Full text of DOI:10.1093/gerona/56.1.B33

Journal of Gerontology: BIOLOGICAL SCIENCES
Copyright 2001 by The Gerontological Society of America
2001, Vol. 56A, No. 1, B33–B37
Effects of Chronic Food Restriction and Exercise
Training on the Recovery of Cardiac Function
Following Ischemia
Tom L. Broderick,1 William R. Driedzic,2 Melissa Gillis,3 Jacqueline Jacob,4 and Terry Belke4
1Department of Physiology, Midwestern University, Glendale, Arizona.
2Ocean Sciences Centre, St. John’s Campus Memorial University of Newfoundland, St. John’s.
3Department of Biology and Biochemistry, Mount Allison University, Sackville, New Brunswick.
4Department of Psychology, Mount Allison University, Sackville, New Brunswick.
Clinical and experimental data suggest that exercise training (ET) and food restriction (FR) improve cardiovas-
cular function. However, the effects of long-term FR or FR in combination with ET on the recovery of cardiac
function following ischemia have not been determined. Male Wistar rats were assigned to ad libitum-fed, FR, ad
libitum-exercise, and FR–exercise groups. Mechanical function of isolated working hearts was assessed in re-
sponse to increases in afterload resistance and following global no-flow ischemia. At low workload, there was a
significant FR effect on aortic flow as well as an interaction between FR and ET on systolic pressure. These ef-
fects remained when hearts were subjected to increases in aortic afterload resistance. During reperfusion of
ischemic hearts, there was a significant FR effect on aortic flow and systolic pressure and a significant ET effect
on diastolic pressure. An interaction between FR and ET on heart rate was also seen during reperfusion. In terms
of percent recovery of heart function following ischemia, FR continued to affect aortic flow, and we observed an
interaction between FR and ET on aortic flow. Our results clearly indicate that the myocardium from the FR an-
imal or the FR, exercise-trained rat is more resistant to ischemia.
OOD restriction (FR) has elicited a great deal of inter-
est because it increases life span and delays the devel-
determined in hearts perfused in the absence of fatty acids
(6). Blood levels of fatty acids are elevated in patients in the
clinical setting of reperfusion and are known to potentiate
ischemic injury secondary to an accumulation of intermedi-
ates of fatty acid oxidation and by inhibition of glucose me-
tabolism (18,19).
In the present study we examined the effects of FR and
ET on the recovery of heart function following ischemia.
We showed that FR, or FR combined with ET, improves
heart function, particularly following ischemic insult.
F
opment and severity of age-related diseases (1–3). FR re-
tards the development of cardiomyopathies and, in some
cases, prevents the physiological decline of myocardial per-
formance that is normally associated with aging (4,5). The
anti-ischemic effects of FR have also been reported, and, as
expected, hearts of FR animals are more resistant to anoxic
injury (6).
The impact of exercise training (ET) on myocardial per-
formance is also of interest, and the benefits of training on
preventing ischemic damage are well documented. Regular
exercise reduces the prevalence of heart disease, decreases
the development of heart complications, and can prevent the
development of non-insulin–dependent diabetes (7–9). ET
improves myocardial tolerance to ischemia in various ani-
mal models by rapidly restoring high-energy phosphates
and by improving hemodynamic function and coronary
flow (10,11). The beneficial effects of FR and ET can be ex-
plained by similar mechanisms of action. Improved insulin
sensitivity (12), enhanced adrenergic sensitivity (13,14), up-
regulation of glucose transporter proteins (15,16), and a fa-
vorable redistribution of blood lipids have been reported
following food restriction as well as ET (17).
METHODS
Animals
Male Wistar rats were used in this study. Rats were as-
signed to four groups: ad libitum-fed (AL), ad libitum-exer-
cise (ALE), FR, and FR–exercise (FRE). Rats were individ-
ually housed in standard plastic cages and kept in a holding
room on a 12-hour light/dark cycle. The AL and ALE rats
were allowed free access to food. Rats in FR conditions
were also maintained on ad libitum feed until their body
weight reached 400 g. The amount of food provided daily
was then reduced to maintain a target weight of 335 Ϯ 10 g.
This was achieved by gradually reducing food intake to
45% of the amount consumed by the AL animals. Restricted
calorie intake was maintained for a period of 8 months. ET,
as described below, was initiated at the onset of weight re-
duction. All animals used in this study were cared for ac-
cording to the recommendations in the Canadian Council on
Animal Care’s Guide to the Care and Use of Experimental
Animals.
To date, few studies have investigated the effects of long-
term FR or of ET combined with FR on myocardial perfor-
mance and recovery of function following ischemia. Al-
though earlier studies have shown that FR increases anoxic
tolerance in hearts (6), further studies are needed to confirm
this beneficial effect using a model of global ischemia. Fur-
ther, the effects of FR on recovery following anoxia were
B33

B34
BRODERICK ET AL.
Running Regimen
Running rates in the ALE group were low at approximately
60 revolutions per hour, and for this reason the running regi-
men was considered voluntary. Rats in the ALE group did not
receive the same training as rats in the FRE group because
motivation to run in AL rats was insufficient to train the ani-
mals to respond for the opportunity to run as a reward.
Rats in the exercise groups ran in standard activity
wheels (Wahmann and Lafayette Instruments Model 86041,
Lafayette, IN) that were 35.5 cm in diameter. A mi-
croswitch attached to the wheel frame recorded wheel revo-
lutions. Wheels were located in soundproof shells equipped
with fans to provide ventilation and to mask extraneous
noise. Retractable levers (Med Associates ENV-112, St. Al-
bans, VT) were mounted at the openings of wheels. The le-
vers extended 1.8 cm into the chamber through an opening
(7 cm ϫ 9 cm) in the center at the base of the wheel frame.
A solenoid-operated brake was attached at the base of the
wheel. When the solenoid was operated, a rubber tip at-
tached to a metal shaft contacted the outer rim of the wheel
and brought the wheel to an immediate stop. Control of ex-
perimental events and data recording were handled by Bor-
land’s Turbo Pascal programs on IBM personal computers
interfaced to the wheel through the parallel port.
FR rats in the exercise groups were trained under condi-
tions that generated high rates of running. The opportunity to
run in a wheel was restricted to 30-second intervals. To ob-
tain these brief opportunities to run, the animals had to press
a lever. Initially the animals were given the opportunity to
run in a wheel for 30 minutes each day for a period of 10
days. Following this period, we used sucrose reinforcement
in standard operant conditioning chambers to train the ani-
mals to press a lever for the opportunity to run. Each lever
press produced 0.1 ml of a 15% sucrose solution. When rats
reliably pressed the lever, reinforcement was shifted from a
fixed-ratio schedule to a variable-ratio schedule. This sched-
ule remained in effect for approximately four sessions, with
each session terminating when 50 sucrose reinforcers were
obtained. After four sessions on the variable-ratio schedule,
sessions in the operant conditioning chamber were discontin-
ued. During this period of lever training, the rats continued
to run in the wheels for 30 minutes each day in addition to
the sessions in the operant conditioning chambers. At this
point, the retractable lever in each wheel chamber was ex-
tended during the wheel-running sessions, and the opportu-
nity to run for 60 seconds was made contingent upon a single
lever press. When the reinforcement requirement was met,
the lever would retract and the brake would release, leaving
the wheel free to turn for 60 seconds. Once 60 seconds had
elapsed, the reinforcement period was terminated by apply-
ing the brake and extending the lever. Each session consisted
of 30 opportunities to run. The schedule of reinforcement
was changed in the following sequence: fixed ratio 1, vari-
able ratio 3, variable ratio 5, variable ratio 9, and variable ra-
tio 15. Subjects remained on each schedule for four sessions
before advancing to the next schedule. Following this train-
ing regime, sessions were conducted daily over a period of 8
months. Each session consisted of fifty-two 30-second op-
portunities to run, for a total of 26 minutes of running time.
Running rates for these animals average about 30 revolutions
for every minute of opportunity to run, which translates into
approximately 1800 revolutions per hour.
Ischemic Heart Perfusions
Following FR and ET protocols, animals were anesthe-
tized with sodium pentobarbital. Their hearts were quickly
excised, placed in ice-cold buffer, and immediately per-
fused in the Langendorff mode via the aorta with Krebs-
Henseleit buffer containing 11 mM glucose and 2.5 mM
Ca2ϩ (pH 7.4, gassed with 95% O2-5% CO2). During this
perfusion, the hearts were trimmed of excess tissue and the
openings of the left atria were cannulated. Hearts were then
switched to the working mode and perfused with Krebs-
Henseleit buffer consisting of 11 mM glucose and 1.2 mM
palmitate prebound to 3% bovine serum albumin. On the
basis of the working mode model, the perfusate enters the
heart via this cannulated left atrium, where it is subsequently
ejected from the left ventricle through the cannulated aorta.
The ejected perfusate enters a compliance chamber and is
pumped by the heart against a chosen aortic overflow
height. After reaching this height, perfusate overflows back
into the perfusion reservoir where it is then recirculated
through an oxygenator with a large inner surface area ex-
posed to 95%O2-5%CO2. After oxygenation, the perfusate
is delivered to the cannulated left atrium where it enters the
left ventricle and is ejected through the aorta.
Hearts were perfused at a constant left atrial filling pres-
sure of 11.5 mm Hg with variable aortic afterload resistances.
Following the initial Langendorff perfusion, hearts were per-
fused at an afterload resistance of 60 mm Hg for 5 minutes.
The aortic afterload resistance was then increased to 90 mm
Hg and maintained for another 5 minutes. Thereafter, the af-
terload resistance was reduced to 75 mm Hg while heart func-
tion was monitored as baseline pre-ischemic function.
Following a 5-minute period at this afterload resistance,
hearts were subjected to 25-minutes of global no-flow
ischemia. This was achieved by clamping off both the aortic
outflow and left atrial inflow lines, which prevented perfu-
sion of the coronary arteries. Following global ischemia,
aortic outflow and left atrial inflow were restored, and
hearts were reperfused for 15 minutes. Heart function, mea-
sured as heart rate and pressure development, was recorded
throughout the normoxic perfusion and at the end of reper-
fusion using a Harvard research grade pressure transducer
in the aortic line interfaced to a flatbed chart recording sys-
tem (Barnstead, Model 2000, Dubuque, IA). Function was
recorded during normoxic and reperfusion conditions at
5-minute intervals over 30 seconds at a chart speed set at 1
cm/s. Aortic flow was measured by time collection of perfu-
sate in the aortic afterload overflow line. Water-jacketed
chambers kept the temperature of the buffer at 37ЊC
throughout the perfusion.
AL rats had continuous access to rat chow. After rats in the
ALE group attained a body weight of 400 g, they were given
the opportunity to run in a running wheel for 60 minutes each
day. Daily sessions were conducted over an 8-month period.
Measurement of Plasma Metabolites
Following excision of rat hearts, blood that pooled in the
chest cavity was collected in chilled tubes containing hep-

EXERCISE AND FOOD EFFECTS ON THE HEART
B35
Table 2. Effects of ET and FR on Heart Function in Response to
Increases in Afterload Resistance
arin and immediately centrifuged. The plasma was collected
and later analyzed for cholesterol and triglycerides using
commercially available kits from Sigma Diagnostics, Oak-
ville, Ontario, Canada.
Heart Rate
(beats/min)
Systolic Pressure
(mm Hg)
Aortic Flow
(ml/min)
Group
80 cm H2O
AL
Statistical Analysis
210 Ϯ 9
201 Ϯ 8
184 Ϯ 9
193 Ϯ 9
102 Ϯ 5
80 Ϯ 3
84 Ϯ 3
103 Ϯ 5
20 Ϯ 2
32 Ϯ 4
20 Ϯ 2
28 Ϯ 3
Statistical significance for comparisons among groups
was determined using a two-way factorial analysis of
variance. A two-way analysis was selected to determine
whether significant ET or FR effects were present. This
method can also establish if there is an interaction between
FR and ET. A value of p Ͻ .05 was considered significant.
All data are reported as mean Ϯ SE.
FR
ALE
FRE
F ratios†
FR effect
Training effect
FR ϫ training
0.01
3.58
1.10
0.02
0.18
24.42*
22.55*
1.98
1.34
120 cm H2O
AL
FR
ALE
FRE
F ratios†
183 Ϯ 13
195 Ϯ 7
178 Ϯ 8
199 Ϯ 8
127 Ϯ 5
109 Ϯ 3
117 Ϯ 4
135 Ϯ 5
12 Ϯ 3
32 Ϯ 3
13 Ϯ 2
28 Ϯ 3
RESULTS
The physical characteristics of the animals are presented
in Table 1. Significant effects of these variables on plasma
lipids were observed, reflecting FR and ET. In fact, there
was a significant FR effect on plasma triglycerides and cho-
lesterol as well as an ET effect on plasma triglycerides.
However, no significant interactions between FR and ET
were seen on the lipid profile. A reduction in body weight
was not observed following exercise in the ALE group,
which likely reflects the low running rates recorded by this
group. Running rates averaged 60 revolutions per hour com-
pared with 1800 revolutions per hour in the FRE group,
which had dramatically lower body weights.
FR effect
Training effect
FR ϫ training
0.03
5.70*
8.56*
0.01
3.62
17.70*
31.83*
2.23
0.01
Notes: Values are reported as mean Ϯ SE for eight to nine hearts for each
group. Hearts were initially perfused at an 11.5 mm Hg left atrial filling pressure
and 60 mm Hg afterload resistance. Following a 5-min period at this workload,
the aortic afterload resistance was then increased to 90 mm Hg. AL ϭ ad libi-
tum-fed; ALE ϭ ad libitum-exercise; FR ϭ food-restriction; FRE ϭ food-
restriction–exercise; ET ϭ exercise training.
*Significant F ratios, p Ͻ .05.
†F ratios of a two-way factorial analysis of variance to determine whether
FR and/or exercise training had an effect on heart function.
FR and ET effects on cardiac performance in response to
changes in afterload are shown in Table 2. When hearts
were perfused at an aortic afterload resistance of 60 mm Hg,
a significant FR effect on aortic flow was observed. There
was also an interaction between FR and ET on systolic pres-
sure. At 90 mm Hg aortic resistance, the significant FR ef-
fect on aortic flow and the interaction between FR and ET
on systolic pressure remained. At this afterload, a training
effect as well as an interaction between FR and ET on heart
rate were observed.
monitored prior to ischemia. As shown in Table 3, under nor-
moxic conditions, there was a significant FR effect on aortic
flow as well as an interaction between FR and ET on heart
rate and pressure development. The benefits of FR were
clearly shown during the reperfusion of ischemic hearts. Sig-
nificant FR effects on heart rate, systolic pressure, and aortic
flow were seen. In terms of percent recovery following
ischemia, significant FR effects were seen on all cardiac pa-
rameters, including aortic flow. In addition, an interaction be-
tween FR and ET occurred with aortic flow (Table 4).
Following the aortic afterload challenge, the afterload re-
sistance was reduced to 75 mm Hg, and heart function was
DISCUSSION
Table 1. Physical Characteristics of Animals
The main findings of this study clearly indicate that
chronic FR, or FR in combination with ET, results in
marked adaptations in contractile properties of the heart.
These adaptations include the ability of hearts to maintain
aortic pump flow in response to increased afterload resis-
tance and improved postischemic recovery of heart function
during reperfusion following ischemia.
Body
Weight (g)
Triglycerides
(mmol/l)
Cholesterol
(mmol/l)
Group
AL
FR
ALE
FRE
F ratios†
617 Ϯ 35
340 Ϯ 1
682 Ϯ 11
388 Ϯ 2
2.7 Ϯ 0.3
0.7 Ϯ 0.2
2.8 Ϯ 0.1
1.3 Ϯ 0.1
3.7 Ϯ 0.1
2.8 Ϯ 0.1
3.8 Ϯ 0.4
2.5 Ϯ 0.2
Despite earlier studies demonstrating that FR reduces the
incidence of cardiomyopathy, the FR effects on myocardial
function and ischemic tolerance has received little attention.
Using intact working heart preparations, the literature
shows that mechanical function of hearts from FR animals
is improved and in some cases even demonstrates a diabetic
type of cardiomyopathy (6,20,21). In regards to ischemic
tolerance, isolated atrial strips from hearts of FR animals are
more resistant to anoxic and reperfusion injury (6). Al-
though our results are consistent with those of Savabi and
Kirsch (6), we extend these observations by demonstrating
that FR increases ischemic tolerance in hearts perfused in
FR effect
Training effect
FR ϫ training
83.77*
4.30*
1.26
59.44*
0.52
2.34
Notes: Body weight, plasma triglycerides, and cholesterol of rats 8 mo fol-
lowing ET and FR. Values are reported as mean Ϯ SE for 8 animals for each
group. AL ϭ ad libitum-fed; ALE ϭ ad libitum-exercise; FR ϭ food-restriction;
FRE ϭ food restriction–exercise; ET ϭ exercise training.
*Significant F ratios, p Ͻ .05.
†F ratios of a two-way factorial analysis of variance to determine whether
FR and/or ET had an effect on plasma lipids. Analysis of body weight differ-
ences were not determined because weight was regulated through food intake
for the FR groups but not in the ad libitum groups, leading to heterogeneity of
varience in weights between groups.

B36
BRODERICK ET AL.
Table 3. Effects of ET and FR on Heart Function Under Normoxic
Conditions and During Reperfusion of Previously Ischemic Hearts
glucose metabolism (18,19). Further, unlike in the current
study, function following anoxic insult was determined us-
ing tissue preparations rather than an intact working heart
where reperfusion recovery could be monitored under phys-
iological loading conditions.
Pressure
Heart Rate
(beats/min) (mm Hg) (mm Hg)
Systolic
Diastolic
Aortic Flow
(ml/min)
Group
The benefits of chronic FR on reperfusion recovery can
likely be explained, in part, by a favorable redistribution of
lipids and cholesterol. Chronic interventions that lessen
plasma lipid levels also favorably alter the reliance of the
heart on fatty acid metabolism (12,22,23). In particular, in-
terventions that decrease the supply of lipids to the heart can
improve glucose metabolism and exert a protective effect
on the heart following ischemia (17,24). In support of these
observations, we show that there was a significant effect of
chronic FR on plasma levels of cholesterol and triglycer-
ides. This may be of importance where glucose utilization is
impaired, such as in the ischemic reperfused heart (25–27).
We can only speculate as to what could be responsible for
the interaction between caloric restriction and ET on per-
cent recovery of heart function following ischemia. One
possibility is that the benefits of ET and FR on cardiac per-
formance occur through common systemic mechanisms. In
support of this, earlier studies have shown that both FR and
ET increase the sensitivity of tissues, particularly of the
heart, to insulin and adrenergic stimulation (12,14,15). FR
and ET attenuate the decrease in myocardial performance
associated with aging (5,7). An increase in insulin sensitiv-
ity attributable to an up-regulation of glucose transporter
proteins and insulin receptor content also occurs in response
to training and caloric restriction (15,28). Interestingly, FR
inhibits the physiological decline in the levels of glucose
transporter proteins associated with aging (29). This may be
relevant in our studies because the duration of the protocols
was based on heart function following long-term FR and ET
in aging rats.
Several physiological and biochemical changes occur in
tissues with chronic FR. In the present study, mechanical
function of the heart during reperfusion is improved follow-
ing FR. Although these changes can be attributed in part to
an improved lipid profile, other metabolic processes in-
duced by FR that have the potential to enhance the heart’s
ability to withstand ischemia should not be excluded. In
fact, a key to the enhanced longevity in the FR laboratory
animal is an increase in mitochondrial antioxidant defenses
(4,30). The increase in heart free-radical production and ox-
idative damage normally associated with aging can be atten-
uated or even prevented with dietary restriction (31). In rat
heart mitochondria, increases in the activity of antioxidant
enzymes, including superoxide dismutase and catalase,
have been reported with FR (31,32). Antioxidant defense is
of important clinical concern, because a burst of oxygen
free radicals immediately upon reperfusion can cause dys-
function of the heart (33).
Normoxic
AL
215 Ϯ 6
192 Ϯ 6
176 Ϯ 8
199 Ϯ 8
117 Ϯ 5
102 Ϯ 2
108 Ϯ 3
121 Ϯ 5
52 Ϯ 3
46 Ϯ 2
43 Ϯ 2
56 Ϯ 3
21 Ϯ 3
36 Ϯ 3
20 Ϯ 2
30 Ϯ 3
FR
ALE
FRE
F ratios†
FR effect
0.01
4.69*
9.85*
0.13
2.07
13.31*
1.18
0.02
13.11*
22.07*
1.36
1.12
Training effect
FR ϫ training
At 15 min reperfusion
AL
183 Ϯ 13
181 Ϯ 9
128 Ϯ 10
193 Ϯ 8
94 Ϯ 11
98 Ϯ 2
78 Ϯ 11
116 Ϯ 3
45 Ϯ 3
48 Ϯ 1
32 Ϯ 5
60 Ϯ 4
6 Ϯ 3
21 Ϯ 4
1 Ϯ 1
FR
ALE
FRE
F ratios†
19 Ϯ 2
FR effect
Training effect
FR ϫ training
8.91*
3.90
10.41*
6.31*
0.02
3.91
0.02
18.35*
0.02
35.12*
1.70
0.24
Notes: Values are reported as mean Ϯ SE for eight to nine hearts for each
group. Hearts were perfused at an 11.5 mm Hg left atrial filling pressure and 75
mm Hg aortic afterload and then subjected to 25 min of global no-flow isch-
emia. Following ischemia, hearts were reperfused for a period of 15 min. AL ϭ
ad libitum-fed; FR ϭ food-restriction; ALE ϭ ad libitum-exercise; FRE ϭ
food-restriction–exercise; ET ϭ exercise training.
*Significant F ratios, p Ͻ .05.
†F ratios of a two-way factorial analysis of variance to determine whether
FR and/or ET had an effect on heart function.
the presence of relevant levels of fatty acids. We chose to
perfuse hearts with elevated levels of fatty acids, because
this is representative of clinical setting of myocardial infarct
(18). High levels of fatty acid are also known to contribute
to postischemic cardiac dysfunction, secondary to the accu-
mulation of intermediates of fatty acid and by inhibition of
Table 4. Effects of ET and FR on Percent Recovery of Heart
Function Following Global No-flow Ischemia
Pressure
Heart Rate
(beats/min)
Systolic
(mm Hg)
Diastolic
(mm Hg)
Aortic Flow
(ml/min)
Group
AL
FR
ALE
FRE
F ratios†
85 Ϯ 5
95 Ϯ 4
73 Ϯ 6
98 Ϯ 4
81 Ϯ 9
97 Ϯ 2
72 Ϯ 10
96 Ϯ 2
92 Ϯ 7
105 Ϯ 2
75 Ϯ 11
105 Ϯ 3
27 Ϯ 10
56 Ϯ 7
6 Ϯ 4
66 Ϯ 7
FR effect
Training effect
FR ϫ training
13.08*
0.83
2.35
7.83*
0.40
0.26
9.14*
1.54
1.45
33.10*
0.56
4.27
Notes: Values are reported as mean Ϯ SE for 8 to 9 hearts for each group.
Hearts were perfused at an 11.5 mm Hg left atrial filling pressure and 75 mm Hg
aortic afterload and then subjected to 25 min of global no-flow ischemia. Per-
cent recovery is shown at 15 min reperfusion. AL ϭ ad libitum-fed; FR ϭ food-
restriction; ALE ϭ ad libitum-exercise; FRE ϭ food-restriction–exercise.
*Significant F ratios, p Ͻ .05.
†F ratios of a two-way factorial analysis of variance to determine whether
FR and/or ET had an effect on percent recovery of heart function following
ischemia.
Several studies have sought to assess the functional re-
sponse of the rat heart to chronic exercise. Although most of
these studies have reported cardiac benefits following train-
ing, others have not always shown an improvement in car-
diac function. These inconsistencies may result from the
type of exercise itself, the intensity and duration of the train-
ing protocol, or even the sex of the animals. In our study,

EXERCISE AND FOOD EFFECTS ON THE HEART
B37
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because recovery was compromised. Low running rates re-
corded in this group could be the reason for this lack of ben-
eficial effect. No benefits on either body weight or circulat-
ing plasma lipid levels were reported. In the FRE group,
however, cardiac adaptations to ET occurred and cannot be
attributed to FR alone. The effects of FR on recovery of
heart function following ischemia can be separated from the
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of fatty acids.
Acknowledgments
This study was supported by grants from the Heart and Stroke Founda-
tion of Canada (TLB), Medical Research Fund of New Brunswick (TLB),
and the National Sciences and Engineering Research Council of Canada,
Grant OGP0017002 (TB). The authors thank Sharon Torcivia for secre-
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Melissa Gillis is currently with the Faculty of Medicine, Dalhousie Uni-
versity, Halifax, Nova Scotia.
Address correspondence to Tom L. Broderick, PhD, Department of
Physiology, Midwestern University, 19555 North 59th Avenue, Glendale,
AZ 85308. E-mail: tbrode@arizona.midwestern.edu
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Received October 21, 1999
Accepted July 18, 2000
Decision Editor: Jay Roberts, PhD