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. Author manuscript; available in PMC: 2013 Jan 1.
Published in final edited form as: J Hand Ther. 2011 Dec 3;25(1):27–37. doi: 10.1016/j.jht.2011.09.003

Effect of Lateral Epicondylosis on Grip Force Development

Amrish O Chourasia 1, Kevin A Buhr 2, David P Rabago 3, Richard Kijowski 4, Curtis B Irwin 5, Mary E Sesto 6
PMCID: PMC3281279  NIHMSID: NIHMS342892  PMID: 22137195

Abstract

Introduction

While it is well known that grip strength is adversely affected by lateral epicondylosis (LE), the effect of LE on rapid grip force generation is unclear.

Purpose

The purpose of this study was to evaluate the effect of LE on the ability to rapidly generate grip force.

Methods

Twenty-eight participants with LE (13 unilateral and 15 bilateral LE) and 13 healthy controls participated in this study. A Multi-Axis Profile dynamometer was used to evaluate grip strength and rapid grip force generation. The ability to rapidly produce force is comprised of the electromechanical delay and rate of force development. Electromechanical delay is defined as the time between the onset of electrical activity and the onset of muscle force production. The Patient Rated Tennis Elbow Evaluation (PRTEE) questionnaire was used to assess pain and functional disability. Magnetic resonance imaging was used to evaluate tendon degeneration.

Results

LE-injured upper extremities had lower rate of force development (−50 lbs/sec, CI [−17, −84]) and less grip strength (−7.8 lbs, CI [−3.3, −12.4]) than non-injured extremities. Participants in the LE group had a longer electromechanical delay (+59%, CI [29,97]) than controls. Peak rate of force development had a higher correlation (r=0.56)(p<0.05) with PRTEE function than grip strength (r=0.47) (p<0.05) and electromechanical delay (r=0.30)(p>0.05) for participants with LE.

Conclusion

In addition to a reduction in grip strength, those with LE had a reduction in rate of force development and an increase in electromechanical delay. Collectively, these changes may contribute to an increase in reaction time, which may affect risk for recurrent symptoms. These findings suggest that therapists may need to address both strength and rapid force development deficits in patients with LE.

Introduction

Lateral epicondylosis (LE), a prevalent musculoskeletal disorder of the common extensor tendon, is associated with significant individual and societal costs.1-5 LE is characterized by microtears, collagen degeneration and angioblastic proliferation of the common extensor tendon.6-8 LE may affect the muscle fiber type composition9, neural drive10 and stiffness of the muscle tendon complex.11,12 Pain at the lateral aspect of the elbow is a primary symptom of LE.13 This pain is often exacerbated by gripping activities with grip strength often impaired.14,15

While important, measures of strength and pain may not provide information about other important aspects of upper extremity function that may be affected by LE, such as sensorimotor function. The sensorimotor system includes the sensory, motor and central integration and processing components and is important in maintaining postural control and functional joint stability.16,17 Sensorimotor deficits have been observed in musculoskeletal conditions including patellofemoral pain syndrome,18 low back pain,19 shoulder disorders20 and neck pain.21 Specific to LE, sensorimotor and motor performance deficits observed include a longer reaction time16,22,23 and less muscle tendon stiffness and damping.11,12 A decrease in stiffness and damping during rapid loading is associated with greater displacement of the upper extremity, increased strain and risk of injury.12 Such evidence highlights a need to investigate other aspects of upper extremity function that may be affected by LE.

Reaction time may be of particular importance in preventing injury when reacting to rapid loading.24 Two components that may contribute to the observed increase in reaction time in LE are rate of force development and electromechanical delay. Rate of force development is considered to be a measure of the ability to rapidly generate strength25 and is an important component for joint stability and postural control.26,27 Rate of force development is important as one’s ability to rapidly develop force not only influences the accelerations of the body but also dictates how the body interacts with objects. For example, a greater rate of force development is associated with higher functional performance in the upper extremity28 as well as the lower extremity.29 Conversely, injury can result in reduced rate of force development. Prior research found 33–54% lower rate of force development in women with neck pain compared to those without.26 In addition, rate of force development had a stronger association with self-reported pain than maximal strength.26

Electromechanical delay may also be affected by injury.30 Electromechanical delay is defined as the time between the beginning of electromyographic (EMG) activity and the beginning of force development. This represents the duration of the excitation contraction coupling in the muscle and the time to take-up the slack in the elastic structures of the muscle tendon unit.31 Altered muscle spindle sensitivity30 and muscle preactivation levels32 may adversely affect electromechanical delay. Hopkins et al30 reported longer peroneal electromechanical delay in patients with functional ankle instability compared to controls suggesting altered muscle spindle sensitivity and muscle preactivation. Vint et al32 reported lower electromechanical delay when exertions are initiated from non-resting levels. It is currently unknown whether electromechanical delay is affected due to LE.

While reductions in grip strength occur in LE,14,15,33 it is unknown whether the ability to rapidly generate force during a gripping activity is similarly affected. Current rehabilitation interventions for LE focus on improvement of strength and reduction in pain. However, an increase in maximal strength is not necessarily associated with an increase in rate of force development and electromechanical delay.27 Hence, restoration of grip strength in patients with LE may not be accompanied with an increase in sensorimotor measures of performance such as rate of force development and electromechanical delay. This may make patients with LE vulnerable to re-injury especially with tasks involving rapid loading during occupational and recreational activities.

While it is important to understand how LE affects sensorimotor function, instrumentation to quantify the components of rate of force development and electromechanical delay is lacking. Grip dynamometers14,15 measure a single, scalar value for grip strength and therefore, are not capable of obtaining rate of force development data. Therefore, a multi-axis profile (MAP) dynamometer which is capable of measuring rate of force development and electromechanical delay was used.34

While reductions in reaction time and grip strength occur due to LE,14,22,23,35 it is unknown whether the ability to rapidly generate force is similarly affected. In addition, most studies to date have excluded patients with bilateral LE.10,16,23,36,37. This may limit generalizability of results since those with LE present may present with bilateral symptoms.4

Clearly there is a need to explore the effect of LE on rate of force development and electromechanical delay in those with unilaterally and bilaterally affected arms. Therefore, the purpose of this study was to evaluate the effect of LE on the ability to rapidly generate grip force. In addition, we accounted for the effect of hand dominance, gender, and age on rapid force generating capacity. The relationship between function, grip strength and rapid force generating capacity was also assessed. A better understanding of the impact of LE on grip function may lead to improved therapeutic interventions for LE as well as possibly reducing the risk of recurrence of LE by addressing deficits in rapid force generating capacity.

Methods

Study design and participants

This study was an add-on to a study designed to assess mechanical parameters of stiffness and damping in participants with LE (+LE) compared to healthy, uninjured controls (−LE). The mechanical parameter results are reported elsewhere.11 The study was a case-control study comparing sensorimotor and motor performance of injured and uninjured upper extremities using data collected in participants with LE (+LE) compared to healthy, uninjured controls (−LE).

A total of 31 individuals with LE were recruited from various outpatient clinics in a Midwestern city from June 2009 to February 2010. (The majority of +LE participants were participating in a therapeutic trial investigating the efficacy of prolotherapy for LE; only baseline measures (pre-injection) are reported in this paper.) Two participants were excluded because they did not meet the eligibility criteria (see figure 1). In addition, data from one +LE participant was not included due to instrumentation failure. Of the 28 eligible participants, 13 had unilateral symptoms and 15 had bilateral symptoms. A control group of thirteen uninjured participants was recruited from the university campus.

Figure 1.

Figure 1

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Flow diagram showing the recruitment process and the reasons for exclusion.

Diagnostic criteria for LE included tenderness to palpation over the lateral epicondyle and/or extensor mechanism and pain present on at least two of the following provocation tests: pain with resisted extension of the wrist or fingers, pain with resisted supination, pain with passive stretch to the wrist extensors or supinator. All participants completed additional screening; those with coexisting or previous medical history of rheumatoid or inflammatory arthritis, chronic pain diagnoses, diabetes mellitus, pregnancy, systemic nervous disease, neuropathy, or acute trauma to the fingers or hands were excluded. Additional exclusion criteria include prior cervical or upper extremity injury, concurrent cervical or upper extremity injury, unresolved litigation and co-morbidities that could interfere with ability to participate in the study. In addition, participants from the comparison group were excluded if they reported any cervical or upper extremity symptoms. Informed consent was obtained for all participants in accordance with the university human subjects institutional review board. Participant characteristics are presented in table 1.

Table 1.

+LE and −LE participant characteristics

Characteristic +LE −LE
Males / Females (n) 17/11 5/8
Age (years) (Mean (SD)) 48.2 (8.4) 44.6 (8.1)
Symptom Duration (years) (Median (Min-Max)) 2 (0.5-10) -
Right = 26; Right = 10;
Hand Dominance (n)
Left = 2 Left = 3
Unilateral / Bilateral Symptoms (n) 13/15 -
Unilateral – Dominant Extremity Symptomatic (n) 11 -
Unilateral – Non-dominant Extremity Symptomatic (n) 2 -
Work Status: Full time (FT)/ Part Time (PT)/ /Not FT = 11; PT =
FT = 24; PT = 4
working (NW) 1; NW = 1
Rehabilitation (Yes/No) 23/5 -
Cortisone Injection (Yes/No) 13/15 -
Visual Analog Scale (0-10) (Mean (SD)) 4.65 (2.3) 0.0 (0.0)
Patient Rated Tennis Elbow Evaluation (0-100)
(Mean (SD))		 38.60 (18.50) 1.77 (2.54)
Grade 0 = 0;
Grade 1 = 8
Grade 0 = 11
MRI (Grade 0 – 3) Grade 2 = 10
Declined = 2
Grade 3 = 9
Declined = 1
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Measures

Pain-free Grip Strength

Pain-free grip strength was evaluated bilaterally using a novel dynamometer called the Multiaxial profile (MAP) dynamometer34 as well as a hydraulic Baseline dynamometer (Fabrication Enterprises, White Plains, NY, USA). In addition to grip strength, the MAP is also able to assess rate of force development. The MAP has been found to demonstrate excellent test-retest reliability (ICC=0.99) and has excellent concurrent validity when compared to the Baseline dynamometer (r=0.88-0.90).34 Pain-free grip strength was used as it is a reliable measure (ICC=0.97)15 of strength in patients with LE and is considered a better measure to assess sensitivity to change than maximal grip strength.33

All participants were seated in a chair with the shoulder flexed at 90 degrees and the elbow in an extended position. This posture has been recommended for evaluation of grip strength in individuals with LE.14,38 Upon receipt of a randomly timed visual stimulus, all participants were instructed to squeeze the handle as quickly and as hard as possible without pain for five seconds. Standardized verbal encouragement and visual feedback of grip force, without numerical values, was provided to the participant. Practice sessions were provided to participants before data collection. The average of the peak force from three replications, performed with 60s rest intervals was used. The signals from the MAP dynamometer were sampled at the rate of 1000 samples/s using a USB 6009 card (National Instruments, Austin, TX, USA).

The geometry of the handles is different for the MAP and Baseline resulting in different grip strength values.34 Thus, to compare results with previous studies, pain free grip strength was also measured with the Baseline hydraulic dynamometer using the same posture and procedure as that used with the MAP.

Rate of force development

Rate of force development was measured bilaterally using the MAP dynamometer output obtained during the grip strength exertion. Rate of force development was calculated by taking the time derivative of the force signal, which was sampled at 1000 samples/s. The time resolution used for calculation of the rate of force development was 1 ms. Peak rate of force development is the maximal value of the time derivative of the force signal and sub-maximal measures of rate of force development were measured at 30ms, 50ms and 100ms from onset. Rate of force development is affected by muscle fiber type and myosin heavy chain composition, viscoelastic properties of the muscle tendon complex and neural drive to the muscle.39 It is theorized that rate of force development at different time intervals is affected differently as a result of these factors; hence rate of force development was evaluated at 30, 50 and 100 ms from onset of contraction as well as peak rate of force development. This protocol for assessing rate of force development is similar to the one used by Aagaard et al25 and Andersen et al39. Practice sessions were provided to participants before data collection. Average of three replications performed with 60s rest intervals was used.

Electromechanical delay

Electromechanical delay was also measured during the grip strength exertion. It was measured bilaterally by simultaneously sampling the MAP dynamometer output and the raw EMG signal from the extensor carpi radialis (ECR) muscle using a 16-channel wireless Noraxon Telemyo 2400 system (Noraxon Inc., Scottsdale, AZ, USA). The time between the onset of EMG and the onset of force is defined as the electromechanical delay (see figure 2). Therefore, the onset of electromechanical delay occurs when electrical activity is measured in the ECR via EMG. The ending point for electromechanical delay is the start of actual force production, which was measured via the MAP dynamometer.

Figure 2.

Figure 2

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Measurement of electromechanical delay (EMD) and rate of force development (RFD) from EMG and force signals

The ECR is comprised of the extensor carpi radialis longus and the extensor carpi radialis brevis muscles. Surface electrodes were placed on the ECR at one third of the distance from the proximal end of a line from the medial epicondyle to the distal head of the radius, with the forearm supinated as recommended by Mogk and Keir.40 This method is similar to the one used by Alizadehkhaiyat et al36 and Snijders et al41 to assess muscle activity of the ECR in patients with LE. The reference electrode was attached to lateral epicondyle of the right elbow. Prior to electrode placement, skin preparation was performed according to SENIAM guidelines.42 Disposable, self-adhesive Ag/AgCl snap dual electrodes with individual electrode diameter of 1cm and inter electrode distance of 2cm manufactured by Noraxon were used. Preamplified EMG leads with a differential gain of 500 connected the electrodes to the wireless transmitter with 16-bit analog to digital converter and bandwidth 10-500Hz. The EMG amplifier characteristics were: gain=1000, input impedance>>100MOhm and the common mode rejection ratio was >100dB. The EMG and force signals were sampled at the rate of 1500 samples/second. Average of three replications was used.

Magnetic Resonance Imaging (MRI)

MR scans were performed on the eleven participants in the −LE group and 27 participants in the +LE group. Two participants in the −LE group and one participant in the +LE group and declined the MR scan. MRI examination was performed using an Artoscan 0.17T extremity scanner (GE Healthcare, Waukesha, WI, USA). Axial and coronal T1-weighted and fluid sensitive short tau inversion recovery (STIR) sequences of the elbow were used for semi-quantitative assessment of disease severity. T1 weighted scan parameters were: TR = 2050ms, TE = 18ms, Slices = 7, Gap = 1.0mm, Thickness = 3.5mm, Readout FOV = 180, Encoding FOV = 180, Samples = 192, Encoding # = 192. STIR scan parameters were: TR = 2050ms, TE = 34ms, TI = 75ms, Slices = 7 Gap = 1.0mm, Thickness = 3.5mm, Readout FOV = 180, Encoding FOV = 180, Samples = 192, Encoding # = 192. A musculoskeletal radiologist who was blinded to group status reviewed MRI examinations. A semi-quantitative grading scale was used to estimate the severity of chronic degeneration and pathologic changes in the common extensor tendon origin.43 The grading scale is as follows:

  • Grade 0 = normal CET which is of uniform low signal intensity on T1-weighted and STIR images.

  • Grade 1 = CET with mild tendinopathy which is thickened and has intermediate signal intensity on T1-weighted and STIR.

  • Grade 2 = CET with moderate tendinopathy which is thinned and shows focal areas of intense fluid-like signal intensity on STIR images which comprise less than 50% of the total cross sectional diameter of the tendon.

  • Grade 3 = CET with severe tendinopathy which is thinned and shows focal areas of intense fluid-like signal intensity on STIR images which comprise more than 50% of the total cross sectional diameter of the tendon.

Visual Analog Scale (VAS)

All participants were asked to rate the average pain intensity in each of the elbows for the previous week using a VAS ranging from “0 = no pain” to “10 = most pain”. Note that for the purposes of ascertaining whether a participant was unilaterally or bilaterally injured, the upper extremity was considered injured if the VAS score was greater than 0.

Patient Rated Tennis Elbow Evaluation (PRTEE)

Participants also completed the PRTEE questionnaire. The PRTEE measures both elbow pain and function44-46 and has demonstrated good test-retest reliability in LE (ICC=0.89).45

Study Sample Size

The original study was powered to detect a difference between +LE and −LE participants in upper extremity mechanical parameters.11 Based on pilot data collected on healthy individuals and participants with injuries comparable to LE, simulated power calculations showed that a mixed effects analysis of n=50 participants, would have 90% power at alpha=0.05 to detect an injury effect of a 10% change in stiffness, the mechanical parameter of primary interest. Ultimately, n=42 eligible participants were recruited, 29 +LE participants and 13 −LE controls.

Statistical Analysis

The effect of injury and extremity dominance on grip strength, rate of force development and electromechanical delay was evaluated using a linear mixed effects model. The mixed effects model permits simultaneous fitting of data for +LE participants with bilateral and unilateral injury and LE uninjured controls to simultaneously estimate the independent effects of extremity dominance and injury. Age and gender effects were accounted for by the model. The α level was set at 0.05. Based on examination of the response variability and model diagnostics, a log-transformation was used for the electromechanical delay response.

The relationship between rate of force development, electromechanical delay, grip strength and PRTEE function, and VAS score was investigated for +LE participants using Pearson correlation coefficients. Correlations were calculated using the more injured extremity in each +LE participant, as evaluated by VAS score, or using the dominant extremity where extremity VAS scores were equal. Data analysis was conducted using the R language and environment for statistical computing (R Foundation for Statistical Computing, Vienna, Austria).

Results

Summary data for sensorimotor and motor performance are presented in table 2.

Table 2.

Mean (SD) values for sensorimotor and motor performance variables. Participants with non-dominant extremity injury (n=2) are not included in the table.

Controls (n=13) Unilateral LE in Dominant
Limb (n=11)		 Bilateral LE (n = 15)
Dominant
Limb		 Non-dominant
Limb		 Dominant
Limb		 Non-dominant
Limb		 Dominant
Limb		 Non-dominant
Limb
Limb Status Non-injured Non-injured Injured Non-injured Injured Injured
Grip Strength
(MAP) (lbs)		 48 (11) 45 (12) 30 (12) 38 (13) 37 (14) 33 (15)
Grip Strength
(Baseline) (lbs)		 98 (27) 94 (28) 49 (25) 86 (19) 67 (32) 53 (40)
Rate of force
development at 30
ms (lbs/s)		 136 (85) 125 (66) 85 (62) 113 (80) 110 (37) 100 (60)
Rate of force
development at 50
ms (lbs/s)		 163 (97) 147 (73) 103 (78) 140 (98) 132 (41) 120 (69)
Rate of force
development at
100 ms (lbs/s)		 181 (85) 160 (67) 116 (80) 157 (96) 150 (46) 137 (72)
Peak rate of force
development
(lbs/s)		 256 (107) 233 (74) 177 (98) 228 (122) 205 (62) 191 (85)
EMD (s) 0.039 (0.008) 0.039 (0.014) 0.061 (0.029) 0.064 (0.024) 0.061 (0.02) 0.065 (0.033)
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Pain-free Grip Strength

As expected injured extremities had lower grip strength compared to non-injured extremities. Overall, a significant effect of injury was observed for peak grip strength regardless of dynamometer used. Using the MAP dynamometer, the injured extremity had, on average 7.8 lbs less grip strength (p<0.001, 95% CI [3.3,12.4]) than the non-injured extremity. A significant effect of extremity dominance was also observed with the dominant extremity having, on average, 2.6 lbs more grip strength than the non-dominant extremity (p=0.046, 95% CI [0.2,4.9]). Figures 3 and 4 show observed Baseline and MAP grip strengths. Handle differences result in an overall 38% difference in grip strength between the MAP and Baseline dynamometers.

Figure 3.

Figure 3

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Mean (SD) of MAP grip strength. Bar graph pairs compare distributions of grip strength as assessed in the N=non-dominant and D=dominant extremity for uninjured controls (n=13), patients with unilateral injury to dominant extremity (n=11), and patients with bilateral injury (n=15). The participants with non-dominant extremity injury (n=2) are not included in these plots.

Figure 4.

Figure 4

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Mean (SD) of Baseline grip strength. Bar graph pairs compare distributions of grip strength as assessed in the N=non-dominant and D=dominant extremity for uninjured controls (n=13), patients with unilateral injury to dominant extremity (n=11), and patients with bilateral injury (n=15). The participants with non-dominant extremity injury (n=2) are not included in these plots.

Rate of Force Development

Observed peak rate of force development values are shown in Figure 5.

Figure 5.

Figure 5

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Mean (SD) of peak rate of force development. Bar graph pairs compare distributions of peak rate of force development as assessed in the N=non-dominant and D=dominant extremity for uninjured controls (n=13), patients with unilateral injury to dominant extremity (n=11), and patients with bilateral injury (n=15). The participants with non-dominant extremity injury (n=2) are not included in these plots.

Peak rate of force development

Significant effect of injury was observed on peak rate of force development. The injured extremity had, on average 50 lbs/sec less peak rate of force development (p=0.007, 95% CI [17,84]) than the non-injured extremity. No significant effect of extremity dominance was observed (p=0.37).

Submaximal rate of force development

Significant effect of injury was observed on submaximal rate of force development at 30, 50 and 100ms from onset. The injured extremity had, on average 29, 36, and 38 lbs/sec less rate of force development at 30ms, 50ms, and 100ms respectively (all p<0.03). No significant effect of extremity dominance was observed (all p>0.3).

Electromechanical Delay

A significant effect of injury was observed on electromechanical delay (p=0.007). However, model diagnostics indicated that the effect of injury on electromechanical delay was best explained by a group effect (+LE/−LE) rather than an injured extremity effect. That is, +LE participants had, on average, a 59% longer electromechanical delay (p<0.001, 95% CI [29,97]) than −LE participants in both extremities, with no evidence that injured extremities had longer electromechanical delay than uninjured extremities in participants with unilateral injury (p=0.14). No significant effect of extremity dominance was observed (p=0.74). Observed electromechanical delay values are shown in Figure 6.

Figure 6.

Figure 6

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Mean (SD) of electromechanical delay. Bar graph pairs compare distributions of electromechanical delay as assessed in the N=non-dominant and D=dominant extremity for uninjured controls (n=13), patients with unilateral injury to dominant extremity (n=11), and patients with bilateral injury (n=15). The participants with non-dominant extremity injury (n=2) are not included in these plots.

Magnetic Resonance Imaging

Participants in the −LE group did not show increased signal intensity in the common extensor tendon and therefore were assigned a score of 0. Participants in +LE group had increased signal intensity in the common extensor tendon region. Eight +LE participants were assigned a score of 1, ten were assigned a score of 2 and nine were assigned a score of 3.

Grip Strength, rate of force development, electromechanical delay and VAS, PRTEE correlations

Correlations between the sensorimotor and motor performance variables and self-report pain and function variables for +LE participants are presented in table 3. The participant’s most injured extremity as assessed by VAS score (or dominant extremity in case of a tie) was used. Significant correlations were observed between grip strength, rate of force development and PRTEE function with peak rate of force development having the highest correlation with PRTEE function (r=−0.56 for peak rate of force development vs. r=−0.47 for MAP grip strength). The correlations between grip strength, rate of force development and self-report pain were significant for the PRTEE pain scale but not for the VAS. Electromechanical delay did not have significant correlation with PRTEE function and VAS.

Table 3.

Pearson correlation coefficients for sensorimotor and motor performance variables and self-report pain and function for more injured extremity in +LE participants

PRTEE PRTEE PRTEE VAS
Function Pain Total
Baseline Grip Strength
(lbs)		 −0.43* −0.42* −0.44* −0.18
MAP Grip Strength (lbs) −0.47* −0.46* −0.37* −0.2
Rate of force development
at 30 ms (lbs/s)		 −0.49* −0.40* −0.32 −0.26
Rate of force development
at 50 ms (lbs/s)		 −0.51* −0.42* −0.34 −0.27
Rate of force development
at 100 ms (lbs/s)		 −0.54* −0.44* −0.36 −0.26
Peak rate of force
development (lbs/s)		 −0.56* −0.46* −0.37* −0.31
Electromechanical delay
(s)		 0.30 0.17 0.19 0.15
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*

(p<0.05)

Discussion

The main finding of this study was that the +LE extremities had a reduction in rate of force development compared to −LE extremities while electromechanical delay was bilaterally lower in +LE participants compared to −LE participants, regardless of unilateral or bilateral LE. The combined deficits in rate of force development and electromechanical delay result in a decrease in ability to rapidly generate grip force. This change may explain the longer reaction times observed in patients with LE.16,22 Another interesting finding was the stronger correlation of rate of force development than pain-free grip strength with self-report function in patients with LE.

Effect of LE injury on the ability to rapidly generate force is similar to decreases observed in other musculoskeletal conditions like neck pain26 and functional ankle instability.30 For example, Andersen et al26 reported a 33-55% lower rate of force development in females with neck pain compared to those without. In the current study +LE extremities had on average 23% lower peak rate of force development compared to −LE extremities. Hopkins et al30 reported that patients with chronic functional ankle instability had on average 42% longer electromechanical delay than matched controls. In the current study, we found that +LE participants had on average 59% longer electromechanical delay than −LE participants.

Interestingly, the effect of injury on electromechanical delay was observed bilaterally for +LE participants, including those with unilateral injury. While electromechanical delay was affected bilaterally, grip strength and rate of force development were not similarly affected. It is possible that that these differences represent a baseline difference in those with LE versus those without. Similarly, Bisset et al16 observed bilateral deficits in reaction time in unilaterally injured participants and speculated that pain may cause cortical reorganization causing the impaired motor task on the injured side to be mapped on the non-injured side. It is plausible that patients with LE may have bilaterally altered motor neuron activity affecting muscle preactivation which results in longer electromechanical delay. Further research is needed to verify this hypothesis.

Pain or the fear of pain may prevent participants with LE from exerting their true maximal pain free effort during a gripping activity. We did inquire whether participants experience pain during testing and pain was not reported. It is possible that the decrease in ability to rapidly generate force and grip strength may be a protective adaptation but we are not able to elucidate this with the current study.

As expected, +LE extremities had less grip strength than −LE extremities, with both the Baseline and MAP dynamometer. The grip strength measurements were performed with the elbow extended as recommended by Dorf et al14 as grip strength is lower in elbow extension than flexion for patients with LE.14,38 MAP dynamometer grip strength magnitude was, on average, 38% lower than the Baseline grip strength measurement. These results are consistent with those reported previously by Irwin and Sesto.34 The difference in grip strength is attributed to the difference in the geometry of the handles of the dynamometers. The fingers are able to wrap around the handles of the Baseline dynamometer in a flexed position, while the metacarpophalangeal joints remain in a neutral position when grasping the MAP. This latter position is considered less biomechanically advantageous thereby causing a reduction in the MAP grip strength.

These findings are important in the context of rehabilitation for patients with LE. Clinicians frequently recommend an active rehabilitation program either alone or in conjunction with other treatments for LE.47 However, based on different exercises used as part of the rehabilitation treatment, different adaptations in motor performance may be observed.48 For example, Bisset et al16 reported reduced sensorimotor deficits despite improvements in grip strength following physical therapy treatment aimed at resolution of symptoms and improvement in grip strength and endurance.

Collectively both electromechanical delay and rate of force development are similarly affected by training. In general, the ability to rapidly produce force is most affected by exercises that incorporate a velocity dependent component and not solely resistive strengthening. It has been reported that following sensorimotor training involving balancing exercises on unstable bases an increase in the lower extremities ability to rapidly generate force is observed, while no increase in the maximal strength is observed.27,48 Conversely, following resistance training, strength improved considerably while minor increase in the rate of force development was observed.49 This suggests different adaptations for rate of force development and strength based on type of training. Grosset et al50 found that for the lower extremity, 10 weeks of plyometric training caused an increase in electromechanical delay while endurance training lead to shorter electromechanical delay. Rehabilitation interventions that address the recovery of both, rapid generation of force and maximal strength, may be more likely to benefit patients than those that focus solely on maximal strength. This may be particularly important to individuals who are returning to activities that involve rapid and forceful loading. Further research is needed to verify this hypothesis.

Limitations

The participants in this study were participating in a therapeutic trial and one of the inclusion criteria for this trial was that the participants have refractory LE. As a result, this study involved a small sample of participants with chronic LE. It is plausible that the reductions in sensorimotor and motor performance observed may be amplified in this sample because of the chronic nature of the condition. Therefore, the results of this study may not be generalizable to patients with LE of lesser duration. Further studies involving a larger number of participants with varied duration of symptoms may help elucidate the effect of LE on rate of force development and electromechanical delay in a more general LE patient population.

Only the radiologist was blinded to the status (case vs. control); the other assessors were not blinded and it was possible that they could affect the performance of the participants during various measurements. To minimize assessor bias during measurement, a standard operating procedure was developed and used. To investigate assessor bias for measurement of sensorimotor variables, two assessors calculated the variables from collected data and their intra-class correlation coefficient was found to be 0.99.

Conclusions

In addition to lower grip strength, +LE extremities have a lower rate of force development than non-affected (−LE) extremities while electromechanical delay is bilaterally reduced in participants with LE compared to controls. Collectively these changes may contribute towards increased reaction time in those with LE. These findings suggest that therapists may need to address both strength and ability to rapidly generate force in patients with LE. In patients with LE, it is plausible that improvements in rapid force generation may be associated with greater improvement in function than maximal strength but further research is required to address this hypothesis.

Acknowledgments

Funding Sources Drs. Sesto, Chourasia, and Buhr received support from the University of Wisconsin Clinical and Translational Science Award (NIH/NCRR 1 UL1RR025011). Dr Irwin was a postdoctoral fellow in the Department of Biomedical Engineering at the University of Wisconsin when this study was conducted and was partially supported by a T32 Women’s Health and Aging Research and Leadership Training Grant from the National Institute on Aging (AG000265). Dr.Rabago was partially supported by the American Academy Family Practice Foundation’s Research Committee Joint Grant Awards Program (G0810).

Footnotes

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Level of evidence: Not applicable

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Amrish O. Chourasia, Department of Biomedical Engineering, University of Wisconsin – Madison. 2107 Engineering Centers Building 1550 Engineering Dr Madison, WI 53706, USA amrishc@gmail.com Phone: 1-608-313-4166.

Kevin A. Buhr, Department of Biostatistics and Medical Informatics, University of Wisconsin – Madison. 211 WARF Office Building 610 Walnut Street Madison, WI 53726, USA buhr@biostat.wisc.edu Phone: 1-608-265-4587.

David P. Rabago, Department of Family Medicine, University of Wisconsin – Madison. Delaplaine Ct 1100 777 S Mills St Madison, WI 53715, USA david.rabago@fammed.wisc.edu Phone: 1-608- 845-9531.

Richard Kijowski, Department of Radiology, University of Wisconsin – Madison. Box 3252 Clinical Science Center-E3 600 Highland Ave Madison, WI 53792, USA r.kijowski@hosp.wisc.edu Phone: 1-608-264-3247.

Curtis B. Irwin, Trace Research and Development Center University of Wisconsin – Madison. 2106 Engineering Centers Building 1550 Engineering Dr Madison, WI 53706, USA irwin@cae.wisc.edu Phone: 1-608-263-5485.

Mary E. Sesto, Department of Orthopedics and Rehabilitation, University of Wisconsin – Madison. 2104 Engineering Centers Building 1550 Engineering Drive Madison, WI 53706, USA.

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