1

Table of Contents
Patient Profile

Risk Classification

Follow Up

Supplements

Special Considerations

Hypertension

Dyslipidemia

Exercise Testing

Pulmonary Function

Cardiovascular Fitness

Muscular Strength

Flexibility

Exercise Prescription

10

Goals

11

Patient Education

13

References

15

Appendix

21

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Patient Information
Karol is a 49-year-old Caucasian female who volunteered to participate in
the wellness program. She currently has a sedentary lifestyle and occupation as
a secretary. The client self-reports ankle edema, which is more, pronounced at
the end of the day and during the summer months. The client reported feeling
fatigued as well as shortness of breath with mild exertion. The client also selfreports knee, ankle, hip, foot, hand, right elbow and lower back pain all at a 5 out
of 10 scale. Over the past 5 years, Karol has been diagnosed with hypertension,
dyslipidemia and angina. However she is currently not taking any prescribed
medications for her hypertension and hypercholesterolemia.
According to the measurements taken during Karols intake, she was 1.63
meters and 127.91 kilograms, which classifies her as class III obese, because
her body mass index (BMI) is 48.40 kg/m 2. She is classified as stage 1
hypertensive because of her blood pressure reading of 140/90. Her resting heart
rate of 82 bpm, which is within normal ranges. She is classified has having
dyslipidemia because of her total cholesterol of 218 mg/dL and HDL of 25 mg/dL.
She is however on no medication for her hypertension and dyslipidemia. All of
Karols laboratory test results are confirmed values.
TABLE 1. Anthropometrics
Height
Weight
BMI

1.63 m
127.91 kg
48.40 kg/m2 *

BMI: body mass index

M: meters
Kg: kilograms
*BMI classification of class III obese according to ACSM

TABLE 2. Hemodynamics
Resting BP
Resting HR

140/90 mmHg
82 bpm

BP: blood pressure

BPM: beats per minute

HR: heart rate

TABLE 3. Blood Profile

HDL
TC
Ratio= TC/HDL

25 ml/dL
218 ml/dL
8.72

HDL: high density lipoproteins

TC: total cholesterol FBG: fasting blood glucose

Risk Classification
According to ACSM guidelines, Karol would be classified as high risk
because she is symptomatic. Karol is considered symptomatic because of her
angina, ankle edema and fatigue. According to her Framingham risk classification

3
score, she has a 10% chance of having an MI in the next 10 years. Karols other
cardiovascular risk factors are as follows: hypertension, obesity, dyslipidemia and
sedentary lifestyle.
Follow Up
Future follow-ups that should be done with Karol are a personality test and
a psychosocial survey. Karols main barrier to exercise is staying motivated. A
personality test would allow the clinician to know based on Karols personality
what would motivate her to stay active. A psychosocial survey should be done
because there is usually an underlying psychosocial issue with weight gain. The
survey would also allow the clinician to gain knowledge how supportive Karols
family is and if she has any encouragement or social support at home.
Supplements
Karol is currently not taking any prescribed medications. When a client is
taking multiple supplements there is an increased risk for interactions. However
she does take a variety of vitamins. It is important that her physician is aware of
all her supplements and daily dosage.
Karol is currently taking Mega Red/Omega 3 Krill Oil. Krill oil use as a
supplement to lower blood lipids is increasing in popularity (17). The decrease in
blood lipids is mainly attributed to the omega-3- long-chain polyunsaturated fatty
acids (n-3- PUFAs), in particular to eicosapentaenoic acid (EPA) and
docosahexaenoic acid (DHA), which is abundant in fish and seafood. The effects
of n-3 PUFAs on various risk factors of cardiovascular disease are well
documented. In large systematic reviews, consistent reductions in triglyceride
(TG) levels following consumption of n-3 PUFAs have been demonstrated as well
as increases in levels of high-density lipoprotein (HDL) cholesterol (4, 29). Krill oil
has also been found to reduce joint pain in arthritis. Multiple studies have proven
EPA and DHA to trigger secretion of anti-inflammatory prostaglandins and
interleukin-6 resulting in a decrease of C-reactive protein (CRP) and tumor
necrosis factor (TNF) (62, 58, 65). As well as its needed effects, omega-3polyunsaturated fatty acids may cause unwanted effects that require medical
attention. Karol needs to be aware of side effects such as cough, shortness of
breath irregular heartbeat, headache, tightness in her chest, and unusual
tiredness.
A magnesium supplement is also one of the supplements in Karols daily
routine. Magnesium is an essential element that is crucial to hundreds of
physiologic processes in humans. Inadequate intake of magnesium has been
linked to various adverse health outcomes, including hypertension,
cardiovascular disease, and hypercholesterolemia (2). Research has shown that
there is dose-dependent relationship between blood pressure and magnesium
supplementation. Specifically, research has found a 4.3mmHg reduction in
systolic blood pressure (SBP) and a reduction of 2.3 mmHg in diastolic blood
pressure (DBP) for each 10 mmol/day of magnesium (18, 79). A magnesium
deficiency is also associated with hyperlipidemia. Research has found that
magnesium supplementation decreases both triglycerides and low-density

4
lipprotein (LDL) (52). Along with magnesiums needed effect, it may also
causome some unwanted effects. Karol should be aware that although rare,
dizziness and shortness of breath are side effects of magnesium (2).
Karol is also currently taking Niacin daily. Niacin, a broad-spectrum lipid
regulating agent, has been shown to exert multiple favorable effects on
cholesterol metabolism, including reduction of total cholesterol, triglycerides
(TG), very low-density lipoprotein (VLDL), LDL, lipoprotein (a), and augmentation
of HDL (36). Research has shown that niacin is associated with a 15-35%
increase in HDL and 20-50% decrease in triglycerides and a 5-25% reduction in
LDL (21, 11, 48). Niacin produces large, rapid decreases in TG levels by
inhibiting release of fatty acids from adipose tissue as well as hepatic synthesis
of fatty acids and TG (36). Reduced TG synthesis is postulated to enhance
hepatic degradation of apo B, the major lipoprotein component of VLDL, thereby
reducing VLDL production and hence levels of LDL (33). The reduction in TG
availability also results in production of smaller VLDL particles, with subsequent
inhibition of small dense LDL production. Niacin may elevate HDL levels primarily
by suppressing the hepatic removal of apo A-I, which increases levels of apo A-I
as well as large apo A-I containing HDL particles (36, 34). Niacin also appears
not to inhibit hepatic removal of cholesterol esters, and so preserves the ability of
retained apo-A-I to augment reverse cholesterol transport. Niacin may also cause
unwanted side effects. Karol needs to be aware that darkening of urine, loss of
appetite, severe stomach pain and yellowing of eyes and skin, although rare may
occur when taking niacin.
Psyllium husk is another supplement that is apart of Karols daily routine.
Psyllium is a natural, soluble fiber derived from the husks of psyllium seeds. In
recent years, psyllium has been shown to lower blood cholesterol by stimulating
the conversion of cholesterol into bile acid and then increase bile acid excretion
(20). It may also decrease the intestinal absorption of cholesterol (20, 75).
Studies have found that individuals with mild to moderately high blood
cholesterol, who ate a low-fat diet and consumed 10.2 g of psyllium a day for
over eight weeks, reduced total cholesterol by 4% and LDL by 7% (3). Studies
have also found that using psyllium-enriched cereal that provided 10 to 12g of
psyllium a day reduced total cholesterol by 5% and LDL by 9% (53). Common
side effects that Karol needs to be aware of are abdominal fullness and minor
bloating.
Special Considerations
Overweight/obesity is an important modifiable risk factor for cardiovascular
disease (CVD) and other chronic diseases (63). Excess weight has been shown
to be associated with increased prevalence of hypertension and dyslipidemia. In
general, the prevalence of hypertension, high blood cholesterol, low HDL, and
high total cholesterol to HDL ratio increase with increasing BMI, as does the
combined prevalence of both hypertension and dyslipidemia. These relationships
are found among men and women in all race/ethnic groups and in most age
groups (51).

5
Hypertension
The worldwide prevalence of obesity and associated cardiometabolic
disease has increased dramatically in the past 2-3 decades, rapidly becoming
major challenged to the health care systems. Current estimates indicate that
greater than 1 billion people in the world are overweight or obese (82). In the
United States, at least 65% of adults are overweight and approximately one-third
of adults are obese with a BMI greater than 30 kg/m 2 (50). Associated with
obesity is a cascade of metabolic and cardiovascular disorders, including
hypertension, a primary mediator of obesity-induced cardiovascular disease.
Population studies show that excess weight gain predicts future development of
hypertension, and the relationship between BMI and blood pressure appears to
be nearly linear in populations throughout the world 26). Some studies suggest
that excess weight gain may account for 65-75% of human essential
hypertension (25). Moreover, clinical studies indicate that weight loss is effective
in primary prevention of hypertension and in reducing BP in most hypertensive
individuals (73). Although the importance of obesity as a major cause of essential
hypertension is well established, the physiological and molecular mechanisms
that mediate the BP effects of excess weight gain are only beginning to be
illuminated.
Notable changes, in addition to increased BP, include increases in cardiac
output and heart rate as well as activation of the sympathetic nervous system
(SNS) and renin-angiotensin-aldosterone system (RAAS). Rapid weight gain also
stimulates renal tubular sodium reabsorption, and obese subjects require higher
than normal BP to maintain balance between intake and renal excretion of
sodium, indicating impaired renal pressure natriuresis (26). Three factors are
especially important in increasing renal sodium reabsorption, impairing pressure
natriuresis, and causing the initial rise in BP during rapid weight gain: 1)
increased SNS activity, 2) activation of the RAAS, and 3) physical compression of
the kidneys by fat accumulation within and around the kidneys and by increased
abdominal pressure due to accumulation of excess visceral fat. These
mechanisms are closely interrelated and interact to raise BP in obese subjects.
For example, SNS activation and physical compression of the kidneys both
cause activation of the RAAS, and pharmacological blockade of either the RAAS
or the SNS attenuates obesity-induced hypertension by at least 5060% (15, 27).
When obesity is prolonged over many years, however, renal injury may
exacerbate hypertension and make it more difficult to control with
antihypertensive drugs (28).
Several observations indicate that increased SNS activity contributes to
obesity hypertension (26, 27). 1) SNS activity, especially renal sympathetic nerve
activity (RSNA), is increased in obese subjects; 2) pharmacological blockade of
adrenergic activity lowers BP to a greater extent in obese compared with lean
subjects; and 3) denervation of the kidneys markedly attenuates sodium retention
and hypertension in obese experimental animals. In obese hypertensive patients,
combined - and -adrenergic blockade for 1 month reduced ambulatory BP
significantly more than in lean essential hypertensive patients (80). These

6
findings suggest that increased adrenergic activity contributes to the
development and maintenance of obesity hypertension in humans (26, 27).
Obesity does not cause mass activation of the SNS. Instead, increased
SNS activity in various tissues is modest and appears to be differentially
controlled in obesity. For example, cardiac SNS activity is normal or reduced in
obese compared with lean subjects, and increased heart rate is due mainly to
decreased parasympathetic activity rather than increased SNS activity (28). In
contrast, SNS activity is increased in the kidneys and skeletal muscles of obese
hypertensive subjects (15, 27). However, obesity-induced increases in SNS
activity are mild and not sufficient to cause vasoconstriction of the kidneys or
other organs, although they do stimulate renin secretion and increase renal
sodium reabsorption (28, 15, 27).
A promising mediator of obesity-induced SNS activation is leptin, a peptide
hormone secreted by adipocytes in proportion to the degree of adiposity. Leptin
crosses the blood-brain barrier (BBB) via a saturable receptor-mediated transport
system (9). The short form of the leptin receptor (LRa), highly expressed in brain
microvessels, is believed to be one of the important transporters (9). However,
other factors modulate leptin transport across the BBB, and in obesity, the
efficiency of leptin uptake by the brain is reduced (9). High levels of triglycerides,
which inhibit BBB leptin transport, may at least partially explain this reduced
efficiency of leptin transport in obesity, but the mechanisms involved are still
uncertain (9).
Leptin binds to its receptors in various regions of the central nervous system
(CNS), including the hypothalamus and brainstem, where it activates neural
pathways that decrease appetite and increase SNS activity and energy
expenditure (27,64). Evidence that leptin is a powerful controller of energy
balance comes from studies in mice and humans that demonstrate that missense
mutations of the leptin gene or leptin receptor (LR) cause extreme early-onset
obesity (23). However, mutations of the leptin gene in humans are rare, and there
is little evidence that LR mutations contribute significantly to excess weight gain
in most obese people. Yet, obesity may cause resistance to the anorexic effects
of leptin, perhaps analogous to obesity-induced resistance to the metabolic
effects of insulin (23). To the extent that resistance to the anorexic effects of
leptin occurs in obese subjects, impaired feedback regulation of appetite could
perpetuate or amplify weight gain.
Dyslipidemia
The hallmark of dyslipidemia in obesity is elevated fasting and
postprandial triglyceride (TG) in combination with the majority of small dense LDL
and low HDL (59, 38). Hypertriglyceridemia may be the major cause of the other
lipid abnormalities since it will lead to delayed clearance of the TG-rich
lipoproteins and formation of small dense LDL (10,31).
Lipolysis of TG-rich lipoproteins is impaired in obesity by reduced mRNA
expression levels of lipoprotein lipase (LPL) in adipose tissue reductions in LPL
activity in skeletal muscle and competition for lipolysis between VLDL and
chylomicrons (13, 40). Increased postprandial lipidemia leads to elevated levels
of FFA, resulting in detachment of LPL from its endothelial surface (61, 37). LPL

7
may remain attached to VLDL contributing to further TG depletion. The exchange
of TG from these remnants for cholesterol-esters from HDL, ultimately leads to
the formation of small dense LDL (10,31). In the presence of
hypertriglyceridemia, the cholesterol-ester content of LDL decreases, whereas
the TG content of LDL increases. However, the increased TG content within the
LDL is hydrolyzed by hepatic lipase, which leads to the formation of small, dense
LDL particles. The development of small dense LDL in obesity is mainly due to
increased TG concentrations and does not depend on total body fat mass (74).
Small dense LDL are relatively slowly metabolized with a five day residence time,
which enhances its atherogenicity (54).
Remnants of chylomicrons and VLDL are involved in the development of
atherosclerosis (12). Several investigators have demonstrated an association
between TG-rich lipoproteins and remnant cholesterol levels with the presence of
coronary, cerebral, and peripheral atherosclerosis (69, 68, 59). In addition to a
direct detrimental effect by chylomicron remnants on vessels, impaired
endothelial function after an oral fat load and after infusion of artificial TG-rich
lipoproteins have been described (40, 76, 45). This phenomenon may take place
by elevated levels of FFA, which are generated by the action of LPL mediated
lipolysis (72). Other mechanisms of remnant-mediated atherogenesis, which may
play a role in obesity, comprise the postprandial activation of leukocytes,
generation of oxidative stress and production of cytokines (40, 1,14).
HDL metabolism is also strongly affected by obesity because of the
increased number of remnants of chylomicrons and VLDL together with impaired
lipolysis. The increased number of TG-rich lipoproteins results in increased
cholesterylester transfer protein (CETP) activity, which exchanges
cholesterolesters from HDL for TG from VLDL and LDL (16). Moreover, lipolysis
of these TG-rich HDL occurs by hepatic lipase resulting in small HDL with a
reduced affinity for apolipoprotein A1 (apo A-I), which leads to dissociation of apo
A-I from HDL. This will ultimately lead to lower levels of HDL-C and a reduction in
circulating HDL particles with impairment of reversed cholesterol transport (16).
In summary, excess weight gain is a major cause of hypertension and
dyslipidemia. Activation of the SNS plays a key role in increasing renal sodium
reabsorption, impairing pressure natriuresis, and raising BP in obese subjects. As
well as, higher levels of triglycerides lead to a decrease in clearance of LDL and
particles and a decrease in HDL.
Exercise Testing
Before pre-exercise testing was performed, the client wore a Metria
lifestyle patch for 1 full week to assess her baseline physical activity level, steps
per day, and sleep duration. Based on information gathered during the initial
interview and clients stated goals, exercise tests where chosen to assess her
physical fitness level.
Pulmonary Function Test
Obesity can cause various deleterious effects to respiratory function, such
as alterations in respiratory mechanisms, decrease in respiratory muscle strength

8
and endurance, decrease in pulmonary gas exchange, lower control of breathing,
and limitations in pulmonary function tests and exercise capacity (22, 41, 42, 44,
67). These changes in lung function are caused by extra adipose tissue in the
chest wall and abdominal cavity, compressing the thoracic cage, diaphragm, and
lungs. The consequences are a decrease in diaphragm displacement, a
decrease in lung and chest wall compliance, and an increase in elastic recoil,
resulting in a decrease in lung volumes and an overload of inspiratory muscles
(41). These changes are worsened by an increase in the BMI (35). This may be
the cause of Karols shortness of breath and constant cough. To rule our
respiratory and lung function Karol underwent a pulmonary function test.
The evaluation of pulmonary function was performed by spirometry.
Spirometry is considered the gold standard for pulmonary testing. Spirometric
testing has been shown to be valid, reliable and reproducible (39). However
spirometric testing requires total cooperation and forced maximal efforts, which
are needed for an accurate test result, and this may be difficult to obtain (39).
The evaluated parameters were forced vital capacity (FVC), forced expiratory
volume in one second (FEV1) and the FEV1/FVC ratio. Karol was given one
practice trial and three recorded trials. Karols best trial was used to compare to
her predicted values. Karols predicted values were as follows: 3.16 L, 2.57 L,
84%. Karols values of her best trial were, 3.18 L, 2.8 L, 88%, which excedded
her predicted values. Because Karol exceeded her predicted values, it can be
concluded that Karols respiratory function is above average. Karols respiratory
function was not reassessed at the mid-point or during the post-testing because
she was already above average.
Cardiovascular Fitness
Evidence-based research has shown that cardiorespiratory fitness (CRF)
determined by measured oxygen uptake, is an independent predictor of
cardiovascular events and death in women (24,1,7). Maximal oxygen
consumption (VO2max) is considered a gold standard for assessing CRF and is
typically ascertained using a symptom-limited graded exercise test or cycle
ergometer exercise test. However, VO2max protocols are not always feasible or
appropriate. As a result, alternative methods have been developed. Submaximal
protocols require individuals to exert a lower effort and then utilize prediction
equations that are based on measured parameters, such as, age, gender, and
exercise heart rate, to estimate CRF. Ebbeling and colleagues developed a
single stage submaximal treadmill walking (EbbTM) protocol to estimate
VO2max. The EbbTM protocol allows participants to self-select the walking speed
until they reach a pre-determined heart rate (50-70% of age predicted maximum
(30). This differs from other submaximal treadmill protocols that require predetermined walking speeds, which do not account for individuals differences in
gait, potentially reducing participants comfort level. Furthermore, the EbbTM is a
single-stage protocol (30). Overall, the EbbTM has high test-retest reliability and
validity with VO2max for middle-aged women (30). Karols fitness and comfort
levels as well as the reliability and validity of the test were all factors considered
when choosing the proper protocol.

9
Karols cardiorespiratory fitness was assessed during both the pre- and
post-testing appointments. During the pre-test Karol reached 50% of her agepredicted heart rate at a speed of 2.6 mph. Based on the prediction equation
Karols VO2max was calculated to be 27.38 ml/kg/min, which is classified as very
poor. During the post-testing Karol reached 50% of her age-predicted heart rate
at a speed of 3.2 mph. Based on the prediction equation, Karols VO 2max for the
post-testing was 31.54 ml/kg/min, which is classified as poor. Karols
cardiorespiratory fitness improved overall. Factors that could have also helped to
increase her cardiorespiratory fitness level are comfort level and motivation.
Karol has stated that she does not feel comfortable exercising in front of others.
When pre-testing was being administered there were at least 4 other individuals
in the gym, this could have made her nervous and uncomfortable which would
have lead her to reach her predicted heart rate quicker. During the post-testing
Karol was the only client in the gym, which could have made her more
comfortable to exert a greater effort. During post-testing there was also two
clinicians in the room providing encouragement, whereas during pre-testing there
was only one clinician.
Muscular Fitness
Karol expressed interest in toning her upper body, so upper body strength
was assessed. Reliable and valid evaluation of hand strength can provide an
objective index of general upper body strength (60). The power grip is the result
of forceful flexion of all finger joints with the maximum voluntary force that the
subject is able to exert under normal biokinetic conditions. The synergistic action
of flexor and extensor muscles and the interplay of muscle groups is an important
factor in the strength of the resulting grip. People are generally limited by their
strength when exerting force. Strength is a muscles capacity to exert maximal
effort or resist maximal opposing force. Grip strength is correlated with the
strength of the upper extremity and general strength of the body and therefore is
often adopted in clinical practice as an objective measure of upper extremity
function (66, 5). Overall, the handgrip test was chosen for Karol because of its
generalizability, reliability and validity to upper body strength.
Karols handgrip strength was assessed during both the pre- and posttesting appointments. During the pre-test Karols handgrip was 30 kg for both her
right and left hand. For a 49-year-old woman, 30 kg is considered average.
During the post-testing Karols handgrip actually declined. Karols handgrip test
results were 28 kg for both her right and left hand during the post-testing.
However, 28 kg is still classified as average for a 49-year-old woman. Overall,
Karols handgrip/upper body strength stayed relatively the same. Handgrip is
influenced by many factors such as, sleep, nutrition and time of day. Any of these
factors could have influenced Karols handgrip strength during post-testing to
give her a lower score.
Flexibility
Karols sedentary job as a secretary requires her to be sitting at a desk for
most hours of the day. As Karol is sitting in her office chair, her hamstring
muscles are inactive and are held at a shortened length. Over time the
hamstrings will stay at the shortened length, ultimately decreasing Karols range

10
of motion (78). Karol also complains of lower back pain and this could be due to
her shortened hamstrings. Shortened hamstrings are associated with lower back
pain because the tight hamstrings stop the hips from flexing during forward
bending; this forces the lower back to bend beyond its strongest middle range
(78). The modified back saver sit-and-reach (MBSSR) was the protocol chosen
for Karol. The MBSSR was chosen because it is a reliable test for hamstring
flexibility in women (r=0.23-0.54). With the MBSSR, one leg is assessed at a time
and Karol will be able to do the test sitting on a bench/ mat table instead of fully
getting on the floor (32).
Karols hamstring flexibility was assessed during pre-, mid- and posttesting appointments. Karol was given one practice trial and three recorded trials
for each leg. During the pre-testing Karol was able to reach 8 inches on her left
leg and 9 inches on her right leg. These results classified her flexibility as
needing improvement. During the midpoint testing Karol reached 10 inches on
her left leg and 9 inches on her right leg. These results classified her flexibility
as fair. During the post-testing Karol was able to reach 10 inches for her left
leg and 10 inches on her right leg. These results classified Karols hamstring
flexibility as fair. Overall, Karols hamstring flexibility increased by 14%. Karol was
noticing the results and this seemed to keep her motivated to do the flexibility
exercises.
Exercise Prescription
Based on Karols exercise test results it was determined that
cardiovascular and flexibility should be the focus of her exercise prescription.
Results from the lifestyle patch were used to set Karols goals for steps/week.
Karol was also given a BodyMedia armband to wear for at least 23 hours
throughout the exercise program. The armband recorded steps/day, calories
consumed, calories burned, physical activity, and sleep duration.
Karols initial exercise prescription consisted of her ambulating on the
treadmill at 40% of heart rate reserve (HRR) three days per week. Treadmill was
chosen as the mode of exercise because Karol had access to a treadmill and
research supported treadmill walking as a safe mode of exercise for obese
women. Research has found that walking at a relatively slow speed (~1.67 mph)
up a moderate incline (6-7) helps reduce the risk of musculoskeletal
injury/pathological disease while providing cardiovascular stimulus in obese
adults (19, 43). However, Karol was not compliant with walking on the treadmill
and expressed interest in resistance training. Karols exercise program was
adjusted to include circuit training 3 days per week where Karol would step for 1
minute and then do 1 minute of resistance training instead of walking on the
treadmill. Research found that combined training (aerobic training plus muscular
resistance training) decreased body fat and increased lean body mass as well as
increase heart and muscle strength in middle-aged obese women (57, 70).
Research also found that combined training is more effective in reducing visceral
fat than food intake restriction (56). The resistance training exercises included:
frontal raise, lateral raise, two-handed triceps extension, and dumbbell side bend.
Frontal and lateral raise were given to work Karols front and outer portion of her

11
shoulders. Triceps extension was given to work on the back of Karols arms
where she has most of her muscle wasting. The dumbbell side bend was given to
work on Karols obliques. After the circuit was implemented and a behavioral
contract was signed, compliance was no longer an issue. Flexibility exercises for
Karols hamstrings and quadriceps as well as pelvic tilts were also included in her
exercise program. Karol was instructed to perform the flexibility and pelvic tilt
exercises 5-7 days per week. Karol was given the pelvic tilts to help stabilize her
core and reduce her lower back pain (46). Karols exercise prescription also
included a daily step goal. From the lifestyle patch, it was determined that Karol
was averaging around 7,000 steps per day. Karols initial goal was to accomplish
7,000 steps per day for the first week.
Throughout the program Karols exercise and daily step goals were
progressed. Exercise intensity for the circuit was increased by 5% every other
week. On the off week, when exercise intensity was not increased, duration of
resistance training was decreased to 30 seconds. Karols step goal was
increased by 10% every week. The last two weeks of the program, Karols
compliance became an issue, because she was becoming busy and more
stressed at work. She still did her pelvic tilt and flexibility exercises but did not do
the circuit training. Therefore, for Karols 6-week summer exercise program the
starting point is where she became non-compliant. Her summer exercise
program is then progressed in the same fashion as her 10-week program. During
the summer exercise prescription Karol will reach 15,000 steps/day. Once 15,000
steps/day is reached the goal will become to maintain the 15,000 steps.
Goals
TABLE 4. Goal Setting
Pre
Goals
Weight
282 lbs
W.C.
46 inches
VO2max
27.39 ml/kg/min
8.75 inches,
MBSSR
9.25 inches
Calories/day
PA
Leisure PA

1,889 calories
Sedentary

18-Mar
280 lbs
N/A
N/A
10.25 inches,
9.75 inches
1,739
calories
90 min/week

7,000 steps

7,500 steps

W.C.: Waist Circumference

MBSSR: Modified Back Saver Sit-And-Reach

Post
283 lbs
46.5 inches
31.53 ml/kg/min
10.5 inches,
10 inches

262 lbs
42 inchers
4.14 ml/kg/min
1.75 inches,
.75 inch

1,739 calories
90 min/week
11,313
steps/day

Cut out 300 calories

Increase PA 150 min/week
10,000 steps/day

12
Based on Karols initial interview, lifestyle patch and pre-test results
goals were made, which can be seen in Table 4. A modest weight loss of 2
pounds per week is deemed safe by research (77). So overall, Karols goal was
to lose 20 pounds within the 10-week exercise program. To help with the weight
loss Karol was also going to cut out 300 calories from her diet and burn 200
calories with exercise, for a total of 500 calories less per day. This level of
calories reduction is associated with an average weight loss of 1 pound (47). It
was also calculated that Karols basal metabolic rate was 1,889 calories/day, so
Karol needs to be consuming 1,739 calories/day to help with her weight loss (8).
A 10-pound decrease would equate to losing 4 inches off of her waist, so a goal
of 42 inches was set. Weight loss goals were however not met at the end of the
10-week program. Next time, nutrition would be more of a focus point. A goal was
also set to increase Karols steps/day to 10,000 steps, which she met and
exceeded. General goals were also made to increase Karols cardiovascular
fitness and flexibility, which were also accomplished. Karols goals were modified
for her summer program. Karols summer goals for weight loss, physical activity
and flexibility can be seen below in Table 5, 6 and 7. One of Karols goals for the
Summer is to tone her upper body. Based on my clients physical activity level
and body type she may not experience a significant change within the 6-week
program to require a SMART goal involving upper body circumference
measurements. However, baseline upper body measurements should be done
for future comparisons. 6-week measurements will be based on adherence and
weight loss. The overall goal will be to build her confidence, overall strength and
her ability to do everyday tasks.
TABLE 5. Summer Weight Loss Goal
S
Lose 10 pounds by the end of the 6-week program by increasing
physical activity and reducing caloric intake.
M
Lose 1.5 lbs per week to accumulate a total weight loss of 10 lbs.
A
R
T

Reduce caloric intake by 300 calories and burn 200 calories through
physical.
Make conscious food decisions at every meal and reduce sedentary
time.
Achieve goal weight of 273 lbs. by the end of the 6-week exercise
program.

13

TABLE 6. Physical Activity Goal

S
Perform 30 min of moderate intensity exercise 3 days per week.
M
A
R
T

Track total time of moderate intensity exercise as well as number of

circuits completed.
Moderate intensity exercise can be accumulated through circuit or
household chores.
Accumulate 30 minutes of moderate exercise through circuit,
household chores or being active with family.
At the end of the 6-week program be able to withstand 30 minutes
of moderate intensity exercise continuously.

TABLE 7. Flexibility Goal

S
Improve flexibility by stretching, focusing on lower body 5-7 days per
week.
M
Weekly self-assessments may be done to assess improvements with
flexibility. My client can compare how much farther she can reach her
fingers past her toes each week.
A
Accumulate 60 seconds per exercise 5-7 days per week.
R
T

Patient

Can do stretches in the morning, at work or in the evening. Stretches

can be done any where there is a wall and chair available. Take short
breaks during work to get up to walk and stretch throughout the day.
Progressively hold stretch longer to hold a stretch for 60 seconds
continuously. However, do not hold stretch longer than 60 seconds.
Education
Throughout the exercise program various patient education brochures
were given to Karol. Karol was provided with brochures regarding, time
management, stress management and the importance of sleep. Patient
education was based on Karols initial interview, Metria lifestyle patch and
BodyMedia armband.
In the initial interview, Karol identified time as a barrier for exercise. Karol
was provided a brochure on time management skills (Appendix A). The brochure
included short- and long-term tips for managing time as well as three different
websites for further resources. The websites included a time management guide,
seminars, books and articles about time management and a schedule template,
so Karol could plan out her day. The patient education could have been tailored
to Karol more. The brochure could have included tips to help her manage her
time during work and also in her personal life. The brochure could have also
addressed the effects of getting involved in too many projects and the importance
of knowing when to say no. Not managing her time wisely could be leading to her
stress.
During the initial interview, Karol identified her stress level as a 6 out of
10. Karols stress could be a contributor to her weight. During prolonged stress

14
the body will release excess cortisol, a hormone critical in managing fat storage
and energy use in the body. Cortisol also is known to increase appetite (6). When
individuals are stressed they tend to reach for fattening comfort foods, such as
muffins, pastries, doughnuts and cookies. These foods are laden with
carbohydrates. Individuals choose the foods loaded with carbohydrates because
carbohydrates raise the bodys serotonin levels, which are the bodys feel-good
chemical (81). This is why it is important for Karol to learn how to manage her
time and reduce her stress levels. The brochure that was provided for Karol
contained long-term effects of stress on the body as well as short- and long-term
techniques to deal with stress (Appendix B). The patient education could have
been enhanced and more useful if there was an app that helped her
manage/reduce her stress. Karols stress levels may also be affecting her sleep.
Based on her BodyMedia armband, Karol was getting roughly 5 hours a
sleep a night. Multiple pathways likely mediate the relationship between sleep
and obesity. An upregulation of the activity of orexin neurons and changes in
appetite-regulating hormones may affect food intake. It has been previously
shown that ghrelin, a hormone promoting hunger, increases with sleep restriction,
whereas leptin, a hormone contributing to satiety perception, decreases (49, 55,
71). Additionally, sleep loss could affect energy balance by decreasing both
exercise and nonexercise energy expenditure. Leptin by itself increases energy
expenditure; therefore, changes in leptin after sleep deprivation would affect both
caloric intake and energy expenditure. Energy expenditure in sleep loss has
been poorly studied, but it is conceivable that sleepiness and fatigue increase
sedentary behavior and therefore decrease exercise-related energy expenditure
under real life conditions (49,55,71). Based on the importance of sleep, Karol
was provided a brochure for sleep hygiene (Appendix C). The brochure
explained short- and long-term effects of sleep deprivation on the body. The
brochure also provided tips to getting a good night sleep as well as instructions
for a sleep app. The app can track sleep movement, noise and sleep cycle. This
app will provide Karol another source for her to see how long she is sleeping and
the quality of sleep she is getting each night.

15

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