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J Pain. Author manuscript; available in PMC 2015 July 09.
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Published in final edited form as:

J Pain. 2014 June ; 15(6): 656–663. doi:10.1016/j.jpain.2014.02.008.

EXERCISE-INDUCED MODULATION OF PAIN IN ADULTS WITH

AND WITHOUT PAINFUL DIABETIC NEUROPATHY
Matthew T. Knauf and Kelli F. Koltyn
Department of Kinesiology, University of Wisconsin-Madison

Abstract
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The purpose of this study was to examine exercise-induced pain modulation in diabetic adults with
painful diabetic neuropathy (PDN) compared to diabetic adults without PDN. Eighteen adults
diagnosed with Type 2 diabetes with and without PDN (mean age of 49 yrs) completed two
sessions. During the familiarization session, participants completed questionnaires, were
familiarized with the pain testing protocols, and completed maximal isometric contractions.
During the exercise session, experimental pain testing was completed before and following
exercise consisting of three minutes of isometric exercise performed at 25% MVC. Ratings of
perceived exertion (RPE) and muscle pain (MP) were assessed every 30 seconds during exercise.
Results indicated RPE and MP during exercise were significantly higher (p < 0.05) for diabetic
adults with PDN vs diabetic adults without PDN. Diabetic adults with PDN did not experience
changes in thermal pain ratings following exercise while diabetic adults without PDN reported
significantly lower pain ratings following exercise. It is concluded that diabetic adults with PDN
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experienced high levels of muscle pain during exercise and a lack of exercise-induced hypoalgesia
following exercise in comparison to diabetic adults without PDN who experienced lower levels of
muscle pain during exercise and a hypoalgesic response following exercise.

Keywords
diabetes; neuropathic pain; exercise-induced analgesia

INTRODUCTION
One of the most common complications of diabetes is neuropathy which may result in pain,
loss of mobility and amputation.1 Research indicates that adults with painful diabetic
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neuropathy have annual health care costs almost three times higher than costs for matched
control populations.2 Painful diabetic neuropathy (PDN) has proven difficult to treat and in
the majority of patients, existing therapies for neuropathic pain are far from effective.3 It is
well-established that lifestyle changes which include exercise can significantly reduce the
prevalence of diabetes and associated complications such as neuropathy, however, very little
research has focused on the effects of exercise on PDN. Results from several animal studies

Correspondence should be sent to: Kelli F. Koltyn, Ph.D., 2000 Observatory Drive, University of Wisconsin-Madison, Madison, WI
53706-1121, [email protected], Telephone: (608) 262-4234, Fax: (608) 262-1656.
Discolsures:There are no conflicts of interest with this study, none of the authors have anything to disclose.
 Knauf and Koltyn Page 2

suggest that an exercise training program reduces behavioral symptoms of neuropathic pain
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and tactile sensitivity.28, 37, 38, 40 In addition, one human study indicated improvements in
neuropathic symptoms and cutaneous nerve fiber branching following an exercise training
program.20

Despite the limited number of studies conducted examining the impact of exercise on pain in
individuals with PDN, there is research indicating that exercise is associated with an
attenuation of pain in healthy individuals,11, 16, 22, 23, 25, 35 and investigators have typically
found hypoalgesia (diminished pain in response to a noxious stimulus) occurs during and/or
following an exercise session. Various modes of exercise have been used including aerobic
exercise (e.g., cycling, running), resistance exercise (e.g., weight lifting), and isometric
exercise (e.g., static muscular contraction), and results indicate that exercise-induced
hypoalgesia (EIH) occurs during and/or following a single exercise
session.5, 16, 22, 23, 24, 25, 35 Limited research is available, however, examining changes in
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pain after an immediate (i.e., acute) bout of exercise in individuals with PDN. In fact, there
are reports that individuals with chronic pain (e.g., fibromyalgia, temporomadibular
disorders) may experience a hyperalgesic response during and/or following an exercise
session,18, 26, 32, 42 and it has been suggested that this hyperalgesic response may be a
reflection of endogenous pain modulatory system dysfunction.32,34,42 Whether these results
generalize to individuals with PDN is currently unclear. Further research is needed to
expand our understanding of the impact of exercise on PDN. Thus, the purpose of this study
was to examine exercise-induced pain modulation in diabetic adults with and without
painful diabetic neuropathy.

MATERIALS AND METHODS

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Participants
All protocols, methods, and procedures were approved by the Health Sciences Institutional
Review Board (IRB) at the University of Wisconsin – Madison. Adults (18 – 60 yrs)
clinically diagnosed with type 2 diabetes mellitus with and without PDN by their primary
care physician were recruited to participate in this study. Exclusion criteria included: 1) any
acute medical or psychiatric illness, 2) uncontrolled chronic medical conditions (e.g.,
hypertension, heart disease, hypercholestrolemia, hyperglycemia, etc.), 3) upper extremity
neuropathy or arthritis that limits exercise, 4) neuropathies from other causes than diabetes,
and 5) cognitive or reading impairments which would preclude completing the
questionnaires. Participants were recruited from university hospital and clinics, diabetes
clinics, and community health care centers. Prior to participating in the study, informed
consent was obtained from each participant. Participants who enrolled in this study
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completed two sessions (i.e., familiarization and exercise sessions) and were paid $25 for
completing both sessions.

Procedures
Familiarization Session—During the familiarization session, participants completed an
informed consent document and a packet of questionnaires which consisted of: 1) a
Demographic, Pain, and Health History, 2) a 24-Hour Health History, 3) the Short Form

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McGill Pain Questionnaire (SF-MPQ),31 4) the Profile of Mood States (POMS),30 and 5) the
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International Physical Activity Questionnaire (IPAQ).6, 13, 15 In addition, participants

completed three neuropathic pain questionnaires including the Neuropathic Pain
Questionnaire (NPQ),27 the painDETECT(PD-Q),14 and the Neuropathic Pain Symptom
Inventory (NPSI)8 in order to assess various aspects of neuropathic pain (e.g., symptoms,
gradation of pain, the pain course pattern, etc).

Upon completion of the packet of questionnaires, participants were exposed to the thermal
stimuli in order to familiarize them with the pain testing to be completed in the exercise
session. A thermal stimulus using a computer controlled Medoc Sensory Analyzer (CHEPS
model) was applied to the thenar eminence of the dominant hand and volar suface of the
dominant forearm. Two different thermal protocols were used because the manner in which
stimuli are applied can influence responses (e.g., Type-III vs Type-IV responses). One
protocol that was used was the Ramp and Hold protocol which activates predominantly
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Type-III (Aδ) nociceptors.51 Stimulus response functions of the volar surface of the forearm
were determined by rapidly increasing the thermode temperatures (10 – 20°C/sec) from a
baseline of 32 – 35°C to four different peak temperatures ranging between 42 – 49°C and
holding the temperature for four seconds. The second protocol involved administration of
brief, repetitive suprathreshold heat pulses that evoked Type-IV (C-fiber) pain summation
(i.e., temporal summation). A thermode was programmed to deliver pulses that rapidly rise
from an adapting temperature to a peak temperature of 51°C at a rate of 30°C/sec, remain at
this level for 0.25sec, and then return to baseline at a rate of 30°C/sec. Ten heat pulses were
delivered to the thenar eminence of the hand according to the adjusted protocol described by
Staud et al. (2006).42 The temperature of the thermode increased during the first four stimuli
in this manner: 35°C (baseline) to 45°C (peak temperature) by 30°C/pulse (1st stimulus),
36°C to 47°C (2nd stimulus), 37°C to 48°C (3rd stimulus), 38°C to 49°C (4th stimulus). The
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baseline and peak temperatures of the 6 remaining stimuli were 38°C and 51°C. During
exposure to the thermal stimuli, participants rated late sensations of pain (approx 1 second
after each pulse) using a 0 – 100 numerical scale.41, 49 Participants then completed a
recovery period (sat quietly for 3 minutes). Following the recovery period, participants
completed the two thermal testing protocols again to ensure that the protocols were set and
participants were familiar with the testing to be completed in the exercise session.

Finally, participants were asked to squeeze a hand dynamometer with their dominant hand at
their maximum strength for five seconds two times, with a two minute interval between the
two trials. The average of the two maximum strength values was used to compute the
participant’s 25% MVC for the next session. Prior to leaving, participants were given a
pedometer to wear for 5 consecutive days (Saturday – Wednesday) to record the number of
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steps taken per day, as well as a physical activity log to record any exercise performed on
those days.

Exercise Session—In the isometric exercise session, participants returned the pedometer
and physical activity log, and then completed a 24-Hour Health History and the Short Form
McGill Questionnaire (SF-MPQ). Participants then underwent thermal pain testing prior to
exercise. Next, participants squeezed the hand dynamometer at their respective 25% MVC
for 3 minutes. Participants were asked to rate their muscle pain and perceived exertion every

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30 seconds during exercise using validated rating scales. Exercise-induced muscle pain was
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assessed during the exercise session using a pain intensity scale.10 The scale developed by
Cook et al. (1997) consists of 11 vertically aligned numerical responses that range from 0 to
10, with verbal descriptors attached to nine numerical responses. This scale represents a
continuum from no pain sensation to unbearable levels of pain, and allows participants to
use a number greater than 10. The pain intensity scale has been shown to be a reliable and
valid measure of muscle pain during exercise.10 In addition, perceived exertion was assessed
using the Ratings of Perceived Exertion (RPE) scale. The RPE scale developed by Borg
(1998) consists of 15 vertically aligned numerical responses that range from 6 – 20, with
verbal descriptors attached to nine numerical responses. The RPE scale has been shown to
be a reliable and valid measure to assess an individual’s perceived exertion during exercise.7
Immediately following the isometric exercise session, the participants underwent
experimental pain testing once more and then completed the SF-MPQ.
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Statistical Analyses—Descriptive statistics were computed for the neuropathic pain

measures and independent samples t-tests were performed to analyze whether there were
differences between groups. Muscle pain responses and RPE were assessed every 30
seconds during the 3 minute isometric exercise session and the data were analyzed with a 2
(groups) × 6 (time: every 30 seconds during isometric exercise) ANOVA. For the Ramp and
Hold protocol, participants rated pain intensity before and following exercise to four
different temperatures, and this data were analyzed with a 2 (groups) × 2 (trials: pre and
post) × 4 (temperatures) mixed ANOVA. For the Temporal Summation protocol,
participants rated pain intensity before and following exercise to 10 heat pulses, and this
data were analyzed with a 2 (groups) × 2 (trials: pre and post) × 3 (ratings 1, 5, and 10)
mixed ANOVA. The data for the SF-MPQ (Visual Analog Scale, Present Pain Index, and
SF-MPQ Total), were analyzed using a 2 (groups) × 2 (trials) repeated measures ANOVA.
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The data for the pedometers were analyzed using a 2 (groups) × 5 (days) repeated measures
ANOVA. The data for the POMS were analyzed using independent samples t-tests to
determine if there were differences between groups. The data for the IPAQ were analyzed
using a Mann-Whitney U Test, in order to determine differences between groups. The level
of statistical significance was set at α = 0.05 for all analyses. Post-hoc analyses were
performed if significant main effects or between group differences were observed and
Bonferroni corrections for multiple comparisons were made.

RESULTS
Eighteen individuals diagnosed with Type 2 diabetes with and without PDN who
participated in this study had a mean age of 49 yrs (sd = 11). Six men and 12 women
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participated in this study and the racial/ethnic composition of the sample included 11
Caucasian participants, 3 African American participants, 3 Asian participants, and one
Latino participant. All of the participants reported taking insulin in order to control Type 2
diabetes, and participants with PDN reported taking a variety of medications to treat painful
neuropathy including: gabapentin, amitritylene, acetomenophen, nortryptyline, and
amlodipine. Results indicated significant group differences for the Neuropathic Pain
Questionnaire, Neuropathic Pain Symptom Inventory, and painDETECT Questionnaire (p

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< .05). No significant group differences were found for age, duration of diabetes, and BMI
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(p > 0.05). The baseline data for the participants are summarized in Table 1.

Muscle Pain Ratings During Exercise

Muscle pain was assessed every 30 seconds during exercise. The results indicated that
diabetic adults with PDN rated muscle pain significantly higher (p < 0.05) in comparison to
diabetic adults without PDN. The results for muscle pain ratings are summarized in Figure
1.

Ratings of Perceived Exertion

Ratings of perceived exertion were measured every 30 seconds during exercise. The results
indicated that RPE increased significantly during exercise for both groups (p < .01). In
addition, diabetic adults with PDN rated isometric exercise as more effortful at 180 seconds
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during exercise in comparison to diabetic adults without PDN (p < .05).

Experimental Pain Ratings: Ramp & Hold and Temporal Summation Protocols
For the ramp and hold protocol, experimental pain ratings were assessed before and
following exercise (i.e., trials) using four separate temperatures (43°C, 45°C, 47°C, and
49°C). The results indicated that diabetic adults with PDN rated experimental pain
significantly higher (p < 0.05) than diabetic adults without PDN. Further, pain ratings for all
four temperatures decreased significantly (p < 0.05) following exercise in diabetic adults
without PDN, but there were no changes in pain ratings following exercise in diabetic adults
with PDN. The results for the four temperatures are summarized in Figure 3.

For the temporal summation protocol, experimental pain ratings for the first, fifth and tenth
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pulses were analyzed before and following exercise. The results indicated that temporal
summation pain ratings were significantly lower (p < 0.05) following exercise for the
diabetic adults without PDN, however, for diabetics with PDN no significant differences
were found after exercise. The results for temporal summation of heat pain are summarized
in Figure 4.

Current Pain
Current sites of pain were assessed with the Demographic, Pain, and Health History
questionnaire and included: dental pain (PDN = 5, No PDN = 3), headaches (PDN = 4, No
PDN = 4), back pain (PDN = 5, No PDN = 3), knee pain (PDN = 3, No PDN = 3), and
shoulder or neck pain (PDN = 2, No PDN = 0). In addition, the SF-MPQ was completed
before and following exercise. The SF-MPQ assesses total pain with affective and sensory
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descriptors, a visual analog scale (VAS), and a present pain index (PPI). The results
indicated that ratings were significantly lower following exercise for diabetic adults without
PDN for the SF-MPQ total, VAS, and PPI; however, for diabetic adults with PDN only PPI
ratings were significantly lower following exercise. The results for the VAS, PPI and SF-
MPQ Total are summarized in Table 2.

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Physical Activity
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Physical activity levels were measured via self-report (i.e., IPAQ) and with a pedometer
(i.e., steps per day). Results indicated diabetic adults with PDN reported significantly more
Total MET-mins/wk on the IPAQ in comparison to the diabetic adults without PDN (p <
0.01), However, no significant differences were found in the other activity domains of the
IPAQ. Results for the IPAQ data are summarized in Table 3.

Participants wore a pedometer for 5 consecutive days (Saturday – Wednesday). The

pedometer data were cleaned prior to analyzing the data, and any individuals who did not
meet the following criteria were not included in the analysis: 1) minimum of 500 steps per
day, 2) pedometer worn for minimum of 10 hours, and 3) steps per day count less than
20,000. Only one individual was excluded from the analysis due to failing to meet the above
criteria. Results indicated no significant differences (p > 0.05) between diabetic adults with
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PDN (mean = 5765 steps/day, sd = 3044) in comparison to diabetic adults without PDN
(mean = 4795 steps/day, sd = 2594).

Profile of Mood States (POMS)

Mood states were assessed at baseline using the POMS (i.e., how participants felt over the
past week including the day they came in for testing). Results indicated no significant
differences between diabetic adults with or without PDN for tension, depression, anger,
vigor, fatigue, confusion, or total mood disturbance (p > .05). The results from the POMS
are summarized in Table 4.

DISCUSSION
The purpose of this study was to examine the influence of exercise on endogenous pain
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modulation in adults with PDN compared to diabetic adults without PDN. The results from
this study indicated that experimental pain responses following exercise differed between
the two groups of diabetic adults who participated in this study. Experimental pain ratings
were found to decrease significantly following exercise for the diabetic adults without PDN
indicating that EIH occurred following exercise.

Very little research has been conducted examining EIH in diabetic adults. The results from
this study indicated that pain ratings for the ramp & hold protocol (predominantly Type III
fiber responses) were found to be significantly lower following exercise. In addition, pain
ratings for the temporal summation protocol (predominantly Type IV fiber responses) were
also found to be lower following exercise. In fact, it appears that temporal summation did
not occur following exercise since the temporal summation protocol was not rated as painful
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following exercise (ratings < 20). Further, general levels of pain on the day of testing as
measured by the SF-MPQ were also found to be lower following exercise in the diabetic
adults without PDN. The results from this study are in agreement with results from research
conducted with healthy adults. For example, there are reports that healthy adults experience
EIH following a similar exercise paradigm.21, 46

In contrast, the diabetic adults with PDN did not experience a decrease in experimental pain
ratings following exercise indicating that EIH did not occur. Also, general levels of pain on

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the day of testing did not change significantly (with the exception of the PPI). These results
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are in agreement with results from research conducted with other chronic pain conditions.
For example, some investigators have reported that women with fibromyalgia (FM) do not
experience EIH following an exercise session.26, 29 In addition, lack of an EIH response has
also been reported for adults with temporomandibular jaw disorder (TMD),32 adults with
chronic whiplash associated disorders,47 and Gulf War veterans with chronic
musculoskeletal pain.12 As for temporal summation, it appears there is only one other study
conducted examining the influence of exercise on temporal summation of second pain.
Vierck et al. (2001) found that temporal summation ratings increased following exercise for
women with FM in comparison to a decrease in temporal summation ratings following
exercise for healthy women.49 It has been hypothesized that that this lack of EIH may reflect
endogenous pain modulatory system dysfunction.34,43 Investigators have suggested that this
dysfunction may be the result of an active deficiency of inhibitory mechanisms or enhanced
facilitation that overrides inhibition.29, 34,42
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In addition, results indicated that muscle pain during exercise was significantly higher for
diabetic adults with PDN. By the end of the three minute exercise bout, diabetic adults with
PDN reported very strong pain while the diabetic adults without PDN rated their muscle
pain as moderate. These results are in agreement with studies conducted with chronic pain
patients in which participants with a chronic pain condition experienced hyperalgesia during
exercise compared to healthy controls. For example, Cook et al. (2010) reported that Gulf
War veterans with chronic musculoskeletal pain rated muscle pain intensity significantly
higher during aerobic exercise in comparison to healthy Gulf War veterans.12 Also, there
have been several studies conducted with fibromyalgia patients using an isometric exercise
protocol, and results indicate that FM patients rated muscle pain significantly higher than
healthy controls.19, 26, 29, 42 The results from these studies suggest dysfunction in regulation
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of nociceptive processes, thus leading to increases in naturally occurring muscle pain during
exercise.12

The mechanisms underlying dysfunction of the endogenous pain modulatory system in

chronic pain conditions are poorly understood. While the pain in patients with PDN is
believed to originate in the peripheral nervous system, central nervous system mechanisms
also contribute to the maintenance of neuropathic pain possibly through central
sensitization.4, 9, 48 Experimental and clinical studies indicate that neuronal and afferent
fiber hyperexcitability is a key factor in the development of neuropathic pain.17, 36 Central
neuronal hyperexcitability underlying neuropathic pain is usually explained by increased
input from the periphery.50 Contributing to the hyperexcitability may be decreased activity
in endogenous pain inhibitory systems, and research with other chronic pain conditions (e.g.,
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FM, TMD) provides evidence for endogenous pain modulatory system dysfunction.32, 42 It
has been suggested that this dysfunction may be due to a deficiency in the pain inhibitory
system or there may be enhanced facilitation that overrides inhibition.32, 42 Therefore, more
research on the mechanisms underlying dysfunction of the endogenous pain modulatory
system in adults with chronic pain warrants further investigation.

Physical activity levels were assessed both subjectively (i.e., IPAQ) and objectively (i.e.,
pedometer). Results from the IPAQ indicated that the only group difference was the IPAQ

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Total MET-mins/wk; however, groups were not significantly different on the individual
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domains of the IPAQ. Diabetics with PDN reported higher levels of physical activity in
comparison to diabetics without PDN. This finding was somewhat unexpected; however,
this result may be due to clinicians prescribing exercise to prevent further complications and
potential amputations as a result of PDN. In contrast, the results from the pedometer data
indicated the two groups did not differ in physical activity levels. The mean number of steps
per day indicated that the Type 2 diabetic adults without PDN could be categorized as
“sedentary” and the Type 2 diabetic adults with PDN could be categorized as “low active”
according to guidelines published by Tudor-Locke & Bassett (2004).45 This is in agreement
with previous reports indicating that Type 2 diabetic adults are not regularly active.33, 39, 44
Further research is needed examining strategies to increase physical activity levels in
diabetic adults with and without PDN.

Several limitations of the present study should be acknowledged. First, the sample size in
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this study was small and diabetes disease severity was not assessed. Thus, further research is
needed with larger sample sizes and groups matched on disease severity. Also, in the
absence of a control condition, the possibility of experimental artifacts (i.e., regression to the
mean, effect of multiple testing, etc) contributing to the observed hypoalgesic responses
cannot be entirely discounted. Future research examining changes in pain perception
following exercise in adults with and without neuropathic pain should incorporate random
assignment of participants into both exercise and control conditions to control for these
potential experimental artifacts.

In summary, the results from this study can only be generalized to men and women with
Type 2 diabetes with and without PDN. The results are in agreement with other investigators
who found that individuals with other chronic painful conditions (e.g., fibromyalgia,
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temporomandibular disorders, chronicwhiplash associated disorders) did not experience an

attenuation of pain during or following an exercise session.26, 32, 42, 47 However, the
mechanisms underlying dysfunction of the endogenous pain modulatory system remain
unclear. Thus, additional research is needed in this area. It is concluded that diabetic adults
with PDN experienced high levels of muscle pain during exercise and a lack of EIH
following exercise in comparison to diabetic adults without PDN who experienced lower
levels of muscle pain during exercise and a hypoalgesic response following exercise.

Acknowledgements
We would like to thank Dr. Miroslav Backonja for his helpful comments and insight.

This study was funded by the UW-Madison Virginia Horne Henry Fund. All authors participated in the conduct of
this study.
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PERSPECTIVE
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Very little research has been conducted examining the impact of exercise on pain
modulation in diabetic adults with PDN. This study provides support that adults with
PDN exhibit exercise-induced endogenous pain modulatory system dysfunction.
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Figure 1.
Means and Standard Errors for Muscle Pain Ratings During Exercise (Muscle Pain Ratings
scale = 0 – 10). *Denotes significance at the p < .05 level.
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Figure 2.
Means and Standard Errors for Ratings of Perceived Exertion During Exercise (RPE = 6 –
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20). *Denotes significance at the p < .05 level.

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Figure 3.
Means and Standard Errors for Ramp and Hold. *Denotes significance at the p < .05 level.
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Figure 4.
Means and Standard Errors for Temporal Summation of Heat Pain. *Denotes significance at
the p < .05 level.
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Table 1

Means and Standard Deviations for the Baseline Data

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Diabetics PDN

M (SD) M (SD)

Age (yrs) 46 (13) 53 (7)

Duration of Diabetes (yrs) 6 (6) 6 (3)
Duration of PDPN (yrs) 0 (0) 3 (2)
Blood Pressure (SBP/DBP mmHg) 119/76 (13/3) 119/75 (11/5)
Heart Rate (bpm) 71 (2) 72 (2)
BMI (0 – 100) 38 (10) 34 (9)

NPQ (−1.41 – 10.00)* −1.41 (0) 0.32 (1.2)

NPSI (0 – 100)* 0 (0) 18 (10)

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PD-Q (0 – 35)* 0 (0) 13 (5)

PDN = Painful Diabetic Neuropathy; SBP = Systolic Blood Pressure; DBP = Diastolic Blood Pressure; BMI = Body Mass Index; NPQ =
Neuropathic Pain Questionnaire; NPSI = Neuropathic Pain Symptom Inventory; PD-Q = painDETECT Questionnaire; M = Mean; SD = Standard
Deviation; yrs = Years; bpm = Beats Per Minute; mmHg = Millimeters of Mercury
*
Denotes significance at the p < .05 level.
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Table 2

Means and Standard Deviations for the VAS, PPI, and SF-MPQ Total
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Diabetics PDN

Pre Post Pre Post

M (SD) M (SD) M (SD) M (SD)

VAS (mm 0 – 100) 13.22 (13.85) 7.56 (9.66)* 18.11 (16.14) 11.89 (13.16)

PPI (0 – 5) 1.00 (0.71) 0.67 (0.50) * 1.33 (0.71) 1.00 (0.50)*

SF-MPQ Total (0 – 45) 2.44 (1.94) 1.22 (1.30)* 4.00 (3.96) 3.33 (2.24)

PDN = Painful Diabetic Neuropathy; Pre = Pre-exercise; Post = Post-exercise; M = Mean; SD = Standard Deviation
*
Denotes significance at the p < .05 level.
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Table 3

Medians and Interquartile Ranges for the IPAQ

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IPAQ Category Diabetics PDN

M (IR) M (IR)

IPAQ Job-Related (MET-mins/wk) 0 (0 – 800) 0 (0 – 311)

IPAQ Transportation (MET-mins/wk) 149 (0 – 805) 495 (165 - 1213)
IPAQ Housework (MET-mins/wk) 90 (45 – 720) 610 (169 – 1860)
IPAQ Recreation (MET-mins/wk) 80 (0 – 396) 429 (8 – 689)
IPAQ Walking (MET-mins/wk) 495 (149 – 842) 1336.5 (396 – 2400)
IPAQ Moderate Intensity (MET-mins/wk) 620 (45 – 840) 940 (327 – 2130)
IPAQ Vigorous Intensity (MET-mins/wk) 0 (0 – 440) 0 (0 – 0)
IPAQ Sitting Time (mins/wk) 2730 (1260 - 4200) 3120 (2070 – 4035)
IPAQ Total (MET-mins/wk) 980 (540 - 2091)* 2799 (2505 – 3228)*
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IPAQ = International Physical Activity Questionnaire; PDN = Painful Diabetic Neuropathy; MET-mins/wk = Metabolic equivalence minutes per
week; M = Mean; IR = Interquartile Ranges (25th and 75th); PDN = Painful Diabetic Neuropathy
*
Denotes significance at the p < .05 level.
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Table 4

Means and Standard Deviations for the POMS data

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Diabetics PDN

M (SD) M (SD)

Tension 11.56 (6.41) 7.11 (4.14)

Depression 12.78 (10.53) 5.67 (5.20)
Anger 9.00 (8.25) 4.56 (3.21)
Vigor 13.11 (5.49) 16.78 (3.87)
Fatigue 7.67 (6.06) 7.78 (4.14)
Confusion 9.00 (5.66) 4.78 (2.49)
Total Mood Disturbance 136.89 (33.08) 113.11 (11.78)

POMS = Profile of Mood States; PDN = Painful Diabetic Neuropathy; M = Mean; SD = Standard Deviation
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