humans, female trained distance runners demonstrate increased LPL

activity and improved triglycerides compared to controls (Podl et al., 1994). Taken

6
together, LPL activity is regulated by energy demand of surrounding tissue. LPL

activity, and other regulators, can contribute to CVDs.

Nitric Oxide and Endothelin-1

The antagonistic regulators of blood vessel diameter, nitric oxide (NO) and

endothelin-1, undergo differing gene regulation and expression during prolonged

sedentary behavior. During exercise, NO is released from the endothelial cells that

line the walls of arteries due to increased shear stress. Shear stress is created

when arterial blood flow increases. NO, a powerful vasodilator, increases vessel

diameter to accommodate the increased blood volume to be delivered to

exercising muscle (Zhang et al., 2006). Exercise also results in down-regulated

expression of endothelin-1, a vasoconstrictor. Numerous studies report the ability

of exercise to decrease expression of endothelin-1 (Maeda et al., 2001; Maeda et

al., 2003; Van Guilder, Westby, Greiner, Stauffer, & DeSouza, 2007). However,

after engaging in long bouts of sedentary activity, NO expression and

bioavailability remain unchanged (Donato et al., 2009; Thosar, Johnson, Johnston,

& Wallace, 2012). In contrast, sedentary bouts, in conjunction with aging, can

result in overexpression of endothelin-1 (Donato et al., 2009) to suggest that

sedentary activity problems with blood pressure may be a result of overexpression

of endothelin-1 rather than decreased NO. This overexpression of endothelin-1

can contribute to hypertension and ultimately lead to structural changes to the

vasculature, making it less elastic and accepting of increases in blood volume

(Marti et al., 2012).

7
1.3.4 Physical Activity Recommendations

Increased energy expenditure is associated with a variety of health

indicators which range from reductions in blood pressure (Sriram, Hunter, Fisher,

& Brock, 2014), weight management (Muller, Enderle, & Bosy-Westphal, 2016),

and improvement of plasma triglycerides (Hirose et al., 2015). In principal,

increased energy expenditure triggers increased energy production in the form of

adenosine triphosphate (ATP). Production of ATP is primarily through glucose and

fat oxidation (Rosen & Spiegelman, 2006). An increase in fat oxidation has the

potential to decrease body adiposity, ultimately improving weight, body mass index

(BMI), and waist circumference (Esposito et al., 2003; Kelley, Goodpaster, Wing,

& Simoneau, 1999). Protein oxidation constitutes a small percentage of total

energy production, typically reserved for extreme circumstances (Dickerson,

Guenter, Gennarelli, Dempsey, & Mullen, 1990). Recently, the ACSM released

new guidelines for maintaining fitness in normal, healthy adults. Included in the

recommendation are guidelines for maintaining cardiorespiratory health by

engagement in 150 minutes of moderate exercise per week, 75 minutes of

vigorous exercise per week, or any combination moderate or vigorous of exercise

that results in energy expenditure of 500-1000 MET minutes per week or greater

(Garber et al., 2011). Moderate or vigorous physical activity will not result from

working at a standing desk for set amount of time.

8
1.3.5 Increased Physical Activity and Positive Health Outcomes

Engagement in physical activity and exercise as recommended by the ACSM

can help to produce a variety of positive health outcomes. Training induced

improvements can improve oxygen delivery to the muscular tissue via increased

capillary density (Mandroukas et al., 1984; Warburton, Nicol, & Bredin, 2006). In

combination with improvement in muscle oxidative capacity via proliferation of type

I muscle fibers (Schiaffino & Reggiani, 2011), VO2max can increase (Mandroukas

et al., 1984; Warburton, Gledhill, & Quinney, 2001). In addition, interventions

aimed at increased physical activity, namely moderate and vigorous intensity, is

able to reduce or prevent increased fat percentage in children (Ruiz et al., 2006),

men (King, Haskell, Young, Oka, & Stefanick, 1995), premenopausal women

(Trapp, Chisholm, Freund, & Boutcher, 2008) and postmenopausal women (Irwin

et al., 2003). However, light physical activity can produce some of the same health

benefits as moderate or vigorous activity.

1.3.6 Light Physical Activity and Human Health

Light physical activity is defined as any activity capable of utilizing 3.5

kilocalories per minute or an energy expenditure of 1.5 – 3.0 METs (American

College of Sports Medicine, 2013; Healy et al., 2007). Common examples of light

physical activity includes easy walking or biking. This physical activity category is

of particular importance to older individuals and is associated with physical health

(Buman et al., 2010). When compared to sedentary behavior, light physical activity

revealed the ability to significantly reduce both central and brachial blood

9
pressures (Gerage et al., 2015). With the health benefits of light activity, there

remains the question of whether standing is enough to produce an energy

expenditure equivalent to at least 1.5 METs and have an impact on blood pressure

and arterial stiffness (i.e. ability of arteries to expand and recoil with each cardiac

cycle).

1.4 Arterial Stiffness

1.4.1 Normal Arterial Function

In young, healthy individuals, the arteries of the cardiovascular system

possess a large amount of distensibility, or the ability to stretch. During systole,

fresh, oxygenated blood is ejected from the left ventricle of the heart, passes

through the aortic semilunar value, into the aorta. The addition of new blood

volume to systemic circulation causes the aorta to stretch. The ability of the aorta

to stretch inhibits excessive increases in blood pressure (London & Guerin, 1999).

As the heart enters diastole, negative or decreased pressure within the ventricle

causes the aortic values to close. The elastic recoil of the aorta allows for the

preservation of both blood flow and diastolic pressure (Michel E Safar, 2004). In

addition to blood ejection into systemic circulation, the heart contraction produces

a pulse wave that travels through the vasculature. This pulse wave is also called

the palpable pulse, which can be felt most commonly at the wrist or neck. Reflected

pulse wave timing in reference to systole and diastole can either be beneficial or

detrimental to the heart.

10
 Pulse Wave Reflection

With each cardiac cycle, a pulse wave is sent through the vasculature

during systole. This wave travels forward through the aorta. As the aorta begins to

branch into smaller arteries and arterioles, the initial pulse wave sends a forward

wave into the smaller arteries, but also sends a reflected wave back toward the

heart (London & Guerin, 1999). The reflected waves have the potential to cause

additional stress on the aorta in older individuals or individuals who have

abnormally high arterial stiffness for their age. Increased arterial stiffness has the

potential risk of being pathological as stiffness can affect the timing of when the

reflected waves return to the aorta (Mayet & Hughes, 2003). In a young, healthy

individual, the reflected wave arrives during diastole, when the reflected wave can

Figure 1.1. Wave reflection associated with low arterial stiffness (top BP waveform) and wave
reflection associated with high arterial stiffness (bottom BP waveform). Reflected waves arise
from artery branch points or areas of stiffness within the vasculature. Reflected waves during
systole (e.g. bottom waveform) can place added stress on the heart.

11
help to further perfuse the coronary arteries to aid with oxygen delivery to the

myocardium (Kelly, Daley, Avolio, & O'Rourke, 1989; London & Guerin, 1999). In

an older or unhealthy individual, the reflective wave returns during systole and

further increases the blood pressure in the aorta. Over a long period of time, the

added stress can lead to further stiffening of the aorta and increases in the aortic

systolic pressure and decreases in aortic diastolic pressure. This forces the heart

to generate more and more force with each heart contraction and increased stress

on the vasculature with larger changes in pulse pressure.

1.4.2 Methodological Development

While brachial blood pressure is still considered an excellent screening tool

for cardiovascular diseases and serves as an accurate predictor of future

cardiovascular events, blood pressure varies within the arterial division of the

cardiovascular system (Carmel M. McEniery, Cockcroft, Roman, Franklin, &

Wilkinson, 2014). A healthy individual’s aortic systolic pressure is normally lower

than the corresponding brachial blood pressure due to artery distensibility changes

in periphery and vessel radius (Roman et al., 2009). However, instances arise

where brachial blood pressure values are normal, or near normal, and the aortic

blood pressure is comparable to the brachial blood pressure (Carmel M McEniery

et al., 2008). This discrepancy may be evident from differing levels of stiffness of

the large arteries elevating central blood pressure (Michel E Safar, Levy, &

Struijker-Boudier, 2003). This discovery outlines the need for direct assessment of

aortic blood pressure as an independent risk factor for cardiovascular disease.

12
 A variety of techniques exist for the assessment of arterial stiffness in

humans. Invasive measures include implantation of aortic catheters, which are

equipped with pressure transducers to obtain measures of blood pressure at the

level of the heart (Chen et al., 1998; Currie et al., 1985; Kawaguchi, Hay, Fetics,

& Kass, 2003). Early work in the animal model confirmed pressure within the aorta

was equivocal to pressure in the left ventricle during systole as blood is ejected

into systemic circulation (Wiggers, 1928). In an effort to determine a less invasive

technique of determining aortic blood pressure, radial artery catheterization can be

used to generate aortic blood pressure via a generalized transfer function to

generate an aortic blood pressure waveform. Actual and computer modeled aortic

wave forms prove comparable and reliable (Chen et al., 1997; Pauca, O’rourke, &

Kon, 2001). The new technique termed applanation tonometry, which is proven to

be reliable and repeatable, is now wildly used for cardiovascular research (Crilly,

Coch, Bruce, Clark, & Williams, 2007; Papaioannou et al., 2004; Wilkinson et al.,

1998).

1.4.3 Applanation Tonometry

Arterial stiffness is measured through two main techniques associated with

applanation tonometry. Pulse wave analysis (PWA) is a rapid recording where a

tonometer records pressure waves of an artery of interest, most often the radial

13
 Figure 1.2. Applanation tonometry, the process of flattening out an artery of interest against a hard
surface, like bone, to obtain pulse-wave recordings. A general transfer function can generate the
estimated aortic blood pressure waveform.
artery. SphygmoCor computer software is used to analyze characteristics of the

pulse wave. When calibrated to a brachial blood pressure, this measure can

provide estimates of the blood pressure waveform in the aorta, via generalized

transfer function, to generate aortic blood pressure (systolic, diastolic, mean, and

pulse pressure), which are confirmed against aortic and radial catheterization (Adji,

Hirata, Hoegler, & O’Rourke, 2007; Chen et al., 1997). Additionally, an aortic

augmentation index is calculated from the characteristics of the pulse wave. This

14
 Figure 1.3. Sample pulse wave analysis (PWA) recording of the radial artery following
calibration with brachial BP. Via generalized transfer function, pulse wave characteristics can
estimate aortic SAP, DAP, MAP, and PP.

is defined as the quotient of the aortic augmentation pressure (i.e. aortic systolic

pressure – blood pressure at inflection point, AIx) and aortic pulse pressure. This

index can also be normalized to 75 heart beats, however there is debate as to

when to use the normalized value vs. the non-normalized value (Stoner et al.,

2014). However, AIx is recognized to be dependent on heart rate, body height, and

blood ejection duration (Townsend et al., 2015).

Another technique under the classification of applanation tonometry is pulse

wave velocity, where pulse wave speed can be estimated. Carotid-femoral pulse

wave velocity (cfPWV) is often considered the gold standard indicator of

cardiovascular health assessed with applanation tonometry, where a 1.0 m/s

increase in velocity increases the risk of a cardiovascular event by 15%

(Vlachopoulos, Aznaouridis, & Stefanadis, 2010). This measurement is done in

15
 Figure 1.4. Sample pulse wave velocity (PWV) recording of cfPWV. Based on pulse wave
distance, time delay of pulse creation to pulse arrival is recorded at carotid and femoral sites. A
speed in meters per second is calculated.

tandem with an electrocardiogram recording. Each R wave of the ECG serves as

the creation of the pulse wave. Two pulse sites are referenced where the distance

from the suprasternal notch (i.e. location of the aorta) to each pulse site is

measured. The tonometer is placed over the artery to examine when the pulse

wave arrives. The time delay is calculated from the pulse wave creation (i.e. R

wave) and the pulse wave arrival (i.e. waveform upstroke) for each cardiac cycle.

The data collection software uses the distance from the aorta and time delay of

pulse wave arrival to calculate the pulse wave velocity (Doupis, Papanas, Cohen,

McFarlan, & Horton, 2016). A cfPWV below 10 m/s is considered to normal,

whereas upwards of 10 m/s may be indicative of arterial stiffness within the

vasculature (Van Bortel et al., 2012).

16
1.4.4 Pathological Associations with Arterial Stiffness

Arterial stiffness is associated with a variety of cardiovascular diseases

including hypertension, atherosclerosis, etc. There has long been a debate on

whether arterial stiffness is the precursor to hypertension or if the inverse is true.

A review by Franklin addressed this concern where he suggested an interplay

between hypertension and arterial stiffness (Franklin, 2005), now termed a “vicious

cycle”. High arterial stiffness can induce incident hypertension (Tomiyama &

Yamashina, 2012). Left untreated, rapid increases in arterial stiffening occur, which

can further increase the severity of hypertension (Franklin et al., 1997). Long term

stress on arterial walls triggers vascular remodeling, which is can be categorized

as, hypertrophic, hypotrophic, or eutrophic, corresponding to increase, decrease,

or unchanged amount of new tissue in the blood vessel (Mulvany et al., 1996;

Schiffrin, 2012). Inward eutrophic and hypertrophic remodeling are common within

smaller arteries undergoing the stress of hypertension (Schiffrin, 2012). Inward

eutrophic remodeling leads to decreased size of the vessel ultimately leading to

decreased lumen diameter. Inward hypertrophic remodeling also reduces the

lumen diameter via increased lumen endothelial growth. Large artery stiffness is

characterized by outward hypotrophic growth where the lumen diameter is

increased (Schiffrin, 2012). Over time, the elastin within the vessels is broken down

and replaced with less compliant, dense collagen (O'rourke, 1990). This

phenomenon explains, in part, why stiff arteries produce increases in pulse

pressure and disruptions in blood flow (Renna, de Las Heras, & Miatello, 2013). In

addition, chronic stress on arterial walls can lead to inflammation (Booth et al.,

17
2004), where the inner layers of the vasculature are not replaced or undergo the

same remodeling process as other arterial layers. Inflammation within the

vasculature can lead to the buildup of LDL cholesterol, which can exacerbate the

progression of atherosclerotic plaque formation (Libby, 2012).

Another pathological aspect of arterial stiffness includes the potential of end

organ damage. Common examples include the kidney, brain and heart (Gary F

Mitchell, 2008). As stated, the disruptions in blood flow from vascular remodeling

contributes to more of a pulsatile blood flow rather than a constant flow. Decreased

myocardial perfusion is evident in individuals with high arterial stiffness, where

reflected pulse waves arrive to the heart during systole, rather than diastole,

increasing the risk of myocardial ischemia from increased contractility and

decreased oxygen availability (Kelly et al., 1989; London & Guerin, 1999).

Increased pulsatility to the brain and kidney puts added stress on the

microvasculature. Within the kidney, the glomerulus vasculature becomes

damaged, which can allow large molecules like proteins into the urine (M. E. Safar,

Nilsson, Blacher, & Mimran, 2012). Within the brain, there are associations

between high arterial stiffness and beta-amyloid plaque deposition. Because of the

decrease in blood vessel integrity from increases in pulsatility, the vasculature acts

comparable to the kidney, allowing larger substances move across the blood brain

barrier, which may contribute to the progression of Alzheimer’s disease (Singer,

Trollor, Baune, Sachdev, & Smith, 2014).

18
1.5 Factors Influencing Arterial Stiffness

1.5.1 Non-Modifiable Risk Factors

Numerous studies have reported the relationship between age and arterial

stiffness (Benetos et al., 2002; Vaitkevicius et al., 1993; Wen et al., 2015). The

Framingham Heart Study cohort data showed age was a strong predictor of both

cfPWV and reflected wave transit time (i.e. time from reflection to arrival at the

heart). PWV increased with age, whereas the reflected wave time decreased. This

phenomena may contribute to arterial stiffness related SAP and pulse pressure

(PP) increases. (G. F. Mitchell et al., 2004). In addition, there is data to further

suggest arterial stiffness progression throughout the aging process independent

of hypertension status (Vaitkevicius et al., 1993). However, interventions exist to

ameliorate age related increases in arterial stiffness. Other non-modifiable risk

factors include sex and ethnicity. African-American men appear to have increased

central blood pressure, intima-media thickness, and carotid beta-stiffness as

compared to age matched Caucasian men (Heffernan, Jae, Wilund, Woods, &

Fernhall, 2008). In addition, African-American men appear to have increased

baseline aortic stiffness as compared to Caucasian men (Heffernan, Jae, &

Fernhall, 2007). Sex differences of arterial stiffness show women have increased

arterial stiffness following menopause compared to men (Coutinho, Borlaug,

Pellikka, Turner, & Kullo, 2013), consistent with increased prevalence of

hypertension as women age (Oparil & Miller, 2005).

19
1.5.2 Modifiable Risk Factors

Interventions to improve aerobic capacity are common within the scientific

community and range in focus from cognition (Colcombe & Kramer, 2003) to

cardiovascular health (Warburton et al., 2006). One cross-sectional study

demonstrated the ability of increased aerobic capacity to significantly lower levels

of arterial stiffness when compared to sedentary controls (Vaitkevicius et al.,

1993). Another modifiable factor is maintenance of a healthy body composition.

Increased abdominal visceral fat in obese individuals is associated with increased

arterial stiffness (Sutton-Tyrrell et al., 2001; Zebekakis et al., 2005), whereas

interventions that decrease obesity also can improve arterial stiffness (Goldberg,

Boaz, Matas, Goldberg, & Shargorodsky, 2009). Easy to implement interventions

include increasing physical activity throughout the day, and use of an alternative

workstation, which can increase energy expenditure and potentially to improve

arterial stiffness (Hamasaki, Yanai, Kakei, Noda, & Ezaki, 2015).

1.6 Alternative Workstations

1.6.1 Examples of Alternative Workstations

Sedentary behavior in the workplace is a problem. A variety of new, active

workstations were created and are now widely used. These new workstations

range from a standing desk, to a biking workstation, to a treadmill desk. The main

goal of each alternative workstation is to breakup prolonged seated periods and

improve energy expenditure throughout the workday (Torbeyns, Bailey, Bos, &

Meeusen, 2014). However, the implementation of new workstations created new

20
questions to answer. Productivity was a large concern especially when alternative

desks were bought for employees rather than in the home. Is the worker as

productive while standing, walking, or biking as compared to remaining seated

(Karol & Robertson, 2015)? Do the alternative workstations truly provide a

significant benefit to health (Torbeyns et al., 2014)? Each question was warranted

to justify investment in a new workstations to ensure there would be no harm to

the employee or company productivity.

1.6.2 Standing Desk

Perhaps the easiest and simplest of all active workstations, the standing

desk, is one of the most popular to encourage reduced sitting time while at work.

Most who readily use a standing desk report the desire to move more throughout

the day, which is consistent with the principal of active workstations (Levine &

Miller, 2007). In addition, there is little evidence to suggest office programs, like

intermittent walking, effectively promote a reduction in sedentary time due to poor

adherence (Chau et al., 2010). By providing an option of an active workstation like

a standing desk, workplace sedentary time and perhaps productivity and health

could improve.

1.6.3 Standing Desks and Productivity

Standing workstation productivity was one of the first questions to be posed

to the scientific community. The question was of particular interest to employers,

whereas an investment in a standing workstation that decreased productivity would

21
be irrational from a financial perspective. The most frequent test of productivity at

workstations are typing performance tests. Two studies report no differences in

typing performance (Drury et al., 2008; Ebara et al., 2008). Another study provided

evidence of increased productivity with changes in posture like standing, but longer

standing time decreased productivity, driven by employee fatigue (Hasegawa,

Inoue, Tsutsue, & Kumashiro, 2001). A recent study of a Texas call center, who

implemented a standing desk intervention, saw increased productivity (up to 50%)

in the form of successful phone calls at months one and six (Garrett et al., 2016).

In summary, the majority of research into standing desk productivity provided

support for their implementation into the workplace given only long bouts of

standing decreased workplace productivity. If a standing desk can both boost

productivity and improve employee health, the purchase can be financially justified.

1.6.4 Standing Desks and Health

In an effort to reduce sitting time throughout the day, researchers have

inferred that replacement of sitting with standing for part of the workday will

positively impact human health and decrease biomarkers for certain

cardiovascular or metabolic disorders. A recent study published by Winkler et al

(2017), reported improvements in a variety of health variables. Standing was

associated with improvements in triglycerides, HDL cholesterol, and fasting

glucose via a 12- month program to promote more standing throughout the

workday (Winkler et al., 2017). HDL cholesterol improvement was documented to

increase as much as 4.68 mg/dL (Alkhajah et al., 2012). An increase of this

22
magnitude can improve HDL cholesterol from a range indicative of increased risk

of heart disease (18.74 mg/dL) to an acceptable level (21.08 mg/dL) (Stone et al.,

2014). There is no current evidence on standing desk ability to improve resting

blood pressure, only one study reports blood pressure is increased during standing

rather than sitting (Cox et al., 2011). However, there is differing literature to

suggest standing is not enough to provide positive health outcomes like

improvements in body composition and blood pressure (Carr, Swift, Ferrer, &

Benzo, 2016). Furthermore, moderate or vigorous physical activity will not result

from working at a standing desk for set amount of time. Perhaps standing

throughout in the workday is enough to achieve light physical activity.

1.6.5 Standing Desks and Energy Expenditure

A recent review reported that the use of standing desks produced increases

in energy expenditure ranging from 4.1 to 20.4 kcal/hr or VO2 of 0.18 to 0.90

mL/kg/min (MacEwen, MacDonald, & Burr, 2015). Yet, an important question

remains. Is the increase in energy expenditure able to produce light physical

activity compared to physical activity associated with seated desks? Given 1 MET

is 3.5 mL/kg/min, an average 75 kg individual would produce at most an additional

¼ of a MET by standing. However, standing at the work place puts workers at

higher likelihood to walk more at work, which could, indirectly, increase energy

expenditure to as much as 119 kcal/hr or 1.5 METs (Levine & Miller, 2007).

23
1.7 Standing Desks and Arterial Stiffness
Current research into energy expenditure of workstations employed indirect

calorimetry analyses to determine specific caloric use and substrate metabolism.

In one study, utilization of a standing desk increased energy expenditure by 7.5

kcal/hour when compared to a seated desk control (Roemmich, 2016). In addition,

increased light physical activity in older individuals is correlated with improved

carotid-femoral PWV (Yuko Gando et al., 2010), but could a standing desk be

enough to promote physical and cardiovascular well-being if light physical activity

is achieved?

1.7.1 Acute Effect of Standing Desk on Arterial Stiffness

Very few studies exist which examine the effect of standing desks on arterial

stiffness. One study observed the effects of using a standing desk during one

stimulated workday, but alternated between sitting and standing throughout the

day. The study revealed acute changes in carotid-ankle PWV compared to the

seated control group. However, no changes were seen in carotid-femoral PWV

(Bethany Barone Gibbs et al., 2017). No current research has examined the

chronic effects of standing desk use during a normal work day.

Thus, the purpose of this study is to determine the chronic effect of standing

desk use on arterial stiffness vs. seated sedentary controls. We hypothesized that

individuals who chronically stand at work would demonstrate lower arterial stiffness

than those that chronically sit at work.

24
2 Methods

2.1 Participant Information

Fifty-five participants were recruited from the Michigan Tech and Houghton,

Michigan community. Of the 55 participants, 50 (42 females, 8 males) were

enrolled in the study. Twenty-six participants were chronic users of a seated desk

(21 females, 5 males: age 42 ± 11 years, BMI 25 ± 4 kg/m2) and 24 chronic

standing desk users (21 females, 3 males: age 45 ± 12 years, BMI 25 ± 5 kg/m2)

via self-report questionnaire. Standing desk users must have used a standing desk

for at least 8 weeks (desk use 2 ± 1 years, 19 ± 16 months). All participants were

free of any diagnosed cardiovascular or metabolic diseases. All women were

screened for particular phase of

menstrual cycle in an effort to

have equal groups of early

follicular, mid-luteal, and post-

menopausal women within the

seated and stranding desk

groups. This study was approved

by the Michigan Technological

University Institutional Review

Figure 2.1. Study schematic of enrollment.
Board (M1457). All participants Hypertension: ≥140/90 mmHg, Aortic Pulse
Pressure (aPP): >50mmHg
provided written informed consent

prior to study enrollment.

25
2.2 Procedures
Participants arrived to Michigan Tech’s Clinical and Applied Human

Physiology Lab following a fast for at least three hours and abstaining from

exercise and caffeine for at least 12 hours prior to the scheduled orientation and

testing sessions. During the orientation session, participants completed an

informed consent form, participant information sheet, and a Godin Leisure Time

Questionnaire (i.e. quantify physical activity habits outside of normal workday).

Height, body mass, and body fat percentage were recorded. Participants were

instructed to lay supine and quiet on an exam table for five minutes. Up to three

brachial blood pressure recordings were taken with an automated

sphygmomanometer to screen for potential hypertension (i.e. ≥140/≥90 mmHg).

Preliminary arterial stiffness measures were taken via a pulse wave analysis

recording of the radial artery following calibration of the SphygmoCor system with

the brachial blood pressure. Participants with an aortic pulse pressure of ≥50

mmHg were excluded from the study due to a potential increased risk of

atherosclerotic plaque (Oliver & Webb, 2003; Roman et al., 2009). Aerobic fitness

was estimated via a Rockport Walk Test on a treadmill within the lab.

Following the orientation session, participants reported back to the laboratory

for their scheduled testing session. Each were instructed to lay supine and refrain

from talking for five minutes on an exam table. Using an automated

sphygmomanometer, three brachial blood pressures were obtained, with each

measurement separated by one minute. Duplicate pulse wave analysis recordings

26
were collected from the radial pulse site for 10 cardiac cycles, with operator indices

above 80. An operator index above 80 is considered satisfactory by the

manufacturer and indicates maintenance of pulse height and limited variation of

the systolic and diastolic portions of the waveform. Three electrodes were placed

on the participant’s chest. Two at the shoulders near the collar bone and one on

the bottom portion of the rib cage on the left side of the body to capture lead II of

an ECG. Three regional pulse wave velocity measures (carotid-radial, femoral-

dorsalis pedis, carotid-femoral) were performed to assess arterial stiffness within

the arm, leg, and central region of the body. Measures of distance (mm) were taken

from the suprasternal notch (aorta location) to the pulse site of interest (carotid,

radial, femoral, or dorsalis-pedis). Recordings were executed in duplicate, where

recordings having a standard deviation of <10% were kept for analyses.

2.3 Measurements

2.3.1 Body Fat Percentage

Body Fat percentage was measured with a bioelectrical impedance scale

(BC-418 Segmental Body Composition Analyzer; Tanita, Tokyo, Japan).

Participants were instructed to remove shoes and socks and place their feet on the

metal pads on the scale. Medal handles were also held at the participant’s side

during the recording. Each were instructed to remain still as the electromagnetic

wave passed through their body. Impedance is indicative of adipose tissue given

the hydrophobicity of adipose cells and the lipids they possess. Other tissues like

27
muscle are water rich and result in low impedance. Whole body and regional

assessments of fat percentage were obtained.

2.3.2 Rockport Walk Test

To estimate aerobic fitness, a Rockport walk test was administered to

estimate a VO2peak score, given ease of test administration and reliability with

actual VO2peak via graded exercise test (Kline et al., 1987). Participants completed

a physical activity readiness questionnaire (PAR-Q; Canadian Society of Exercise

Physiology) prior to the test and then were instructed to perform a three minute

submaximal walking warm-up at a 1% grade on the laboratory treadmill, which

produces similar results to track administration (Nieman, 1999). Directly following,

participants were instructed to walk one mile as fast as possible, without running,

at a 1% grade. A ten second heart rate, test time, and modified Borg rating of

perceived exertion were collected at conclusion of the test. Weight (lbs), age

(years), sex (1=men, 0=women), time (minutes), and minute heart rate were

entered into the following regression equation: VO2peak = 132.853 – (0.00769 *

weight) – (0.3877 * age) + (6.315 * sex) – (3.2649 * test time) – (0.1565 * heart

rate) (American College of Sports Medicine, 2013). Participants were instructed to

cool down ad libitum for at least two minutes.

2.3.3 Blood Pressure

Following five minutes of supine rest, a brachial blood pressure recording

was taken with an automated sphygmomanometer (Omron HEM-907XL; Omron

28
Health Care, Kyoto, Japan). Blood pressure recordings was performed in triplicate

during the testing session. The average blood pressure was used to calibrate

arterial stiffness data collection software.

2.3.4 Pulse Wave Analysis

An average brachial blood pressure was entered in the SphygmoCor data

collection software (SphygmoCor; AtCor Medical, Sydney, Australia) for calibration

purposes. The tonometer probe was placed over the radial artery by flattening out

the artery and pressing it against the carpals of the wrist. Following probe

adjustment to find a strong reading and eliminate systolic and diastolic variation,

the probe was kept still for approximately 10-12 seconds to capture ten radial pulse

waves. This technique was done in duplicate to ensure consistent quality

recordings. The software analyzed the radial pulse wave via a generalized transfer

function to generate an aortic pulse wave, aortic blood pressure values, and aortic

augmentation indices.

2.3.5 Pulse Wave Velocity

Three electrodes, two at the shoulder region and one on the bottom, left side

of the rib cage, were placed to obtain lead II of an ECG. Measurements of straight-

line distance (mm) were recorded from the suprasternal notch to two pulse sites of

interest to examine carotid-radial, femoral-dorsalis pedis, and carotid-femoral

pulse wave velocities. Each pulse wave reading was gated to the R-wave of the

ECG to calculate the time delay between pulse creation at the heart and to arrival

29
at the pulse site. The change in the distance (proximal – distal in reference to aorta)

is divided by the change in time delay (proximal – distal time delay) to provide a

speed in meters per second. Duplicate readings with a standard deviation ≤10%

were kept for data analysis.

2.4 Data and Statistical Analyses

Data were exported from the SphygmoCor system to a Microsoft excel file

and then to SPSS. Initially, normality tests were conducted on the variables of

age, VO2peak, and fat percentage. Two participant’s data were excluded from

analysis due to non-normally distributed VO2peak scores. Forty-eight participants,

twenty-four chronic seated desk users (19 females, 5 males: age 41 ± 10 years,

BMI 25 ± 4 kg/m2) and 24 chronic standing desk users (21 females, 3 males: age

45 ± 12 years, BMI 25 ± 5 kg/m2) were used for final analysis. Differences in age,

estimated VO2peak, BMI, fat percentage, blood pressure (SAP and DAP), and heart

rate between seated and standing groups were assessed using independent

samples t-tests. We used a median analysis to classify participants by age, aerobic

fitness (VO2peak), and fat percentage (i.e. young v. old, high fitness v. low fitness,

etc.) for additional secondary analysis of cfPWV. Each pulse wave velocity was

averaged with corresponding value in preparation for statistical analysis using

commercial software (SPSS 25.0, SPSS, Chicago, IL). Results are expressed as

mean ± SD (Streiner, 1996). Means were considered significantly different when

P ≤ 0.05 (i.e. two-tailed test).

30
2.4.1 Power Analysis

An additional analysis was performed to ensure adequately powered sample

size to produce 1 m/s differences in cfPWV, where 1 m/s reductions of cfPWV may

reportedly reduce CVD risk by 15% (Vlachopoulos et al., 2010). Power analysis

software (G*Power 3.1.9.2, Kiel, Germany) was used to determine proper effect

size for total sample power of 0.8, alpha of 0.05, and equal allocation ratio. Effect

size was determined via group means and group standard deviations. A difference

of 1 was selected between group means based on the findings of Vlachopoulos et

al. (2010). A standard deviation of 1.2 was selected from The Reference Values

for Arterial Stiffness Collaboration via cfPWV reference value of 40-49 year old

individuals with normal blood pressure (n = 562) (Collaboration, 2010). A

computed effect size of 0.8333 was achieved with a sample size of n = 48.

31
3 Results

3.1 Participant Characteristics

Participant demographic values between seated and standing groups are

shown in Table 3.1. Age, VO2peak, Godin score, height, weight, body mass index

(BMI), fat percentage, systolic arterial pressure (SAP), and heart rate (HR) were

all similar between seated and standing groups. However, diastolic arterial

pressure (DAP) was significantly higher in the standing group.

Table 3.1. Participant Characteristics: Seated vs. Standing

Seated Standing
Variable (n = 24, 19 female) (n = 24, 21 female) P Value

Age (years) 41 ± 10 45 ± 12 0.238

VO2peak (mL/kg/min) 39 ± 8 34 ± 10 0.124
Godin (score) 61 ± 63 47 ± 22 0.311
Height (cm) 167 ± 8 167 ± 8 0.961
Weight (kg) 70 ± 12 71 ± 13 0.704
BMI (kg/m2) 25 ± 4 25 ± 5 0.860
Fat Percentage 28 ± 8 30 ± 8 0.356
SAP (mmHg) 113 ± 8 115 ± 11 0.529
DAP (mmHg) 66 ± 5 71 ± 7* 0.008
HR (beats/min) 59 ± 11 63 ± 9 0.208

Values are means ± SD; n, number of participants; Godin, Physical Activity

Questionnaire activity score; BMI, Body Mass Index; SAP, systolic arterial
pressure; DAP, diastolic arterial pressure; HR, heart rate. *Significantly different
from corresponding seated value, P < 0.05

32
3.2 Carotid-Femoral Pulse Wave Velocity
Figure 3.1 compares carotid-femoral pulse wave velocity (cfPWV) or arterial

stiffness in the central region of the body when categorized by seated and

standing. No differences were detected between seated and standing groups (p =

0.474). Figure 3.2 shows participants separated into categories of young v. old,

low fitness v. high fitness, and high fat v. low fat, where a median analysis

generated two groups for comparison in each respective category (i.e. age, fitness,

and fat percentage). Carotid-femoral pulse wave velocity was significantly higher

in older participants (Panel A) when compared to younger (p=0.002). High fitness

and low fat percentage (Panel B and C, respectively) had significantly attenuated

cfPWV when compared to low fitness and high fat percentage (p<0.001 and

p=0.022, respectively).

10
cfPWV (m/s)

2
Seated Standing
(n = 24) (n = 24)

Figure 3.1 Carotid-femoral Pulse Wave Velocity (cfPWV) when classified by

seated v. standing (p = 0.474). Result is mean ± SD

33
 10 A
*

cfPWV (m/s)
8

2
Younger Older
(n = 24) (n = 24)

10 B
cfPWV (m/s)

8
*
6

2
Low Fitness High Fitness
(n = 24) (n = 24)

10 C
cfPWV (m/s)

8
*
6

2
High Fat Low Fat
(n = 24) (n= 24)

Figure 3.2 Carotid-femoral Pulse Wave Velocity (cfPWV) classified using

traditional factors such as age (Panel A; median = 42.0 years, p = 0.002), fitness
(Panel B; median = 36.0 mL/kg/min, p < 0.001), and fat (Panel C; median =
28.7%, p = 0.022). Results are means ± SD. *Significantly different from
corresponding value, P < 0.05
34
3.3 Peripheral Pulse Wave Velocity
Figure 3.3 represents carotid-radial pulse wave velocity (panel A; crPWV) and

femoral-dorsalis-pedis pulse wave velocity (panel B; lPWV). Both recordings

represent arterial stiffness in the arm and leg respectively. Both analyses saw no

significant difference between seated and standing groups (p = 0.133 and 0.661,

respectively).

10 12
crPWV (m/s)

8 10

lPWV (m/s)
6 8

4 6

2 4
Seated Standing Seated Standing
(n = 24) (n = 24) (n = 22) (n = 24)

Figure 3.3 Carotid-radial pulse wave velocity (crPWV) and Leg Pulse Wave
Velocity (lPWV) when classified by seated v. standing (P = 0.133 and 0.661)
Results are means ± SD

35
4 Discussion
To our knowledge, this is the first study to examine chronic use of a standing

desk throughout a normal workday. cfPWV, crPWV, and lPWV were not different

between chronic seated and standing desk workers. Secondary analysis of

traditional factors of age, aerobic fitness, and fat did produce significant differences

in cfPWV between groups (i.e. younger v. older, low v. high fitness, high v. low fat)

The results of this study were not in support of our hypothesis, where cfPWV of

individuals who used a standing desk for at least 50% of the day was not lower as

compared to seated desk controls. However, our results do confirm the influence

of age, aerobic fitness, and body fat on arterial stiffness. The findings of this study

further advance the field of both inactivity physiology and alternative workstations.

4.1 Carotid-Femoral Pulse Wave Velocity

As stated previously, cfPWV is considered to be the gold-standard of

assessing cardiovascular health where a 1 m/s decrease is associated with a 15%

reduction in CVD risk (Vlachopoulos et al., 2010). The comparison between seated

and standing groups revealed little difference between cfPWV, possibly due to lack

of achieving light physical activity while working at a standing desk. Light physical

activity may trigger NO release (Niebauer & Cooke, 1996) and some degree of

endothelin-1 suppression (Nyberg, Mortensen, & Hellsten, 2013). The relationship

between light physical activity and cfPWV has been demonstrated in older

individuals (i.e. 65-85 years old), but not young (van de Laar et al., 2010). There

is some evidence to suggest only vigorous activity is correlated with improved

36
arterial stiffness in young adults, rather than habitual moderate and light physical

activity (van de Laar et al., 2010). Working to reduce other CVD factors such as

hypertension and dyslipidemia can also work to prevent age related increase in

arterial stiffness (Benetos et al., 2002).

Arterial stiffness is known to increase with age (Benetos et al., 2002;

Vaitkevicius et al., 1993; Wen et al., 2015), which is supported by our results. Over

time, arteries undergo a process called remodeling where vessel wall elasticity

decreases and the diameter of the vessel lumen can increase (Mulvany et al.,

1996). Increases in arterial stiffness lead to increased SAP, while increases in

vessel lumen diameter via outward remodeling decreases DAP (Mulvany et al.,

1996; Schiffrin, 2012). The opposing changes in SAP and DAP results in increased

pulse pressure (Schiffrin, 2012). Increased pulse pressure, especially aortic, is

indicative of CVD like atherosclerosis and other cerebrovascular disease like an

ischemic stroke due to interrupted blood flow (Townsend et al., 2015).

Many studies have noted the association between increased physical activity

and decreased arterial stiffness (Vaitkevicius et al., 1993; Zieman, Melenovsky, &

Kass, 2005). We believe the decreased cfPWV in those with higher aerobic fitness

in the present study to be a robust finding, as fitness was based on the Rockport

Walk test results independent of exercise and physical activity habits. Another

possible explanation is individuals who engage in regular physical activity expose

vasculature to higher levels of shear stress triggering the expression and

production of eNOS and NO, respectively. This increased vessel diameter and

37
bioavailability of NO is associated with reduced cfPWV (Gilligan et al., 1994;

Wilkinson et al., 2002).

Promotion of healthy body composition is another factor associated with

arterial stiffness. Those with higher overall body fat in the present study

demonstrated significantly higher cfPWV. Increased fat percentage is reportedly

associated with decreased distensibility of both the aorta and femoral arteries

(Ferreira et al., 2004). Additionally, increased percentage of fat/adipose tissue

produces molecules like adipokines and leptin. Specifically, leptin’s effect on

arterial stiffness seems dose dependent with percentage body fat including both

visceral and subcutaneous fat. However, adipokine levels vary independent of

body fat, but are still associated with increased arterial stiffness (Windham et al.,

2010). Visceral or perivascular fat’s ability to release adipokines into circulation

can promote vascular endothelial dysfunction, leading to arterial stiffness

(Villacorta & Chang, 2015). While body composition and fat percentage are related

to arterial stiffness, decreased fat percentage may not always result in improved

arterial stiffness. Both amount and distribution of the adipose tissue within the body

may be the larger player in arterial stiffness regulation.

4.2 Carotid-Radial and Leg Pulse Wave Velocity

Previous work on the acute effects of standing desk use show significant

reductions in carotid-radial and carotid-ankle pulse wave velocities (Bethany

Barone Gibbs et al., 2017). Inherently, the nature of pulse wave velocity recordings

38
in the periphery (i.e. arm and leg) provide an indication of the stiffness of some of

the muscular arteries. Muscular arteries aid in filtering excess pulsatility throughout

the cardiovascular system and various end-organs (Zarrinkoob et al., 2016). Given

the similarity of both groups in the crPWV and lPWV reading, pulsatility should also

be similar between groups. However, perhaps sit to stand transition, and walking

more throughout the day may only impact the arterial stiffness of the periphery

rather than the central region of the body. Sitting for more than three hours is

shown to impair superficial femoral artery flow mediated dilation (Thosar, Bielko,

Mather, Johnston, & Wallace, 2015). Chronic impairment of arterial flow can lead

to decreased NO production via decreased shear stress leading to increased

arterial stiffness (Wilkinson et al., 2002). Future work warrants investigation

whether lPWV increases during prolonged sitting and the potential relationship to

cfPWV or crPWV.

4.3 Limitations
One limitation in the present study in the lack of control of the menstrual

cycle. Menstrual cycle status is reported to influence arterial stiffness. Pulse wave

velocity measures are at the lowest during the mid-luteal phase (Madhura &

Sandhya, 2014) following ovulation, and higher during early follicular (Ounis-Skali,

Mitchell, Solomon, Solomon, & Seely, 2006). Additionally, the onset of menopause

appears to accelerate the age related increases of arterial stiffness when

compared to age-matched women who still possess their menstrual cycle (Moreau

& Hildreth, 2014). We did record menstrual cycle status and this potential limitation

39
should be minimized by the similar distribution of women in each phase/status (i.e.

early follicular, mid-luteal, perimenopause, and postmenopause). Distributions

were 41%, 23%, 6%, and 29% in seated participants and 25%, 30%, 5%, and 40%,

respectively in standing participants.

4.4 Implications
The present study did not detect any differences in PWV between seated and

standing desk participants. The current study suggests standing for at least 50%

of a normal workday may not be enough to produce an effect on arterial stiffness.

If light physical activity is achieved while using a standing desk, this may not result

in decreased arterial stiffness in younger populations. There is a suggestion that

only moderate and/or vigorous physical activity can improve arterial stiffness in

younger populations (van de Laar et al., 2010). However, older individuals can

reduce their arterial stiffness with increased light physical activity (Y. Gando et al.,

2010). In contrast to employee health, standing is reported to increase productivity

(Garrett et al., 2016; Hasegawa et al., 2001). By this measure, perhaps the

purchase of a standing desk can still be justified, independent of arterial stiffness

improvement. On the contrary, further research into the cardiovascular health

effects of standing desk use is warranted.

4.5 Future Directions

Plenty of opportunities exist in the realm of arterial stiffness and standing desk,

or alternative work stations. Cross-sectional designs have inherent draw back by

40
comparing data across individuals rather than to the same person. Future work

should initiate a standing desk intervention to examine if/when arterial stiffness is

affected from standing for most of the day after controlling for physical activity

minutes outside of work. Additionally, longitudinal studies should be built from

initial cross-sectional designs to determine if chronic standing desk can

significantly attenuate arterial stiffness during the aging process compared to the

seated desk controls.

4.6 Summary
Workplace standing desks and active workstations, in general, are in popular

demand in the office, where the effects on human health are largely unknown. The

present study comparing chronic standing desk users and chronic standing desk

users did not find any differences in cfPWV, crPWV, or lPWV. However, secondary

analysis of traditional factors of age, aerobic fitness, and fat revealed significant

differences between young and old, low and high aerobic fitness, and high and low

fat percentage. This finding further supports arterial stiffness increases with age,

and promotion of exercise and healthy body composition can work to ameliorate

age related increases in arterial stiffness. Standing for at least 50% of the workday

does not appear to directly influence arterial stiffness based on our initial cross-

sectional analysis.

41
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55
A Appendix A – Raw Data
A.1 Participant Characteristics
Table A.1. Subject Characteristics Raw Data
Part. # Age Sex VO2peak Godin Height Weight BMI Fat % SAP DAP HR

1 25 F 45.8 52 156 83.0 34.0 36.1 108 72 64

2 54 F 35.6 96 163 64.4 24.4 24.6 126 77 67
3 48 F 28.4 37 173 68.5 23.0 24.3 119 77 64
4 38 F 39.5 21 160 56.3 21.7 30.2 112 69 57
5 34 M 50.9 44 168 73.9 26.2 39.6 122 81 62
6 44 M 41.9 51 167 81.7 29.0 32.7 120 73 60
7 47 F 24.5 62 172 72.6 24.1 33.6 134 81 59
8 56 F 26.0 203 163 57.1 21.5 25.6 107 54 61
9 50 F 37.8 26 161 58.5 22.1 33.1 107 61 54
10 32 F 42.1 25 160 74.9 29.3 37.1 96 64 77
11 56 F 34.9 39 180 71.4 22.0 34.7 106 62 50
12 22 F 47.6 18 165 96.2 35.3 44.2 105 69 66
13 25 F 57.1 21 164 56.8 20.8 18.7 107 66 51
14 41 M 35.0 54 185 103 29.8 24.0 114 72 49
15 46 F 33.8 91 180 80.5 24.7 14.8 122 70 40
16 45 M 48.2 55 167 60.8 21.6 20.5 123 67 60
17 42 F 36.3 125 167 82.4 29.3 20.7 105 71 49
18 29 F 41.9 15 158 82.4 33.2 40.5 110 61 54
19 37 M 51.8 26 169 74.9 26.1 34.8 113 74 49
20 35 F 31.4 290 158 76.1 30.7 41.6 116 64 53
21 35 F 30.9 81 179 65.7 20.5 12.3 129 78 59
22 57 F 11.2 29 171 90.4 31.2 46.2 129 78 67
23 57 F 31.0 49 167 78.9 28.1 39.6 115 75 67
24 53 F 33.4 41 162 62.3 23.6 25.0 133 79 51
25 34 F 38.5 49 162 65.5 24.8 24.8 109 68 51
26 38 F 30.8 50 170 67.1 23.2 30.2 109 69 72
27 50 F 32.7 52 162 59.6 22.6 25.4 125 68 60
28 47 F 39.6 77 175 72.4 23.6 31.2 105 60 67
29 55 F 26.3 54 154 60.3 25.5 24.8 134 65 69
30 47 F 30.6 83 162 68.5 26.3 36.6 123 73 71
31 51 F 29.2 36 175 64.3 20.9 24.6 115 65 49

56
 32 63 F 27.2 30 178 101 32.1 29.5 112 67 64
33 36 F 36.3 21 160 51.2 20.0 19.7 115 63 75
34 35 F 19.8 39 185 83.6 24.6 21.0 111 64 41
35 39 M 51.3 12 170 65.5 22.6 29.2 102 60 58
36 63 F 40.0 42 155 47.2 19.6 24.9 103 66 59
37 56 F 16.2 40 168 63 22.4 31.1 110 62 59
38 31 F 35.1 55 184 79.1 23.3 15.0 117 61 53
39 27 M 55.7 28 157 71.7 28.9 31.8 110 68 64
40 61 F 32.1 45 166 84.6 30.6 44.4 109 69 54
41 42 F 37.7 43 175 76.5 33.7 33.7 108 66 49
42 62 F 28.7 25 160 70.1 21.8 28.2 120 74 66
43 32 F 41.9 17 167 60.4 22.6 26.9 115 65 82
44 52 F 11.3 72 160 57.8 27.4 39.9 135 86 72
45 50 F 23.5 45 158 80.8 32.1 42.5 127 88 69
46 61 F 14.9 56 161 69.5 26.7 37.8 102 64 64
47 27 F 42.7 47 173 55.1 18.5 18.5 115 72 93
48 42 F 38.2 15 162 58.5 22.1 25.9 93 60 68
49 28 M 45.1 26 173 79.3 26.6 23.9 123 74 75
50 37 F 46.3 54 169 62.2 21.8 24.8 103 69 56
Part. = Participant; Age = Years; VO2peak = mL/kg/min; Godin = Physical
Activity Questionnaire; Height = cm; Weight = kg; BMI = Body Mass Index
(kg/m2); SAP= Systolic Arterial Pressure (mmHg); DAP = Diastolic Arterial
Pressure (mmHg); HR = Heart Rate (beats/min)

57
A.2 Rockport Walk Test
Table A.2. Rockport Walk Test Raw Data
Participant Weight Age Sex Code Time Heart Rate VO2peak
1 183 38 0 15.23 150 30.84
2 142 50 0 15.35 126 32.71
3 151 47 0 14.25 108 39.59
4 124 55 0 18.00 108 26.32
5 163 47 0 14.42 156 30.61
6 180 51 0 14.55 144 29.21
7 159 63 0 15.10 126 27.20
8 126 25 0 13.53 150 45.82
9 129 54 0 14.32 126 35.57
10 165 48 0 15.78 138 28.41
11 157 36 0 15.27 132 36.29
12 212 35 0 18.30 150 19.76
13 125 38 0 12.80 174 39.47
14 226 39 1 11.80 108 51.26
15 177 34 1 12.78 126 50.90
16 134 63 0 12.05 120 40.00
17 182 44 1 13.68 138 41.88
18 182 56 0 18.48 132 16.18
19 165 31 0 15.18 150 35.10
20 168 47 0 17.03 138 24.53
21 145 27 1 11.47 156 55.70
22 199 57 0 27.4 132 11.2
23 174 56 0 15.36 138 26.02
24 137 61 0 15.20 108 32.11
25 144 50 0 12.59 150 37.78
26 148 32 0 14.17 132 42.14
27 131 56 0 14.23 126 34.86
28 160 42 0 13.49 144 37.72
29 133 22 0 13.18 150 47.59
30 151 62 0 14.38 138 28.66
31 142 25 0 11.72 108 57.10
32 223 41 1 14.87 144 35.02

58
 33 113 46 0 15.60 138 33.82
34 184 45 1 11.55 138 48.25
35 144 42 0 14.57 138 36.31
36 104 32 0 14.42 150 41.91
37 139 29 0 15.10 126 41.92
38 174 37 1 13.38 102 51.75
39 158 35 0 17.17 126 31.37
40 187 35 0 15.18 156 30.95
41 169 57 0 13.25 150 31.04
42 133 53 0 14.98 126 33.42
43 127 34 0 14.38 156 38.50
44 178 50 0 17.60 120 23.52
45 155 52 0 22.5 102 11.3
46 153 61 0 19.25 126 14.85
47 121 27 0 13.22 174 42.67
48 129 42 0 16.07 102 38.23
49 175 28 1 13.62 162 45.06
50 137 37 0 12.57 132 46.27
Weight = lbs; Age = years; Sex Code, Female = 0, Male = 1; Time = Minutes;
Heart Rate = beats/min; VO2peak = mL/kg/min

59
A.3 Pulse Wave Velocity Raw Data
Table A.3. Pulse Wave Velocity Raw Data
Participant cfPWV crPWV lPWV
1 8.05 9.1 6.0
2 7.25 9.3 7.8
3 6.3 7.7 8.2
4 7 7.4 7.2
5 6.65 10.4 9.8
6 7 7.1 8.6
7 9.9 8.3 10.4
8 5.55 6.3 7.7
9 6.8 7.0 11.6
10 8.7 7.9 ---
11 5.3 6.9 8.2
12 5.75 7.2 10.0
13 5.85 7.5 9.5
14 7 10.5 11.3
15 5.6 7.7 9.4
16 7.15 6.7 10.4
17 5.8 9.2 7.3
18 8.6 8.6 6.3
19 6.2 7.5 9.0
20 7.65 7.8 11.4
21 5.25 7.7 8.2
22 9.9 8.8 9.1
23 6.55 8.4 10.3
24 6.55 8.0 9.4
25 6.7 6.6 8.7
26 8.4 9.5 9.9
27 6.1 7.2 8.4
28 4.95 6.9 10.0
29 9.3 8.5 11.3
30 5.95 7.8 10.0
31 8.8 9.8 9.0
32 6.05 8.1 8.5

60
 33 6 9.0 5.6
34 5.75 7.1 8.2
35 4.7 7.1 9.6
36 6.15 6.6 9.8
37 6.95 7.0 9.2
38 5.05 7.1 ---
39 5.5 10.1 8.2
40 6.25 6.8 9.1
41 6.4 8.0 9.4
42 6.6 7.7 7.7
43 7.1 9.3 7.5
44 6.8 7.4 9.3
45 5.7 8.6 7.1
46 6.15 8.6 8.6
47 8.5 10.8 8.5
48 5.8 9.5 10.1
cfPWV = Carotid-Femoral PWV; crPWV = Carotid-Radial PWV; lPWV = Leg
PWV; --- = Missing Data Point

61
B Appendix B - Statistical Analyses

Table B.1a - Descriptive Statistics for Age

Condition N Mean Std. Deviation Std. Error Mean

age 1.00 24 41.0833 10.45037 2.13317

2.00 24 45.0000 12.18338 2.48692

Table B.1b - Independent Samples T-Test for Age

Levene's Test
for Equality of
Variances t-test for Equality of Means

95% Confidence
Interval of the
Sig. Difference
(2- Mean Std. Error
F Sig. t df tailed) Difference Difference Lower Upper

ageEqual 1.172 .285 - 46 .238 -3.91667 3.27646 - 2.67851

variances 1.195 10.51184
assumed

Equal - 44.958 .238 -3.91667 3.27646 - 2.68264

variances not 1.195 10.51597
assumed

Table B.2a – Descriptive Statistics for VO2peak

Condition N Mean Std. Deviation Std. Error Mean

VO2max 1.00 24 38.5149 8.46315 1.72753

2.00 24 34.2419 10.34880 2.11244

62
Table B.2b – Independent Samples T-Test for VO2peak
Levene's Test
for Equality of
Variances t-test for Equality of Means

95%
Confidence
Interval of the
Sig. Difference
(2- Mean Std. Error
F Sig. t df tailed) Difference Difference Lower Upper

VO2maxEqual .838 .365 1.566 46 .124 4.27301 2.72888 - 9.76596

variances 1.21993
assumed

Equal 1.566 44.257 .125 4.27301 2.72888 - 9.77181

variances not 1.22578
assumed

Table B.3a – Descriptive Statistics for Godin Leisure Time Questionnaire

Condition N Mean Std. Deviation Std. Error Mean

Godin 1.00 24 61.3333 63.44728 12.95112

2.00 24 47.3125 21.84372 4.45883

Table B.3b – Independent Sample T-Test for Godin Leisure Time Questionnaire
Levene's Test
for Equality of
Variances t-test for Equality of Means

95% Confidence
Interval of the
Sig. Mean Std. Error Difference
(2- Differenc Differenc
F Sig. t df tailed) e e Lower Upper

GodinEqual 4.840 .033 1.024 46 .311 14.02083 13.69718 - 41.59183

variances 13.55016
assumed

Equal 1.024 28.377 .315 14.02083 13.69718 - 42.06146

variances not 14.01979
assumed

63
Table B.4a – Descriptive Statistics for Height
Condition N Mean Std. Deviation Std. Error Mean

height 1.00 24 167.1042 8.44931 1.72471

2.00 24 166.9875 7.95227 1.62325

Table B.4b – Independent Sample T-Test for Height

Levene's Test
for Equality of
Variances t-test for Equality of Means

95% Confidence
Interval of the
Mean Std. Error Difference
Sig. (2- Differenc Differenc
F Sig. t df tailed) e e Lower Upper

heightEqual .027 .871 .049 46 .961 .11667 2.36845 - 4.88411

variances 4.65078
assumed

Equal .049 45.832 .961 .11667 2.36845 - 4.88458

variances not 4.65125
assumed

Table B.5a – Descriptive Statistics for Weight

Condition N Mean Std. Deviation Std. Error Mean

weight 1.00 24 69.8821 11.98086 2.44558

2.00 24 71.2458 12.73926 2.60039

64
Table B.5b – Independent Sample T-Test for Weight
Levene's Test
for Equality of
Variances t-test for Equality of Means

95% Confidence
Interval of the
Mean Std. Error Difference
Sig. (2- Differenc Differenc
F Sig. t df tailed) e e Lower Upper

weightEqual .041 .840 -.382 46 .704 -1.36375 3.56972 - 5.82172

variances 8.54922
assumed

Equal -.382 45.828 .704 -1.36375 3.56972 - 5.82245

variances not 8.54995
assumed

Table B.6a – Descriptive Statistics for BMI

Condition N Mean Std. Deviation Std. Error Mean

BMI 1.00 24 25.2583 3.98943 .81434

2.00 24 25.4792 4.62892 .94488

Table B.6b - Independent Samples T-Test for BMI

Levene's Test for
Equality of
Variances t-test for Equality of Means

95% Confidence
Interval of the
Difference
Sig. (2- Mean Std. Error
F Sig. t df tailed) Difference Difference Lower Upper

BMI Equal .264 .610 -.177 46 .860 -.22083 1.24737 - 2.29000

variances 2.73166
assumed

Equal -.177 45.019 .860 -.22083 1.24737 - 2.29147

variances not 2.73314
assumed

65
Table B.7a – Descriptive Statistics for VO2peak
Condition N Mean Std. Deviation Std. Error Mean

Overall_Fat 1.00 24 27.9792 7.82715 1.59771

2.00 24 30.1333 8.16635 1.66695

Table B.7b – Independent Samples T-Test for VO2peak

Levene's Test
for Equality of
Variances t-test for Equality of Means

95%
Confidence
Interval of the
Sig. Difference
(2- Mean Std. Error
F Sig. t df tailed) Difference Difference Lower Upper

Overall_FatEqual .348 .558 - 46 .356 -2.15417 2.30898 - 2.49357

variances .933 6.80191
assumed

Equal - 45.917 .356 -2.15417 2.30898 - 2.49380

variances not .933 6.80213
assumed

Table B.8a – Descriptive Statistics for SAP

Condition N Mean Std. Deviation Std. Error Mean

SAP 1.00 24 113.2500 8.43002 1.72077

2.00 24 115.0000 10.55009 2.15353

66
Table B.8b – Independent Samples T-Test for SAP
Levene's Test for
Equality of
Variances t-test for Equality of Means

95% Confidence
Interval of the
Difference
Sig. (2- Mean Std. Error
F Sig. t df tailed) Difference Difference Lower Upper

SAPEqual 1.964 .168 -.635 46 .529 -1.75000 2.75658 - 3.79871

variances 7.29871
assumed

Equal -.635 43.864 .529 -1.75000 2.75658 - 3.80601

variances not 7.30601
assumed

Table B.9a – Descriptive Statistics for DAP

Condition N Mean Std. Deviation Std. Error Mean

DAP 1.00 24 66.3750 5.30637 1.08316

2.00 24 71.4583 7.30681 1.49150

Table B.9b – Independent Samples T-Test for DAP

Levene's Test for
Equality of
Variances t-test for Equality of Means

95% Confidence
Interval of the
Difference
Sig. (2- Mean Std. Error
F Sig. t df tailed) Difference Difference Lower Upper

DAPEqual 2.786 .102 - 46 .008 -5.08333 1.84331 - -

variances 2.758 8.79373 1.37294
assumed

Equal - 41.981 .009 -5.08333 1.84331 - -

variances not 2.758 8.80334 1.36333
assumed

67
Table B.10a – Descriptive Statistics for HR
Condition N Mean Std. Deviation Std. Error Mean

HR 1.00 24 59.0833 10.99769 2.24489

2.00 24 62.9583 9.25710 1.88960

Table B.10b – Independent Samples T-Test for HR

Levene's Test for
Equality of
Variances t-test for Equality of Means

95% Confidence
Interval of the
Difference
Sig. (2- Mean Std. Error
F Sig. t df tailed) Difference Difference Lower Upper

HR Equal 1.631 .208 - 46 .193 -3.87500 2.93430 - 2.03144

variances 1.321 9.78144
assumed

Equal - 44.699 .193 -3.87500 2.93430 - 2.03609

variances not 1.321 9.78609
assumed

Table B.11a – Descriptive Statistics for cfPWV (Seated v. Standing)

Condition N Mean Std. Deviation Std. Error Mean

aorticPWV 1.00 24 6.5896 1.25516 .25621

2.00 24 6.8542 1.28299 .26189

68
Table B.11b – Independent Samples T-Test for cfPWV
Levene's Test
for Equality of
Variances t-test for Equality of Means

95%
Confidence
Interval of the
Difference
Sig. (2- Mean Std. Error
F Sig. t df tailed) Difference Difference Lower Upper

aorticPWVEqual .015 .902 - 46 .474 -.26458 .36637 - .47289

variances .722 1.00205
assumed

Equal - 45.978 .474 -.26458 .36637 - .47290

variances not .722 1.00206
assumed

Table B.12a – Descriptive Statistics for crPWV (Seated v. Standing)

Condition N Mean Std. Deviation Std. Error Mean

armPWV 1.00 24 7.8271 1.06066 .21651

2.00 24 8.3250 1.19209 .24334

Table B.12b – Independent Samples T-Test for crPWV

Levene's Test
for Equality of
Variances t-test for Equality of Means

95%
Confidence
Interval of the
Sig. Difference
(2- Mean Std. Error
F Sig. t df tailed) Difference Difference Lower Upper

armPWVEqual .622 .434 - 46 .133 -.49792 .32571 - .15770

variances 1.529 1.15354
assumed

Equal - 45.386 .133 -.49792 .32571 - .15794

variances not 1.529 1.15378
assumed

69
Table B.13a – Descriptive Statistics for lPWV (Seated v. Standing)
Condition N Mean Std. Deviation Std. Error Mean

legPWV 1.00 22 9.0159 1.31515 .28039

2.00 24 8.8354 1.44902 .29578

Table B.13b – Independent Samples T-Test for lPWV

Levene's Test
for Equality of
Variances t-test for Equality of Means

95%
Confidence
Interval of the
Difference
Sig. (2- Mean Std. Error
F Sig. t df tailed) Difference Difference Lower Upper

legPWVEqual .934 .339 .441 44 .661 .18049 .40931 -.64443 1.00541

variances
assumed

Equal .443 43.997 .660 .18049 .40756 -.64089 1.00188

variances not
assumed

70
Table B.14a – Median Analysis for Age
Statistic Std. Error

age Mean 43.0417 1.64569

95% Confidence Interval for Mean Lower Bound 39.7310

Upper Bound 46.3524

5% Trimmed Mean 43.0139

Median 42.0000

Variance 129.998

Std. Deviation 11.40168

Minimum 22.00

Maximum 63.00

Range 41.00

Interquartile Range 18.25

Skewness .085 .343

Kurtosis -.994 .674

Table B.15a – Descriptive Statistics for cfPWV (Younger v. Older)

AGE_GROUP N Mean Std. Deviation Std. Error Mean

aorticPWV 1.00 24 6.1875 1.06007 .21639

2.00 24 7.2562 1.24029 .25317

71
Table B.15b – Independent Samples T-Test for cfPWV
Levene's Test
for Equality of
Variances t-test for Equality of Means

95%
Confidence
Interval of the
Sig. Difference
(2- Mean Std. Error
F Sig. t df tailed) Difference Difference Lower Upper

aorticPWVEqual .926 .341 - 46 .002 -1.06875 .33305 - -

variances 3.209 1.73914 .39836
assumed

Equal - 44.911 .002 -1.06875 .33305 - -

variances not 3.209 1.73958 .39792
assumed

Table B.16a – Median Analysis for VO2peak

Statistic Std. Error

VO2max Mean 36.3784 1.38535

95% Confidence Interval for Mean Lower Bound 33.5914

Upper Bound 39.1653

5% Trimmed Mean 36.4279

Median 35.9500

Variance 92.122

Std. Deviation 9.59801

Minimum 14.85

Maximum 57.10

Range 42.25

Interquartile Range 11.40

Skewness .024 .343

Kurtosis -.109 .674

72
Table B.17a – Descriptive Statistics for cfPWV (Low v. High Fitness)
FIT_GROUP N Mean Std. Deviation Std. Error Mean

aorticPWV 1.00 24 7.3313 1.35477 .27654

2.00 24 6.1125 .80478 .16427

Table B.17b – Independent Samples T-Test for cfPWV

Levene's Test
for Equality of
Variances t-test for Equality of Means

95%
Confidence
Interval of the
Sig. Difference
(2- Mean Std. Error
F Sig. t df tailed) Difference Difference Lower Upper

aorticPWVEqual 8.224 .006 3.789 46 .000 1.21875 .32165 .57130 1.86620

variances
assumed

Equal 3.789 37.435 .001 1.21875 .32165 .56727 1.87023

variances not
assumed

73
Table B.18a – Median Analysis for Fat Percentage
Statistic Std. Error

Overall_Fat Mean 29.0563 1.15290

95% Confidence Interval for Lower Bound 26.7369

Mean
Upper Bound 31.3756

5% Trimmed Mean 29.0741

Median 28.7000

Variance 63.800

Std. Deviation 7.98751

Minimum 12.30

Maximum 44.40

Range 32.10

Interquartile Range 10.40

Skewness .076 .343

Kurtosis -.609 .674

Table B.19a – Descriptive Statistics for cfPWV (Low v. High Fat Percentage)
FAT_GROUP N Mean Std. Deviation Std. Error Mean

aorticPWV 1.00 24 6.3104 .92748 .18932

2.00 24 7.1333 1.42986 .29187

74
 Table B.19b – Independent Samples T-Test for cfPWV

Levene's Test for

Equality of
Variances t-test for Equality of Means

95% Confidence
Std. Interval of the
Mean Error Difference
Sig. (2- Differen Differen
F Sig. t df tailed) ce ce Lower Upper

aorticPEqual 5.116 .028 - 46 .022 -.82292 .34789 - -.12264

WV variances 2.365 1.52319
assumed

Equal - 39.44 .023 -.82292 .34789 - -.11949

variances not 2.365 3 1.52634
assumed

75

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