predicting maximal voÂ² in exercise-induced asthmatics

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Ithaca College Theses

2004

Predicting maximal vo² in exercise-inducedasthmatics using albuterolKerry A. KerfootIthaca College

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PREDICTING MAXIMAL V02 1N

EXERCISE―INDUCED ASTHMATICS USING ALB■「 llEROL

A Masters Thesis presented to the Faculty of the

Graduate Program in Exercise and Sport Sciences

Ithaca College

In partial ilillment ofthe reqlllrements for the degree

Master of Science

by

Kerv A.Kerfoot

September 2004

Ithaca CollegeSchool of Health Sciences and Human Performance

Itlacu New York

CERTIFICATE OF APPROVAL

MASTER OF SCIENCE THESIS

This is to certiff that the Thesis of

Kerry Kerfoot

Submitted in partial fulfillment of the requirements for the

Degree of Master of Science in the School ofHealth Sciences and Human Performance

Thesis Adviser:

Committee Member:

Candidate:

Chair,

Graduate Progtam:

Dean of Graduate Studies:

Date:

ABSTRACT

This study investigated the ability to predict morimal oxygen consumption (VO2) using

the YMCA submaximal cycle test in people with exercise induced asthma (EIA) using

albuterol (AL). In order to investigate this relatiomhip, heart rafe ftIR) at rest and during

ttnee stages of submaximal testing was measured and amlyzed. Predicted maximal VO2,

derived from steady state HR dtring stages 2 and 3 of submaximal testing on AL and on

placebo (PL), was compared with measured maximalY0z from a rnaximal cycle test

while on AL. Peak flow prior to submarimal testing with AL use and with PL use was

also analyzed. The zubjects included six males and five females aged 18-35 years.

Rdsults revealed AL caused a significant increase (p < .05) in I{R at rest and during stage

I of submaximal testing, however, no effect was seen during stages 2 afi 3. Results also

showed there was a significantly greater peak flowwith AL than PL at rest. Ultimately,

there was no significant difference found betweenpredicted maximal VO2 using AL or

PL and measured maximal VO2 using AL. Following this, a separate analysis was done

on predicted maximal VO2 compared to measured maximal VO2 for the subjects who

used the same submaximal workloads (\VI,) (U = 6) when on AL and PL, and also for

those who used dif,[erent WL (U:5) during stages 2 and3. Agarn, there was no

significant difference found in these groups for predicted vs. measured maximal VO2.

These results indicate that predicted maximal VO2 from submaximal testing with AL or

with PL equally predicts measured maximal VO2 in people with EIA. However, given

the error often seen in predicting maximal VO2 from submaximal testing, sometimes

greater than7soh, caution should be used when prescribing exercise from these tests in

people with EIA.

ACKNOWLEDGMENTS

The investigator wishes to express her sincere appreciation to everyone involved in

the completion of this study:

1. Dr. Gary A. Sforzo, my thesis advisor, for all his guidance, advice, and

encouragement throughout the investigation.

Z. Dr. Jeffiey Ives for his watchful eye and his encouragement when I needed it the

most.

3. Gerard Dunphy for his advice, expertise, and help with supplies for the

investigation.

4. Wai Kwong Hui, my friend, for his patience while teaching me how to use the gas

analyzer equipment and all of his help with subject recruitment and data collection.

5. Patricia and William Kerfoot, my parents, for their tireless encouragement and for

the example they set for me on the importance of pursuing knowledge.

6. Chris Kerfoot, my brother, for he is always an inspiration.

7. Ben Howell, my fianc6, for his support.

8. The Schering Pharinaceuticals Company for supplying the placebo inhalers.

lV

TABLE OF CONTENTS｀

ABSTRACT.……………….・ ……………………………………………¨̈ ¨̈………・・… …̈……………………

ACKNOWLEDGMENTS.… ………………………………………………………………………

LIST OF TABLES.… …………………・・…………………・・… …̈………・・̈・・………・・……………・・̈ …̈・

Chapter

l.mODUC■ ON.…………………………………・・……・・……………………………… …̈………

Statelnent ofthe Pwpose......¨ ¨̈ ¨̈ ¨̈・・・・̈ ¨̈ ¨̈ ¨̈ ¨̈・・̈ …̈……̈ ………・

Scope ofthe PЮblem...¨ ¨̈ ¨̈ ・̈・̈ …̈…̈ ¨̈ ………………・・・・……………………・・̈ ¨

Hypothesis ofthe Study… ……… …… ……… … …… … ……… …

Dettnition ofTerIIns.… ………………………………………………̈ ………………・

Assmptions ofthe Study… …………………………………………………・・……

Delimitatiolls ofthe Study… ……………………………………………………

Limitations ofthe Study… …… ……… ……… … …… … …………

2.REVIEW OF L11■RAШ .………………………………………………………………

Sublllaxilllllal Exercise Testmg.¨ .̈.¨¨̈ ・̈・"¨ ・̈・̈・・̈・・̈ …̈…………・・̈・・・・・ 7

Autollonuc ContЮ l ofHcart Ratc.… ………………Ⅲ……………・・………・・…… 9

Exercise― Induced Asthma。 ……………・・………………・…… ・̈………・…… 10

Effect Albuterol has on Hcart Rate...¨ ¨̈ ・̈・̈ ¨̈ ………………・・・・̈ ¨̈ ¨̈ 。̈ 12

Exercise Testing ofPeople With Asthma vs.

People Without Asthma

Albuterol and Maximal Exercise Testing 20

Summary 2l

Ｃ晰“　　・Ш　　　・Ⅳ　　　̈Ｖ・・‐

1

3

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4

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5

5

6・

7

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V

3. METHODS .............

Selection of Subjects

Procedures for Data Collection

I'reatment of Data

SummarY

RESULTS

Heart Rate AnalYsis ....;....."

Peak Flow AnalYsis

VO2 Max Analysis """"""""""'

SummarY

22

22

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27

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37

39

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44

4.

5。 DISCUSS10N.………………̈・・… …̈……………・・…………・・…………………………………・・“̈ ・̈・・・

Erect ofAlbutcrol on Hcart Rate.....… …・・̈・・̈ ¨̈ ・̈・̈ ¨̈ ・̈・̈・・̈ ¨̈ ……・

Effect ofAlbuterol on Predictmg卜ね対mal V02.………………………

Practtal Applicatbn.… ……………………………………………………

Su―ary.¨ ..¨ ……..¨ ・̈・̈ ¨̈ ・̈・̈ ……………・・̈ ¨̈ ¨̈ ¨̈ ¨̈・・̈………………̈…・・・・̈

6。 SUMMARY,CONCLUSIONS,AND RECOMMENDAT10NS。 …………..¨ ・̈・・

SummarY " 47

Conclusions 48

Recommendations for Further Study 48

REFERENCES ......... 50

APPENDICES

RECRIIITttNT FLYER...,¨ ¨̈ ¨̈・・̈・・̈ ………̈ …̈………̈・・̈ ̈ 55

MEDICAL HISTORY FORM.… ………………………………… 56

４５

　

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Vl

C.

D。

E.

F。

G.

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H.

INFORMED CONSENT FORM.… … …̈……..………………………

PARICIPAT10N FORM.… …..… ..… ……… …̈………・・………・・̈

PRE‐EXERCISE TEST INSTRUCTIONS.…………………̈ ¨̈

INHALER USAGE INSTRUC■ONS.… ………………………

WORKLOAD SEWING GLIDE

FOR YMCA CYCLE TEST。 …………………………………・・,…

GRAPH FOR DE‐RMINING V02

WITH YMCA CYCLE TEST.… …………………………………・

RAW DATA― HEART RATE.… …… …̈…………̈ ………・・"¨ …̈…

RAW DATA― PEAK FLOW.……… …̈……・・……………・・……。

RAW DATA― V02.…………………………………………………

I.

J.

K.

Vll

LIST OF TABLES

Tablc

l. ANOVA Su―ary Table for HR at Rest and Stage l.… ……………………………

2.HR Dcscript市e Data.… …………………………………………………………………………

3.ANOVA Su― ry Table for HR at Stage 2 and Stage 3.… ………………・・:………

4.Pcak Flow Descriptive Data.……………… ……………… ……… … ………・

5。 Su― ry Table ofOne‐Way ANOVAs for Differences h

V02 1nax.… ………………………………………………………………………………………

6.V02 1nax Descriptive Data。 …………………………………………………………………・

Ｃ晦

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36

38

Vlll

Chapter l

INTRODUC■ON

It tt gencraly agreed that tetting lnaxIIllal oxygen∞nsumption Ⅳ 02 111a⇒ iS the

lnost accu口te method tO assess Cardiovascular capacity.Once cardiOVascular capaciy is

determmed,m appropnate exerciSe prescription for heakh and iness can be made.

Although屁ⅨiIIlally tetting V02ヽ the pretred techniquc,constramts related to time,

budget,or personnel oflen lead tO Subllllaxillllal testing belng perforlned instead.

Submaximaltestmg usually involVes a prediction ofV02 111ax based on heart rate(HRy,

and this method iS very llsenll for repeated meastre studies.However,submaxilllal

te■ing in cedaln populatiorls may llot proサ ide an accurate assessment ofcardiovascular

capacity.In other words,the V02 1nax predicted ibm submaxlmalte■ing e飲)■s lnght

difFer in results wtth that recorded durng maxlmal testing on the salne person.There is

reason to believe that asthコ ■■ics are a subgroup ofthe population slyeptible to ｀

inaccurate submaxlmal tett results.The ramlicatiorls for an exercise prescription based

on fauly subrrlaxllnaltesting are atthe least a waste oftllne att potentially may lead to

dangerous exercise recolnmendations for the asthnatic.

There iS a need to mvestigate ifthe linear relatiolllship that e対sts between submaxitnal

and lrlaxlmal tt h nOrlnal populatbns holds true in special populatiolls,such as those

wih exercise=induced asthma cIA)。 EIA is a self‐ limited episode ofairway obstrllction

that occurs during or after physical act市 ity(Sanders,1997).Cllrrently more than 7%of

the general population arc amicted with EIA.´ EIA is typically treated with one 9fseveral

beta agonists.AlbuteЮ lis a sho■ duration(2-4 hollr),relatiVely selective,beta‐ 2

adrenergic bronchodilator that is corrmonly prescribed.However,albuterol has been

2

shown to evoke changes in tIR (Hanratty, Silk, & Riddell, 1999; Silke, Hanraffy, Veres,

& Riddell, 2000) and blood pressure (BP) @remmer, Crane, & Beasley, 1996; Ferro,

Hall, Dickerson, & Brown, lggl),which are two key factors used to develop an exercise

prescription. Accurate submaximal testing relies on accurate exercise HR for the

prediction ofVO2 max. Furthennore, the effect albuterol has on HR and BP seems to be

related to exercise intensity and underlying adrenergic tone. The albuterol influence will

typically be most prominent at the start of an exercise test (low adrenergic tone), and

during the middle of an exercise test (moderate adrenergic tone), but disappear near

maximal effort (high adrenergic tone) (Fleck, Luci4 Storms, WallactU Vint, &

Zimmerman, 1993;Grove & Lipworttr, 1996;Grove, McFarlane, & Lipworttt, 1995).

However, subjects in these previous studies of albuterol were nonasthmatic.

It is reasonable to believe the albuterol influence on HR and BP related to adrenergic

tone will be comparable between asthmatics and nonasthmatics. However, subjects with

EIA have their own unique attributes, which may also affect HR and BP, possibly leading

to an exercise responsiveness unlike that of the nonasthmatic. Subjects with EIA have a

decreased oxygen (Oz) ventilation/perfusion ratio, decreased hemoglobin saturation,

decreased aerobic metabolisnr, and increased lactic acid formation (Handley, Morley, &

Vaickus, 1998; Jagod4 Shephard, Sevit4 & Joseph, 1997). With the rezulting decreased

availability of oxygen to the working muscles and build-up of lactic acid, an increase in

HR may result. Also, chronic use of albuterol rezults in a cross-sensitization between beta

I and beta 2 cardiac receptors (Ferro, Kaumann, & Browu 1995). Beta-l adrenoceptors

are the predominant cardiac adrenergic receptors with beta-2 adrenoceptors comprising

the other 10-50% (Physician's Desk Reference, 2002). Accordingly, chronic use of

albuterol may alter normal beta-l response to acute inhalation of a relatively selective

beta-2 agonist in people with EIA.

Given the unique cardiovascular responses by those with EIA, the HR observed during

the YMCA submaximal cycle test when moderate levels of adrenergic tone are present,

may be very different from people without asthma. Because the prediction of maximal

VO2 is based on HR taken duru4 the middle of this cycle test, when IIR should be

affected by albuterol, and because people with asthma would seem to have an even

greater HR response than people without asthm4 one could expect inaccurate predictions

of maximal VO2 resulting from zubmorimal tests on people with ElA. It is unclear if

results attained from zubmaximal testing of patients with EIA who use albuterol are

acceptable for safe and effective exercise prescription.

Statement of the Purpose

The purpose of this study was to investigate the ability to predict maximal VO2 using

the YMCA submaximal cycle test in subjects with EIA while on albuterol and while

using a placebo.

Scope of the Problem

An attempt was made to find out ifthere is any effect of using albuterol on HR during

stages of a submaximal cycle test in subjects with EIA. Furthermore, if albuterol does

alter HR during cycle testing, an attempt was made to investigate if this effect had

psychological origins by using a placebo.

For this purpose each participant performed two submaximal cycle tests, one using

albuterol and one using a placebo. HR was recorded, using a Polar HR monitor, during

each stage of YMCA submaximal cycle testing. Each participant also performed one

maximal cycle test using a modified Astrand protocol. Maximal testing was performed

with the use of albuterol.

The findings of this study will provide information about the accurate assessment of

aerobic capacity in individuals with ElA. Results from this work can then be considered

when creating exercise prescriptions for this population. A more accurate assessment of

aerobic capacity leads to more accurate exercise prescription thus reducing the risks of a

potentially harmful or inefficient exercise prescription being made.

Hwothesis of the Study

The following null hypothesis was identified:

H0: There will be no significant difference between predicted maximal VO2 of

subjects with EIA performing the YMCA submaximal cycle test on albuterol or using

placebo. Both submaximal tests will equally predict rnaximal VO2 as measured using a

maximal cycle test on albuterol.

Definition of Terms

The following terms that were used in this study are herein defined:

1. EIA: Exercise-induced asthma is a reversible airway obstruction that occurs during

or after exertion; its symptoms include cough, wheezing, dyspnea, and/or chest tightness.

2. Moderately active: A person who performs cardiovascular exercise 3-5 times per

week for 20 minutes or more per workout.

3.VOz max: The highest rate of orygen consumption and use that can be achieved at

maximal physical exertion.

4. Kilogram-meters (kgm): The amount of work required to lift one kilogram one

meter.

5

5. Low-moderate intensity (Sage l): The intensity level of exercise a person

experiences cycling during stage I of the YMCA submaximal cycle test. The workload

setting for stage I is equal to 150 kgm.

6. Moderate intensity (stage 2): The intensity level of exercise a person experiences

cycling during *age2of the YIVICA zubmaximal cycle test. The workload setting for

stage2 is based on steady state HR achieved durrng stage I and may ftInge from 300 kgm

to 750 kgrn

7. Moderately-high intensity (stage 3): The intensity level of exercise a person

experiences cycling during stage 3 of the YMCA submaximal cycle test. The workload

setting for stage 3 is determined by the workload setting used for stage2 and may ftmge

from 450 kgm to 900 kgtn

Assumptions ofthe StudY

The following assumptions concerning the study were made:

l. Subjects followed the proper technique for fully administering ao albuterol dose as

explained in the pre-testing handout.

2.There is a linear relationship that develops between HR and workload when HR

levels are between I l0 bpm to 150 bpm dunng YMCA submaximal testing on albuterol

and using placebo.

Delimitations of the Study

The following were the delimitations of the sfudy:

l. Submaximal YMCA cycle tests were performed only on people with EIA.

2. Only moderately active 18-35 year old males and females with EIA diagnosed for at

least six months were allowed to participate in this study.

6

3. Only people with EIA using albuterol were tested.

Limitations of the Study

The following limitations were made for this study:

l. A submaximal YMCA protocol cycle test may be the only submaxirnal exercise test

where these results apply.

2. Results of this study may only apply to moderately active l8-35 year olds with EIA

diagnosed for at least six months.

3. Results of this study may only apply to people with long-standing EIA treated with

albuterol for at least six months.

Chapter 2

REVIEW OF LITERATURE

Submaximal exercise testing can be performed in the general population to assess

cardiovascular fitness. Once cardiovascular fitness is assessed, an appropriaie exercise

prescription can be provided to an individual. SLUmaximal exercise testing relies heavily

on HR, but some medications may affect HR. Persons with EIA often use albuterol, a

&ta-2 agonist, which may increase HR during exercise testing. Most previous studies

using albuterol and exercise testing were performed on non-asthmatics to assess the

possibility of albuterol being used as a performanceenhancer. There have been no studies

performed on people with EIA using albuterol during YMCA submaximal testing

designed specifically to see how albuterol may impact predicted maximal VO2. This

chapter reviews the Iiterature pertinent to this study. Specifically, this chapter includes

the following sections: (a) submaximal exercise testing, (b) autonomic control of IIR, (c)

exercise-induced a^*hma, (d) effect albuterol has on H& (e) exercise testing of people

with asthma vs. people without asthmq (f) albuterol and maximal exercise testing, and

(g) summary.

Submaximal Exercise Testing

Subrnaximal exercise testing using the YMCA submaximal cycle test can be used to

predict maximal aerobic capacity. Submaximal exercise testing is commonly used to

assess aerobic capacity in large groups, such as gym members, wellness program

participants, and health fair participants. This type of testing is popular due to its relative

low cost and high safety for large goups.

The methodological objective of the YMCA submaximal test is to obtain two heart

rates between I l0-150 beats per minute (bpm). There is a linear relationship between HR

and workload between these two heart rates for most people. When the HR is less than

I l0 bpnr, many external stimuli can affect the rate (e.g., talking, laughter, nervousness).

However, once the HR climbs between I l0-150 bpnl external stimuli should no longer

affect the I{R, and a linear relationship develops. If the HR climbs above 150 bpnr, the

relationship between tIR and workload becomes curvilinear. Thus, the objective of a

submaximal test is to obtain two steady state heart rates behreen I l0 bpm and 150 bpm

at two different workloads in order to establish a linearity between HR and workload for

the person being tested.

Once the test is complete, the two steady state heart rates are plotted against their

respective workloads and a straight line is drawn through the two points and extended to

the person's predicted maximal HR(220-age). A vertical line dropped at the point which

the diagonal line intersects the horizontal predicted maximal HR line represents the

maximal working capacity for that participant. The maximal physical workload can then

be used to predict a person's maximum oxygen uptake (Nieman, 1995).

So, what happens when albuterol is used by a person with asthma prior to exercise

testing? If albuterol affects HR during the middle of exercise testing (moderate levels of

adrenergic tone) then the slope of the line betrveen the two heart rates may be altered,

thus leading to an inaccurate prediction of a maximal workload and maximal aerobic

capacity. The following four scenarios might occur. If albuterol causes the slope to

increase then submaximal VO2 will underpredict maximal aerobic capacity. If albuterol

causes the slope to decrease then submaximalYoz will overpredict maximal aerobic

capacity.If the slope stays the same, but both heart rates are higher, then submaximal

testing will underpredict maximal aerobic capacity. If the slope stays the salne, but both

heart rates are lower, then submaximal testing will overpredict maximal aerobic capacity.

Autonomic Control ofHeart Rate

The sinoatrial (SA) node is normally the pacemaker of the heart because it has the

fastest spontaneous depolarization to threshold. When the SA node reaches thneshold, an

action potential is initiated that spreads tlroughout the heart, inducing the heart to

contract or have a"heartbeat". The inherent rate at which the heart would beat under

just SA node control would be approximately 100 bpm. However, the autonomic systenr,

primarily controlled by the cardiovascular control center located in the b,rain stem,

decreases this rate through parasympathetic control.

The parasympathetic nerve to the heart, the vagus nerve, primarily innervates the

atriunU especially the SA and atrioventricular (AV) nodes. When parasympathetic

activity is stimulated it causes the heart to beat less frequently, the time is slowed

between atrial and ventricular contraction, and the atrial contraction is weaker.

The cardiac sympathetic nerves supply the atri4 including the SA and AV nodes, as

well as influencing the ventricles. Sympalhetic stimulation also triggers a release of

epinephrine from the adrenal medulla. Epinephrine augments the sympathetic nervous

system actions on the heart. The resulting effect of sympathetic stimulation on the heart is

to increase I{R, speed up the time between atrial and ventricular contractioq decrease

conduction time throughout the heart, and to increase the force of contraction. During

exercise the sympathetic nervous system is responsible for increasing HR to meet the

need for greater blood flow. During submaximal exercise testing, two steady state heart

rates need to be recorded between 110-150 bprn In order for tIR to rise substantially

10

above 100 bpnU the sympathetic system needs to be activated (Sherwoo4 1993).

Therefore during submarimal testing, the sympathetic system is important to the increase

in HR.

Exercise-Induced Asthma

EIA occurs in approximately 7% of the population and is most common among active

children, adolescents, and young adults. EIA occurs when vigorous physical activity

triggers airuray narrowing in people who have heightened bronchial reactivity. EIA is a

reversible airutay obstruction that occurs during or after exertion EIA limits exercise

performance and can be a source of great discomfort. The pathophysiology of EIA is still

unknown. However, two theories offer explanations for EIA. They are the water loss

theory and the heat-exchange theory.

The water loss theory states that when dry cold air is inspired through the nose,

pharyna and first seven generations of bronchi, it is warmed and humidified before it

reaches the sensitive alveolar membranes. During vigorous exercise however, most

breathing occurs through the mouth thus bypassing upper airway conditioning. The

upper airways of the lungs are then required to contibute water vapor from the surface

Iiquid of the respiratory epithelium to saturate inspired air. This loss of water fiom the

epithelium of the bronchial mucosa dries the airway, changing the osmolarity, pH, and

temperature ofthe perciliary fluid. Hyperosmolarity of the airways is believed to cause

the release of bronchoactive mediators that may include histamine, leukotrienes, and

prostoglandins released from mast cells and/or epithelial cells. The resulting

bronchoconstriction may be the primary mechanism accounting for EIA (Lacroix, 1999).

The heat-exchange theory may account for why EIA often occurs after exercise is

terminated. This theory holds that increased ventilation during vigorous exercise cools

the airways. Once exercise has stopped, the respiratory epithelium is re-warmed via the

bronchial vasculature dilating and engorging with warm blood. Hlperemia of the

bronchial vascular bed impinges and narrows the airway. Engorged vessels may also

leak, leading to mediatbr release and bronchosprum. Accordingly, post-exercise EIA may

result from airways narrowed by exercise hyperemia and mediator-induced

bronchoconstriction (Lacroix" I 999).

Normally, airways dilate during exercise, allowing airflow to meet increased muscular

oxygen demands. Bronchodilation is thought to result from decreased cholinergic activity

in the airways as exercise begins. In people with EIA an above normal increase in

circulating concentrations of catecholamines may play a role in improper bronchodilation

when exercising because they do not allow for proper b'ronchodilation. In people with

EIA ffiial bronchodilation is diminished, and bronchoconstriction develops after 6 to 8

minutes ofvigorous exercise. The maximal decrease in pulmonary function typically

occurs about 15 minutes after exercise begins (Lacroix, 1999). To counteract the

bronchoconstriction brought on by vigorous activity in people with EIA" they self-

administer albuterol 20 minutes prior to starting exercise. Albuterol is a relatively

selective beta2-adrenergic agonist causing brronchodilation. Although albuterol helps to

relieve bronchoconstriction fiom EIA" it may also increase HR and BP in many

asthmatics. This can potentially become problematic when exercise testing asthmatics

because it is important to have a normal HR response to incremental increases in

workload.

12

Effect Albuterol has on Heart Rate

Beta 2-adrenoceptors are the predominant adrenergic receptors in bronchial smooth

muscle and beta l-adrenoceptors are the predominant receptors in the heart. There are

also beta 2-adrenoceptors in the human heart comprising 10-50% of the total'beta

adrenoceptors @hysician's Desk Reference, 2002). The precise function of these

receptors in the heart is not yet established, however it is known that albuterol can

stimulate the beta 2 receptors in the heart. In additiorU albuterol is only relatively

selective for beta 2 receptors; meaning that albuterol will also mildly stimulate beta I

receptors in the heart.

Thus, it seems understandable that several studies have found an increase in HR at rest

with the use of albuterol and salbutamol @remmer et al., 1996; Dhand et al., 1996;

Hanratty et al., 1999;Lin, Sauter, Newmarl Sirleal Walters, & Tavakol, l993;Ramsdell,

Colice, EkholnL & Klinger, 1998; Silke et al., 2000; Williams, Weiner, Reiff, Swensorl

Fuller, & Hughes, 1994). Salbutamol is another nirme used for albuterol in the brand

rurme inhalei Ventolin. Bremmer et al. (1996) compared the effect albuterol versus

fenoterol (another beta agonis| had on HR in eight healthy subjects. They found that

albuterol behaves as a partial agonist at beta-receptors when compared with fenoterol.

Albuterol at avery high dose, I1.6 puffs, was found to elicit hn increase in resting HR of

32.5 bprn When inhaled at doses currently recommended for severe asthmq albuterol

also caused an increase in I{R, however, it was found to result in less severe maximum

cardiac and metabolic effects than fenoterol. Lin et al. (1993) continually administered

0.a mglkgnr of albuterol in nebulized form to sev.en adult asthmatics over a four hour

time period. One subject withdrew after three hours due to developing supraventricular

13

tachycardia. A mean increase in resting HR of 16.3 percent was observed for the entire

group. Williams et al. (1994) administered 5 mg salbutamol, 5 mg adrbnaline, and

placebo to six subjects and monitored their HR response. He found an increase in IIR

after both salbutamol and adrenaline. Ventricular ectopic beats and a short run of

parasySole were recorded on ECG in two patients after using salbutamol and in one

patient after using adrenaline. Dhand et al. (1996) treated 12 mechanically ventilated

patients with increasing.doses of albuterol every l5 minutes. The doses used were 4, 8,

and 16 puffs. Resting HR significantly increased after a cumulative dose of 28 puffs.

Ramsdell et al. (1998) tested 22palientsby administering doses every 30 minutes of 1, l,

2,4, and 8 puffs for a total of l6 puffs of albuterol. They found a significant dose

response for albuterol with regard to resting HR In two separate studies Hanratty et al.

(1999) and Silke et al. (2000) administered single oral doses weekly of salbutamolto 17

and 49 subjects, respectively, and recorded resting HR variability over short and long

term periods. They both found significant increases in tIR with the use of salbutamol

versus with the use ofplacebo when compadng data using scatterplots. Scatterplots are

graphs that can be used in studies to compare each subject's average hourly HR in bpm

after using salbutamol or placebo. HR data was gathered using continuous holter

monitoring over an eight hour period of time during sleep.

There is only one study that found no significant change in resting HR when albuterol

was administered. In this study, l0 subjects were administered 20 mg of salbutamol, l0

mg salmeterol (long-lasting beta-agonist), or placebo, and then had them wear holter

monitors for a24 hour time period. The testing occurred on three non-consecutive days.

14

HR did increase on average 7 bpm in the salbutamol group, however the change in HR

was found to be non-significant (Bagnato, Mileto, Gulli, & Oriti, 1996).

Multiple studies have shown increases in HR with the use of albuterol during all or

some stages of exercise testing (Fleck et al., 1993; Grove et al., 1995; Heir & Stemshaug,

1995;Ingemann'Hansen, Bundgaard, Halkjaer-Kristensen, Siggaard-Anderserq &

Weeke, 1980; McCaffrey, Riddell, & Shanks, 1988; Violante, Pellegrino, Vinay, Selleri,

& Ghinamo, 1989). Fleck et al. (1993) cycle tested 21 highly trained competitive road

cyclists, who did not have asthma, using submaximal workloads of 150, 200,225,250,

275,300 wafis, and at maximum workload. Each subject was administered either

albuterol or placebo (36 mg) 15 minutes prior to testing. Heart rate was significantly

greater with albuterol at 200,225, and 250 watts, but at 150,275, and 300 watts no

significant albuterol effect was found. Blood lactate was also found to be higher in

albuterol versus placebo at275 watts. RPE and VO2 were unchanged in albuterol versus

placebo groups at each stage. Grove et al. (1995) conducted a study on eight untrained

subjects, who did not have asthma using 2,4, and 8 mg of salbutamol. Heart rate was

recorded at rest and at maximal exercise. The conclusions ofthe study found that during

rest salbutamol produced an increase in HR consistent with beta 2 agonism. However, at

maximal exercise, salbutamol did not increase HR

Violante et al. (1989) exercise tested seven untrained subjects, who did not have

asthma, using a progressive treadmill test with the use of salbutamol 0.4 m/kg over 20

minutes followed by 0.3 rng/kglh. The progressive test was started with a 5 km/h speed at

0%o grade for three minutes. Thereafter, the speed was kept constant but the incline was

increased by 2.5% every minute until exhaustion. A seven minute recovery period at a

15

speed of 3 km/h followed testing. They noted an increase in IIR with the use of

salbutamol over placebo during 0o/o, 5%o,15%o gade, and during two and seven minute

recovery time periods. Heir et al. (1995) tested 17 highly trained endurance athletes, who

did not have asthmq during a treadmill run to exhaustion at ll0%o of rnaximal VO2 with

the use of salbutamol0.5 mg/kg or placebo. During high intensity running they found HR

was slightly higher in the salbutamol group, however, at maximal capacity there was no

difference in HR. Ingemann-Hansen et al. (1980) cycle tested five young untrained men,

with EIA, using salbutamol or placebo at workloads corresponding to 50%o,75%o, and

I2O% of maximal capacity. Maximal cycle and treadmill tests were also performedat a

workload corresponding to 100%of maximal capacity. After salbutamol use, a higher HR

and mean blood pressure G\AP) in relation to VO2 were found when compared to

placebo, however the slope of HR/VO2 relationship and MBPA/O2 was unaffected.

McCaftey et al. (1988) recorded HR during sleep, resting supirie position, and exercise

after eight untrained male volunteers without asthma took 8 mg of salbutamol. Exercise

consisted of a three minute step test where HR was measured five seconds into the

recovery period. They found an increase in HR in all three conditions with the use of

salbutamol.

To summarizethe studies mentioned above, two studies (Fleck et al., 1993; Heir et al.,

1995) used highly trained subjects. Both studies found HR was affected during exercise

testing but unchanged at maximal capacity. Fleck et al. (1993) found f:[R was increased

with the use of albuterol during cycle workloads between200-250 watts but unchanged at

cycle workloads higher than 275 watts. Heir et al. (1995) noted HR was slightly higher

during high intensity running (ll0% of max) during the first four minutes of treadmill

16

testing but salbutamol no longer affected HR when testing duration lasted longer than

four minutes. Subjects fatigued between 4 and l0 minutes oftesting. Both studies used

subjects who did not have asthma.

The other four studies (Grove et al., l99l;Ingemann-Hansen et al., 1980; McCaffiey

et al., 1988; Violante et al., 1989) did not use highly trained subjects. All of these studies

found an increase in HR at rest. Violante et al. (1989) found an increase in tIR during

some stages oftesting, whereas McCaftey et al. (1988) and Ingemann-Hansen et al.

(1980) found an increase in tIR during all stages of exercise testing. Grove et al. (1995)

recorded HR only at rest and maximal exercise and found HR to be increased at rest but

not at maximal exercise. In all ofthe above studies the only group to use asthmatics was

Ingemann-Hansen et al. (1980).

A few studies showed no increases in HR with the use of albuterol during exercise

testing (Carlsen, Ingier, Kirkegaard, & Thyness,1997; Freeman, Packe, & Cayton, 1989;

Robertson, Simkins, O'Hickey, Freman, & Cayton, 1994; Schmidt, Diamant, Bundgaard,

& Madsen, 1988). In order to investigate the effect beta 2-agonists had on exercise

performance, Schmidt et al. (1988) tested eight asthmatics using an incremental exercise

test on a treadmill after the use of salbutamol given five minutes prior to testing. No

significant difference was found in total work time, maximal lactate concentration, I{R,

or rate of perceived exertion (PJE). Another sdy, also trying to see if beta agonists

caused an improvement in performance studied l8 highly trained athletes, aged 17-30

years. Salmeterol, salbutamof or placebo were administered. Salmeterol is a long-acting,

highly selective, beta 2-agonis. After a l0 minute warm-up, anaerobic threshold was

measured then a brief graded exercise test to exhaustion was performed. No significant

17

differences were found for ventilation, oxygen uptake, or HR at anaerobic threshold or at

maximum performance between placebo and the bta-2 agonists (Carlsen et al., 1997).

Freeman et al. (1989) investigated the effect of nebulised salbutamol on maximal

exercise perforrr,ance in eight men with mild asthma. Exercise tests, maximal and

submaximal, were performed on a cycle ergometer after 5 mg salbutamol or placebo were

administered. They concluded there were no significant differences in maximal workload,

oxygen uptake, I{R, or ventilation after salbutamol. However, during submaximal

progressive exercise the RPE was reduced and oxygen pulse was reduced due to a small

and non-significant increase in HR. Robertson etal. (1994) had eight asthmatic men

perform progressive maximal cycle tests after taking salmeterol0.5 mg, salbutamol 2 ^9,

or placebo. They were trying to see if single dose sahneterol affects exercise capacity in

asthmatic men Cardiorespiratory, hemodynamic or subjective responses to progressive

maximal exercise tests were not different with salmeterol, salbutamol, or placebo, nor did

endurance capacity change with any treatment modality. However, blood lactate levels,

after 15 minutes of exercise were signifrcantly higher with salbutamol, but not with

salmeterol, when compared with placebo.

One study showed a decrease in I{R with the use of albuterol during exercise testing in

a highly trained group but not in a moderately trained group (Ienna & McKenzie,1997).

They studied 17 female and male subjects, nine highly trained, and eight moderately

trained. Salbutamol or placebo was administered before undergoing an exercise test

including four continuous five minute increments representing 25,50,75, and 90% of the

subject's maximal VO2. No differences were found between groups at any stage of

exercise with respect to VO2, minute ventilation (VE), RE& fIR, or Yo saturation (SaO2).

18

However, irmong the highly trained Broup, the mean HR for the four exercise conditions

was significantly higher when using placebo. No differences were found in lactic acid

during exercise or in recovery, but peak expiratory flow rate was significantly higher with

the use of salbutamol.

When looked at collectively, there is a trend in the research that suggests that the

increase in IIR caused by albuterol use may be dependent on different intensity levels of

exertion (i.e., rest, low-moderate, moderate, moderately-higtu and maximal exercise). A

study (Grove et al., 1995) was designed to compare the effect salbutamol had on HR

during two different levels of adrenergic tone, low tone found at rest and high tone found

during maximal exercise. Subjects' heart rates were recorded during low tone (rest) and

high tone (maximal exercise) after inhalation of salbutamol. The study found that in a

state of low adre:rergic tone (rest) salbutamol produced effects consistent with beta-2

agonism such as an increase in HR. In contrast, in a state of increased tone (maximal

exercise) salbutamol produced trfa-z selective antagonism with no effect on HR. Other

research studies when looked at in light of different levels of adrenergic tone, appear to

indicate similar findings. In the Fleck et al. (1993) study, albuterol was shown to have an

effect on HR during cycle ergometry testing between 200-250 watts, but at 150,275,300

watts, and maximal work no effect on HR was found. Another study, using salbutamol,

showed no changes in IIR at anaerobic threshold which would be considered moderately-

high levels of adrenergic tone (moderately high exercise) or high levels of tone (maximal

exercise) (Carlsen et al., lggT).In general these studies indicate albuterol may affect HR

during rest and moderate intensity exercise, with the effect decreasing during moderately-

19

high intensity exercise and ceasing to have an effect at maximal exercise. However, these

three studies were all performed on non-asthmatics.

Exercise Testing of People With Asthma vs. People Without Asthma

Testing of asthmatics differs from testing non-asthmatics in several,ways. First, those

with EIA have a lesser peak expiratory flow rate (PEFR), even after albuterol use. After

an initial60 Limin rise in PEFR for 30 minutes after albuterol inhalation, a substant tal25

L/min drop occurs over the next 30 minutes followed by another substantial 60 L/min

drop in PEFR from hours 5 to 12 @agnato et al., 1996).

Second, people with EIA have a decreased O2 ventilation/perfusion ratio, and

therefore have decreased hemoglobin saturatio4 leading to decreased aerobic metabolism

and increased lactic acid formation The decreased 02 ventilation/perfusion ratio occurs

because bronchospasm and mucous plugging in asthmatics obstruct both inspiratory and

expiratory airflow. This airflow obstruction is not uniforrn, leading to mismatching of

ventilation to perfusion. This mismatch is the major cause of hlpoxemia in asthma.

Mismatch increases minute ventilation, which increases the work of breathing,

ultimately, increased work with decreased oxygen supply results in anaerobic metabolism

and a buildup of lactic acid (Jagoda et al^, 1997).

A third difference in testing exercise-induced asthmatics is that they have physiologic

adaptations that have occurred in response to chronic use of beta agonists/antagonists.

For example, with regular use of salbutamol, there is a progressive decline of protective

efficacy and a corresponding intensification of airway resporisiveness (Hancox et al.,

2002). Also existing from chronic use is a cross-sensitization between beta-l andbeta-2

cardiac receptors. Cardiac bta-2 adrenergic sensitization can be induced in normal

20

subjects prospectively by beta-l blocker freatment (Ferro et al., 1995). Activation of beta-

1 receptors would impact HR.

Albuterol and Maximal Exercise Testing

The present study tested the affect albuterol had on HR inpeople with EIA during a

commonly used submaximal test and how this might impact estimated maximal aerobic

capacity. However, to be able to make this comparison, it must be assumed that albuterol

does not alter maximal VO2 achieved from exercise testing.

The research unanimously has reported that albuterol (salbutamol) does not.have an

effect on maximal exercise performance in people with asthma. Schmidt et al. (1988)

concluded that the release of an inhaleAbeta-2 agonist (salbutamol) for use in

competitive events is justified with no ergogenic effect seen in eight subjects they

maximally tested. Supporting this finding, Freeman et al. (1989) staled that salbutamol

may reduce the severity ofEIA" but once again no ergogenic effect on maximal exercise

performance was shown when administered to eight subjects with asthma and eight

zubjects without asthma. And finally, another study was conducted in 1980 (Ingemann-

Hansen et al., 1980) that involved five males with EIA using salbutamol. When testing

these men at 50%o,75%o, and 120% of maximalVoz, and having them perform a

maximal cycle and a maximal treadmill test, a higher HR in relation to VO2 was found

with those using salbutamol. However, even with an increase in HR at 50%o,75Yo,and

120% of maximal aerobic capacity, they found no significant difference in maximal VO2

when subjects used salbutamol vs. placebo.

21

Summar.v

In summary, submaximal exercise testing using the YMCA cycle test is useful in large

populations for predicting maximal aerobic capacity. By recording steady state HR

during progressively challenging stages of cycle testing a predicted maximal capacity can

be derived. This test, however, might not be accurate for all populations. People with EIA

use albuterol, a relatively selective beta-2 agonist, to reverse bronchiole constrictive

airway obstruction caused by heightened bronchial reactivity. Research studies show a

strong bonnection between albuterol and an increase in HR during rest and possibly

during exercise. Studies have also shown this effect to disappear during or near maximal"

effort. Most studies used untrained sirbjects without asthma however a few used highly

trained subjects, and a few use people with asthma. This variety in training level and in

subject health (asthmatic vs. non-asthmatic) may account for some of the differences in

findings on whether or not albuterol affects HR during exercise. Studies show tlmrtVo2

max is not affected by albuterol use, however, it is unclear if the prediction of VO2 max

from submaximal HR is impacted by albuterol.

Chapter 3

METTIODS

The methqds used in this study are explained in this chapter. It includes the following

sections: (a) selection of subjects, O) procedures for data collection, (c) treatment of the

dat4 and (d) summary.

Selection of Subjects

Subjects included 1l moderately active males and females, aged 18-35 years, with a

documented history of EIA" but otherwise healthy. All subjects were volunteers solicited

through recruitment flyers (Appendix A) posted at Ithaca College and Cornell University

fitness facilities. AII subjects were screened prior to exercise'testing. The screening

involved a detailed medical history form (Appendix B), case review by an Ithaca College

exercise physiologist, and resting hemodynamic assessments (i.e., BP, IIR). All subjects

agreed to participate in uriting through informed consent fornrs (Appendix C). Subjects'

physicians were sent participation forms (Appendix D) to facilitate any necessary

communications befween Ithaca College staffand the participants' physicians. Subjects

were excluded fiom this study if they presented any contraindications to exercise testing

as defined by the American College of Sports Medicine (ACSM, 2000). Subjects who

could not perform a cycle test because ofphysical limitations were also excluded from

the study.

Each subject performed maximal exercise testing with gas analysis and a rescue

inhaler was present during all testing for potential emergency situations. Prior to testing,

each subject was provided with pre-exercise test instructions'(Appendix E), and inhaler

usage instructions (Appendix F). Testing was terminated voluntarily at any time by the

22

23

subject, or by the tester if any signs or symptoms warranting test termination developed

(ACSM, 2000). Procedures for the niaximal cycle test are detailed below but followed a

customary protocol including monitoring of metabolic gasses, Fm, BP, and rating of

perceived exertion (RPE) throughout the test. An established emergency plan was in

effect during all testing periods in accordance with guidelines listed by the American

College of Sports Medicine (ACSM, 2000).

Procedures for Data Collection

Testing for each subject included two subma:rimal cycle tests using the YMCA

protocol (Nieman, lg95). One test was performed with inhaled albuterol and one with

inhaled placebo. Placebo inhalers were provided by Schering Pharmaceuticals Company

(Kenilwortb NI). Placebo inhalers looked the same and had the same taste as albuterol

inhalers. Albuterol inhalers were purchased from Warrick Pharmaceuticals Company

(Reno,I.W). A maximal cycle test using a modified Astrand protocol (Nieman, 1995)

was also performed with inhaled albuterol. A double-blind, crossover design was used

during submaximal testing. Neither the subject nor experimenter knew ifthe inhaler

contained albuterol or placeb<1. The submaximal test protocol included four sequential

parts: l) pre-exercise rest (10 minutes);2) albuterol or placebo administration followed

by rest (20 minutes); 3) YMCA submaximal cycle test and;4) recovery (10 minutes).

Each subject performed one submaximal iest with albuterol and the other with placebo.

Albuterol or placebo was self-administered in the physician-recommended dose of two

puffs, 9 mg eactq 20 minutes before exercise. Each canister of albuterol contains a

microcrystalline suspension of albuterol, USP in propellants with oleic acid. Each

actuation delivers 9 mg albuterol, USP from mouthpiece. During the submaximal test

24

(part 3), RPE, IIR, and BP were measured each stage in accordance with YMCA testing

instructions (Niemarq 1995). For parts 1,2, arrd 4 of the test protocol, I{R, BP, and RPE

were recorded at five minute intervals.

Each submaximal cycle test included several continuous three minute stages starting at

150 kgr/min. Workload settings for stages 2,3,and 4 (if needed) were determined by

steady state HR achieved during cycling at stage I (150 kgn/min) (Appendix G).

Submaximal testing continued until two steady state heart rates between 110 bpm and

150 bpm during two different stages were obtained (Niemerl 1995). These two heart

rates could thenbe graphed to determine predicted maximal VO2 (Appendix H). During

each stage the subject was asked to rate hiVtrer shortness of bneath on a l-4 scale. The

scale was set up so that 1 equals no shortness of b'reat[ 2 equals mild shortness of breath

3 equals moderate shortness of breath, and 4 equals severe shortness of breath. In an

effort to keep exercise testing modalities as similar as possible, metabolic gasses were

monitored on a continuous basis, as described below, throughout submaximal and

maximal exercise testing. Peak expiratory flow rate was recorded using a self-test peak

flow meter prior to albuterol or placebo administration, 20 minutes after albuterol or

placebo administratiorU and 10 minutes after each exercise test.

Submaximal testing occurred twice, once with the use of albuterol (18 mg total)

before testing, and once with the use of placebo before testing. The only difference in the

protocol between the two submaximal tests was h the substance taken prior to testing.

However, due to the nature of the YMCA submaximal cycle test, different workloads for

testing may have been used when using albuterol versus testing when using placebo. For

example, if a subject using placebo had a steady state HR of less than 80 bpm during

25

stage 1 of the cycle test, that subject's following workloads for stages 2,3, arrd 4, would

be respectively 750 kgnr, 900 kgrn, and 1050 kgrrl If the same subject now using

albuterol had asteady state HR of greater than 100 bpm during stage I of the cycle test,

that subject's following workloads for stages 2,3, and 4 would be 300 kgrn, 450 kgrn,

and 600 kgnr, respectively. Submaximal testing was performed with half ofthe subjects

tested first with albuterol and the other half tested first with placebo. For each subject,

submaximal testing took place at different times during the same day with at least six

hours between submaximal tests, or were tested on different days.

The testing for maximal aerobic capacity was assessed at least 24 hours after both

submaximal cycle tests were completed. Two puft of albuterol (9 mg each) were taken

twenty minutes prior to nraximal testing. Peak expiratory flow rate was measured just

before exercise testing began. Heart rate was continually monitored throughout the entire

test. Rate of perceived exertion and shortness of breath were monitored during each

stage. The maximal testing protocol for females started at 300 kgu/min, increased to 450

kgn/min after two minutes, then increased by 150 kgn/min every three minutes until

maximal aerobic capacity was reached (Niemaq 1995). Modmal testing for males started

at 600 kg/mnL increased to 900 kgr/min after two minutes, then increased by 300

kgm/min every three minutes until maximal aerobic capacity was reached. Peak

expiratory flow'rate was also measured immediately after testing. Metabolic gasses were

measured dunng maximal testing using a TrueMar 2400 metabolic measurement system

by Parvo Medics (Salt Lake City, UT) and standard protocols. Subjects wore headgear to

support ventilation hoses and also wore a noseclip. Expired air was transferred via

ventilation hose into a gas at:m.lyzer where ventilatory and gas exchange variables were

26

continuously monitored and recorded during exercise testing. Maximal aerobic capacity

was determined by taking the highest VO2 obtained once the subject had reached a

plateau in VO2 with an increase in workload, or once a subject had met at least two of the

following criteria: RPE equaled or reached above 17 on the RPE scale; HR was within

+l- l1%age-predicted max and/or no longer continurld to rise with increasing workload;

and RER equaled or reached above 1.1. Leg frtigue causing pre-mature cessation of

testing is a concern when using maximal cycling tests, however if criteria listed above are

met, the test is considered a valid assessment of maximal VO2.

Treatment of Data

Data analysis involved comparison of steady state HR during comparable stages of

submaximal cycle testing after albuterol versus after placebo. This comparison yielded

information on whether a HR difference existed between testing subjects with EIA while

using albuterol or while using placebo. Dataamlysis also involved comparison of PEFR

prior to submaximal testing with the use of albuterol or with the use of placebo.

Differences between predicted maximal VO2 obtained from submaximal testing with

albuterol and placebo versus maximal VO2 obtained from maximal testing were also

assessed. Finally, if albuterol increased IIR enough during repeated submaximaltesting

to place subjects into different workload settings for stages 2,3, and 4 of the YMCA

cycle test, then two additional analyses were performed. One analysis was used to

compare predicted VO2 max fromtesting with albuterol and placebo with measured VO2

max using only subjects with comparable workloads. The second analysis was used to

compare actual and predicted VO2 for subjects with different workloads during the two

submaximal tests.

27

Statistical analysis involved lwo 2 x2 repeated measures analysis of variance tests

(ANOVAs) for inspecting heart rate differences with repeated measures on both the

condition (i.e., albuterol vs. placebo) and time (i.e., rest vs. stage I or stage 2 vs. stage 3)

factors. PEFR prior to submaximal testing was analyzed using a paired T-test. A one-way

repeated measures AIiOVA was used to compare predicted maximal VO2 from

submaximal testing using albuterol with placebo predicted VO2 max and with measured

maximal VO2 using albuterol. Following this, if albuterol increased HR enough to place

a subject into a different workload sefting for stages 2,3, and4 of the YMCA cycle test

than with placebo then two one-way repeated measures ANOVAs were run. The two one-

way repeated measures A}IOVAs were used to compare predicted maximal aerobic

capacrty with measured maximal capacity for the subject who l) had the same workload

when submaximally tested with albuterol as when submaximally tested with placebo

during stages 2,3, and4 of submaximal cycle testing, and 2) had a different workload

when tested submaximally with albuterol as when tested submaximally with placebo

durrng stages 2,3, and4 of cycle testing. Post-hoc Tukey HSD analyses were used to

further inspect any differences detected by ANOVA analyses.

Summary

The methods of this study were detailed in this chapter. Methods included the

selection of subjects, methods of data collection, and treatment of data. Subjects included

1 I moderately active males and females aged l8-35 years. Each subject underwent two

submaximal (one with albuterol and one with placebo) and one maximal (with albuterol)

cycle test. HR during zubmaximal testing with albuterol and with placebo was recorded

to obtain predicted maximal VO2 using the YMCA prediction technique. Data were

|

| ＼

28

statistically ar:rrlyzed to determine if albuterol caused any difference in HR or altered

maximal VO2 predictability. It was through these methods that the appropriateness and

zrccuracy of maximal VO2 prediction using HR-dependent, submaximal YMCA cycle

testing, in patients with EIA was investigated.

Chapter 4

RESULTS

This study was conducted to investigate the accuracy of predicting maximal VO2

using the YMCA submaximal cycle test in subjects with EIA while on albuterol or on

placebo. In order to investigats [his, six analyses were completed. HR at rest, stage 1,

stage2,and stage 3 were al:mrlyzelJ using two2x2repatedmeasures ANOVAs. A

paired T-test was used to compare peak flow values. A one-way repeated measures

ANIOVA was used to compare VO2 max predictions under the various conditions (i.e.,

predicted maximal VO2 using albuterof predicted nraximal VO2 using placebo,

measured maximal VO2 using albuterol). Following this, two one-way repeated measures

ANIOVA5 were run cornparing predicted maximal aerobic capacities with measured

maximal capacrty for zubjects who used the sane workloads on both YMCA submai'imal

tests and for those who had different workloads during stages 2,3, and 4 of submaximal

testing..sections in this chapter describe the resulting data and include: (a) IIR,nalysis,

(b) peak flow analysis, (c) VO2 max analysis, and (d) summary.

Heart Rate Analysis

Restrng HR and steady state HR during stages 1,2, and 3 of the zubmaximal YMCA

cycle test were recorded for each subject on albuterol and on placebo. Raw data for HR

for all subjects dwing rest and stages 1,2, and 3 can be found.in Appendix I. As

expected, and indicated in Table l, a significant increase in HR was found fiom rest to

stage I (p <.05). More importantly, noted in Table l, a significantly greater HR when

using albuterol was noted compared to placebo at rest and during stage I (p < .05).

However, the effect albuterol had on HR over time did not significantly change from rest

29

30

Table 1

ANOVA Summary Table for HR at Rest and Staee I

Source ofVarlation SS df MS F p

Time

Error I

Med

Enor 2

Time x Med

Error 3

3654.57 1 3654.57 167.50 0.00+

218。 18 10 21.82

270.02 1 270.02 6.74 0.03*

400.73 10 40.07

31.11 1 31.11 3.22 0.10

96。64 10 9.66

Note. Time: rest and stage I of cycle testing; Med : albuterol and placebo.

+p < .05; There was, as expected, a significant (main effect) increase in mean HR from

rest to stage I during submaximal cycle testing due to an increase in cycling

workload.

*p < .05; There was a significantly (main effect) greater mean HR in albuterol than

placebo across rest and stage I during submaximal cycle testing.

to low level exercise as shown in Table I because the interaction (Time x Med) was not

significant (p > .05).Table 2 displays the descripive data for HR at rest and at steady

state HR during stages 1,2, arrd 3 of the cycle testing when subjects exercised at

workloads that were the same on both trials. During rest and stage l, all zubject (n: I l)

data were amlyzsdbecause workload settings, or lack of workload as is the case at rest,

were the same. There was a significant main effect of albuterol on HR across both rest

and stage l.

Dudng the YMCA submaximal cycle test, steady state HR during stage I is used to

determine the resistance settings for stage 2,3, and 4 if needed. Ultimately, the cycle test

is terminated once two steady state heart rates between I l0 bpm-I50 bpm have be-en

achieved during two separate stages. These two steady state heart rates are then used to

estimate maximal VO2. All of the subjects whose data were arr.lyzel for HR reached

steady state HR between 110 bpm-l50 bpm during stage2 and stage 3. When arulyzrng

the effect albuterol had on HR during stages, some subjects (U: 5) were set at different

workloads during stages 2 and3 of their albutbrol and placebo trials. This required a

separate analysis of data for these subjects because only subjects with equal workloads (q

= 6) during stages 2 and3 could be used for comparison of HR in this repeated measures

design study. Data from zubjects with,different workloads (n: 5) were used for VO2

max comparisorq but not in HR analyses for stages 2 and3. The increase in HR that

albuterol caused during stage I for 5 of I I subjects put those five into a lower workload

setting for stages 2 and3. Therefore, only data for six subjects were analyz-ed when

- comparing HR during stage 2 and stage 3 as depicted in Table 3. Table 3 shows a

significant increase in HR with increased workload, as expected, from stage2 to stage 3

31

32

Tablc 2

1‐IR DescriptiVe Data

Condition N Min Max Mcall SD

HR rest albuterol

HR rest placebo

HR stage I albuterol

HR stage I placebo

HR stage 2 albuterol

HR stage 2 plasebo

HR stage 3 albuterol

11

11

11

11

6

6

6

6

55

53

76

77

113

114

125

124

98

79

110

106

134

124

157

159

75。27ホ十

68.64ホ+

91.82*+

88.56ネ+

124.50∧

118.33∧

141.67∧

138.50∧

10.67

8.65

10.51

9.17

8.60

4.50

13.88

12.68HR stage 3

Note. fIR: heart rate measured in beats per minute (bpm).

During rest and stage I all zubject (n: I l) fR data was arprlyzrld because

workload settings, or lack of a workload setting as is the case at rest, were the same.

During stages 2 and 3, only HR data from subjects (n: 6) cycling at the same workload

on albuterol and placebo trials were analyzed.

*p < .05; There was a significantly (main effect) greater mean IIR in albuterol than

placebo across rest and stage I dwing submaximal cycle testing.

+p < .05; There was, ils expected, a significant (main effect) increase in mean HR

from rest to stage I during submaximal cycle testing due to an increase in cycling

workload.

T < .05; There was, as expected, a significant (rnain effect) increase in mean HR from

stage2to stage 3 during submaximal cycle testing due to an increase in cycling

workload.

a^53

(p <.05).However, there was no significant difference in tIR for albuterol versus

placebo during stage 2 and stage 3 (p > .05). It is also shown in Table 3 that the

interaction (Time x Med) for HR was not found to be signifrcant (p > .05).

Peak Flow Analysis

peak flow was analyzed using a paired T-test for all eleven subjects. These data were

collected 20 minutes after albuterol and placebo ffialation but before cycle testing. Raw

data for peak flow values may be found in Appendix J. Peak flow levels were

significantly greater after treatment with albuterol versus treatment with placebo (Table

4). Descriptive data for peak flow may be found in Table 4'

VO2 Ma:< Analysis

predicted maximal 02 uptake was determined twice for each subject using the

yMCA cycle test, once with the use of albuterol and once with the use of placebo. Each

subject also underwent a maximal cycle test to determine maximal VO2 via indirect

calorimetry while using albuterol. Raw data for predicted and measured VO2 can be

found in Appendix IC,Maximal VO2 measured for each of the eleven subjects was then

compared to each subject's predicted maximal VO2 fromthe submaximal albuterol and

placebo trial (Table 6). No significant difference for VO2 max was found between the

conditions when compared using a repeated measures one-way ANOVA. Following this,

two additional repeated measures one-way ANOVA analyses were also run comparing

predicted maximal aerobic capacity with measured maximal capacity for the subjects

who l) had the same workload (U:6) when submaximally tested with albuterol as when

submaximally tested with placebo during stages 2 and 3 of cycle testing, and 2) had

different workload (n: 5) when tested submaximally with albuterol as when tested

34

Table 3

ANOVA Suln― Table for IIR tt Stage 2 and Sta2e 3

Sollrcc ofVarlation SS df MS F p

Time 2090.67 1 2090.67 37.22 0.00*

Error 1 280。83 5 56.17

Med 130.67 1 130.67 1.75 0.24

Enor 2

Time x Med

Error 3

327。 83 5 74.57

13.50 1 13.50 3.38 0。 13

20.00 5 4.00

Note. Time = stage2 vs. stage 3 of cycle testing

Med: albuterol vs. placebo

*p < .05; There was, zls expected, a significant main effect for an increase in HR from

stage}to stage 3 due to an increase in cycling workload.

35

Table 5

Peak Flow Descrわ tive Data

SD SEM

albuterol

lacebo

Note. Peak flow levels measured in liters per minute-

*p < .05; Mean peak flow was significantly higher in subjects when administered

albuterol vs. placebo based on a paired T-test.

455.91ホ

425。91*

94.57

115.99

５２

　

９７

８．

　

４

．

２

　

　

３

Tablc 6

SS df Sig。

l)All subjects

Error

2)Subjects with same

workloads

Error

3 )Subjects with differentworkloads

7.70

617.20

0.18

523.13

13.34

7.71

61.72

0。 18

104.63

13.34

22.07

0.13 0.731

10

1

５

　

　

　

１ 0.61 0.48

Error 88.26

Note。 1)ANOVA ona■ 1l sutteCtS・

2)ANOVA on only sutteCtS(ュ =6)lMth eqllal workloads durmg由電es 2 and 3 of

albuterol and placebo mals.

3)ANOVA on only sllttects(■ =5)宙th direrent workloads dllring s●ges 2 and 3 of

albuterol and Placebo mals.

36

0.00 0。97

37

submaximally with placebo during stages 2,3, aurrd4 of cycle testing. These two

additional analyses were done to show that VO2 predictions were not affected by

alterations in IIR from different workload settings for stages 2 arrd 3 of submaximal

te$ing. Both of these enalyses showed no difference in prediction between albuterol,

placebo, and measured maximal VOz. Predicted and measured marimal VO2 values for

all zubjects are seen in Table 7. Although predicted maxirnal VO2 derived fiomtesting

with albuterol and testing with placebo were equal predictors of measured marimal VO2,

they were actually equally poor predictors. In the majorrty of subjects testd predicted

'ma:rimal VO2 from submaximal testing with albuterol and placebo differed by greater

tbaals%from measured maximal VO2. Maximal VO2 for zubjects can be foud in

Appendix K.

Summary

The statistical information in this section discussed the effect on HR at rest and during

submaximal cycle testing with subjects on and offalbuterol. Of note was a significant

increase in IIR with the use of albuterol at rest and during low level exercise of stage I of

the YMCA zubrnaximal cycle test. At higher intensity levels of exercise (stage 2 and

stage 3), however, there were no signfficant differences in HR between albuterol and

placebo. Peak flow was also measured and found to not be significantly affected by

albuterol prior to exercise testing. Also found were no signifrcant differences between

predicted VO2 using albuterol or placebo and maximalV}zusing albuterol ufuether

examining all subjects (n = 1l), sanre workload zubjects (u:6) or subjects with different

workloads (a = 5).

38

Table 7

V02 111ax Descrintive Data

SDV02 MaxAlbuterol pred.

Placebo pred.

Measured

Same workloadsalbuterol Pred.placebo Pred.Measured

Different workloadsalbuterol Pred.placebo Pred-Measured

11

11

11

24.4

24.7

24.9

30.8

27.9

41.6

24.4

24.7

24.9

61.8

60.4

53.2

61.8

60.4

53.2

48.8

49.9

45。4

41.89

40.84

40。 71

45。 11

43.33

44.87

38.03

37.87

35。72

11.42

11.60

7.30

12.92

11.86

4.29

9.13

11.82

7.29

６

６

６

５

５

５

Note. Values ofVO2 rxD( expressed in ml&ymin'

Albuterol pred. : predicted marimal VO2 using albuterol; Placebo pred. : predicted ,

maximal VO2 using placebo; Measued = manimal VO2 using albuterol'

Same workloads : datafiom subjects with..q*iworkloads ontheir albuterol and

placebo cyile tests during stages 2 afr3'

Different workloads = datafrom zubjects with different workloads ontheir albuterol and

placebo cycle tests dudng stages 2,3, and 4'

ChaPter 5

DISCUSSION

The purpose of this study was to investigate ability to predict maximal VO2 using the

yMCA submaximal cycle test in people with EIA using albuterol or placebo. Heart rate

recorded during submaximal testing on albuterol and on placebo was used to analyze this

relationship. This chapter contains a discussion of the results reported in chapter 4'

Sections in this chapter include the following: (a) the effect of albuterol on H& (b) the

effect of albuterol on predicting maximalVo2, (c) practical applicatiorU and (d)

summary.

Effect of Albuterol on Heart Rate

Heart rate during rest is controlled by the depolarization rate of the SA node but if HR

control was left solely to the inherent depolarization rate of the SA node then resting HR

would be about 100 bprn However, the autonomic nervous system modifies this rate,

decreasing or increasing the number of beats by stimulating parasympathetic or

sympathetic control, respectively. Thus, average resting HR for men is between 67-70

bpm and for women 7}'71bpm (Nieman, 1995).

Some medications alter average resting HR when used in certain populations. For

example, asthmatics using albuterol are shown to have higher resting heart rates than with

placebo @hand et al., 1996;Fleck et al., 1993; Gadomski, Aref, el Diq el Sawy, Khallaf,

& Black, 1994;Lin et a1.,1993;Rakhmanin4 Kearns, & Farrar, 1998; Rohr, Spector,

Rachelefsky ,I(at1& Siegel 1986). Findings of the current study agreewith these results

and show increased resting HR with the use of albuterol. In the current study, after

albuterol use, resting HR was an average of 7 bpm higher (75.3 bpm +/'lO.7 bpm for

39

40

albuterol vs. 68.6 bpm +/- 8.7 bpm for placebo) than after placebo use. Albuterol is a

short duration(2-4 hour), relatively selective beta-2 adrenergic bronchodilator,

commonly prescribed to people suffering from EIA. It is administered as a preventative

medication 20 minutes prior to exercise. It is thought that the increase in HR with the use

of albuterol could be related to albuterol treing only relatively selective forbeta-2

receptors. Accordingly, albuterol rnay stimulate beta I receptors found in the heart

resulting in increased HR at rest.

When administering a submaximal exercise test, any changes to HR from a normal

response are very important. This is because a normal linear HR response from rest

through incrementally increasing stages is assumed for accurate VO2 max prediction. In

normal individuals, when increasing from rest to low-moderate exercise, there is a need

for bltered management of blood flow. In response to this need, sympathetic control is

increased and there is a release of epinephrine (Sherwood, 1993). The combination of

increased sympathetic conhol and epinephrine release cadse HR to increase to match the

demand for greater blood flow during changing levels of exercise intensity from one

stage of submaximal testing to another.

During low-moderate intensity exercise, as in the current study, HR in EIA sufferers

was elevated when using albuterol cornpared to placebo. Findings from two other sfudies

performed at low-moderate exercise seem to contradict the findings of this study,

however, training level, time between drug administration and exercise were different

from the current study. One of these studies, conducted by Ienna &McKerzie (1997),

found a higher mean HR in highly trained people with EIA using placebo versus

salbutamol dtuing an exercise test. This differs from the current study where subjects

,41

were moderately active but not highly trained. In Ienna & McKenzie's (1997) second

group of individuals who were moderately trained, they found no change in HR with

salbutamol at any exercise intensity. Their findings differ from the present study, possibly

because salbutamol was administered only l5 minutes prior to testing. [n the present

study, albuterol was administered 20 minutes prior to testing. There was a signihcant

increase in PEFR found in both studies. Another study, performed by Schmidt et al.

(1988), also found no change in HR with the use of salbutamol versus placebo during

low-moderate exercise. Once again, these contrary findings may be due to the timing of

drug administration. In their study, salbutamol was administered only five minutes before

exercise testing b"guru instead of the recommended20 minutes for salbutamol to reach its

full effect.

The increase in HR with the use of albuterol at rest qnd during low-moderate exercise

intensity (stage l) observed dwing the present study had implications when using the

yMCA submaximal cycle test. This is because the workload settings for stages 2,3,and

4 are determined by the steady state HR duing low-rnoderate exercise (i.e., stage 1). For

nearly half of the subjects tested in the present study, albuterol caused an increase in HR

that required a lower workload setting for stages 2,3, and4 than in their placebo trial. For

example, if a subject using placebo hadaHR during stage I of 85 bprq the following

workload settings for stages 2, 3 , and 4 would be 2.0 kp,2-5 kp, and 3.0 kp, respectively.

If the same subject, now using albuterol, had an elevated HR during stage I of 95 bpnl

the workload settings for stages 2, 3, arrd 4 would be lowered to 1.5'kp, 2.0 kp, and 2.5

kp, respectively. Lower workload settings should theoretically produce lower steady state

HR during stages 2,3, and4. This should alter the two points needed to predict maximal

42

VO2, but this does not necessarily mean that the predicted VO2 would be affected' The

two HR points, in combination with the slope generated by these two points, determines

predicted maximal VO2.

As a person progresses from moderate to moderately-high exercise intensitY, the

demand for increased muscle blood flow continues to rise resuhing in an even greater

cardiac sympathetic control and more release of epinephrine causing further increase in

HR. When HR climbs above I l0 bpm as with moderately-high levels of exercise, Inany

external stimuli such as talking, laughter, and nervousness, cease to have an effect on HR

(NiemarL 1995). With the effect of such external stimuli at a minimum, a linear

relationship develops between HR and workload when HR rises above I l0 bpm but

below 150 bpm. This linear relationship that develops is the reason YMCA submaximal

exercise testing can be used to predict maximal VO2.

However, if albuterol significantly increases HR during moderate and/or moderately-

high intensity exercise as it did during rest and low-moderate intensity exercise, the linear

relationship formed between HR and workload would be affected and cause an altered

prediction of rnaximal VO2.

In the present study, at moderate and moderately-high intensity exercise workload

settings, there was no.significant effect of albuterol on HR. A study conducted by

Robertson et al. (1994) supports the findings of the present study during moderate and

moderately-high intensity exercise. They had eight asthmatic men perform progressive

maximal cycle tests after taking salmeterol0.5 mg, salbutamol 2 mg,or piacebo. Their

purpose was to examine the effects of a single dose of sahneterol on exercise capacity in

asthmatic men. Cardiorespiratory, hemodynamic or subjective responses to progressive

43

maximal exercise tests were not different with salmeterol, salbutamol, or placebo, nor did

endurance capacity change with any treatment.

Other research studies have noted an albuterol efFect on HR during rest and very high

intensity exercise, with the effect "disappearing at maximal exercise. Fleck et al. (1993)

reported an increase in subjects' HR with the use of albuterol during the middle stages of

cycle ergometry testing with workload settings of 200, 225, and 250 watts, but not during

the beginning or ending levels of testing correspondrng to workloads of 150, 275, and

300 watts. In the present study, only one subject cycled at a workload as high as 150

watts dgrihg stage 3 of testing. All ofthe other subjects cycled at workloads less than 150

watts. Similar to Fleck et al. (1993), Carlsen et al. (1997) found salbutamol to have no

effect on HR at anaerobic threshold or maximal exercise testing levels. And, Grove et al.

(1995) noted salbutamol increased HR during rest in his subjects but not at maximal

exercise. The lack of an increase in HR with albuterol use found dunng very high and

maximal exercise may be due to advanced sympathetic activation and increased

circulating catecholamines. At levels of high sympathetic activatiorl HR rise may be

attenuated due to activation of baroreceptors and vagal-mediated slowing of the HR

(Klabunde, 1999). This may explain why albuterol ha.s been shown in many studies to

increase HR at rest and low exercise intensities but no longer cause an increase in HR

during high intensity or maximal exercise levels. However, this is just a speculation. And,

although several studies have been performed at rest and high intensity exercise, very

little is known about the effect albuterol has on HR during moderate to moderately high

workload settings used specifically during YMCA zubmaximal testing in the present

study. According to this study, albuterol affects HR during rest and low-moderate

44

intensity exercise (150 kgm) but does not seem to impact HR during moderate (300-750

kgm) or moderately-high intensity exercise (450-900 kgm). Once more information is

gained as to exactly when during exercise testing albuterol ceases to influence I{Ft, then

further speculation on physiological mechanisms can occur.

In the present study, albuterol did not significantly affect HR during moderate to

moderately high workload settings. This indicates that HR predicted maximal aerobic

capacity in people with EIA is likely to produce similar results with albuterol or placebo.

Effect of Albuterol on Predicting Maximal VO2

For the purpose of this study, the predicted maximal VO2 of all subjects, both on

albuterol and on placebo, were compared to actual measured maximal VO2 of all subjects

on albuterol. The positioning ofthe two HR points and the slope of the line created by

those points between I l0 bpm-150 bpm during submaximal tesing determines the

YMCA cycle test predicted maximal VO2.Ifthe slope of the HR line flattens during the

test, there will be a higher predicted maximal YOz.If the slope of the HR line rises more

sharply, the result is a lower predicted maximal VO2.

In subjects whose cycle test workloads were the same on the albuterol and placebo

trials, findings from this study showed albuterol had no significant affect on the slope of

the line or on the positioning of the HR points (i.e., albuterol had no affect on HR at

either ofthe two points). This resulted in similar predictions of VO2 max when using

albuterol or placebo. More surprisingly, there was also no difference between predicted

VO2 max and measured VO2 max in subjects who used different workloads on their two

YMCA cycle trials.

45

The predicted maximal VO2 from the albuterol and placebo trials equally predicted

measured maximal VO2. However, there was a substantial amount of over and

underprediction of melured mzximal VO2 from submaximal testrng of people with EIA.

YMCA submaximal cycle testing usually produces predicted maximal VO2 readings

from 5-15% of actual measured maximal VO2 (Nieman, 1995). In almost hutf (n = 5) of

the subjects in the present study, their predicted maximal VO2 from submaximal testing

with albuterol and with placebo differed from measured maximal VO2 by more than

lsyo. And, in three additional subjects, one of the two predicted maximal VO2 from

submaximal testing with either albuterol or placebo dif,lered from measured by greater

tl;61nl5%. This should lead to further research examining why, in a majority of people

with EIA, predicted maximal VO2 differed by greater tharr- lsyo from measured maximal

VO2 when using the YMCA submaximal cycle test.

Due to the observation of increased HR in people with EIA using albuterol during rest

and low-moderate intensity exercise, further research is warranted when using alternate

exercise testing protocols where subjects VO2 max is derived from HR during rest and/or

low-moderate exercise. For example, if the step test is used to predict aerobic capacity,

HR recovery is recorded over a fixed time period post-test. If albuterol elevates HR

during the recovery period (rest), inaccurate cardiovascular prediction could occur

(Johnsoq 1998).

Practical Application

The frndings of this study suggest that submaximal exercise testing of people with

EIA using the YMCA cycle test provides similar results whether on or offalbuterol.

These results equally, but often poorly, predict marimal aerobic capacity whether or not

へ

46

albuterol is used by people with EIA. Therefore, it is with some caution that exercise

prescriptions derived from submaximal testing should be used in the special population of

people with EIA.

Summary

In summary, this chapter discussed the role albuterol plays in increasing HR at rest

and during low-moderate exercise above the normal increase in HR attributed to

autonomic control and how that may affect YMCA submaximal exercise testing. This

chapter also discussed the effect albuterol had during the two critical stages of

submaximal testing when steady state heart rates are recorded. Albuterol was found not to

affect HR during those two stages. Because of this, maximal VO2 was equally predicted

when using placebo or albuterol during the YMCA cycle test. However, predicted

maximal VO2 predicted maximal VO2 equally poorly with albuterol and placebo trials.

Therefore, caution should be used with exercise prescriptions based on submaximal

testing for the special population of people with EIA.

ChaPter 6

SUMMARY, CONCLUSIONS, AND RECOMMENDATIONS

Summary

The purpose ofthis study was to investigate the ability to predict maximal VO2 from

submaximal testing using albuterol and placebo. Consequently, the effect albuterol had

on HR during stages of YMCA submaximal cycle testing in subjects with EIA was also

examined. The subjects were males (n:6) and females (n: 5) aged 18-35 years. The

study consisted of three testing sessions. Two ofthe sessions included submaximal

testing with albuterol or placebo. The third session was a maximal cycle test to measure

VO2 max while on albuterol. Predicted maximal VO2 from zubmaximal testing was

derived from steady state HR during stages 2 and 3 of YMCA submaximal cycle testing.

Two 2 x2 repeated measures ANOVAS were used to investigate the affect albuterol

and placebo had on HR during submaximal testing. InadditiorU a dependent samples T-

test was used to compare peak flow values in albuterol and placebo conditions. Results

revealed albuterol caused a significant increase in HR at rest and during stage I of

submaximal testing, however, no effect was seen during *age2 and stage 3. Results also

showed there was a significant increase in peak flow between the two groups prior to

testing. A one-way repeated measures ANOVA was used to examine differences in

predicted maximal VO2 from submaximal testing using albuterol and placebo and

measured maximal VOz. There was no significant difference found between predicted

maximal VO2 between albuterol, placebo, and measured maximal VO2. Following this,

two repeated measures one-way ANOVA analyses were used to compare predicted

maximal VO2 with measured maximal VO2 for the subjects who had the same

47

workloads, and for those who had different workloads when tested submaximally on

albuterol and on placebo. AgarU there was no significance found between groups.

Conclusions

The results of this study support the following conclusions:

l. During submaximal exercise testing using the YMCA protocof HR is higher at

rest and during stage I (low-moderate exercise) of testing with the use of albuterol in

subjects with EIA However,'during stages 2 and 3, I{R is not affected by the use of

albuterol.

Z. Because HR is not a^ffected by albuterol during stages 2 and 3 of submaximal

testing, predicted maximal vo2 was also not affected by albuterol.

3. A YMCA submaximal cycle test with people with EIA using albuterol or placebo

equally predicted measured rnaximal VOz-

4. Given the error often secn in predicting m:ximal VO2 from submaximal testing,

sometimes greater thanllyo,caution should be used when prescribing exercise from

these tests in people with EIA.

Recommendations for Further StudY

This investigation led to these r.ecommendations for further study:

l. A study should be conducted with alarger number of subjects because the effect

albuterol had on HR during stage I oftesting caused the subjects to be divided into two

groups for analysis. Additional power of analysis might yield new findings.

2. A study should be conducted examining why predicted maximal VO2 differed

from measured maximal VO2 by greater thminl5%o in people with EIA.

49

3. A study should be conducted with subjects using one of the new drugs commonly

prescribed to treat asthma containing a long-acting beta'Z agonist ard a steroid.

4. A study should be conducted with subjects using one of the new combination

drugs mentioned above in combination with albuterol prior to exercise.

5. Studies should be conducted in which subjects peiform other submaximal

exercise tests in which HR recorded during rest and/or low-moderat;e exercise is used for

predicting aerobic capacitY.

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asthma-the effect of beta 2-adrenoreceptor stimulation. Scandinavian Journal of

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Ienna T. M., & McKenzie, D. C. (1997). The asthmatic athlete: metabolic and

ventilatory responses to exercise with and without pre-exercise medication-

International Journal of Sports Medicine,lS, 142-148'

Jagoda A., Shephar{ S. M., Spevitz, A., &Joseph (1997). Refractory asthmq part l:

Epidemiology, pathophysiology, pharmacologic interventions. Annals of Allergy.

Asthma and Immunology ,2g, 262'274.

Klabunde, R. E. (1999). Cardiovascular physiology concepts [On-line]. Available:

cvphysiologY.com

Lacroix, V. J. (1999). Exercise-induced asthma. The Physician and Sports Medicine,

27, 1-12.

Liq R. Y., smith A. J., &Hergenroeder, P. (1993). High serum albuterol levels and

tachycardia in adult asthmatics treated with high-dose continuously aerosolized

albuterol. Chest, lO3, 221-225.

McCaftey, P. M., Riddell, J. G., & Shanks, R. G. (1988). The selectivity of xamoterol,

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ICI I 18,551. Journal of cardiovascular Pharmocology, I l, 543-551.

McKinley Health Center (2002). How to use your metered-dose inhaler the right way

[On- line]. Available : http ://www.mckinley. uiuc' edu

Niemaru D. C. (19951. Fitrr"r, *d Srort, M"di.ir"' A H"ulth R.lut"d Arrtou"lt 13ra

ed.). Palo Alto, CA: Bull Publishing Company'

53

physician's Desk Reference (2002). PDR (566 ed.). Montvale, NJ: Medical Economics

CompanY.

Ramsdell, J. W., Colice, G.L., EkAokn,8.P., & Klinger, N' M' (1998)' Cumulative

dose response study comparing IIFA-134a albuterol sulfate and conventional CFC

albuterol in patients with asthma. Aruurls of Asthma Allergy and Immunology, &1,

593-599.

Robertson, W., Simkins, J., O'HickeY, S' P', Freeman, S', & Cayton' R'M' (1994)'

p6e5 single dose salmeterol affect exercise capacity in asthmatic men? European

Respiratory Journal, 7, 1978-1984.

Rohr, A. S., Spector, S. L., Rachelefsky, G' S', Kata R' M'' & Siegel' S' C' (1986)'

Efficacy of parenteral albuterol in the treatment of asthma' Comparison of its

metabolic side effects with subcutaneous epinephrine. Chest, 89, 348-351'

Rakhamanina, N. Y., Kearns, G.L., & Farrar, H' C' (1998)' Hpokalemia in an

asthmatic child from abuse of albuterol metered dose inhaler. Pediatric Emergency

Care, 14, 145-147.

Sanders, S. F. (1997). Exercise induced asthma in athletes. American College of Sports

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Cardiovascular Drugs and Therapy,14, 433-M0'

Sherwoo4 L. (1993). Human Physiology: From Cells to Systems. (2'd ed:)' St' Paul,

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ITHACA COLLEGE LIBRARY

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Pharmacology, 7, 235-241.

54

Append破 A

RECRIIIMNT FLYER

DO YOU EXERCISE REGULARLY AND ⅡAVE EXERCISE INDUCEDASTⅡ MA(EIA)?

IF SO.¨ "¨"ARE YOU INTERESTED IN FINDING OUT FREE OF CⅡ ARGEWⅡAT OTⅡERS WOIILD PAY OVER Sl,000 FOR?

FIND OUT:

● YOUR PERSONALIZED MAXIMAL AEROBIC CAPACITY(V02 MAX)● YOUR BL00D PRESSURE G助 ,AND ⅡEART RATE(Htt RESPONSES TO

EXERCISE FOR FREE!

IF YOU MEET EACⅡ OF TⅡE REQUIREMENTS LISTED BELOWPLEASE CALL ME:KERRY KERF00T 254‐ 2985

0R EMAIL ME AT:KK253oCORNELL.EDUFOR MOREINFORMA■ ON RECARDING PARTICIPATINC IN MY STUDY

● medically diagnosed with EIA for at least the past s破 months

● used am albutemlinhaler(geneHc9 Pmventil,or Ventomm)priOr to exe“ ise for at

least the past siI IE10nthS

● age 18‐35● perform cardiovascular exercise 3‐ 5X's per week 20 mino or more per workout

session for at least the past six IE10nthS

● in generally g∞ d health

mT YOU WILLBE ASKED TO DO:

DAY l)Orientation Session(1/2h→DAYS2&3)SubmaXimal erOrt cyCle test(l hr eaCh) .DAY 4)Maximal erort cycle test(lh→Note: Order oFdays and tinles are nexible,‐(Dne submaxilmal cycle test wi‖ be perfomed withoutthe use ofyour inhaler‐DuHng each exercise test you will wear a breathing valve so that we can measure

your oxygen consumption‐Ifat any time you elect to use yourinhaler,you l■ ay do so

YOUR PARICIPAHONIN tt STUDY WILL HELP US TO DETERM□ MEA MOREACCIMTE METHOD FOR PRESCRIBING EXERCISE PROGRAMS FOR AS口 EMATICS

FOR MOREINFO PLEASE CALL OR EMAIL ME:Kenv Kerfoo1 254‐ 2985 or

kk253@comell・ edu

55

Append破 B

MEDICAL IIIISTORY FORM

Nanle

Date

**Dr.'s Name +*Dr.',s # ----------

1. Approximately how long have you had asthma?

2. Please list all allergies (po[en, dust, foo4 medications, etc.)

3. Please list all ctgrent rnedications (asthm4 allergy, and other prescription medicines,

over the counter medicines, etc.)

4. Have you ever been hospitalized due to severe asthma or exercise-induced asthma?

If .!es" than please list the dates and durations of hospitalizations below

*IN TI{E LAST TWO WEEKS......*

5. *How often do you use your b'ronchdilator medications? @roventil, Ventolin,

albuterol, Brethine, terbutaline, etc.)

#Days per week?

Time of Day you use them? (circle one) Morning Noon Night Only

M exercise

#Total Doses per week?

How long have you been taking each? Yrs? Mo.'s? Wk.'s?

6. *How often do you have wheezing, chest tightness, shortness of breath or prolonged

coughing not related to exercise?

#Days per week?

Please rank the severity of the symptoms from l-4 (1: least severe)

7. *How often do you have wheezing, chest tightness, shortness of breattr, or prolonged

coughing caused by exercise?

#Days per week?

Please rank the severity of these symptoms from l-4 (l: least severe)

56

57

g. +How often do you have wheezing, chest tightness, shortness of breath, or prolonged

coughing at night?#Days per week?

Please rank the severity of.these symptoms from l-4 (l: least severe)

g. Have you recently been diagnosed or treated for any injury or infectious diseases?

(cold, flr1 mononucleosis, chickenpox, etc.) If '!es" then when?

10. What types of exercise, sports or physical activities do you regrilarly engage in?

11. How often do you exercise and approximately for how long per session? (i.e- 20

minutes three times per weelq etc.)

12. Has your exercise pattern changed significantly in the past 6 months?

l3.Indicate "Y'or "lrl" next to each of the following items below

Do you smoke? lf uY',then for how long ?

Do you have high blood Pressure?

Does anyone in your family have high blood pressure?

Do have high cholesterol?

Does anyone in your frmily have high cholesterol?

Do you have Diabetes? If "Y', then when diagnosed, and what type do

you have?

Do you have heart problems? If "Y', then what type, and when diagnosed?

Does anyone in yow frmily have heart probtems? If "Y', then what t)'pe, and

when diagnosed?

Appendix C

INFORMED CONSENT FORM

Purpose of the Studyfhis stgdy is being conducted to determine if exercise testing of asthmatic subjects

using albuterol underpredicts exercise capactty.

BenefitsThis study may help veriry the continued use of ctrrent exercise tests or encourage the

revision of apopular fitness test to improve ottrcorne qualfy for individuals with exercise

induced asthma. Your participation will involve sound evaluation techniques and

equipment used pre, during, and post, two functional capacity tests. All testing associated

trith thir study will be done free of charge and the results will be provided to you if you

so request.If you would like this ffirmation sent to you please write your name and

address below:

What vou will be asked to do

You will be asked to perform one maximal cycle test with albuterol (AL), and two

zubmaximal cycle tests using the YMCA protocol one with AL, and one without- The

zubmaximal test protocol includes four sequential parts: l) Pre-Exercise [Resting (10

min)]; 2) ALor Placebo (PL) Administration [Resting (20 min)]; 3) YI\4CA Submaximal

Bike Test ('h" min); 4) Recovery (10 min). AL or PL will be self administered in the

doctor recommended dose via distributor recommended protocol, 2 putrs 20 min before

exercise. As a precaution a rescue inhaler will be present during all testing for any

emergency situations should they arise.

Each submaximal cycle test will include continuous exercise starting at a low intensity

until a moderate intensity is achieved at ufiich point the test will be stopped. Throughout

this cycle test (part 3 only) your IIR, blood pressure @P), and rate of perceived exertion

111PE) wil be determined. Also during each stage you will be asked to rate your shortness

of breath on a l-4 scale. During exercise you will wear head gear with a mouthpiece to

allow us to collect exphed gasses. Before and after testing you will be asked to blow into

a Peak Flow meter which will help us to assess your lung functionMildmal testing will follow the same protocol as submaximal testing except the test

will be stopped after maximal effort has been achieved.

Risks associated with participationAs you are probably aware, there is always a risk of injury involved with exercising.

The risk is slightly greater during the marimal exercise test. The submaximal cycle tests

also pose some risk to the individual especially since one will be performed whileunmedicated. We hope to minimize all risks by only allowing you to participate afteryour physician and our staffhas cleared you. Furthermore, well-trained exercise

physiologists will be conducting both cycle tests with at least one being CPR/Adult First

Aid certified. The most common symptoms of EIA include shortness of breath

58

辮靱猾流増i鸞驚鸞 ∬test,and need treatment,a rescuc inhaler will

認 :蹴出結翼脆1群e ttthe EКrctt Physbby Ltt Room

謝躙瀕藻冨男:助.G.A.Sbrzo 27牛 3359

WildrawJ lЮ m the studv

Participation in this■ dyお volmtary and you may wihdraw at any tlIIle ifyou so

choose。

11l be mantaned in con■ )lete conndence。

infomatbL Allrepo■ing ofthis

l group fo...L You or yollr name wili never

be associated with thiS infomatiOn in any負肛 e disc10Sures.

I have read the above and understand the content.I acknowicdge dntl aln 18 years of

age or older and agree to parttipate in this studyo PLase sign and date bebw.

(Stnaturel(date)

Initial here

Append破 D

PARHCIPA■ON FORM

Ithaca College-Graduate ProgramDept. ofExercise and Sport Sciences

Date

Dear Doctor,

I am writing to inform you that your patient, , has volunteered

for participation in a study of exercise-induced asthma (EIA), albuterol (AL), and graded

exercise testing.

As I am sure you are aware, alongside a growing public awiueness for the many health

benefits associated with exercise is an ever-increasing number of people suffering from

asthma. As I am also sure you are aware, AL iS commonly used in the prevention and

treatment ofthe bronchospasms related to EIA. However, of concern is the fact that AL

may elicit many other physiologic responses other than just bronchodilation These

responses may include changes in heart rate (tIR), blood pressure @P), and lactic acid

(LA) production These three parameters are used by exercise physiologists to create

proper and safe exercise prescriptions for the public. In order to provide EIAs with safe

and effective exercise prescriptions, there is a need to assess the accuracy ofour exercise

tests for this special population Therefore, the purpose of this study is to verif the

continued use of a commonly used exercise test, the YMCA cycle test, or to encourage

the revision of this popular fitness test to improve outcome quality.

Yor.n patient will visit the Exercise Physiology Lab at Ithaca College for three sessions

total: One maximal with AL, one submaximal with AL, and one submaximal without AL.

60

6l

These tests will be conducted by trained exer6ise physiologists in an environment where

precautions have been taken to ensure your patient's safety (emergency plarg rescue

inhaler). Your patient will be excluded from this study if shelhe: l) needs inhaler for

anything other tban EIA 2) is on any other asthma medications or any other medications

that contraindicate an exercise test 3) has had any worsening of symptoms in the past two

weeks 4) has ever been hospitalized for asthma 5) has a Peak Flow of less than 80% just

prior to exercise testing 6) cannot perform a cycle test because of any physical

limitations. Attached please find the formthat your patient has signtrd which more

completely describes the exercise procedures.

My education includes BS in Exercise Science/Fitness and Cardiac Rehabilitation

from Ithaca College in Ithac4 l.IY. I have worked in the fitness field for the past five

years performing extensive exercise testing and exercise prescription on healthy and

diseased individuals including asthmatics. I have also corryleted an internship in Cardiac

Rehabilitation Phase I, II, m, and IV at Lourdes Hospital in Binghamton, NY. My

certffications include HFI, CP& and Adult First Aide. Dr. Sforzo, my advisor, has done

numerous research projects over the past 20 yrs. including work with asthnatic subjects.

I am also conzulting with Gerard Dunphy, a board certified physician's assistant with

over 14 yrs. ofprimary care eryerience.

To allow your patient to participate please retum the form below in the self-addressed

stanrped envelope before 。Contactlne Wih any quettions at(60つ 256‐

5375.Or call Dr.Sforzo at(60η 27牛3359 weekdays hm 9 AM to 5 PM.Thank you for

your collsideration。

Sincerely;

Kerr),Ann Kerfoot, BS, HFI

PLEASE TEAR OFF A}ID RETURN THIS PORTION WITH YOUR RESPONSE

My patient can ParticiPate

My patient cannot ParticiPate

Physician's Signature Date

-l

Appendix E

PRE.E)GRCISE TEST INSTRUCTIONS

You are scheduled to complete a n@dmum effort exercise test; your performance

depends upon adherence to ttrese instnrctions:

l. Do not perform heavy exercise in the 24 hours preceding your test.

2. Do not drink alcohol.for 12 hours preceding your test.

3. Do not use caffeine or nicotine for 3 hours preceding your test.

4. Do not eat for 3 hours preceding the test.

5. Do not eat any food tbat may cause you discomfort the day ofthe test.

6. Avoid over-the-counter medications for the 12 hours prereding the test. (However,

cancel the appointment if you are ill and treat yourself accordingly; we can

reschedule.)

7. Wear comfortable clothing (shorts and a t-shirt recommended) and sneakers.

8. Do not use inhaler (albuterof VentolirU or Proventil) 4 hours or less prior to exercise

test time. If you do use inbaler during this time then please call to reschedule

appointment.

63

に夢Shjdm認獅品錨蹄

Using an inhaler seems simple, but most patients do not use it the right way. When you use yourinhaler the wrong way, less medicine can get to your lungs. (Your doctor may give you other types ofinhalers). For the next two weeks, read these steps aloud as you do them 'or ask someone to read

them to you. Ask your doctor or nurse to check how well you are using your inhaler. Use your inhalerin one of the three ways pictured below (A and B are best, but C can be used if you have trouble withA and B).

STEPS FOR USING YOUR INHALER

Gettino Readv

1. Take off the cap and shake the inhaler.2. Breathe out allthe way.3. Hold our inhaler the way your doctor said (A, B or C below).

Breathe ln Slowlv

4. As you start breathing in slowly through your mouth, press down on the inhaler one time. (lfyou use a holding chamber, first press down on the inhaler. Within five seconds, begin tobreathe in slowly.)

5. Keep breathing in slowly, as deeply as you can.

Hold Your Breath

6. Hold your breath as you count to ten slowly, if you can.7. For inhaled quick-relief medicine (beta2-agonists), wait about one minute between puffs.

There is no need to wait between puffs for other medicines.

Append破 F

INHALER USAGE INSTRUCT10NS

How to Use Your Metered-Dose lnhaler the Right Way

A. Hold inhaler one to twoinches in front of yourmouth (about the width oftwo fingers).

B. Use a spacer/holdingchamber. These come inmany shapes and can beuseful to any patient.

C. Put the inhaler in yourmouth. Do not use forsteroids.

CLEAN YOUR INHALER AS NEEDED

Look at the hole where the medicine sprays out from your inhaler. lf you see "powder" in or aroundthe hole, clean the inhaler. Remove the metal canister from the L-shaped plastic mouthpiece. Rinse

only the mouthpiece and cap in warm water. Let them dry overnight. ln the morning, put the canister

back inside. Put the caD on.

64

Appendix G

WORKLOAD SETTING GUIDE FOR YMCA CYCLE TEST'

Guide to Setting Workloads on Bicycle Ergometer

1stworkload

2ndworkload

3rdworkload

4thworkload

Dl劇10ns:

1.Setthe lrst workload at 150 kgm′min(0。 5 Kp).

2. r the HR in the third rnin is

:器冨雲訛翼鵬翻T器避」1:.踊li5蹴0 90to100,setthe se∞ nd 10ad at 450 kgm(1.5 Kp);

・ greater than(>)100,Setthe second load at 300 kgm (1.O Kp).3. Setthe third and fourth(if required)loadS according to the loads in the co!umns below the

second loads.

棚蹴躙 ∬ぢrT鑑継鶴 ∴甜靴 y。

150 kgmO.5 Kp

750 kgm2.5 Kp

HRくHR 100

65

APPendix H

GRAPH FORDETERMINING VO2 WITH YMCA CYCLE TEST2

御

働

ｍ

口

”

ＨＲ

WORKLOAD(k― l

MAX 02U「rAKE(υ mlKCAL uSED oヒロИm)

APPROX MET ttEL(br132 b)APPROX MET LEVEL(Oor176 b)

獅５．０枷圏‐６．０

鰤４．６劉鯛‐５．０

ｍ４．２２．．０１８．０‐４．０

口”‐９．０‐６．７‐３．０

ｍ３．６‐７．５‐５．３‐２．０

鰤”‐６．０‐４．０‐１．０

側２．０‐４．０・２．７‐０・０

ｍ劉

‐０・５‐０・００．０

「“９．０３．７“

輌“““０・０

輌”６．００．０５，０

ｍ”４．５４．７４．０

口０・６””３，０

10502.4

12.0

1139,0

,From Graph for determining VO2 max from submaximal heart rates obtained during the

YMCA's suUmarimal bicycle test. D. C. Nieman, 1995, Fitness and Sports Medicine: A

Health RelatedApproacn, Sil ed.,p.86. Copyright 1995 by Palo Alto, CA: Bull

Publishing Company.

DRrnOpas

l.P:ot thO HR of the 2workloads YO『 Sug theWOrk(k9耐 min).

2.Determ:no lho Bubled:8max HR :ine by

琳徽柵at th:6 ValuO.

3.Draw a ‖nO through

智精悧 1譜 :席¶

000・

4昴肌∬恥露繊

max workload and 02uptako.

66

APPendix I

RAW DATA _ IMART RATE

A) IIR on AL and PL Trials at Rest and During Stage I

Rest HR A Rest HR P ST l IIR A STl HR P

０

１

１

２

３

４

５

６

７

８

９

１

１

777275

667275

9855748480

7458

70.53747l7957697476

9l9493

808488

ll07687

r05102

857790808488947795

10698

B) HR on AL and PL Trials During ST 2, ST 3, and ST 4

ST2HR A ST2 HR P ST3HR A ST 3 11R P ST4 HR A ST411R P

105

116

134r23131

116120130

tt2113

116

lllt25tl4il6124ll5120124117

tt7137

113

135

156135

148125t4tr57126129138

t24152t34132148

t24r45159

137

t34t54

127

Note. Data are expressed in bpm.

HR:heartrate;\A:albuterol;P:placebo;STl:stagelofcycletesting;ST2:stage

2 of cycle testing; ST 3 = stage 3 of cycle testing; ST 4 : stage 4 of cycle testing.

*denotes subjects with same workload settings for albuterol and pkicebo trials

(stages 2 ard3).

67

3*4*

l1

APPendix J

RAW DATA _ PEAK FLOW

Peak Flow Prior to Submaximal Testing on AL and on PL for all Subjects

Pcak Fbw AL Peak Fbw PL

０

１

１

２

３

４

５

６

７

８

９

１

１

3404502804205005754505505s0520380

280370240370500595420560490520340

Note. AL: albuterol; PL: placebo.

Data are expressed in L/min.

68

Append破 K

RAW DATA― V02

Predicted l山ⅨiIIlal V02 on AL and on PL alld Mcasured Maximl V02 on AL for au

SutteCtS 、

Subject# Po Maxo AL P.lv`LEXし PL M.レLⅨo AL

ホ

ホ

　

＊

　

中

　

＊

　

　

　

中

　

　

　

ｎｖ

■１

１

２

３

４

５

６

７

８

９

１

１

48.8

42.8

34.5

61.8

30.8

59.5

24.4

39。 5

35.2

“

.7

39.0

49.9

45。2

40.5

54。2

27.9

60.4

25。6

37.0

24.7

40.0

4.0

35。 1

45.4

“

.8

“

。7

42。441.6

24.9

53.2

36.8

42.5

36.4

Note. P. Max. AL: predicted rnaximal VO2 using albuerol; P. MalL PL : predicted

modmal VO2 using placebo; M. Ma:<. AL: rneasured maximal VO2 using albuterol.

*denotes subjects with conparable workloads during ST II and ST III.

Data are expressed in mltkg/min.

69

predicting maximal voÂ² in exercise-induced asthmatics

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