Lai Byron thesis 2014

1CALIFORNIA STATE UNIVERSITY, NORTHRIDGE
An Investigation of the Post-Exercise Hypotensive Response Following an Acute Bout of
Aquatic and Overground Treadmill Walking in People Post-Stroke
A thesis submitted in partial fulfillment of the requirements
For the degree of Master of Science in Kinesiology
By
Byron Lai
May 2014
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The thesis of Byron Lai is approved:
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Professor Mai Narasaki-Jara, MS
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Date
_________________________________________
Dr. Vrongistinos Konstantinos, PhD
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Date
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Dr. Taeyou Jung, PhD, ATC, CAPE, Chair
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Date
California State University, Northridge
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DEDICATION
To my parents Simon and Laurie
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ACKNOWLEDGEMENTS
I would like to acknowledge Dr. Taeyou Jung, Mai Narasaki-Jara, and Dr.
Konstantinos Vrongistinos for giving me a direction and purpose in life, whilst allowing
me to grow as a professional in the field of Adapted Physical Activity. I would also like
to thank my father for supporting me through every step of my journey. Without the aid
of these individuals none of this would be possible.
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TABLE OF CONTENTS
Signature page
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Dedication
iii
Acknowledgements
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List of Tables
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List of Figures
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Abstract
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Section 1: Introduction
1
Literature Review
4
Stroke
5
Hypertension in Recurrent Stroke
9
Aerobic Exercise and Post-Exercise Hypotension in Health Adults
12
Treadmill Exercise
16
Aquatic Exercise and Post-Exercise Hypotension
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Section 2: Methods
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Participants
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Instrumentation
21
Procedure
23
Analysis
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Section 3: Results
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Section 4: Discussion
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Resting Blood Pressure
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Matched Intensity
35
Post-Exercise Hypotension
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Limitations and Future Studies
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Conclusion
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References
40
Appendix A: Informed Consent
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Appendix B: Fugl-Meyer Lower Extremity Assessment
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Appendix C: Raw Data
60
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LIST OF TABLES
Table 1
Participant Characteristics
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Table 2
Oxygen Consumption During Exercise
30
Table 3
Blood Pressure
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Table 4
Mixed Model Anova Diastolic Blood Pressure Post-Exercise
61
Table 5
Mixed Model Anova Systolic Blood Pressure Post-Exercise
62
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LIST OF FIGURES
Figure 1
Hourly Systolic Blood Pressure Post-Exercise
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Figure 2
Hourly Diastolic Blood Pressure Post-Exercise
33
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ABSTRACT
An Investigation of the Post-Exercise Hypotensive Response Following an Acute Bout of
Aquatic and Overground Treadmill Walking in People Post-Stroke
By
Byron Lai
Master of Science in Kinesiology
BACKGROUND: While exercise is a universal recommendation for long term
prevention and/or maintenance of hypertension, less is understood about the immediate
effects of blood pressure (BP) following a single bout of exercise, otherwise known as
post-exercise hypotension. The purpose of this study is to investigate the effects of a
single-bout of ATW and OTW on the magnitude and duration of post-exercise
ambulatory BP in people post-stroke.
METHODS: 7 people post-stroke participated in a cross-sectional comparative study.
Ambulatory BP was monitored for up to eight hours after a bout of aquatic treadmill
walking (ATW) and overground treadmill walking (OTW), performed on separate days.
Mean systolic and diastolic BP values were compared between both exercise conditions
and a day when no exercise was performed (control).
RESULTS: Mean ambulatory systolic BP following ATW was reduced by 5% compared
to the control day (p < 0.01) and displayed a systematic trend in reduced BP compared to
OTW (p = 0.051). Mean ambulatory diastolic BP values following OTW and ATW were
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reduced by 6% and 7% respectively, compared to the control day (p <0.01). ATW
demonstrated a reduction of 6% in mean systolic BP at the eighth hour of exercise
compared to baseline (p < 0.05).
CONCLUSION: This study demonstrated that people post-stroke are able to lower their
BP, under free living conditions, for up to nine hours following a single bout of ATW. In
addition, ATW may promote nighttime dipping of systolic BP in people post-stroke.
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Section 1: Introduction
Recurrent strokes are a leading cause of death in individuals post-stroke and responsible
for approximately one-fourth of all annual stroke cases in the United States (Go et al.,
2013). While hypertension is established as a key indicator of a first stroke occurrence, it
has recently been identified as a high risk factor for recurrent stroke (Brown, Lisabeth,
Roychoudhury, Ye, & Morgenstern, 2005; Furie et al., 2011). In addition, hypertension is
associated with a shorter life expectancy and an elevated risk of cardiovascular disease
(Arima & Chalmers, 2011). Current guidelines recommend that BP should be lowered to
less than 140/90 mmHg to reduce recurrent stroke risk (Chobanian et al., 2003; Mancia et
al., 2007). Arima et al. (Arima & Chalmers, 2011) suggest that all persons post-stroke
should receive blood pressure (BP)-reduction treatments irrespective of their baseline
level of BP.
Prevention of hypertension after an acute stroke is the most effective approach to
reduce recurrent stroke risk (Patarroyo & Anderson, 2012). Rodger et al. (1996) have
reported that a reduction of either systolic BP by ten mmHg or diastolic BP by five
mmHg can reduce the risk of a recurrent stroke by 38% and 28%, respectively. Exercise
is often recommended as a means to manage hypertension. It has been reported that
exercise can also reduce BP for an immediate duration following a single bout of
exercise, a concept known as post-exercise hypotension (PEH) (Kenney & Seals, 1993).
Limited studies have documented PEH in people post-stroke.
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Treadmill exercise is commonly used as an effective method to elicit a PEH
response in adults with hypertension (Gomes Anunciacao & Doederlein Polito, 2011).
Previous studies showed that both systolic and diastolic BP can be reduced after treadmill
exercise (Quinn, 2000; Wallace, Bogle, King, Krasnoff, & Jastremski, 1999). These
studies have also suggested that these reductions of BP after exercise can be sustained for
up to 4-11 hours. The precise duration and intensity of exercise to facilitate a PEH
response of significant magnitude and duration remains unclear. Some studies have
suggested that the most prominent PEH response follows moderate-to-high intensity
exercise (at the level of 40-70% peak oxygen consumption) with durations of 15-30
minutes (Guidry et al., 2006; Quinn, 2000). This intensity of treadmill exercise may be
beneficial for people post-stroke who aim to lower their levels of BP. The treadmill is
commonly used to promote cardiovascular fitness and gait rehabilitation in people poststroke. It may be particularly appealing to people post-stroke with hypertension as
treadmill walking can help manage hypertension while addressing other goals of
rehabilitation.
Aquatic treadmill walking (ATW) may provide clinicians with an alternative
mode of exercise to manage hypertension in individuals post-stroke. Compared to
overground treadmill walking (OTW), ATW has been reported to reduce post-exercise
BP in greater magnitude in healthy adults with normotension (Rodriguez et al., 2011).
Unfortunately, no studies have examined post-exercise ambulatory BP in persons with
stroke. The purpose of this study is to investigate the effects of a single-bout of ATW and
OTW on the magnitude and duration of post-exercise ambulatory BP in people poststroke. This information may help clinicians and researchers advance their understanding
2
of BP patterns following aerobic exercise in people post-stroke and eventually develop
effective strategies of managing hypertension.
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Literature Review
Arterial hypertension, otherwise known as high BP, is a leading cause of death in
developed countries and increases an individuals’ risk for cardiovascular events including
stroke. Nearly 26% of the adult population in the United States is hypertensive
(Association, 2012). Hypertension is characterized by elevated pressure on the walls of
the arteries which causes the heart to work harder to pump blood through the body.
Hypertension is regarded as a resting BP of greater than 140 mmHg systolic and 90
mmHg diastolic (Huntzinger, 2008). Lowering BP is the primary means of preventing
coronary artery disease for people with high blood pressure (Huntzinger, 2008).
Hypertension often has no perceivable symptoms or warning signs. Thus it is important to
regularly monitor BP.
Ambulatory BP monitoring (ABPM) is the assessment of BP under normal living
conditions. ABPM has been established as an important measure for future occurrences of
stroke or cardiovascular events (Bastos, Bertoquini, Silva, & Polonia, 2006; CastillaGuerra, Fernandez-Moreno Mdel, Espino-Montoro, & Lopez-Chozas, 2009; Lip et al.,
1997). ABPM allows clinicians to measure circadian BP rhythms, declines in BP at later
hours of the day. This also allows clinicians to measure BP dipping, the difference in
nighttime and the following daytime blood pressure values. Lack of a circadian BP
rhythm can be associated with future occurrence of stroke and coronary events in people
with hypertension (Bastos et al., 2006). ABPM has also been recognized as a powerful
tool for the prediction of cardiovascular incidents in the stroke population (Jain,
Namboodri, Kumari, & Prabhakar, 2004b).
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Stroke
Definition and Characteristics
Stroke is defined as a cerebrovascular event, caused by abnormalities in cerebral
blood flow that can result in death of brain tissue ("National Institute of Neurological
Disorders and Stroke. Stroke: Hope Through Research," 2012). Stroke is a leading
disability in the United States and can result in acute coma, syncope, chronic
physiological and neurological impairments, and even death.
The level of physiological and neurological impairment following a stroke varies with
the location, severity, and duration of cerebral damage (Bowman & Giddings, 2003).
Following a stroke, many symptoms may occur simultaneously that affect locomotor,
visual, visuospatial, verbal, or sensory function skills (Durstine, Moore, Painter, &
Roberts, 2009). Hemiparesis is a common physical deficit following a stroke, which
causes partial or complete paralysis of one side of the body. Hemiparesis occurs from
damage to the cerebellum, which can result in a reduced number of motor units to
perform movement ("National Institute of Neurological Disorders and Stroke. Stroke:
Hope Through Research," 2012). Muscle spasticity, stiffness or rigidity of the muscle, is
also a common impairment among people post-stroke and is closely related to
hemiparesis. Muscle spasticity is caused by a speed dependent hyper-active muscle
stretch reflex, which may restrict locomotion. Muscle spasticity is not directly related to
the severity of post-stroke symptoms (Sommerfeld, Eek, Svensson, Holmqvist, & von
Arbin, 2004). Hemiparesis hinders the gait pattern of people post stroke, which increases
the energy cost of walking (Chen, Patten, Kothari, & Zajac, 2005). Inefficient gait
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patterns in the stroke population limit community ambulation. However, even with
relatively efficient gait, it is estimated that one-third of people post-stroke are not able to
walk independently outside of their home (Lord, McPherson, McNaughton, Rochester, &
Weatherall, 2004). If individuals post-stroke do not have the ability to walk
independently, only 23% of them are able to recover independence through rehabilitation
(Jorgensen et al., 1995). Consequently, gait restoration is a primary focus during stroke
rehabilitation.
Classifications
The two main categories of strokes are ischemic and hemorrhagic strokes: a blockage
or rupture of blood vessels to the brain ("National Institute of Neurological Disorders and
Stroke. Stroke: Hope Through Research," 2012). Approximately 80% of the stroke
incidences worldwide are ischemic stroke and 20% are hemorrhagic stroke (Donnan,
Fisher, Macleod, & Davis, 2008). Ischemic strokes umbrella three different sub-types of
stroke occurrences: thrombosis, embolism, and stenosis (Judd, 2005). A thrombotic stroke
occurs when a formed blood clot attached to the walls of an artery grows large enough to
block blood flow. When a large blood clot detaches from a wall and travels through
circulation, it may become wedged into a cerebral artery, which is called an embolic
stroke. Stenosis is an abnormal narrowing of blood vessels which can distort blood flow
to the brain. Stenosis generally occurs through the formation of plaque on the walls of the
arteries that can hinder blood flow. Moreover, abnormal blood flow to the brain can cause
minor stroke like symptoms. A transient ischemic attack is a relatively short episode of
neurological malfunction caused by lack of cerebral blood flow that does not result in
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tissue death (acute infarction). Ischemia (lack of cerebral blood flow) that lasts less than
24 hours is classified as a transient ischemic attack (Warlow, Sudlow, Dennis, Wardlaw,
& Sandercock, 2003). Approximately one-third of Americans who experience a TIA each
year will have an acute stroke, which may be more severe and require higher levels of
rehabilitation, in the near future ("National Institute of Neurological Disorders and Stroke.
Stroke: Hope Through Research," 2012).
Hemorrhagic strokes are classified as ruptured blood vessels that result in bleeds
surrounding or within areas of the brain. In a typical brain, blood flow does not come into
direct contact with brain tissue. However, when cerebral blood vessels are ruptured,
increases in intracranial pressure result from the direct accumulation of blood flow which
can damage neurological function (Bowman & Giddings, 2003). Although there are
numerous ways hemorrhages (ruptures to blood vessels) can occur, a common cause is a
bleeding aneurysm ("National Institute of Neurological Disorders and Stroke. Stroke:
Hope Through Research," 2012). An aneurysm is a swelling of a cerebral artery.
Overtime, the walls of these aneurysms develop weak spots that may burst under high
arterial blood pressure. Hemorrhagic strokes can also occur through broken arterial walls.
High plaque content that lines the insides of the walls of the artery decreases elasticity.
When arterial walls lose elasticity, the walls are prone to cracks and tears that can result
in a rupture. Furthermore, if a hemorrhage occurs in the subarachnoid space that separates
the arachnoid membrane from the pia membrane (subarachnoid hemorrhage), bleeding
can occur that contaminates the cerebrospinal fluid that can lead to overwhelming brain
damage. Although subarachnoid hemorrhages are relatively rare and do not account for a
large number of stroke-related deaths, they account for a large portion of young mortality
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when compared to ischemic stroke (Johnston, Selvin, & Gress, 1998). Since hemorrhagic
strokes can occur from increased cerebral pressure on arterial walls, it may be important
to monitor BP during exercise.
Etiology and Incidence
The onset of stroke is associated with numerous risk factors including, alcohol
consumption, inactivity, obesity, type-two diabetes, cigarette smoking, and hypertension
(Ezzati et al., 2002; Ohira et al., 2006). A study by Ohira and colleagues (Ohira et al.,
2006) found that hypertension had the greatest power to predict the incidence of ischemic
strokes. Not surprisingly, hypertension is also the most important risk factor for onset of
all types of stroke in able-bodied adults (Ohira et al., 2006). Furthermore, it appears that
the cardiovascular fitness level, denoted by maximal oxygen consumption (VO2max), is
inversely associated with decreased risk of stroke in healthy adult males. A study by Kurl
and colleagues (Kurl et al., 2003), demonstrated that men with higher maximal oxygen
consumption were at a decreased risk of stroke compared to men with lower levels of
maximal oxygen consumption. Increasing cardiovascular fitness and maintaining healthy
levels of blood pressure are important to decrease risk of stroke in healthy able-bodied
adults.
Stroke will continue to be a prevalent disability in the future. As of 2008, there are
greater than 7,000,000 people in the United States who have had a stroke (Association,
2012). It is estimated that by the year 2030, prevalence of stroke will increase 24.9% from
2010, which results in an additional four million people who will have had a stroke
(Heidenreich et al., 2011). Second strokes, recurrent strokes, are responsible for about
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23% of the overall stroke occurrence rate in people post-stroke (Association, 2012).
Research on the prevention of stroke and recurrent stroke will continue to be important
due to the steady prevalence rate of stroke.
Hypertension in recurrent-stroke
Although hypertension is regarded as the primary risk factor for occurrence of a
stroke in able-bodied adults, there is less knowledge correlating hypertension with
increased risk of a person having a recurrent stroke. About 25% of individuals who have
recovered from a first stroke may have a recurrent stroke within 5 years (Stroke, 2004).
Each recurrent stroke may increase an individual’s risk of severe disability or even death.
Normal BP is characterized by higher values in the daytime as compared to nocturnal
values. This decline in blood pressure during later hours of the day is termed nighttime
dipping. People with ischemic stroke have been found to lack night time dipping of BP
(Jain et al., 2004b), which may result in a high-load of stress on the organs. BP reduced at
later hours of the day in people post-stroke may result in a protective effect on cerebral
circulation.
Blood Pressure Range for Reduced Risk of Recurrent Stroke
Recent literature suggests there is a range of systolic BP that may reduce the risk of
recurrent stroke in people who have already experienced a first stroke. A post-hoc
analysis of a multi-center clinical trial by Ovbiagele and colleagues (Ovbiagele et al.,
2011), examined the relationship between high BP and recurrent stroke among 20,330
participants from 35 different countries. Their data found that systolic BP lower than 120
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mmHg and greater than 140 mmHg is associated with an increased risk of recurrent
stroke. Similar results have been presented in a previous study (Irie, Yamaguchi,
Minematsu, & Omae, 1993). Contrary to stroke guidelines that recommend a systolic BP
lower than 140 mmHg (Stroke, 2004), these results suggest that the ideal range for
systolic BP in people post-stroke may lie between 120 mmHg and 140mmHg. A year
later Ovbiagele and colleagues (Ovbiagele, 2012) supported these findings with further
analysis of a trial among 3680 participants. Their results were similar: people with resting
systolic BP lower than 120 mmHg or greater than 140 mmHg were associated with an
approximate 9-10% increased risk of recurrent stroke (Ovbiagele, 2012). This
recommended range of BP is known as the J-curve. Although clinical trials exhibit the
importance of the systolic blood pressure J-curve in people post-stroke, there appears to
be no guidelines that recommend elevating systolic blood pressure when below 120
mmHg. This is due to conflicting results from other literatures that have found no
association between low systolic BP and recurrent stroke (Arima et al., 2006; Dorresteijn
et al., 2012; Turnbull & Collaboration, 2003). Current ongoing clinical trials are being
performed to investigate the systolic blood pressure range of 120-140 mmHg, known as
the J-curve, with reduced risk of recurrent stroke. While many trials have provided
sufficient data surrounding systolic BP post-stroke, it appears there is no direct
association between diastolic blood pressure and increased risk of recurrent stroke.
Reducing Blood Pressure in People Post-Stroke
Reducing high BP in people post-stroke may decrease risk of recurrent stroke and
other cardiovascular incidents. In an analysis of a four-year clinical trial, Arima and
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colleagues (Arima et al., 2006) found that drug-induced therapy to reduce blood pressure,
among 6105 people with various types of stroke, reduced the risk of recurrent stroke.
These results were seen at even lower levels of systolic BP (<120mmHg). These results
conflict with the J-curve theory. Their results also exhibited reduced secondary outcomes
including coronary heart disease, congestive heart failure, and major vascular events.
Turnbull and the Blood Pressure Lowering Treatment Trialists’ Collaboration found
similar results (Turnbull & Collaboration, 2003) from analysis of 29 randomized trials.
Among 162,341 participants, their results suggest that any common form of drug-induced
blood pressure therapy may lower the risk of cardiovascular events. Consequently,
reducing BP among people post-stroke with hypertension may reduce the risk of recurrent
stroke and other cardiovascular events. In addition, these trials suggest treating BP at
lower systolic levels (<120mmHg) may be safe for people post-stroke, which contradicts
the J-curve theory. Whether exercise alone can reduce the risk of recurrent stroke, as
compared to drug-induced therapy, has yet to be investigated.
Data from various clinical trials, has found systolic BP of greater than 140 mmHg
associated with increased risk of a recurrent stroke and cardiovascular events in people
post-stroke. Although some studies have shown poor outcomes associated with systolic
blood pressure levels less than 120 mmHg, there is still no consensus or guidelines that
recommend elevating BP when below 120 mmHg.
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Aerobic Exercise and PEH in Healthy Adults
Exercise is a non-pharmacological method of long term BP reduction in people with
hypertension. However, the immediate effects of exercise on BP are less established.
Following exercise, BP can decrease beyond pre-exercise resting levels, otherwise known
as post-exercise hypotension (PEH). By lowering BP throughout the day, there may be a
reduced strain on organs and reduced risk of cardiovascular events. Consequently, longer
durations of PEH are more clinically significant towards individuals with hypertension.
Aerobic exercise has been documented to reduce ambulatory BP post-exercise, which
includes systolic and diastolic BP, up to 11 hours after exercise compared to a day with
no-exercise in people with hypertension (Quinn, 2000; Wallace, Bogle, King, Krasnoff, &
Jastremski, 1997; Wallace et al., 1999). Other studies (Kaufman, Hughson, & Schaman,
1987; MacDonald, Hogben, Tarnopolsky, & MacDougall, 2001; Moraes et al., 2007b;
Pontes et al., 2008) suggest shorter durations (30-120 minutes) of PEH in people with
hypertension. However, there is some discrepancy as to whether aerobic exercise is able
to reduce post-exercise BP compared to BP levels pre-exercise. Few studies exhibit
reductions in systolic BP after exercise compared to pre-exercise (Pescatello, Fargo,
Leach, & Scherzer, 1991; Pescatello et al., 1999). While many studies have found no
significance in systolic BP compared to pre-exercise levels (Brandao Rondon et al., 2002;
Ciolac et al., 2009; Quinn, 2000; Wallace et al., 1999), but did find significance compared
to a day without exercise. There are also some studies (Guidry et al., 2006; Pescatello et
al., 2004; Syme et al., 2006) that have found an increase in systolic BP compared to preexercise resting values, although these results were still lower than a day without exercise.
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Moreover, diastolic BP has been found to be lower post-exercise when compared to a day
without exercise (Brandao Rondon et al., 2002; Quinn, 2000; Wallace et al., 1999).
There appears to be no literature that has found significant reductions or increases in
diastolic blood pressure when compared to pre-exercise levels in people with
hypertension (Gomes Anunciacao & Doederlein Polito, 2011). There is solid evidence
that aerobic exercise can reduce blood pressure compared to a day without exercise in
people with hypertension. However, there is not enough evidence that aerobic exercise
can reduce blood pressure compared to pre-exercise resting blood pressure. These
conflicting results may be due to differences in methodology which include: mode,
intensity, and duration of exercise, as well as the pre-existing level of hypertension among
participants.
Intensity of Exercise and PEH
Aerobic exercise, alone or combined with resistance exercise, is more effective at
reducing BP after exercise in higher magnitude and duration compared to resistance
exercise (Keese, Farinatti, Pescatello, & Monteiro, 2011), but the intensity of exercise
does not appear to affect the significance of PEH. A study by Pescatello et al. (Pescatello
et al., 1991) examined ambulatory BP for 13 hours following an acute bout of aerobic
exercise at different intensities in 6 people with hypertension. Their results suggest that
ambulatory BP following aerobic exercise was lower than a day without exercise and that
the intensity of exercise (40% versus 70% maximum VO2) did not affect the extent to
which BP was reduced. The sample size of this study was relatively small. Although there
are few studies that have suggested the intensity of exercise affects the magnitude of the
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PEH response (Forjaz et al., 2000; Wallace et al., 1997), the majority of the literature
finds no such relationship (Brandao Rondon et al., 2002; Ciolac et al., 2009; Guidry et al.,
2006; Pescatello et al., 1999; Quinn, 2000). Consequently, aerobic exercise of at least a
light-to-moderate intensity may lower BP for a clinically significant amount of hours
following exercise, as opposed to a day where no exercise was performed in people with
hypertension.
Duration of Exercise on PEH
The duration of exercise does appear to affect the magnitude of PEH. However, there
is currently not enough literature to support that shorter (10-20 minutes) or longer
durations (40-50 minutes) of exercise are optimal for reductions in BP post-exercise. A
report by MacDonald and colleagues (MacDonald, MacDougall, & Hogben, 2000)
demonstrated that there is no difference in PEH when comparing shorter (10 minutes) and
longer (30 minutes) durations of exercise. Their results suggest that 10 minutes of
exercise is sufficient to elicit a PEH response in eight borderline hypertensive
participants. However, results from a study by Mach and colleagues (Mach, Foster, Brice,
Mikat, & Porcari, 2005) demonstrate greater durations of exercise promote higher
reductions in BP post-exercise. Guidry and colleagues (Guidry et al., 2006) also found
longer durations (30 minutes) of exercise had greater reductions in diastolic BP postexercise compared to shorter durations (10 minutes). Although there appears to be a
relationship between the duration of exercise and reduction in BP post-exercise, more
research needs to be conducted on larger populations of people with hypertension.
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Pre-existing Levels of Blood Pressure on PEH
Pre-existing levels of blood pressure may affect the magnitude of the PEH response.
A study by Wallace and colleagues (Wallace et al., 1997) demonstrated that hypertensive
adults had greater reductions in blood pressure after exercise compared to people whom
are normotensive. After 50 minutes of treadmill walking, people with hypertension were
able to sustain a reduction in systolic blood pressure for up to 11 hours compared to a day
without exercise (control day). Diastolic blood pressure was also reduced for
approximately 6 hours following exercise compared to the control day. Normotensive
participants had no significant reduction in blood pressure post-exercise compared to the
control day. These results have been confirmed with other literature (Forjaz et al., 2000;
Pescatello et al., 1991). Consequently, both the magnitude and duration of PEH was more
significant among people with hypertension. Since there is sufficient evidence that PEH
can occur in people who are normotensive (Liu et al., 2012; Syme et al., 2006), the
exercise stimulus administered by Wallace and colleagues (Wallace et al., 1997) may not
have been sufficient to elicit a PEH response in normotensive adults. People with
hypertension may require a lower exercise intensity to elicit a PEH response. It is
important to consider the pre-existing levels of resting blood pressure in research
participants when analyzing the literature.
Mode of Exercise and PEH
Aerobic treadmill exercise (Brandao Rondon et al., 2002; Forjaz et al., 2000; Moraes
et al., 2007a; Pescatello et al., 1991; Pescatello et al., 1999) and stationary cycling
(Kaufman et al., 1987; Quinn, 2000; Wallace et al., 1997, 1999) are the most common
modes of exercise used in studies to elicit a PEH response in people with hypertension.
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To the best of my knowledge there is no literature that compares the PEH response of
treadmill exercise to stationary cycling. Both treadmill exercise (Quinn, 2000; Wallace et
al., 1999) and stationary cycling (Pescatello et al., 1991; Pescatello et al., 1999) have been
shown to elicit a significant PEH response in people with hypertension. The mode of
exercise performed may not be significant as long as the duration and intensity of exercise
are sufficient to elicit a PEH response.
Treadmill Exercise in Stroke
Treadmill exercise has been recently gaining popularity among the stroke population
and is a safe and effective form of cardiovascular exercise at even high intensities
(Brouwer, Parvataneni, & Olney, 2009; Globas et al., 2011; Macko, DeSouza, et al.,
1997; Macko, Katzel, et al., 1997; Tang A, 2010). Treadmill exercise is also commonly
used for gait rehabilitation. Benefits from gait-induced treadmill therapy include,
improved walking symmetry (Harris-Love, Forrester, Macko, Silver, & Smith, 2001;
McCain, Smith, Polo, Coleman, & Baker, 2011), increased walking speed (Globas et al.,
2011), reduced energy cost of walking (Macko, DeSouza, et al., 1997), and improved
functional mobility (Macko et al., 2005), in people post-stroke. However, overground
treadmills possess physical limitations for people post-stroke, particularly in the early
recovery phase of rehabilitation. The Copenhagen stroke study (Jorgensen et al., 1995)
found that out of 1196 participants post-stroke, 28 percent had a moderate to severe level
of disability and 20% of participants were not able to recover walking function within 11
weeks. It may be hard for people post-stroke with moderate to severe disability to perform
overground treadmill walking. People post-stroke have been shown to expend
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approximately twice the energy cost during walking compared to healthy-efficient gait
(Danielsson, Willén, & Sunnerhagen, 2007; Platts, Rafferty, & Paul, 2006). Furthermore,
overground treadmill walking requires a high energy cost and has been shown to require
more energy expenditure than floor walking at a matched speed in people post-stroke
(Brouwer et al., 2009). If a primary goal during rehabilitation is to elicit a PEH response
in people post-stroke with hypertension, a rehabilitator may require a mode of aerobic
exercise people post-stroke can perform for 10-20 minutes that is easier to achieve than an
overground treadmill.
Aquatic Exercise
Aquatic treadmill exercise can elicit a similar cardiovascular response to an
overground treadmill in various populations (Brubaker, Ozemek, Gonzalez, Wiley, &
Collins, 2011; Greene et al., 2009). Furthermore, Park and colleagues (Park et al., 2010)
examined the effects of aquatic and overground treadmill exercise on gait and physical
function of people post-stroke. Their data found that both the aquatic and the overground
treadmill were able to improve gait and physical function of people post-stroke. However,
the aquatic treadmill had a higher positive impact on improved weight bearing of the
affected leg, improved time of stance phase, and a greater emotional aspect, than
overground treadmill exercise.
The aquatic treadmill may also be a safer environment for people post-stroke due to
the physiological properties of water. Water buoyancy during aquatic exercise alleviates
body weight, which decreases impact force on joints, muscles, and bones (Bartels et al.,
2007). At slow treadmill speeds, water buoyancy has also been suggested to reduce the
17
energy cost of aquatic treadmill walking compared to overground treadmill walking in
people with arthritis (Hall, Grant, Blake, Taylor, & Garbutt, 2004). Water buoyancy can
alleviate different percentages of body weight at various water depths. Approximately
50% of body weight is supported with the water depth located at the anterior superior iliac
spine, 75 to 80% at the xiphoid process, and 90% at the seventh cervical vertebrae (Bates
& Hanson, 1996). Hydrostatic pressure, the perpendicular pressure exerted to the surface
of an object under water, and water density, may also improve balance and stabilize joints
during water immersion (Bates & Hanson, 1996). A study by Matsumoto and colleagues
(Matsumoto, Kawahira, Etoh, Ikeda, & Tanaka, 2006) found that warm-water therapy
around 41 degrees is effective at reducing spasticity in people post-stroke. The aquatic
environment is a safe alternative method of cardiovascular exercise and gait therapy. For
these reasons aquatic exercise is a common mode of exercise during rehabilitation.
Aquatic Exercise and PEH
There are few studies that have compared the effectiveness of aquatic and land-based
aerobic exercise on the PEH response in healthy adults. A study by Pontes and colleagues
(Pontes et al., 2008) examined the effectiveness of pool floor running to overground
running on the PEH response of 16 people with hypertension. Their results suggest that
pool floor running promoted a similar PEH response to overground running. 4 years later,
a study by Rodriguez et al. (Rodriguez et al., 2011) compared the effects of a single-bout
of acute overground treadmill walking versus aquatic treadmill walking in 12 healthy
adults and 11 healthy-trained adults. Their results suggest that aquatic treadmill walking
elicited a greater reduction in BP for an hour following exercise in a controlled laboratory
18
setting. In addition, their findings imply that people who are un-trained (lower fitness
level indicated by maximum oxygen consumption, VO2max) have greater reductions in
BP following exercise compared to people who are trained. These results suggest that
people post-stroke, whom have lower aerobic capacities compared to healthy adults, may
show greater reductions in BP compared to healthy adults and may also exhibit greater
reductions in BP following exercise on an aquatic treadmill as opposed to an overground
treadmill. A year later, Terblanche and colleagues (Terblanche & Millen, 2012) examined
the magnitude and duration of PEH following aquatic and overground treadmill exercise
in 21 males and females with various levels of hypertension. They found that both the
aquatic and overground treadmill exhibited a PEH response of similar magnitude. Both
daytime and nighttime BP values were significantly lower than a day without exercise
(control day). However, the duration of PEH following aquatic treadmill exercise lasted
only 9 hours compared to 24 hours following overground treadmill exercise. Their results
also suggest that aquatic treadmill exercise is safe mode of exercise for men and women
with hypertension. Although these studies (Rodriguez et al., 2011; Terblanche & Millen,
2012) have documented significance in PEH while comparing aquatic and overground
treadmill exercise, both of these studies have errors with how the exercise intensity was
matched between both treadmills. Terblanche and colleagues used heart rate and rate of
perceived exertion (RPE) to correlate a specific percentage of oxygen consumption (VO2)
to monitor the intensity of exercise between both treadmills. Rodriguez and colleagues are
vague about how exercise intensity was monitored, but it appears they also used heart rate
to monitor the intensity of exercise. Since heart rate correlated to oxygen consumption
(VO2) has been found to differ by approximately 9 beats per minute between an aquatic
19
and overground treadmill (Hall et al., 2004), heart rate alone will not provide an accurate
matched intensity between an aquatic and overground treadmill. It may be best to match
the intensity of exercise by assessing gas-by-gas analysis of VO2 along with heart rate
between both treadmills.
Recent studies have indicated that aquatic treadmill exercise may reduce blood
pressure post-exercise in healthy adults (Rodriguez et al., 2011; Terblanche & Millen,
2012). However, no studies have compared the effects of aquatic and overground
treadmill exercise on ambulatory blood pressure in people post-stroke. This knowledge
may help rehabilitation professionals advance their understanding of PEH to provide nonpharmaceutical interventions for the management of BP in people post-stroke. Thus the
purpose of this study is to investigate the magnitude and duration of the PEH response to
a single-bout of aquatic treadmill exercise and overground treadmill exercise in people
post-stroke. We hypothesize that that aquatic treadmill exercise may elicit a greater PEH
response compared to overground treadmill exercise in people post-stroke.
20
Section 2: Methods
Participants
A total of 7 participants post-stroke were recruited for this study from a
university-based aquatic therapy program. The mean age of participants in this study was
56.57 ± SD years (range: 36-67 years) and the average time post-stroke 4.85 ± SD years.
All participants in this study were classified with normotensive levels of resting BP, and
no participants were using anti-hypertensive medication throughout the study. Participant
characteristics are summarized in Table 1.
In order for participants to be included they had to meet inclusion criteria: a
medical diagnosis of stroke, a minimum of six months post-stroke, and a minimum age of
35. Participants were excluded from the study if they had a resting systolic BP greater
than 140 mmHg or less than 90 mmHg, a resting diastolic BP above 89 mmHg or below
60 mmHg, cardiovascular complication, and acute injury or surgery within the last six
months. All participants were asked to refrain from smoking or drinking caffeinated
drinks on days of data collection. The study protocol was approved by the institutional
review board of the university. Participants’ informed consent and medical clearance
were collected prior to data collection.
21
Instrumentation
To compare BP responses between two exercise modes, an aquatic treadmill
(AquaGaiter, FERNO, Ohio, 2003) and an overground treadmill (Gait Trainer Treadmill
II, BIODEX, USA, X) were utilized. The water depth of aquatic treadmill walking was
adjusted to the height of the xiphoid process of each participant using a movable floor
pool. (KBE Bauelemate, GmbH & Co., Wilhelmshaven, Germany, 2003). The pool
temperature was held consistently at 33 degrees Celsius.
An ambulatory BP monitor (ABPM-05, Meditech Inc, USA) was used to record
all BP measurements. Validity and reliability of the instrument have been established
according to the British Hypertension Society protocol (Barna, Keszei, & Dunai, 1998).
The ambulatory BP monitor was secured to the waist of each participant and programmed
to record data every 15 minutes for up to nine hours after exercise. BP data were stored in
the instrument and later transferred to processing software (Meditech Software REF) for
analysis. Participants were allowed to assume their activities of daily living while
wearing the BP monitor.
A telemetric metabolic system (K4b2, COSMED Inc., Rome, Italy, 1998) was
used to match the intensity of exercise between the two exercise modes. The validity and
reliability of the portable system have been previously established (Art et al., 2006;
Duffield, Dawson, Pinnington, & Wong, 2004). Participants wore a harness to fasten the
portable unit to their chest while they were performing OTW. The unit was secured
inside of a waterproof case and placed on a nearby dry deck for the ATW condition.
22
Procedure
All participants completed 25 minutes of walking on an aquatic and overground
treadmill on two separate sessions. Each exercise session consisted of five minutes of
warm-up, 15 minutes of walking at 70% of peak oxygen consumption (VO2peak), and
five minutes of cool-down. Participants came to the laboratory for a total of five visits:
the initial visit, two days of familiarization, and two exercise sessions.
The initial visit consisted of anthropometric data collection, a Fugl-Meyer Lower
Extremity Assessment, and a modified sub-maximal exercise test performed on a
stationary cycle (Eng, Dawson, & Chu, 2004). Participants were then given an
ambulatory BP monitor and instructed to record their BP on a separate day without
exercise (control day).
During the control day, participants were instructed to rest for the initial hour of
BP measurement, which was designated as their pre-exercise baseline. Following the
initial hour of rest, participants were informed to resume their activities of daily living
while BP was measured every 15 minutes for the next twelve hours. Exercise journals
were completed by participants to document hourly activity during BP readings.
Following the control day, participants came to the laboratory for two familiarization
visits and two exercise data collection sessions.
A familiarization session was provided on a separate day at least 48 hours prior to
each exercise data collection session. During familiarization sessions seated and standing
BP was measured in water and on land, in order to check the possible influence of water
submersion or change of body position on BP. Participants rested in a seated position for
23
ten minutes while their BP was recorded. In addition, resting BP was measured in a
standing position for ten minutes. Following a total of twenty minutes of rest, participants
then performed a graded walking test on either an aquatic or overground treadmill in
random order, to ensure that each participant could safely walk at 70% of their VO2peak.
Participants returned to the laboratory on two separate sessions for exercise data
collection: one walking session on an aquatic treadmill and the other on an overground
treadmill. Since BP varies throughout different periods of the day, all participants were
instructed to arrive in the laboratory between nine-11am. Prior to exercise, participants
remained seated for ten minutes while their BP was recorded three times at the fifth and
tenth minute of rest. The average of these measurements was designated as the preexercise baseline. Participants then walked on a treadmill for 25 minutes, which consisted
of a five-minute graded warm-up and cool-down, and 15 minutes of exercise at
approximately 70% of each participant’s VO2peak. In order to maintain this intensity of
exercise, speed adjustments were made based on the real-time collection of breath-bybreath oxygen consumption (VO2) data. In addition, heart rate (HR) and Borg’s rating of
perceived exertion (RPE) (Borg, 1982) were monitored.
After completion of each walking trial, participants were asked to wear an ABPM,
and BP values were recorded for a total of nine hours after exercise. The first hour was
recorded in a seated resting position under laboratory conditions. For the next eight hours
participants were allowed to resume their daily activities while wearing an ABPM, which
automatically recorded BP every 15 minutes. Participants were instructed to record their
hourly activity in exercise journals, which were later used to monitor their hourly
activities. Upon completion of the first exercise session, participants then revisited the
24
laboratory a week later to perform the same experimental procedures under the second
walking condition that was randomly selected.
Systolic and diastolic BP measurements were recorded from the non-affected arm
of people post-stroke. BP was recorded before (pre-exercise baseline), during, and up to
nine hours post-exercise. BP during exercise was measured immediately after the 15minute exercise period before the five-minute cool-down based on a modified protocol by
Dolbow et al. (2008). During aquatic treadmill walking, a floatation device was used to
support the arm to ensure that the arm was positioned at the level of the heart above the
water.
Analysis
The primary dependent variables included systolic and diastolic BP measured at three
different time phases: pre-exercise baseline, during exercise, and post-exercise. Postexercise BP data were analyzed at five different time points. First, they were compared to
pre-exercise baseline BP across the three conditions (control, ATW, and OTW). Second,
post-exercise data were also compared to pre-exercise baseline BP within each condition.
The main effects across the three conditions were tested with mixed model MANOVAs.
The between-factors were the three test conditions (control, ATW, and OTW) and the
within-factors the repeated measures over time. The within factors were analyzed using
repeated measures ANOVA. All statistical analyses were performed using SPSS
Statistics 22 (IBM Corp., Armonk, NY, USA, 2013).
25
Section 3: Results
All seven participants completed the experimental procedures of this study. The
test conditions did not show differences in pre-exercise resting BP. The mean systolic BP
values of both seated and standing rest in the pool (116.5 ± 11.56 and 120.1 ± 5.59,
respectively) showed no significant differences compared to those on land (114.3 ± 11.63
and 120.07 ± 5.59, respectively). Also, mean diastolic BP values in both seated and
standing rest in the pool (71.78 ± 12.0 and 76.18 ± 8.75, respectively) were not different
from those on land (69.96 ± 10.93 and 79.81 ± 6.80, respectively).
The means and standard deviations of VO2 during OTW and ATW are shown in
Table 2. The matched intensity of exercise between the two exercise conditions was
determined based upon the average of breath-by-breath gas analysis of VO2. Mean VO2
values during the warm-up, exercise and cool-down were not significantly different
between ATW and OTW. In addition, mean energy expenditure during exercise was not
statistically significant between OTW (3.76 ± 1.33) and ATW (3.81 ± 0.96).
Mean BP responses were compared between the pre-exercise baseline and the
first, third, fifth, seventh, and ninth hour post-exercise. Systolic BP responses at each
time phase can be seen for each of the three test conditions in Figure 1. When compared
to the aquatic pre-exercise baseline (115.0 ± 12.69), the ninth hour post-exercise
demonstrated a reduction of 6% in mean systolic BP (F(1,5) = 12.78, p < 0.05). No other
significant differences were found in mean systolic BP and diastolic BP among the six
time phases within each test condition.
26
Mean BP values at each time phase were compared among the three test
conditions, shown in Table 3. At the pre-exercise baseline, mean systolic and diastolic BP
values showed no significant difference among the three test conditions. Additionally,
during exercise and at the first hour post-exercise, mean systolic BP values displayed no
significant difference among each test condition.
When comparing systolic BP at each time phase post-exercise between test
conditions, significant differences were only found at the ninth hour. Mean systolic BP at
the ninth hour following ATW was reduced by 11% (F(1,5) = 14.08, p < 0.01) compared to
that of the control day (122.5 ± 14.18), shown in Figure 1. In addition, OTW displayed a
trend of a 3% reduction of systolic BP at the same hour (118.35 ± 7.07) compared to that
of the control day (F(1,5) = 5.82, p = 0.052).
Similar to the post-exercise response of systolic BP, a significant reduction of
diastolic BP was seen at the ninth hour. At the ninth-hour after ATW, mean diastolic BP
(70.86 ± 13.2) was reduced by 8% (F(1,5) = 12.73, p < 0.01) compared to mean diastolic
BP of the control day (77.2 ± 11.1). Also, OTW showed a 7% reduction of mean diastolic
BP at the ninth hour post-exercise (71.40 ± 9.21) compared to the control day (F(1,5) =
7.71, p <0.01).
In order to compare the mean BP response of the entire post-exercise period
among conditions, BP values from each hour were averaged into a single overall value.
This mean value was then compared between each condition, shown in Figure 3. Overall
post-exercise systolic BP following ATW was 3% lower than that of OTW (t = 4.06, p <
0.05) and 5% to that of the control day (t = 5.11, p < 0.01). OTW did not show a
27
significant difference in overall systolic BP compared to the control day. On the other
hand, mean overall post-exercise diastolic BP following both OTW and ATW were lower
than that of the control day by 6% (t = 4.01, p <0.01) and 7% (t = 4.33, p <0.01),
respectively.
28
Table 1. Participant Characteristics
Measure
n=7
Age (years)
56.57 ± 10.24
Height (cm)
164.44 ± 10.23
Weight (kg)
74.60 ± 16.18
BMI (kg/m2)
27.36 ± 4.67
Gender (M/F)
3:4
Fugl-Meyer Score LA (0-28)
23.71 ± 3.15
Time Post Stroke (years)
4.85 ± 5.07
Sub Max VO2 (ml/kg-1minute-1)
16.37 ± 3.12
Affected Side (right : left)
4:3
M = male; F = female; R = right; L = left; LA = lower
extremity assessment; VO2 = oxygen consumption;
N/A = not applicable. Mean ± SD.
29
Table 2. Oxygen Consumption During Exercise
VO2
(ml/kg-1/min-1)
Condition
Overground Treadmill:
Warm-up
Exercise
Cool-down
8.45 ± 1.46
10.98 ± 1.90
8.45 ± 1.06
Aquatic Treadmill:
Warm-up
Exercise
Cool-down
7.62 ± 0.84
10.59 ± 1.78
6.95 ± 1.24
VO2 = oxygen consumption. Means ± STD.
30
Table 3. Blood Pressure
Systolic BP
(mmHg)
Diastolic BP
(mmHg)
Resting Baseline
120.9 ± 10.41
75.47 ± 10.57
Overall Post-Exercise
120.9 ± 2.30
75.04 ± 2.55
Resting Baseline
117.36 ± 11.77
82.86 ± 14.01
Exercise
137.71 ± 12.15
-
1-hr Post-Exercise
117.43 ± 11.72
73.00 ± 11.54
Overall Post-Exercise
117.67 ± 4.35
* 71.85 ± 1.74
115.0 ± 9.1
71.60 ± 5.36
Exercise
136.14 ± 12.69
-
1-hr Post-Exercise
116.8 ± 10.57
73.60 ± 8.89
Measures
Control:
Overground Treadmill:
Aquatic Treadmill:
Resting Baseline
Overall Post-Exercise
*^ 114.56 ± 4.74
* 71.25 ± 2.54
nd
th
BP = blood pressure; hr = hour; Ambulatory = 2 to 9 hour post-exercise.
* represents significance at p < 0.05 compared to control.
^ represents significance at p < 0.05 compared to overground treadmill.
Means ± SD.
31
Systolic Blood Pressure (mmHg)
Figure 1
Hourly Systolic BP Post-Exercise
140
Control
OTW
ATW
130
120
*
110
100
^
Time Phase (Hours Post-Exercise)
Abbreviations: OTW = overground treadmill walking, ATW = aquatic treadmill walking,
Control = no exercise.
Means.
* represents significance at ( p < 0.01 ) compared to the control day.
^ represents significance within the condition as compared to baseline ( p < 0.05 ).
32
Diastolic Blood Pressure (mmHg)
Figure 2
Hourly Diastolic Blood Pressure Post-Exercise
90
Control
OTW
ATW
80
*
70
60
Baseline
1
3
5
7
9
Hours Post-Exercise
Abbreviations: OTW = overground treadmill walking, ATW = aquatic treadmill walking,
Control = no exercise.
Means.
* represents significance at ( p < 0.01 ) for both the OTW and ATW condition compared
to the control day.
33
Section 4: Discussion
The purpose of this study was to compare the post-exercise hypotensive response
between aquatic and overground treadmill walking at an equivalent intensity. BP was
measured for nine hours after each bout of treadmill walking. These values were also
compared to a day when no exercise was performed. In addition, hourly BP
measurements were compared within each of the three test conditions. Our results
showed that systolic BP may be reduced for up to nine hours following a single session of
aquatic treadmill walking compared to that of overground treadmill walking and a day
when no exercise is performed. On the other hand, both treadmills exhibited a lower
diastolic BP post-exercise compared to a day without exercise. When comparing hourly
BP values within each test condition, aquatic treadmill walking showed a significant
decline in systolic BP at the ninth hour of exercise compared to pre-exercise resting
values. These findings suggest that cardiovascular exercise can elicit clinically
meaningful reductions of BP in people post-stroke.
Resting Blood Pressure
Resting BP responses have been found to remain consistent between land and
water around a temperature of 30 degrees Celsius, with the water at chest-depth
(indicated by the water level at the xiphoid process), in a variety of populations (Cider,
Sunnerhagen, Schaufelberger, & Andersson, 2005; Cider, Svealv, Tang, Schaufelberger,
& Andersson, 2006; Rodriguez et al., 2011). Our results demonstrated similar findings;
resting BP responses showed no significant difference in sitting or standing between the
land and water environment. Although some studies have suggested that water immersion
34
slightly elevates resting BP, these studies were generally performed in higher depths of
water located at the shoulder-neck-level (Kokot, Ulman, & Cekański, 1983; Sugiyama et
al., 1993). The outcomes from this study confirm that water immersion at chest-depth,
between 32 and 34 degrees Celsius, does not alter resting BP responses of people poststroke.
Matched Intensity
To compare post-exercise BP between aquatic- and land-based exercise in
normotensive adults, previous studies have utilized HR to match the exercise intensity
(Rodriguez et al., 2011; Terblanche & Millen, 2012). However, Hall and colleagues
(2004) have reported that walking in water elicits a lower HR compare to walking on
land. This suggests that HR alone may not be reliable for matching the intensity of
exercise between aquatic and overground treadmill walking. Since oxygen consumption
is reported as a valid measure of exercise intensity in people post-stroke (Brouwer et al.,
2009; Fisher & Gullickson, 1978), our study monitored the real-time collection of oxygen
consumption data to match the intensity of exercise between walking conditions.
Post-Exercise Hypotension
(Overall BP reductions aquatic compared to control day and clinical significance)
After participants performed a single session of walking on an aquatic treadmill,
mean BP over nine hours was lower than that of the control day by 6.3 mmHg systolic
and 3.8 mmHg diastolic. Our data are similar to reported reductions in BP post-exercise
of approximately two to 12 mmHg systolic and 2 mmHg diastolic in the general adult
population with hypertension (Cardoso et al., 2010). Furthermore, our results may be
35
clinically meaningful for people post-stroke with hypertension who aim to reduce their
risk of recurrent stroke. It has been reported that a decrease in resting BP of 10 mmHg
systolic or 5 mmHg diastolic BP is associated with a reduced risk of recurrent stroke by
38% and 28%, respectively (Rodgers et al., 1996). Even minimal declines in systolic BP
of as little as two mmHg following aerobic training have been associated with a 4%
decrease in coronary heart disease and 3% decrease in all-cause mortality (Whelton et al.,
2002).
(Comparing treadmills overall and significance of systolic BP reductions)
When examining diastolic BP among the three test conditions, both ATW and
OTW showed a lower overall diastolic BP than a day without exercise. However, overall
systolic BP values post-exercise were significantly lower following aquatic treadmill
walking compared to overground treadmill walking and to a control day. This may be
clinically significant, because systolic BP values are more closely associated to
cardiovascular risk compared to those of diastolic BP (Zanchetti & Waeber, 2006).
Clinical trials have demonstrated that systolic BP is harder to manage through antihypertensive treatment and most responsible for poor rates of BP control (Lloyd-Jones et
al., 2000). The authors reported that 89.7% of people who received anti-hypertensive
treatment were able to regulate their diastolic BP, whereas systolic BP was only
controlled in 49% of all cases.
(Acknowledging that statistical significance between may not mean clinincal
significance)
36
The comparison of overall post-exercise systolic BP between the aquatic and
overground treadmill showed statistical significance. However, the mean difference was
marginal (input mean values later, raw means) and the clinical significance of this
difference appears unclear. Also, these findings are inconsistent with a previous study
that examined post-exercise BP in people with hypertension following aquatic- and landbased exercise. Terblanche & Millen (2012) reported that a single-bout of land-based
exercise reduced post-exercise BP in greater magnitude and duration to that of aquatic
exercise. This difference appeared most prominent after the 11th hour after exercise.
However, their exercise sessions incorporated both a resistance and a cardiovascular
exercise component, which was not matched for intensity between exercise conditions.
The greatest reductions of BP seen in the present study occurred during the eighth and
ninth hour post-exercise, the last two hours of BP monitoring. Since treadmill exercise
has been shown to reduce BP for up to 24 hours after exercise (Terblanche & Millen,
2012), it is possible that greater declines in BP may be seen after longer periods of
monitoring. Thus, future studies should examine longer durations of BP responses to
aquatic and overground treadmill walking at an equivalent intensity.
(Introduction of nighttime dipping in normal adults and significance)
Typical daily BP is characterized by high levels of pressure during the working
hours of the day with BP drops of approximately ten to twenty percent at nighttime. This
concept is known as diurnal variation, or nighttime dipping (Routledge & McFetridgeDurdle, 2007). An absence of dipping during the night can lead to a higher load of BP
throughout the day, which may cause an increased amount of strain on the internal
organs. It is critical to monitor changes in BP from early hours in the day till late at night
37
in order to prevent hypertension-related health complications (Mancia et al., 1997;
Staessen et al., 1999). In addition, nighttime dipping has been identified as an accurate
predictor of stroke, heart failure, and sudden death in elderly individuals with
hypertension (Staessen et al., 1999). People post-stroke have been documented to lack
nighttime dipping of BP (Castilla-Guerra et al., 2009; Jain, Namboodri, Kumari, &
Prabhakar, 2004). Our results were similar in findings: on a day when no exercise was
performed, people post-stroke displayed no decline in BP at nighttime when compared to
morning BP values. On the other hand, after people post-stroke exercised on an aquatic
treadmill between nine to eleven am they were able to reduce their systolic BP by 6% at
nighttime. This suggests that exercise on an aquatic treadmill may promote nighttime
dipping of BP in people post-stroke. Further investigation is warranted to monitor BP for
longer periods of time, possibly through sleep and morning hours of the following day.
(Clinical significance)
Reductions of BP following a bout of treadmill exercise can be viewed favorably
for people post-stroke with hypertension, as it may provide them with an effective
method of managing their BP. The present study recruited only people post-stroke with
normotension. It is possible that we may observe greater declines of BP after exercise in
people post-stroke with hypertension. People with hypertension have been documented to
display a greater reduction in BP after exercise compared to people with normotension
(Wallace et al., 1999). It is necessary to verify whether the findings from the present
study are translatable to people post-stroke with hypertension. Our results provide
clinicians in rehabilitation with a scientific understanding of post-exercise hypotension in
38
people post-stroke, which may assist them with designing and implementing effective
intervention programs.
Limitations
We acknowledge that there are limitations in this study. Since the sample size of this
study was relatively small, this may limit the clinical interpretation of the study
outcomes. Secondly, this study focused on the main effects of acute exercise on BP, but
did not investigate the mechanism of post-exercise hypotension. Previous studies have
shown that hypotension can be induced by a reduction in sympathetic drive (Kulics,
Collins, & DiCarlo, 1999), vascular resistance, and stroke volume (Brandão Rondon et
al., 2002), all of which have been found to be augmented during aquatic exercise
(Gabrielsen et al., 2000; Pontes et al., 2008). Lastly, this study investigated the immediate
response to a single-bout of exercise on BP. Future studies may examine the effects of
long term interventions within this population.
Conclusion
This study was the first to our knowledge to analyze the post-exercise hypotensive
response of people post-stroke. Our results indicate that people post-stroke are able to
sustain a sufficient walking intensity necessary to elicit a significant decline in BP
following cardiovascular exercise. Aquatic treadmill walking showed a greater reduction
of systolic BP over a nine-hour period as compared to overground treadmill walking.
However, further investigation is warranted to validate these findings with a larger
sample size or longer monitoring period. Also, our results suggest aquatic treadmill
walking can elicit a clinically meaningful nighttime reduction in BP. Thus, it is
39
recommend for clinicians to consider using aquatic treadmill walking as a nonpharmaceutical means to regulate BP in people post-stroke.
REFERENCES
Arima, H., & Chalmers, J. (2011). PROGRESS: Prevention of Recurrent Stroke. J Clin
Hypertens (Greenwich), 13(9), 693-702. doi: 10.1111/j.1751-7176.2011.00530.x
Arima, H., Chalmers, J., Woodward, M., Anderson, C., Rodgers, A., Davis, S., Progress
Collaborative Group. (2006). Lower target blood pressures are safe and effective
for the prevention of recurrent stroke: the PROGRESS trial. J Hypertens, 24(6),
1201-1208. doi: 00004872-200606000-00031
Art, T., Duvivier, D. H., van Erck, E., de Moffarts, B., Votion, D., Bedoret, D., Serteyn,
D. (2006). Validation of a portable equine metabolic measurement system. Equine
Vet J Suppl(36), 557-561.
Asahina, M., Asahina, M. K., Yamanaka, Y., Mitsui, K., Kitahara, A., & Murata, A.
(2010). Cardiovascular response during aquatic exercise in patients with
osteoarthritis. Am J Phys Med Rehabil, 89(9), 731-735. doi:
10.1097/PHM.0b013e3181ec957f
American Heart Association. (2012). Heart Disease and Stroke Statistics-2012 update.
Barna, I., Keszei, A., & Dunai, A. (1998). Evaluation of Meditech ABPM-04 ambulatory
blood pressure measuring device according to the British Hypertension Society
protocol. Blood Press Monit, 3(6), 363-368.
Bartels, E. M., Lund, H., Hagen, K. B., Dagfinrud, H., Christensen, R., & DanneskioldSamsoe, B. (2007). Aquatic exercise for the treatment of knee and hip
osteoarthritis. Cochrane Database Syst Rev(4), CD005523. doi:
10.1002/14651858.CD005523.pub2
40
Bastos, J. M., Bertoquini, S., Silva, J. A., & Polonia, J. (2006). Relationship between
ambulatory blood pressure monitoring values and future occurrence of ischemic
cerebrovascular and coronary events in hypertensive patients. Rev Port Cardiol,
25(3), 305-316.
Bates, A., & Hanson, N. (1996). Aquatic Exercise Therapy. Philadelphia: W.B. Sunders
Company.
Borg, G. A. (1982). Psychophysical bases of perceived exertion. Med Sci Sports Exerc,
14(5), 377-381.
Bowman, J. P., & Giddings, F. D. (2003). Strokes: an illustrated guide to brain structure,
blood supply, and clinical signs.: New Jersey: Pearson Education.
Brandao Rondon, M. U., Alves, M. J., Braga, A. M., Teixeira, O. T., Barretto, A. C.,
Krieger, E. M., & Negrao, C. E. (2002). Postexercise blood pressure reduction in
elderly hypertensive patients J Am Coll Cardiol (Vol. 39, pp. 676-682). United
States.
Brouwer, B., Parvataneni, K., & Olney, S. J. (2009). A comparison of gait biomechanics
and metabolic requirements of overground and treadmill walking in people with
stroke Clin Biomech (Bristol, Avon) (Vol. 24, pp. 729-734). England.
Brown, D. L., Lisabeth, L. D., Roychoudhury, C., Ye, Y., & Morgenstern, L. B. (2005).
Recurrent stroke risk is higher than cardiac event risk after initial stroke/transient
ischemic attack. Stroke, 36(6), 1285-1287. doi:
10.1161/01.STR.0000165926.74213.e3
Brubaker, P., Ozemek, C., Gonzalez, A., Wiley, S., & Collins, G. (2011).
Cardiorespiratory responses during underwater and land treadmill exercise in
college athletes. J Sport Rehabil, 20(3), 345-354.
Cardoso, C. G., Jr., Gomides, R. S., Queiroz, A. C., Pinto, L. G., da Silveira Lobo, F.,
Tinucci, T., de Moraes Forjaz, C. L. (2010). Acute and chronic effects of aerobic
and resistance exercise on ambulatory blood pressure. Clinics (Sao Paulo), 65(3),
317-325. doi: 10.1590/s1807-59322010000300013
Castilla-Guerra, L., Fernandez-Moreno Mdel, C., Espino-Montoro, A., & Lopez-Chozas,
J. M. (2009). Ambulatory blood pressure monitoring in stroke survivors: do we
really control our patients? Eur J Intern Med, 20(8), 760-763. doi:
10.1016/j.ejim.2009.09.004
Chen, G., Patten, C., Kothari, D. H., & Zajac, F. E. (2005). Gait differences between
individuals with post-stroke hemiparesis and non-disabled controls at matched
speeds. Gait Posture, 22(1), 51-56. doi: S0966-6362(04)00117-1
41
Chobanian, A. V., Bakris, G. L., Black, H. R., Cushman, W. C., Green, L. A., Izzo, J. L.,
Committee, N. H. B. P. E. P. C. (2003). Seventh report of the Joint National
Committee on Prevention, Detection, Evaluation, and Treatment of High Blood
Pressure. Hypertension, 42(6), 1206-1252. doi: 01.HYP.0000107251.49515.c2
Cider, A., Sunnerhagen, K. S., Schaufelberger, M., & Andersson, B. (2005).
Cardiorespiratory effects of warm water immersion in elderly patients with
chronic heart failure. Clin Physiol Funct Imaging, 25(6), 313-317. doi:
10.1111/j.1475-097X.2005.00633.x
Cider, A., Svealv, B. G., Tang, M. S., Schaufelberger, M., & Andersson, B. (2006).
Immersion in warm water induces improvement in cardiac function in patients
with chronic heart failure Eur J Heart Fail (Vol. 8, pp. 308-313). Netherlands.
Ciolac, E. G., Guimaraes, G. V., VM, D. A., Bortolotto, L. A., Doria, E. L., & Bocchi, E.
A. (2009). Acute effects of continuous and interval aerobic exercise on 24-h
ambulatory blood pressure in long-term treated hypertensive patients. Int J
Cardiol, 133(3), 381-387. doi: 10.1016/j.ijcard.2008.02.005
Danielsson, A., Willén, C., & Sunnerhagen, K. S. (2007). Measurement of energy cost by
the physiological cost index in walking after stroke. Arch Phys Med Rehabil,
88(10), 1298-1303. doi: S0003-9993(07)00440-6 [pii]
10.1016/j.apmr.2007.06.760
Dolbow, D. R., Farley, R. S., Kim, J. K., & Caputo, J. L. (2008). Oxygen consumption,
heart rate, rating of perceived exertion, and systolic blood pressure with water
treadmill walking. J Aging Phys Act, 16(1), 14-23.
Donnan, G. A., Fisher, M., Macleod, M., & Davis, S. M. (2008). Stroke. Lancet,
371(9624), 1612-1623. doi: S0140-6736(08)60694-7
Dorresteijn, J. A., van der Graaf, Y., Spiering, W., Grobbee, D. E., Bots, M. L., Visseren,
F. L., & Group, S. M. o. A. D. S. (2012). Relation between blood pressure and
vascular events and mortality in patients with manifest vascular disease: J-curve
revisited. Hypertension, 59(1), 14-21. doi: HYPERTENSIONAHA.111.179143
Duffield, R., Dawson, B., Pinnington, H. C., & Wong, P. (2004). Accuracy and reliability
of a Cosmed K4b2 portable gas analysis system. J Sci Med Sport, 7(1), 11-22.
Durstine, L., Moore, G., Painter, P., & Roberts, S. (2009). ACSM'S Exercise
Management for Persons with Chronic Diseases and Disabilities (3 ed.). USA.
Eng, J. J., Dawson, A. S., & Chu, K. S. (2004). Submaximal exercise in persons with
stroke: test-retest reliability and concurrent validity with maximal oxygen
consumption. Arch Phys Med Rehabil, 85(1), 113-118. doi: S0003999303004362
42
Ezzati, M., Lopez, A. D., Rodgers, A., Vander Hoorn, S., Murray, C. J., & Group, C. R.
A. C. (2002). Selected major risk factors and global and regional burden of
disease. Lancet, 360(9343), 1347-1360. doi: S0140-6736(02)11403-6
Fisher, S. V., & Gullickson, G., Jr. (1978). Energy cost of ambulation in health and
disability: a literature review. Arch Phys Med Rehabil, 59(3), 124-133.
Forjaz, C. L., Tinucci, T., Ortega, K. C., Santaella, D. F., Mion, D., Jr., & Negrao, C. E.
(2000). Factors affecting post-exercise hypotension in normotensive and
hypertensive humans. Blood Press Monit, 5(5-6), 255-262.
Furie, K. L., Kasner, S. E., Adams, R. J., Albers, G. W., Bush, R. L., Fagan, S. C.,
Kernan, W. N. (2011). Guidelines for the prevention of stroke in patients with
stroke or transient ischemic attack a guideline for healthcare professionals from
the American Heart Association/American Stroke Association. Stroke, 42(1),
227-276.
Gabrielsen, A., Warberg, J., Christensen, N. J., Bie, P., Stadeager, C., Pump, B., &
Norsk, P. (2000). Arterial pulse pressure and vasopressin release during graded
water immersion in humans. Am J Physiol Regul Integr Comp Physiol, 278(6),
R1583-1588.
Globas, C., Becker, C., Cerny, J., Lam, J. M., Lindemann, U., Forrester, L. W., . . . Luft,
A. R. (2011). Chronic Stroke Survivors Benefit From High-Intensity Aerobic
Treadmill Exercise: A Randomized Controlled Trial Neurorehabil Neural Repair.
Go, A. S., Mozaffarian, D., Roger, V. L., Benjamin, E. J., Berry, J. D., Borden, W. B., . .
. Subcommittee, A. H. A. S. C. a. S. S. (2013). Heart disease and stroke statistics-2013 update: a report from the American Heart Association. Circulation, 127(1),
e6-e245. doi: 10.1161/CIR.0b013e31828124ad
Gomes Anunciacao, P., & Doederlein Polito, M. (2011). A review on post-exercise
hypotension in hypertensive individuals. Arq Bras Cardiol, 96(5), e100-109.
Greene, N. P., Lambert, B. S., Greene, E. S., Carbuhn, A. F., Green, J. S., & Crouse, S. F.
(2009). Comparative efficacy of water and land treadmill training for overweight
or obese adults. Med Sci Sports Exerc, 41(9), 1808-1815. doi:
10.1249/MSS.0b013e3181a23f7f
Guidry, M. A., Blanchard, B. E., Thompson, P. D., Maresh, C. M., Seip, R. L., Taylor, A.
L., & Pescatello, L. S. (2006). The influence of short and long duration on the
blood pressure response to an acute bout of dynamic exercise Am Heart J (Vol.
151, pp. 1322 e1325-1312). United States.
Hall, J., Grant, J., Blake, D., Taylor, G., & Garbutt, G. (2004). Cardiorespiratory
responses to aquatic treadmill walking in patients with rheumatoid arthritis.
Physiother Res Int, 9(2), 59-73.
43
Harris-Love, M. L., Forrester, L. W., Macko, R. F., Silver, K. H., & Smith, G. V. (2001).
Hemiparetic gait parameters in overground versus treadmill walking.
Neurorehabil Neural Repair, 15(2), 105-112.
Heidenreich, P. A., Trogdon, J. G., Khavjou, O. A., Butler, J., Dracup, K., Ezekowitz, M.
D., Council on Cardiovascular Surgery and Anesthesia (2011). Forecasting the
future of cardiovascular disease in the United States: a policy statement from the
American Heart Association. Circulation, 123(8), 933-944. doi:
CIR.0b013e31820a55f5
Huntzinger, A. (2008). AHA Releases Guidelines for Hypertension Management in
Adults With or At Risk of CAD. Am Fam Physician, 78(2), 270-276.
Irie, K., Yamaguchi, T., Minematsu, K., & Omae, T. (1993). The J-curve phenomenon in
stroke recurrence. Stroke, 24(12), 1844-1849.
Jain, S., Namboodri, K. K., Kumari, S., & Prabhakar, S. (2004). Loss of circadian rhythm
of blood pressure following acute stroke. BMC Neurol, 4, 1. doi: 10.1186/14712377-4-1
Johnston, S. C., Selvin, S., & Gress, D. R. (1998). The burden, trends, and demographics
of mortality from subarachnoid hemorrhage. Neurology, 50(5), 1413-1418.
Jorgensen, H. S., Nakayama, H., Raaschou, H. O., Vive-Larsen, J., Stoier, M., & Olsen,
T. S. (1995). Outcome and time course of recovery in stroke. Part II: Time course
of recovery. The Copenhagen Stroke Study Arch Phys Med Rehabil (Vol. 76, pp.
406-412). United States.
Judd, S. J. (2005). Brain Disorders Sourcebook (Second ed.). Detroit: Omnigraphics.
Kaufman, F. L., Hughson, R. L., & Schaman, J. P. (1987). Effect of exercise on recovery
blood pressure in normotensive and hypertensive subjects. Med Sci Sports Exerc,
19(1), 17-20.
Keese, F., Farinatti, P., Pescatello, L., & Monteiro, W. (2011). A comparison of the
immediate effects of resistance, aerobic, and concurrent exercise on postexercise
hypotension. J Strength Cond Res, 25(5), 1429-1436. doi:
10.1519/JSC.0b013e3181d6d968
Kenney, M. J., & Seals, D. R. (1993). Postexercise hypotension. Key features,
mechanisms, and clinical significance. Hypertension, 22(5), 653-664.
Kulics, J. M., Collins, H. L., & DiCarlo, S. E. (1999). Postexercise hypotension is
mediated by reductions in sympathetic nerve activity. Am J Physiol, 276(1 Pt 2),
H27-32.
44
Kurl, S., Laukkanen, J. A., Rauramaa, R., Lakka, T. A., Sivenius, J., & Salonen, J. T.
(2003). Cardiorespiratory fitness and the risk for stroke in men Arch Intern Med
(Vol. 163, pp. 1682-1688). United States.
Lip, G. Y. H., Zarifis, J., Farooqi, I. S., Page, A., Sagar, G., & Beevers, D. G. (1997).
Ambulatory Blood Pressure Monitoring in Acute Stroke. Stroke, 28(1), 31-35.
doi: 10.1161/01.STR.28.1.31
Liu, S., Thomas, S. G., Sasson, Z., Banks, L., Busato, M., & Goodman, J. M. (2012).
Blood pressure reduction following prolonged exercise in young and middle-aged
endurance athletes. Eur J Prev Cardiol. doi: 2047487312454759
Lloyd-Jones, D. M., Evans, J. C., Larson, M. G., O'Donnell, C. J., Roccella, E. J., &
Levy, D. (2000). Differential control of systolic and diastolic blood pressure :
factors associated with lack of blood pressure control in the community.
Hypertension, 36(4), 594-599.
Lord, S. E., McPherson, K., McNaughton, H. K., Rochester, L., & Weatherall, M. (2004).
Community ambulation after stroke: how important and obtainable is it and what
measures appear predictive? Arch Phys Med Rehabil, 85(2), 234-239. doi:
S0003999303008943
MacDonald, J. R., Hogben, C. D., Tarnopolsky, M. A., & MacDougall, J. D. (2001). Post
exercise hypotension is sustained during subsequent bouts of mild exercise and
simulated activities of daily living. J Hum Hypertens, 15(8), 567-571. doi:
10.1038/sj.jhh.1001223
MacDonald, J. R., MacDougall, J. D., & Hogben, C. D. (2000). The effects of exercise
duration on post-exercise hypotension. J Hum Hypertens, 14(2), 125-129.
Mach, C., Foster, C., Brice, G., Mikat, R. P., & Porcari, J. P. (2005). Effect of exercise
duration on postexercise hypotension. J Cardiopulm Rehabil, 25(6), 366-369. doi:
00008483-200511000-00010
Macko, R. F., DeSouza, C. A., Tretter, L. D., Silver, K. H., Smith, G. V., Anderson, P.
A., Dengel, D. R. (1997). Treadmill aerobic exercise training reduces the energy
expenditure and cardiovascular demands of hemiparetic gait in chronic stroke
patients. A preliminary report. Stroke, 28(2), 326-330.
Macko, R. F., Ivey, F. M., Forrester, L. W., Hanley, D., Sorkin, J. D., Katzel, L. I.,
Goldberg, A. P. (2005). Treadmill exercise rehabilitation improves ambulatory
function and cardiovascular fitness in patients with chronic stroke: a randomized,
controlled trial. Stroke, 36(10), 2206-2211. doi:
10.1161/01.str.0000181076.91805.89
45
Macko, R. F., Katzel, L. I., Yataco, A., Tretter, L. D., DeSouza, C. A., Dengel, D. R.,
.Silver, K. H. (1997). Low-velocity graded treadmill stress testing in hemiparetic
stroke patients. Stroke, 28(5), 988-992.
Mancia, G., De Backer, G., Dominiczak, A., Cifkova, R., Fagard, R., Germano, G., The
task force for the management of arterial hypertension of the European Society of
Cardiology. (2007). 2007 Guidelines for the management of arterial hypertension:
The Task Force for the Management of Arterial Hypertension of the European
Society of Hypertension (ESH) and of the European Society of Cardiology (ESC).
Eur Heart J, 28(12), 1462-1536. doi: 10.1093/eurheartj/ehm236
Mancia, G., Zanchetti, A., Agabiti-Rosei, E., Benemio, G., De Cesaris, R., Fogari, R.,
Pessino, A. (1997). Ambulatory blood pressure is superior to clinic blood pressure
in predicting treatment-induced regression of left ventricular hypertrophy.
SAMPLE Study Group. Study on Ambulatory Monitoring of Blood Pressure and
Lisinopril Evaluation. Circulation, 95(6), 1464-1470.
Matsumoto, S., Kawahira, K., Etoh, S., Ikeda, S., & Tanaka, N. (2006). Short-term
effects of thermotherapy for spasticity on tibial nerve F-waves in post-stroke
patients. Int J Biometeorol, 50(4), 243-250. doi: 10.1007/s00484-005-0009-4
McCain, K. J., Smith, P. S., Polo, F. E., Coleman, S. C., & Baker, S. (2011). Excellent
outcomes for adults who experienced early standardized treadmill training during
acute phase of recovery from stroke: a case series Top Stroke Rehabil (Vol. 18,
pp. 428-436). United States.
Moraes, M. R., Bacurau, R. F., Ramalho, J. D., Reis, F. C., Casarini, D. E., Chagas, J. R.,
Araujo, R. C. (2007a). Increase in kinins on post-exercise hypotension in
normotensive and hypertensive volunteers. Biol Chem, 388(5), 533-540. doi:
10.1515/BC.2007.055
Moraes, M. R., Bacurau, R. F., Ramalho, J. D., Reis, F. C., Casarini, D. E., Chagas, J. R.,
Araujo, R. C. (2007b). Increase in kinins on post-exercise hypotension in
normotensive and hypertensive volunteers. Biol Chem, 388(5), 533-540. doi:
10.1515/BC.2007.055
National Institute of Neurological Disorders and Stroke. Stroke: Hope Through Research.
(2012, Oct. 2012). from
http://www.ninds.nih.gov/disorders/stroke/detail_stroke.htm
Ohira, T., Shahar, E., Chambless, L. E., Rosamond, W. D., Mosley, T. H., & Folsom, A.
R. (2006). Risk factors for ischemic stroke subtypes: the Atherosclerosis Risk in
Communities study. Stroke, 37(10), 2493-2498. doi:
01.STR.0000239694.19359.88
Ovbiagele, B. (2012). Low-Normal Systolic Blood Pressure and Secondary Stroke Risk. J
Stroke Cerebrovasc Dis. doi: 10.1016/j.jstrokecerebrovasdis.2011.12.003
46
Ovbiagele, B., Diener, H. C., Yusuf, S., Martin, R. H., Cotton, D., Vinisko, R., . . . Bath,
P. M. (2011). Level of systolic blood pressure within the normal range and risk of
recurrent stroke JAMA (Vol. 306, pp. 2137-2144). United States.
Park, S. E., Lee, M., Yoon, B., Lee, B., Shin, H., Choi, W., Min, K. (2010). Comparison
of Underwater and Overground Treadmill Walking Exercise to Improve Gait and
Physical Function in People After Stroke. J Int Acad Phys Ther Res, 1, 120-125.
Patarroyo, S. X., & Anderson, C. (2012). Blood pressure lowering in acute phase of
stroke: latest evidence and clinical implications. Ther Adv Chronic Dis, 3(4), 163171. doi: 10.1177/2040622312450183
Pescatello, L. S., Fargo, A. E., Leach, C. N., Jr., & Scherzer, H. H. (1991). Short-term
effect of dynamic exercise on arterial blood pressure. Circulation, 83(5), 15571561.
Pescatello, L. S., Guidry, M. A., Blanchard, B. E., Kerr, A., Taylor, A. L., Johnson, A.
N., Thompson, P. D. (2004). Exercise intensity alters postexercise hypotension. J
Hypertens, 22(10), 1881-1888.
Pescatello, L. S., Miller, B., Danias, P. G., Werner, M., Hess, M., Baker, C., & Jane De
Souza, M. (1999). Dynamic exercise normalizes resting blood pressure in mildly
hypertensive premenopausal women Am Heart J (Vol. 138, pp. 916-921). United
States.
Platts, M. M., Rafferty, D., & Paul, L. (2006). Metabolic cost of over ground gait in
younger stroke patients and healthy controls. Med Sci Sports Exerc, 38(6), 10411046. doi: 00005768-200606000-00003 [pii]
10.1249/01.mss.0000222829.34111.9c
Pontes, F. L., Jr., Bacurau, R. F., Moraes, M. R., Navarro, F., Casarini, D. E., Pesquero, J.
L., Picarro, I. C. (2008). Kallikrein kinin system activation in post-exercise
hypotension in water running of hypertensive volunteers Int Immunopharmacol
(Vol. 8, pp. 261-266). Netherlands.
Quinn, T. J. (2000). Twenty-four hour, ambulatory blood pressure responses following
acute exercise: impact of exercise intensity. J Hum Hypertens, 14(9), 547-553.
Rodgers, A., MacMahon, S., Gamble, G., Slattery, J., Sandercock, P., & Warlow, C.
(1996). Blood pressure and risk of stroke in patients with cerebrovascular disease.
The United Kingdom Transient Ischaemic Attack Collaborative Group. BMJ,
313(7050), 147.
Rodriguez, D., Silva, V., Prestes, J., Rica, R. L., Serra, A. J., Bocalini, D. S., & Pontes, F.
L. J. (2011). Hypotensive response after water-walking and land-walking exercise
47
sessions in healthy trained and untrained women Int J Gen Med (Vol. 4, pp. 549554).
Routledge, F., & McFetridge-Durdle, J. (2007). Nondipping blood pressure patterns
among individuals with essential hypertension: a review of the literature. Eur J
Cardiovasc Nurs, 6(1), 9-26. doi: 10.1016/j.ejcnurse.2006.05.001
Sommerfeld, D. K., Eek, E. U., Svensson, A. K., Holmqvist, L. W., & von Arbin, M. H.
(2004). Spasticity after stroke: its occurrence and association with motor
impairments and activity limitations. Stroke, 35(1), 134-139. doi:
01.STR.0000105386.05173.5E
Staessen, J. A., Thijs, L., Fagard, R., O'Brien, E. T., Clement, D., de Leeuw, P. W.,
Webster, J. (1999). Predicting cardiovascular risk using conventional vs
ambulatory blood pressure in older patients with systolic hypertension. Systolic
Hypertension in Europe Trial Investigators. JAMA, 282(6), 539-546.
Stroke, N. I. o. N. D. a. (2004, 2012). Stroke: Hope Through Research. from
http://www.ninds.nih.gov/disorders/stroke/detail_stroke.htm
Sugiyama, Y., Miwa, C., Xue, Y. X., Iwase, S., Suzuki, H., Matsukawa, T., Mano, T.
(1993). Cardiovascular function in the elderly during water immersion. Environ
Med, 37(1), 91-94.
Syme, A. N., Blanchard, B. E., Guidry, M. A., Taylor, A. W., Vanheest, J. L., Hasson, S.,
Pescatello, L. S. (2006). Peak systolic blood pressure on a graded maximal
exercise test and the blood pressure response to an acute bout of submaximal
exercise. Am J Cardiol, 98(7), 938-943. doi: S0002-9149(06)01183-0
Tang A, M. S., Oh P, McIlroy WE, Brooks D. (2010). Feasibility and effects of adapted
cardiac rehabilitation after stroke: a prospective trial. BMC Neurol, 10, 40.
Terblanche, E., & Millen, A. M. (2012). The magnitude and duration of post-exercise
hypotension after land and water exercises. Eur J Appl Physiol. doi:
10.1007/s00421-012-2398-5
Turnbull, F., & Collaboration, B. P. L. T. T. (2003). Effects of different blood-pressurelowering regimens on major cardiovascular events: results of prospectivelydesigned overviews of randomised trials. Lancet, 362(9395), 1527-1535. doi:
S0140673603147393
Wallace, J. P., Bogle, P. G., King, B. A., Krasnoff, J. B., & Jastremski, C. A. (1997). A
comparison of 24-h average blood pressures and blood pressure load following
exercise. Am J Hypertens, 10(7 Pt 1), 728-734. doi: S0895-7061(97)00070-8
48
Wallace, J. P., Bogle, P. G., King, B. A., Krasnoff, J. B., & Jastremski, C. A. (1999). The
magnitude and duration of ambulatory blood pressure reduction following acute
exercise. J Hum Hypertens, 13(6), 361-366.
Warlow, C., Sudlow, C., Dennis, M., Wardlaw, J., & Sandercock, P. (2003). Stroke.
Lancet, 362(9391), 1211-1224. doi: S0140-6736(03)14544-8
Whelton, P. K., He, J., Appel, L. J., Cutler, J. A., Havas, S., Kotchen, T. A., Committee,
N. H. B. P. E. P. C. (2002). Primary prevention of hypertension: clinical and
public health advisory from The National High Blood Pressure Education
Program. JAMA, 288(15), 1882-1888.
Zanchetti, A., & Waeber, B. (2006). Hypertension: which aspects of hypertension should
we impact on and how? J Hypertens Suppl, 24(5), S2-5. doi:
10.1097/01.hjh.0000240039.97472.f1
Appendix A
California State University, Northridge
The Effects of Aquatic and Overground Treadmill Exercise on Post Exercise
Hypotension in People Post-Stroke.
INFORMED CONSENT
Introduction
You are being asked to participate in a research study.
Participation in this study is completely voluntary. Please read
the information below and ask questions about anything that you
do not understand before deciding if you want to participate. A
researcher listed below will be available to answer your
questions.
Purpose of the Study
The purpose of this research study is to evaluate the effects of
49
aquatic and overground treadmill exercise on blood pressure
post-exercise in people post-stroke.
Subject Information
You are eligible to participate in this study if you have been
diagnosed with hemiplegic stroke, are a minimum of 6 months
post-stroke, are above 34 years old, are able to participate in
approximately 30 minutes of walking on an underwater treadmill
and overground treadmill, are able to read, communicate, and
follow directions in English. You are not eligible to participate in
this study if you have a resting systolic blood pressure of greater
than 140 mmHg or below 100 mmHg, a resting diastolic blood
pressure of greater than 95 mmHg or below 61 mmHg,
cardiorespiratory complications, or have had surgery within the
last 6 months.
This study will last approximately a week and total 10 hours of
clinical time and 72 hours of ambulatory blood pressure
measurement monitoring which will approximate to a total of 3
days and 10 hours of your time.
Procedures
Upon being recruited for this study, participants will be required
to obtain medical clearance from their primary physician prior to
any participation in this study. Once medical clearance has been
obtained, participants will be instructed to schedule their initial
50
visit. To participate in the study, participants will be required to
bring and wear: a bathing suit, exercise shorts, a shirt, and a
towel.
After participant’s have obtained medical clearance they will be
directed to come to the Center of Achievement through Adapted
Physical Activity (CoA) on the California State University,
Northridge campus for a brief one-on-one explanation of the
significance behind this study as well as an explanation of the
exercise protocol. All data collection and cardiovascular sessions
will be held at the CoA, CSUN.
The initial visit will include: 1) participants’ characteristics will
be recorded and will then be subject to a lower extremity motor
assessment: (FMA-LE, University of Gothenburg, Sweden),
2)participants will perform a maximal exercise test.3)
Participants will be given an ambulatory blood pressure monitor
to assess their blood pressure for 24 hours on a day without
exercise.
After this initial meeting, participants will be randomized to start
with either aquatic or land treadmill testing. The rest of the visits
will occur in random order with a minimum of 48 hours between
exercise sessions. Phone calls will be made to monitor adherence
to ambulatory blood pressure monitor readings.
51
The second visit will consist of two aquatic walking sessions to
ensure safety during treadmill exercise. Data collection
procedures will last approximately 2 hours which will include: 1)
a participant will perform three 5-minute stages of walking on an
overground treadmill. Blood pressure will be measured at the
end of every stage, 2) after a 15 minute break, the participant
will perform a graded treadmill test at slow speed to a treadmill
walking speed at 70% of a participants’ predicted maximum
oxygen consumption (taken from the “initial visit”), 3)
participants will be given an ambulatory blood pressure monitor
to assess their blood pressure for 24 hours on a day without
exercise.
The third visit will consist of two aquatic walking sessions to
ensure safety during aquatic treadmill exercise. Data collection
procedures will last approximately 2 hours which will include: 1)
a participant will perform three 5-minute stages of walking on an
aquatic treadmill. Blood pressure will be measured at the end of
every stage, 2) after a 15 minute break, the participant will
perform a graded treadmill test at slow speed to a treadmill
walking speed at 70% of a participants’ predicted maximum
oxygen consumption (taken from the “initial visit”), 3)
participants will be given an ambulatory blood pressure monitor
to assess their blood pressure for 24 hours on a day without
52
exercise.
The fourth visit will last approximately 2 hours and 15 minutes
which will include: 1) 25 minutes of walking on a land or aquatic
treadmill, 2)1 hour of seated rest, 3) blood pressure will be
analyzed for 24 hours following exercise via 24 hour ambulatory
blood pressure monitor on a day without exercise.
The fourth visit will last approximately 2 hours and 15 minutes
which will include: 1) 25 minutes of walking on a land or aquatic
treadmill. If the participant walked on an overground treadmill
during the fourth visit, the participant will walk on an overground
treadmill during the fifth visit and vice-versa, 2) 1 hour of seated
rest, 3) blood pressure will be analyzed for 24 hours following
exercise via 24 hour ambulatory blood pressure monitor on a day
without exercise, 4) the participant will be debriefed and the lead
graduate researcher will coordinate a day that the Meditech
ABPM-05 can be picked up at their home or dropped off at the
Center of Achievement.
Risks
While you understand that we strive to prevent any possible
complications or injuries, there are risks involved in participation
such as: cardiovascular complications, dehydration, pain,
soreness, falling, drowning, physical/psychological fatigue, skin
irritation, muscle cramps, other water safety issues, dizziness,
53
and nausea. In an attempt to minimalize these risks, certain
precautions will be taken such as: 1) physician clearance will be
obtained to ensure participants do not have any contraindications
for the exercise protocol, 2) participants will be allowed water
when necessary in order to keep themselves hydrated during data
collection, 3) research assistants will be used as active spotters
during the transition from the lobby to the equipment and off of
the equipment back to the lobby at the conclusion of the exercise
session, 4) emergency services (911) will be contacted and
participants will be referred will be referred to their primary care
physician.
Benefits
The benefits of this study will be having participants complete
organized exercise sessions. The knowledge obtained from this
study may contribute to creating an alternate nonpharmacological method of blood pressure regulation in strokesurvivors. The only alternative to participation in this study is
not to participate.
Compensation, Costs,
You will not be paid for your participation in this research study.
and Reimburstment
There is no cost to you for participation in this study. Parking
passes will be provided by the Center of Achievement. You will
not be reimbursed for any out of pocket expenses, such as
transportation fees.
54
Withdrawal
You are free to withdraw from this study at any time. If you
decide to withdraw from this study you should notify the
research team immediately. The research team may also end
your participation in this study if you do not follow instructions,
miss scheduled visits, or if your safety and welfare are at risk.
Confidentiality
All identifiable information that will be collected about you will
be removed at the end of data collection and replaced with a
code.
All virtual research data will be stored on a laptop computer that
is password protected and owned by the Center of Achievement
at California State University Northridge.
All physical records or identifiable information will be kept in a
locked desk in the Center of Achievement through Adapted
Physical Activity in the main office where only the primary
investigator, Byron Lai, and faculty advisor, Dr. Taeyou Jung
have access.
The researcher and faculty advisor named on the first page of
this form will have access to your study records. Any
information derived from this research project that personally
identifies you will not be voluntarily released or disclosed
without your separate consent, except as specifically required by
55
law. Publications and/or presentations that result from this study
will not include identifiable information about you.
The researchers intend to keep the research data until the
research is published and then it will be destroyed.
Concerns
If you have any comments, concerns, or questions regarding the
conduct of this research please contact the research team listed
on the first page of this form.
If you are unable to reach a member of the research team listed
on the first page of the form and have general questions, or you
have concerns or complaints about the research study, research
team, or questions about your rights as a research subject, please
contact Research and Sponsored Projects, 18111 Nordhoff
Street, California State University, Northridge, Northridge, CA
91330-8232, or phone 818-677-2901.
Voluntary
You should not sign this form unless you have read it and been
Participation
given a copy of it to keep. Participation in this study is
voluntary. You may refuse to answer any question or
discontinue your involvement at any time without penalty or loss
of benefits to which you might otherwise be entitled. Your
decision will not affect your future relationship with California
56
State University, Northridge. Your signature below indicates
that you have read the information in this consent form and have
had a chance to ask any questions that you have about the study.
CONSENT
I agree to participate in the study.
___________________________________________________
Subject Signature
__________________
Date
___________________________________________________
Printed Name of Subject
___________________________________________________
Researcher Signature
__________________
Date
_______________________________________________
Printed Name of Researcher
57
Appendix B
FUGL-MEYER ASSESSMENT
LOWER EXTREMITY (FMA-LE)
Date: Assessment of sensorimotor function
Examiner:
ID:
Fugl-Meyer AR, Jaasko L, Leyman I, Olsson S, Steglind S: The post-stroke hemiplegic patient. 1. a method for
evaluation of physical performance. Scand J Rehabil Med 1975, 7:13-31.
E. LOWER EXTREMITY
I. Reflex activity, supine position
0
can be
elicited
2
0
2
none
Flexors: knee flexors
Extensors: patellar, Achilles
Subtotal I (max 4)
II. Volitional movement within synergies, supine
positionsynergy: Maximal hip flexion
Flexor
(abduction/external rotation),
Hip
flexion Knee
flexion Ankle
dorsiflexion
58
non
e0
partial
full
1
2
0
1
2
0
1
2
maximal flexion in knee and ankle
joint (palpate distal tendons to
ensure active knee flexion).
Hip
ext
ensi
on
Extensor synergy: From flexor synergy
add
to the hip
Subtotalucti
II (max 14)
extension/adduction, knee extension
on
III. Volitional movement mixing synergies, sitting
and
ankleknee
plantar
flexion.
Resistance
position,
10cm
from the
edge of the chair/bed
is
applied
to
ensure
active
Knee
extension
Knee
flexion
noboth
active
motion
movement,
evaluate
movement
from
actively or
Ankle
plantar
and strength.
passively
no flexion beyond 90°, palpate tendons of
flexion
hamstrings
extended knee
knee flexion beyond 90°, palpate tendons of
Ankle
no
active motion
hamstrings
dorsiflexion
limited
compare
dorsiflexi
with
on
Subtotal III (max 4)
unaffected
complete
dorsiflexi
side
IV. Volitional movement
with little or no synergy,
on
standing position, hip at 0°
Knee flexion to
90°
hip at 0°,
balance
support is
allowed
Ankle
dorsiflexion
compare
with
unaffected
side
no active motion / immediate and simultaneous
hip flexion
0
1
2
0
1
2
0
1
2
0
1
2
non
e0
partial
full
1
2
0
1
2
non
e0
partial
full
1
less than 90° knee flexion or hip flexion during
movement at least 90° knee flexion without
2
simultaneous hip flexion
no active motion
0
limited
dorsiflexi
on
complete
dorsiflexi
on
1
2
Subtotal IV (max 4)
V. Normal reflex activity supine position, evaluated only if full score of 4 points
achieved on earlier part
Reflex
0 points on
part IV or 2 of 3 reflexes markedly
IV, compare with unaffected
side
activity
hyperactive
knee
1 reflex markedly hyperactive or at least 2
flexors,
reflexes lively maximum of 1 reflex lively,
Achilles,
none hyperactive
patellar
Subtotal V (max 2)
59
0
1
2
Total E (max 28)
E. LOWER EXTERMTY
/28
F. COORDINATION / SPEED
/6
TOTAL E-F (motor function)
/34
Appendix C
Raw Data in PASW Cording Format
Table C1. Mixed model ANOVA mean diastolic blood pressure post-exercise
Table C2. Mixed model ANOVA mean systolic blood pressure post-exercise
Abbreviations used for coding for statistical analysis
Conditions
1
Control
2
Overground Treadmill
3
Aquatic Treadmill
Dependent Variables
BP
Blood Pressure
SBP
Systolic Blood Pressure
DBP Diastolic Blood Pressure
60
Miscellaneous
Hrs
Hours
PE
Post-Exercise
Table C1. Mixed Model Anova Diastolic Blood Pressure Post-Exercise
Condition
1
1
1
1
1
1
1
2
2
2
2
2
2
2
3
3
3
Baseline
71
72
74
58
92
82
79.3
61
78
71.3
56
92.3
69.8
74.5
67.8
76.5
69.7
2_Hrs_PE
66
71
79.25
62
101
86
74
71
95
79
48
89
74.25
64
67
87.67
69
4_Hrs_PE
70
71
80.75
57
93
73
56
67
65
67
73
94
65
66
73
58.25
69
61
6_Hrs_PE
65
78
77.25
64
98
77
53
59
74
71
61
85
78
67
61
68.75
81
8_Hrs_PE
67
84
79.5
61
95
78
76
61
62
72
64.5
91
73
68
55
78
79
3
3
3
3
64.5
82
80.2
73
59
86
90
69
63
84
71
62
61
78
72
68.33
Table C2. Mixed Model Anova Systolic Blood Pressure Post-Exercise
Condition
1
1
1
1
1
1
1
2
2
2
2
2
2
2
3
3
3
3
3
Baseline
115.5
116
123.5
106
139
119
127
100.7
119
119.7
104
125.8
118.5
134.3
106.8
117.5
108
104
129
2_Hrs_PE
115
114
124.5
115
133
130.5
130.5
116
130
126
131
126
116
127.8
107
127
118
105
126
4_Hrs_PE
113.33
119
123.5
119
136
114
102.5
116
107
115
118
120
107
133
115
99
129
104
125
62
6_Hrs_PE
103.25
124
118.5
113
142
117
113
98
117
118
113
123.67
116
133
103
113
101
114
118
8_Hrs_PE
117
115
125.8
107
133
117
143
92
101
113
115
123
117
128
90
101.5
102
104
125.3
58
92
71
63
3
3
124.5
127.8
131
134
126
115
63
111
126
114
121.5