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. Author manuscript; available in PMC: 2018 Jul 1.
Published in final edited form as: J Vasc Surg. 2017 Jul;66(1):178–186.e12. doi: 10.1016/j.jvs.2017.01.051

Muscle strength and control characteristics are altered by peripheral artery disease

Molly N Schieber a, Ryan M Hasenkamp a, Iraklis I Pipinos b,c, Jason M Johanning b,c, Nicholas Stergiou a,d, Holly K DeSpiegelaere b, Jung H Chien e, Sara A Myers a,b
PMCID: PMC5484068  NIHMSID: NIHMS857812  PMID: 28647034

Abstract

Objective

Peripheral Artery Disease (PAD) is a common manifestation of atherosclerosis, characterized by lower leg ischemia and myopathy in association with leg dysfunction. Patients with PAD have impaired gait from the first step they take with consistent defects in the movement around the ankle joint especially in plantar flexion. Our goal was to develop muscle strength profiles to better understand the problems in motor control responsible for the walking impairment in patients with PAD.

Methods

Ninety-four claudicating PAD patients performed maximal isometric plantar flexion contractions lasting 10s in two conditions: pain-free (patient is well rested and has no claudication symptoms) and pain-induced (patient has walked and has claudication symptoms). Sixteen matched healthy Controls performed the pain-free condition only. Torque curves were analyzed for dependent variables of muscle strength and motor control. Independent t tests were used to compare variables between groups and dependent t tests determined differences between conditions.

Results

Patients with PAD had significantly reduced peak torque and Area Under the Curve compared to Controls. Measures of control differed between PAD conditions only. Load rate and Linear Region Duration were greater in the pain condition. Time to peak torque was shorter in the pain condition.

Conclusions

The current study conclusively demonstrates that the plantar flexor muscles of the PAD patient at baseline and without pain are weaker in patients with PAD compared to Controls. With the onset of claudication pain, patients with PAD exhibit altered muscle control strategies and further strength deficits are manifest compared to baseline levels. The myopathy of PAD legs appears to have a central role in the functional deterioration of the calf muscles, as it is evident both before and after onset of ischemic pain.

INTRODUCTION

Peripheral Artery Disease (PAD) is a prevalent vascular disease affecting 8.5 million people in the United States.1 The most common presentation of PAD is intermittent claudication; a condition in which when the patient walks the metabolic demands of the lower limbs exceed the limited supply of blood, causing ischemia and exercise-induced discomfort and pain in the exercising leg. Chronic lower limb ischemia and ischemia-reperfusion introduce biochemical and histological changes in the muscles of the affected legs producing the well described myopathy of PAD.2–4 Involved in this myopathy are dysfunctional mitochondria bioenergetics, increased oxidative damage and fiber type shifting from Type II to Type I.2–9 The myopathic changes are associated with decreased quality of life,10 leg function,11–12 poor health outcomes and mortality in patients with PAD.12–13 Furthermore, the functional effects of the myopathy are most clearly seen in the gait alterations14–22 claudicating patients demonstrate from the first step they take before they experience any exercise-induced ischemia or pain.14–16,18–19 The altered gait profile found in PAD patients presents as decreased muscle power contributions at the ankle, knee, and hip joints. Among these findings, the compromised biomechanics at the ankle joint are the most consistent deficits seen in patients with PAD compared with Controls.15,18,21–22 These alterations include a lack of controlling the downward, plantar flexion motion of the foot upon heel strike,19 decreased ankle power generation during push off,22 decreased plantar flexion impulse,16 decreased energy output during the push-off phase of gait,15 and altered ankle angle variability.14 These findings equate to an overall reduced ability for a patient with PAD to propel themselves forward during the late stance phase of gait and are present from the first step the patients take while they become exacerbated after the onset of claudication pain. Thus, submaximal muscle performance, common in most functional tasks such as gait, has been quantified in detail in patients with PAD. Previous investigations have also shown that patients with PAD have significantly reduced maximal lower extremity strength as compared to Controls,7,23–25 but limited work has investigated muscle strength beyond measurement of peak maximal output. A peak maximal lower extremity strength measurement represents one value in time and alone provides limited insight to the sequence of functions and mechanics that correspond to normal gait or the muscle contraction abilities as a whole in these patients. Incorporating variables beyond peak maximal strength that reflect the collaboration between much and nerve during a contraction, such as torque generated over time and torque variability, may provide a better understanding of the motor control deficits at the ankle contributing to gait dysfunction in these patients.

Our objective was to develop a detailed strength profile of the ankle plantar flexors in patients with PAD before and after the onset of claudication pain and to compare it to that of non-PAD Controls. We hypothesized that patients with PAD have decreased strength output and altered control of the plantar flexor muscles.

METHODS

Participants

The study was approved by the Institutional Review Boards at the Veterans Affairs Medical Center of Nebraska and Western Iowa and the University of Nebraska Medical Center. Informed consent was obtained from all participants prior to data collection.

PAD Group

Ninety-four claudicating patients that were evaluated and diagnosed with PAD in the vascular surgery clinic of the two institutions were recruited (Table I). All patients with PAD were screened and evaluated by one of two board-certified vascular surgeons. Diagnosis of PAD was based on medical history, physical examination, significantly decreased resting ankle-brachial index (≤0.9), and computerized or standard arteriography. Symptomatic claudication in at least one lower extremity during walking was required for inclusion. Exclusion criteria included ambulation-limiting cardiac, pulmonary, neuromuscular or musculoskeletal conditions, rest pain, and history of previous revascularization.

Table I.

Demographics of PAD Subjects

Ankle brachial index:
 Range 0.19–0.9
 Mean 0.54 ± 0.19
Disease Duration (months) 54.4 ± 57.5
Smoking (%)
 Never 0
 Current 58.5
 Former 41.5
Coronary Artery Disease (%) 33.0
Obesity (%) 40.4
Diabetes (%) 33.0
Dyslipidemia (%) 77.7
Hypertension (%) 79.8
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Continuous variables presented as mean ± standard deviation

Control Group

Sixteen Controls of similar age and anthropometric characteristics were recruited through convenience sampling in the community (Table II). Control subjects were screened in a manner similar to subjects with PAD, were excluded for the same criteria, and were required to have an ankle-brachial index >0.9 and no subjective or objective ambulatory dysfunction.

Table II.

Baseline characteristics of PAD and Control subjects

Characteristicsa PAD Control P
No. in group 94 16
Age, y 63.7 ± 7.0 65.2 ± 7.9 0.49
Body mass, kg 89.7 ± 20.0 86.7 ± 13.5 0.57
Body height, m 1.74 ± 0.10 1.78 ± 0.05 0.23
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a

Data is reported as mean ± standard deviation.

Experimental procedure and data collection

Muscle strength was examined through isometric dynamometry using a Biodex (System 4.0; Biodex Medical Systems, Shirley, NY). Isometric contractions are a well-established and reliable technique that is better tolerated by patients compared with an isokinetic measurement.25 All subjects were secured in the Biodex and. were positioned so that the ipsilateral thigh was braced and supported with a knee angle of 30°, which allowed for maximum contribution of the gastrocnemius.26 The ankle was positioned at 90° allowing for maximum torque recruitment at the ankle. To isolate the plantar flexor muscles, the contralateral thigh, waist and chest were secured. The ankle was secured to the Biodex attachment with the axis of rotation of the dynamometer aligned with the subjects’ malleoli.

All Control subjects walked on a treadmill for three minutes as a warm-up. Patients with PAD walked for a maximum of three minutes or less if pain forced them to stop and then rested until they were free of pain. Prior to testing, subjects were allowed to perform submaximal trial-repetitions to get comfortable with the Biodex. Patients with PAD performed pain-free and pain-induced conditions, respectively. During each condition, two repetitions of maximal plantar flexion contraction for a duration of 10 seconds26 were performed on the more diseased leg of PAD patients with bilateral disease or the symptomatic leg of patients with unilateral disease. Two repetitions provide a more representative sample than a single repetition, and are well tolerated by the patients. Controls performed only the pain-free condition with their dominant leg. Each subject was instructed to push as quickly and as hard as possible throughout the entire repetition. During the pain-free condition, patients and Controls rested for one minute between each repetition. This rest period served to prevent the onset of claudication pain in subjects with PAD and to limit the effect of fatigue in Controls. After performing two repetitions of plantar flexion in the pain-free condition, subjects were unstrapped from the Biodex concluding the testing for Controls. Subjects with PAD were tested again in the pain condition, after claudication pain was induced by walking on a treadmill at 2 mph and a 10% incline until the subject reached a moderate level of pain that persisted. Immediately, subjects again performed two maximal contractions of plantar flexion for 10 seconds each, but were only given five seconds of rest between repetitions.

Data Analysis

Each isometric plantar flexion was collected at 100Hz in the Biodex and the resultant torque time series was imported into Matlab (MathWorks, Natick, MA, USA) to calculate dependent variables from custom scripts (see Supplemental Figure I, II, and III for group curves, individual Control subject curves, and all individual PAD curves, respectively). The linear region of each torque curve was identified for a more detailed analysis of torque control during the maximal contraction. The linear region was determined as the region in the torque curve that showed a trend of constant slope. Collectively, these dependent variables provide a clear picture about the ability to control force output during muscle contractions (depicted in Figure I):

  1. Area Under the Curve – total area under the torque curve. This measure is representative of work performed during the contraction.

  2. Peak Torque – average torque produced during the linear region of the contraction.

  3. Time to Peak Torque – amount of time it takes to reach the start of the linear region. Indicates the functional ability of the muscle to produce and maintain maximal torque quickly.

  4. Linear Region Duration – amount of time during the contraction that the linear region is maintained. This timing measure is representative of fatigue during maximum contraction.

  5. Standard Deviation During the Linear Region – calculated during the defined linear region to create a measure of variability. This represents an ability to control a constant muscle contraction.

  6. Load Rate – the rate of torque applied during the first second of the contraction. This timing measure indicates the ability to produce torque rapidly and is indicative of muscle power.

Figure I.

Figure I

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A representative strength curve from the control group with the six calculated dependent variables: Area Under the Curve, Linear Region Duration, Peak Torque, Time to Peak Torque, Standard Deviation of Torque During the Linear Region, and Load Rate.

Statistical Analysis

Means and standard deviations for each variable were calculated. Two independent t tests were utilized to compare PAD conditions independently to Controls and one dependent t test was used to compare PAD pain-free vs. PAD pain. A repeated measures ANOVA was utilized to perform linear trend analysis. Statistical comparisons were performed using SPSS 22.0 software (SPSS Inc, Chicago, I11) and the significance level was set at 0.05.

RESULTS

Group means for age (P = 0.49), body mass (P = 0.57), and height (P = 0.23) were not different between patients with PAD and Controls, verifying that the groups were well matched (Table II).

In comparisons of PAD to Controls, both Peak Torque and Area Under the Curve are greater in Controls than PAD pain-free (PAD-PF) and pain (PAD-P) conditions (Table II, Figure II). No other variables were statistically different between both PAD conditions and the Control group.

Figure II.

Figure II

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Mean and standard deviation graphs for (a) Area Under the Curve, (b) Peak Torque, (c) Time to Peak Torque, (d) Load Rate, (e) Standard Deviation During the Linear Region, and (f) Linear Region Duration. Significance denoted as *p < 0.05; **p < 0.01; ***p < 0.001

Five variables were significant in comparisons between PAD pain-free and PAD pain conditions (Table III, Figure II). Peak Torque, Area Under the Curve, and Time to Peak Torque are all greater in the PAD pain-free condition. Load Rate is larger and the Linear Region is longer in the PAD pain condition. Thus, exercise-induced ischemic pain further reduced strength and changed motor control in the plantar flexors of patients with PAD.

Table III.

Group means for each dependent variable

Variablea Control PAD-PF PAD-P P
C vs. P <0.001b
Area Under the Curve (N · m · s−1)
858.7 ± 237.0 682.4± 274.0 601.5 ± 265.4 C vs. PF 0.01b
P vs. PF <0.001b
C vs. P <0.001b
Peak Torque (N · m) 98.2 ± 27.6 81.4 ± 32.6 69.1 ±28.7 C vs. PF 0.04b
P vs. PF <0.01b
C vs. P 0.06
Time to Peak Torque (s) 3.74 ± 1.22 3.91 ± 1.39 3.09 ± 1.17 C vs. PF 0.67
P vs. PF <0.001b
Standard Deviation C vs. P 0.23
During 3.04 ± 1.53 2.75 ± 2.00 2.54 ± 1.41 C vs. PF 0.49
Linear Region (N · m) P vs. PF 0.23
C vs. P 0.91
Linear Region Duration (s)
5.80 ± 1.42 5.00 ± 1.77 5.85 ± 1.77 C vs. PF 0.06
P vs. PF <0.001b
C vs. P 0.44
Load Rate (N · m · s−1) 197.1 ± 140.8 147.9 ± 88.2 168.3 ± 88.0 C vs. PF 0.19
P vs. PF 0.04b
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a

Data is reported as mean ± standard deviation.

b

Indicates a significant difference (P < .05) between groups

Standard Deviation During the Linear Region yielded no significant comparisons. The linear region of each torque curve was divided into three equal tertile regions for further analysis. Trend analysis revealed a decreasing linear trend for torque variability about the linear region, from beginning to end, in PAD conditions only (Table IV).

Table IV.

Results of Linear Trend Analysis within each linear region section

Groupa Beginning 1/3 (N · m) Middle 1/3 (N · m) End 1/3 (N · m) P
Control 2.13 ± 0.97 2.13 ± 1.45 2.03 ± 1.10 0.756
PAD-PF 1.90 ± 1.35 1.54 ± 1.19 1.47 ± 1.44 0.001b
PAD-P 1.71± 1.05 1.53± 0.92 1.47 ± 1.18 0.041b
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a

Data is reported as mean ± standard deviation.

b

Indicates a significant difference (P < .05).

DISCUSSION

The purpose of this study was to create a more detailed strength profile of the ankle plantar flexors to gain insight into the contribution of the ankle to the identified gait abnormalities in patients with PAD.14–22 Measures of maximal strength and motor control were measured while subjects performed isometric ankle plantar flexions with and without claudication pain and were compared to Controls. Our findings support our hypothesis that significant differences exist in muscle strength profiles between Controls and patients with PAD. As expected, previously reported findings for reduced ground reaction forces and joint powers15–16,18 coincide with the significant differences found for Area Under the Curve and Peak Torque of the plantar flexors in all comparisons. Specifically, patients with PAD exhibited reduced Area Under the Curve and Peak Torque production compared to Controls. The strength differences between Controls and PAD when subjects perform a 10 seconds isometric test immediately after rest and before any exercise-induced ischemia/pain confirm that the weakness in the PAD ankle plantar flexors is related to the well described myopathy of PAD.2,4,9,11,27–28 Furthermore, the introduction of ischemic claudication symptoms altered the motor control strategies of the ankle plantar flexors producing significant differences between PAD conditions.

Our data demonstrate that the plantar flexor muscles of PAD patients have significant functional deficits. These deficits appear related to the neuropathy and myopathy previously described by our group2–4,11,27–28 and others.5–6,31–33 Our work demonstrates that there are functional tests, including the maximal isometric plantar flexion test we are describing in this paper, that can measure and stratify the degree of impairment in the legs of patients with PAD. Such measurements can be used both as diagnostic tools to assess the severity of PAD in each individual patient but also to potentially predict and guide therapy depending on the patient’s presentation. Our group is currently evaluating multiple parameters of this myopathy both as predictors of outcomes after standard therapies (revascularization or supervised exercise), but also in an effort to understand whether therapeutic measures can improve these deficits and to what extent.

Decreased Area Under the Curve

Area Under the Curve is a measure of angular impulse during a contraction and is indicative of work; the smaller area found in patients with PAD indicates they are unable to reach or maintain a similar level of torque output over the same amount of time as Controls. Our results show a decreased total area in PAD torque curves at the ankle plantar flexors and a decreased capacity to complete the same amount of work as Controls. The difference between Controls and patients with PAD in pain-free conditions was exacerbated in pain conditions.

Decreased Peak Torque

Similarly, Peak Torque is highest in Controls and lowest in the PAD pain condition. Our results demonstrate a true deficit in strength at the ankle plantar flexors in patients with PAD before the onset of pain. These findings further document the strength decreases associated with PAD that could potentially contribute to gait deficits during intermittent claudication by reducing total propulsive forces during push off.

Works from other groups are in agreement with our finding of reduced strength in the plantar flexor muscles of patients with PAD.7,12,24 Gerdle et al24 found that patients with PAD produced lower Peak Torque and less contractile work than Controls during submaximal endurance testing of the plantar flexors.24 The methodology was different in the Gerdle et al24 study; subjects performed a set of 30 non-fatiguing isokinetic contractions at 180°sec−1 and a set of 200 fatiguing isokinetic contractions at 60°sec−1.24 Other work by Regensteiner et al7 showed reduced levels of strength in the plantar flexors in patients with PAD that correlated with total calf cross-sectional area and type II fiber cross-sectional area.7 Strength testing in the Regensteiner et al7 study was performed during two sets of five maximal effort isokinetic contractions at 60°sec−1 in pain-free conditions. The single highest torque for the gastrocnemius and anterior tibial muscles was used for analysis.7 However, in a similar study Scott-Okafor et al25, tested strength at the ankle, knee, and hip but only found differences at the dorsiflexors when compared to individuals without PAD.25 Similar to the present study, Scott-Okafor et al25 used isometric testing, but tested plantar flexor strength with the knee at a 90° angle, whereas Regensteiner et al7 tested the ankle with the knee fully extended, and the present study tested the ankle with slight flexion of 30° at the knee. The gastrocnemius crosses both the knee and the ankle joint; therefore, for a given ankle plantar flexion torque the contribution of the gastrocnemius is dependent on the position of the knee. A more flexed knee decreases the overall plantar flexion torque output by minimizing the contribution of the gastrocnemius, the main contributor in plantar flexor contractions29 and is likely the main reason Scott-Okafor et al25 were not able to see the decrease in torque during plantar flexion. Collectively, decreased strength about the ankle in patients with PAD is a common finding and the current study adds to that conclusion.

Measures of motor control at plantar flexors

To our knowledge, this is the first study to investigate muscle strength beyond a measurement of the peak maximal force in patients with PAD. Measures of rate, standard deviation, and timing (including Time to Peak Torque, Standard Deviation During Linear Region, Linear Region Duration, and Load Rate) represent muscle motor control because they assess the ability of a subject to produce a maximal contraction and detail changes in the quality of the contraction over the course of the trial. The differences found in these measures were only in comparisons between PAD conditions. Our data did not demonstrate differences between PAD patients and Controls.

Increased Load Rate in pain conditions

A larger Load Rate indicates rapid torque production during the first second of the isometric contraction. A steeper slope during the first second of contraction would represent this on the torque curve. Load Rate increased in pain conditions for PAD, indicating that the onset of pain altered the initial approach to the contraction to perform more work. It appears that induction of pain produces motor adjustments which lead to the observed faster load rates. It is possible that pain input from sensory endings may change the motor output into the symptomatic muscle leading to increased recruitment of motor units during the first second of the contraction. Another possibility is that once symptoms have been induced the neuromuscular system is sensitized and responds quicker to the nerve impulses for contraction. Irrespective of the underlying mechanism, the capacity of the myopathic tissues to perform more work is not maintained throughout the contraction since our data demonstrated decreased overall Area Under the Curve in pain conditions.

Time to Peak Torque

Time to Peak Torque was measured to assess whether timing differences existed in maximal torque generation in an isometric contraction. PAD pain reached Peak Torque quicker than in pain-free conditions which is likely associated with the concurrent decrease in peak torque observed in the pain condition. Specifically, the PAD patients reach quicker the level of peak torque while in pain because the peak torque is lower than in the pain-free condition and are able to arrive faster to it. Although a quicker response may be the product of a neuromuscular system that is more sensitive to nerve impulses, when it is combined with the finding of lower Peak Torque and Area Under the Curve, it indicates that the presence of symptoms exacerbates the deficit in torque output capabilities in patients with PAD.

Linear Region Duration and Standard Deviation

Linear Region Duration was significantly longer in the PAD pain condition compared to baseline. It appears that because in the pain condition, torque generation was of a lower magnitude, the patients spend more time trying to maintain their torque output because of an inability to generate more.

Standard deviation of the entire linear region elicited no significant comparisons. Due to the large variance within this variable, we investigated variability in maintenance of torque further by dividing the linear region of each curve into three equal tertiles. Linear trend analysis revealed that variability about the linear region decreased in PAD and did not change in Controls. Neuromuscular fatigue is known to affect motor output during an isometric contraction by increasing the amount of variability as a contraction progresses.30 Controls exhibit no trend because a healthy neuromuscular interaction involves recruitment of more motor units to maintain torque within a 10s contraction while the decreasing variability in PAD is an example of less activity within the muscle. Myopathic fiber type shifting from Type II to I2,9 and the neuropathy in PAD muscle that has been shown to decrease conduction velocities and amplitude corroborate this trend.31–33

Possible mechanisms for the strength and motor control deficits at the ankle

The present study confirmed the significant deficits in strength that have been found in the ankle plantar flexors of patients with PAD previously.7,15–16,21–22,25 During gait, the leg of a patient with PAD is unable to generate normal power and produce normal positive work for push-off, indicated by reduced ankle plantarflexion torque and power compared to adults without PAD.7,15–16,18 This gait deficit is present both before and after the onset of claudication pain.16 Patients with PAD also have a reduced ability to produce work during walking, independent of walking speed.15 The deficits in strength and ability to produce work with the plantar flexor muscles are likely key contributors to the gait deficits that have been documented in patients with PAD.

Our findings are the result of maximal isometric strength assessments, which are independent of blood flow, and demonstrate that deficits in patients with PAD relative to Controls reflect the metabolic myopathy and neuropathy that is present in the muscles of patients with PAD.2,4–5 The effects of neuropathy in patients with PAD have been found to include decreased nerve conduction velocities, decreased amplitude of and increased duration of motor unit action potential.31–33 The myopathy in patients with PAD involves defective mitochondrial bioenergetics, oxidative damage, myofiber degeneration and fibrosis of the affected skeletal muscles.2–6,11,27–28,34–35 Increased oxidative damage in PAD muscle is associated with deterioration of the size and shape of myofibers in the gastrocnemius with preference for Type II myofibers while Type I fibers persist and are less damaged.9 Type II fibers are high-energy consumers and are utilized in short explosive movements such as the isometric contraction.36 The change in myofiber type in the gastrocnemius in connection with defective mitochondria and neuropathy demonstrate possible underlying mechanisms for the deficits we are demonstrating in maximal torque generation and performance of effective work at the plantar flexor muscles in patients with PAD relative to Controls. It is evident from our data that the onset of claudication pain affects motor control at the ankle in patients with PAD. It is probable that during exercise-induced ischemia, fatigue, pain, and an increased workload from restricted bioenergetics would alter the control of a muscle contraction, especially at a maximal intensity for ten seconds. To our knowledge, no work with similar measures of motor control in the ankle plantar flexors currently exists to compare our results to other populations and pathologies.

The parameters we have described allow quantitation of the degree of neuromuscular impairment present in the legs of claudicating patients. These parameters delineate the collaboration between muscle and nerve during leg contraction and allow an objective assessment of the neuromuscular health of the leg of each patient at baseline and the way it responds to different treatment modalities. If a patient improves their walking distances after treatment, knowledge of whether the improvement is, or is not, reflected in muscle strength and performance, can help us understand how treatments affect the performance of different muscle groups. Of particular interest would be the possibility that after treatment a patient increases their ability to walk either without a measurable change (or even deterioration) in the performance of his neuromuscular system or with a measurable improvement of certain “unexpected” muscle groups. Based on these examples it becomes obvious that there are many and exciting opportunities for expanding our understanding of the mechanisms involved in PAD pathophysiology but also for taking advantage of these mechanisms to modify current treatments and propose new ones.

Control group size and the use of an isometric measurement instead of isokinetic are possible limitations of this study. Isokinetic testing is more reflective of function because strength is measured through a range of motion, rather than in a static position. However, the differences reported here provide insight into the functional capacity of the muscle. Furthermore, an isometric test was tolerable for our patients in the pain condition and still allowed measurement of the changes that occur because of pain.

Conclusions

Our findings conclusively confirm that the plantar flexor muscles of the PAD patient have a significant functional impairment compared to Controls. Impairments in strength were present at baseline, providing more evidence for the impact of myopathy and neuropathy of PAD on the skeletal muscle of claudicating patients. With the onset of claudication pain, patients with PAD have further decrease in peak strength and altered muscle control strategies at the ankle compared to baseline levels. The ankle joint is of primary importance to proper gait mechanics and patterns, especially during the push off phase in late stance, and thus the deficits we describe have important clinical implications for restoring function. Future biomechanics research in PAD populations should examine the use of strength deficits as predictors of surgical and exercise outcomes.

Supplementary Material

Supplemental Figure I. Average Torque Curves with Standard Deviation Bounds for both groups and conditions.

Supplemental Figure II. Individual Torque Curves for Control subjects 1–16.

Supplemental Figure III. Individual Torque Curves of all PAD subjects in each trial and in pain-free and pain conditions (a) subjects 1–10, (b) subjects 11–20, (c) subjects 21–30, (d) subjects 31–40, (e) subjects 41–50, (f) subjects 51–60, (g) subjects 61–70, (h) subjects 71–80, (i) subjects 81–90, (j) subjects 91–94.

Acknowledgments

Support for this work was provided by funds from the National Institutes of Health (R01AG034995 and P20GM109090), the Veteran’s Affairs Rehabilitation Resources and Development (1I01RX000604), and the National Aeronautics and Space Administration (NASA) Nebraska Space Grant.

Footnotes

Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.

This study was presented at the 2016 Annual Midwestern Vascular Surgical Society Meeting, Columbus, Ohio, September 8–10, 2016 and received the Charles C. Guthrie award.

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Associated Data

This section collects any data citations, data availability statements, or supplementary materials included in this article.

Supplementary Materials

Supplemental Figure I. Average Torque Curves with Standard Deviation Bounds for both groups and conditions.

Supplemental Figure II. Individual Torque Curves for Control subjects 1–16.

Supplemental Figure III. Individual Torque Curves of all PAD subjects in each trial and in pain-free and pain conditions (a) subjects 1–10, (b) subjects 11–20, (c) subjects 21–30, (d) subjects 31–40, (e) subjects 41–50, (f) subjects 51–60, (g) subjects 61–70, (h) subjects 71–80, (i) subjects 81–90, (j) subjects 91–94.

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