Dig Dis Sci (2013) 58:526–533 DOI 10.1007/s10620-012-2372-4
ORIGINAL ARTICLE
Decreased Neuromuscular Function in Crohn’s Disease Patients Is Not Associated with Low Serum Vitamin D Levels Amanda J. Salacinski • Miguel D. Regueiro Craig E. Broeder • Jean L. McCrory
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Received: 5 April 2012 / Accepted: 10 August 2012 / Published online: 5 September 2012 Ó Springer Science+Business Media, LLC 2012
Abstract Background Neuromuscular fatigue is a common complaint in Crohn’s disease (CD) patients. A correlation between serum vitamin D concentrations and neuromuscular function has been found in the elderly or nonambulant populations. Aims The aim of this study was to determine whether CD patients exhibit impaired neuromuscular function and if so, is there a link between vitamin D and neuromuscular function. Methods Crohn’s disease patients (n = 19) with at least one prior small bowel resection and matched controls (n = 19) underwent muscle strength and endurance testing, vitamin D, and nerve function analysis.
A. J. Salacinski (&) Department of Kinesiology and Physical Education, Northern Illinois University, 204 Anderson Hall, DeKalb, IL 60115, USA e-mail:
[email protected] M. D. Regueiro Inflammatory Bowel Disease Center, University of Pittsburgh Medical Center, PUH M2, C-Wing, 200 Lothrop St., Pittsburgh, PA 15213, USA e-mail:
[email protected] C. E. Broeder Exercising Nutritionally LLC, 4225 Naperville Rd, Naperville, IL 60565, USA e-mail:
[email protected] J. L. McCrory Division of Exercise Physiology, Department of Human Performance and Applied Exercise Science, West Virginia University, 8315 Robert C Byrd Health Science Center, South Building, PO Box 9227, Morgantown, WV 26506-9229, USA e-mail:
[email protected]
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Results Knee extension and flexion peak torque (Nm/kg) were greater in the control group than in the CD patients (P = 0.04 and 0.014, respectively. A significant difference was found between fatigue rates of the rectus femoris (P = 0.015) between CD patients and controls, but no difference was found in serum vitamin D levels between groups (P = 0.317). Knee extension and flexion torque measurements, with age as a covariate, were compared with high and low vitamin D levels. Those subjects with high serum vitamin D levels had a significantly greater extension peak torque (P = 0.045) and extension average torque (Nm/kg) (P = 0.014) than those with low levels. Conclusion Crohn’s disease patients with sufficient vitamin D levels experienced a 43 % greater extension peak torque. Although vitamin D deficiency has been associated with neuromuscular dysfunction, there were no differences in serum vitamin D levels between the CD and healthy controls to explain the decreased muscle strength. Keywords Crohn’s disease Vitamin D Muscle strength Fatigue
Introduction Within the past decade, researchers have reported anecdotal neuromuscular fatigue and low bone mineral density in patients with inflammatory bowel disease (IBD), with a higher prevalence in Crohn’s disease (CD) patients [1–4]. The mechanisms underlying the complaints of neuromuscular fatigue are not clearly defined [5–7]. Additionally, although muscle pain and bone pain are the chief complaints of CD patients, the magnitude of impairment in neuromuscular function is unknown [5]. A number of factors are associated with the possible
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decreased function in patients with CD, such as disease activity, nutrient malabsorption, corticosteroid therapy, calcium and vitamin D deficiency, cytokines, and overall poor nutrition [4, 5]. Few studies have focused on the reduced muscle function in patients with CD. Wiroth et al. [7] concluded that CD patients measured during clinical remission still exhibit decreased skeletal muscle strength compared to healthy controls. Norman et al. [8] also noted a decrease in muscle strength in CD patients in remission but observed that it was not present in all muscle groups. Wiroth et al. [7] found decreased leg strength in CD patients, but no difference in handgrip strength. In contrast, other researchers have reported decreased handgrip strength [9, 10]. Serum 25-hydroxyvitamin D [25(OH)D] level is positively correlated to muscle strength and physical function in individuals of all ages, especially the elderly [11–16]. The majority of the research performed to date on the relationship between vitamin D and neuromuscular function has been on older or infirm adults [16, 17]. Interestingly, elderly populations have reduced vitamin and mineral absorption rates [18], similar to CD patients with small intestine infection or resections. According to Grant and Holick [19], serum 25(OH)D levels of \20 ng/mL (50 nmol/L) can be considered deficient, 20–32 ng/mL (50–80 nmol/L) insufficient, and between 32 and 100 ng/ mL (80–250 nmol/L) sufficient. Bischoff-Ferrari et al. [13] found a positive correlation between 25(OH)D level and lower extremity strength in ambulatory older persons. Visser et al. [17] reported that low serum 25(OH)D concentration was related to losses in muscle strength and mass in older individuals over a 3-year time period. The average loss of handgrip strength over the 3-year study period was 7.7 kg [17]. It has been widely accepted that low serum 25(OH)D level is related to poor neuromuscular function [12, 20], but it remains unknown whether the mechanism for this decrement is primarily neural or muscle-related. There are a paucity of studies assessing nerve function in the presence of hypovitaminosis D. Patients with CD, especially those with small bowel resections, are at risk of developing hypovitaminosis D, secondary hyperparathyroidism, and fatigue [1, 2, 4]. No study to date has examined neuromuscular function in relation to vitamin D status in CD patients. Understanding the relationship between 25(OH)D levels and muscular strength, excessive fatigue, nerve conduction velocity, and quality of life in CD may lead to treatment paradigm recommendations to increase vitamin D levels and therefore improve neuromuscular function. Additionally, there currently no objective recommendation for strength training or dietary intake of vitamin D specifically for those patients with CD [21, 22].
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Therefore, the aim of this study was twofold: (1) to examine whether neuromuscular function is reduced in CD patients based on physiological testing; (2) to evaluate whether low 25(OH)D concentrations are present concurrently with neuromuscular dysfunction in CD patients compared to healthy controls.
Methods Subject Characteristics Nineteen individuals with CD having a minimum of at least one small bowel resection and a minimum disease duration of 5 years and 19 gender- and age-matched healthy controls participated in the study. There were nine males and ten females in each group, bringing the total study cohort to 18 males and 20 females, between the ages of 27 and 62 years. The CD patients were recruited from the IBD Center at University of Pittsburgh Medical Center (UPMC) Presbyterian Hospital and were under the clinical care of a single gastroenterologist (MR). The normal healthy controls were recruited via flyers posted in the gastroenterologist’s office, hospital research boards and research email registry, and university advertisement boards, and from the local Pittsburgh community. Subject demographics are shown in Table 1. Inclusion criteria for CD patients were at least one small bowel resection, idiopathic musculoskeletal pain or weakness, and a disease history of at least 5 years. Exclusion criteria for all subjects, regardless of group, included oral vitamin D supplementation, exposure to UVB tanning beds within the last year, history of diabetes, known knee pain or anterior cruciate ligament pathology, and a history of neuromuscular disease. Any individual who had a pacemaker or an intravenous port was excluded, as was any individual who had been diagnosed with severe psoriasis or sprue or had a known neuromuscular disorder. CD patients were excluded if the individuals were currently taking more than 20 mg of metronidazole because of its effects on peripheral neuropathy. Study Protocol The Institutional Review Board of the University of Pittsburgh approved all procedures in the protocol in accordance with the Helsinki Declaration. All patients gave written informed consent prior to all testing procedures. Blood was obtained from each subject for measurement of serum 25(OH)D. All testing of CD patients and matched controls took place during the months of October and beginning of November to control for seasonal variation in serum vitamin D levels.
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Table 1 Subject demographics Group
Age (years)
Mass (kg)
Height (cm)
Body mass index (kg/m2)
Crohn’s patients (n = 19)
44.16 (10.28)
77.30 (19.45)
168.58 (15.27)
27.45 (7.20)
Healthy controls (n = 19)
41.68 (11.19)
78.89 (17.31)
173.26 (11.47)
26.88 (6.17)
Data are presented as mean (SD)
Serum Vitamin D Concentration A licensed phlebotomist obtained a sample of each subject’s blood in order to assess the concentration of serum 25(OH)D. A resting venous blood sample (15 mL) was drawn from a forearm vein and immediately stored at -70 °C in a freezer (Revco Model ULT2186-5, 230 V; Thermo Fisher Scientific, Waltham, MA). The samples were packed in dry ice and shipped to a laboratory at the Boston School of Medicine, under the direction of Dr. Michael Holick, for analysis. Blood serum 25(OH)D levels were analyzed by radioimmunoassay using the gold standard high-performance liquid chromatography technique. Low 25(OH)D levels were considered to be deficient when \20 ng/mL (50 nmol/L) and insufficient when between 20 and 32 ng/mL (50–80 nmol/L) [19]. Muscle Strength Maximal isometric strength of the knee flexors and extensors on the subject’s left side was measured using a customized strength-testing device which included a tension/compression load cell attached to a custom-designed chair (Fig. 1). The device was designed to test the subject’s left side because it is typically the non-dominant side of the lower extremity. Pilot testing in our laboratory has determined that the output of the chair has an interclass correlation coefficient of 0.91 with that of a Biodex dynamometer. The load cell was connected to a National Instruments (Austin, TX) A/D board located inside a computer. Labview 7.0 software (National Instruments) was used to collect the data. The subject was seated such that his/her hip was flexed to 90° and the knee was flexed to 45°. The load cell was positioned just proximal to the malleoli. The subject’s left knee was aligned with the axis of the device. The subject was secured to the chair with straps at the hips and shoulders to prevent extraneous movement. All subjects were instructed to either place their arms in their laps or cross them over their chest, but they were not permitted to hold onto the device. A 5-s resting trial was performed in order to calculate gravity-effect torque. Subjects were asked to perform three repetitions of maximal isometric knee flexion lasting 5 s each. They were provided with standardized encouragement
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Fig. 1 The customized designed strength chair
during the trial, such that the word ‘‘push’’ or ‘‘pull’’ was said loudly to the subject at each second during the test. A 30-s rest interval was allowed between contractions. Subjects then were asked to perform three repetitions, each lasting 5 s, of maximal isometric knee extension; again 30 s were allowed between contractions. Data were collected at 100 Hz and filtered with a fourth-order low-pass Butterworth filter with a cutoff frequency of 10 Hz. Peak torque was calculated as the peak force read by the load cell during the trial multiplied by the distance from the knee to the load cell. Peak torque normalized to body weight was calculated, as well as average torque, and the average torque normalized to body weight for both knee flexion and extension. Muscle Fatigue Fatigue rates of the vastus lateralis (VL) and rectus femoris (RF) on the subject’s left side were assessed by surface
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electromyography (EMG) in accordance with previously used methods [23, 24]. The bipolar Ag/AgCl electrodes were applied to the skin parallel to the alignment of the muscle fibers with an inter-electrode distance of 20 mm. A ground electrode was placed on the skin superficial to the long axis of the tibia on the anterior shin. The approach monitored median frequency from the electrode sites during a sustained sub-maximal contraction. Fatigue was assessed with a Noraxon MyoSystem (model Telemyo; Noraxon USA, Scottsdale, AZ). Subjects were instructed to perform a 60-s submaximal isometric contraction at 60 % of their maximum knee extension torque as assessed previously in the muscle strength tests. The 60 % level was shown to subjects via a computer-generated line on the computer monitor. EMG data were collected at 1,024 Hz. The EMG signal was amplified (gain 500) and filtered (500- to 10,000-Hz band pass Butterworth filter, common mode rejection ratio of 130 dB). Matlab software (Mathworks, Natick, MA) was used to determine the median muscle activation frequency for every second of data. Each muscle activation frequency point was normalized against the initial muscle activation frequency to the maximal voluntary contraction and then plotted, with time on the X-axis and muscle activation frequency on the Y-axis. The slope of this line determined the fatigue rate. The latency and amplitude of peroneal nerve conduction was assessed with an automated electrophysiological neurodiagnostic device (BrevioÒ NCS-Monitor; NeuMed, West Trenton, NJ). The left leg was tested to maintain consistency with the muscular strength and endurance testing data. The active electrode was placed over the belly of the extensor digitorum brevis muscle. The reference was then attached at the side of the small toe, distal to the extensor digitorum brevis muscle, and the ground was attached at the distal tibia. Data Analysis Statistical analysis of the data was performed with SPSS ver. 16.0 (SPSS, Chicago, IL) and JMP 8.0 (SAS, Cary, N.C.) software. The dependent variables included 25(OH)D, isometric knee extension and flexion torque, quadriceps fatigue rates, peroneal nerve latency and amplitude, and an assessment of each subject’s quality of health. Descriptive statistics were generated for each subject, and a two-factor analysis of variance (group 9 gender) for differences between the CD patients and the healthy controls was performed for each of these measured variables. The alpha level set at 0.05 for all statistical analyses. JMP software was used to run secondary analyses using age as a covariate.
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Results The experimental means for the participants in the CD group and control group for each of the measured variables are presented in Table 2. The serum 25(OH)D was not statistically different between the CD patients and the healthy control group (P = 0.317). Only 10.5 % of the CD patients had deficient levels of 25(OH)D and 37 % of the CD patients tested were insufficient. Of the 19 controls, 37 % had sufficient levels of 25(OH)D, while 37 % had insufficient levels. Only one control was deficient in 25(OH)D levels. The controls displayed significantly greater knee extension peak torque (Nm) than CD patients (P = 0.013), with the mean extension peak torque for the CD patients being 29 % less than that of the healthy controls. Similarly, controls demonstrated significantly greater flexion strength (Nm) than the CD patients (P = 0.001), with the mean flexion peak torque (Nm) in the CD patients tested being just more than half that of the healthy controls. When normalized to body weight, the knee extension and flexion peak torque (Nm/BW) was also significantly greater in the control group than in CD patients P = 0.039 and 0.022, respectively). Additionally, there was a significant difference between the fatigue rates of the RF (Hz/s) (P = 0.015), but not the VL (Hz/s) (P = 0.969), between the CD patients and the control patients. The RF fatigue rate of the control group was almost 40 % greater than that of the CD patients. Our assessment of peroneal nerve function revealed no statistical difference between the CD patients and the healthy controls for the latency of peroneal nerve activity (ms) (P = 0.565). However, there was a trend towards significance (P = 0.067) between the nerve signal amplitude (Log amp) of the CD patients and the healthy controls, with the amplitude of the peroneal nerve signal being larger in the control group. For all variables measured there was no gender 9 group interaction. The males were stronger than the females for extension peak torque (Nm) (P = 0.003), extension average torque (Nm) (P = 0.0002), and extension average torque normalized to body weight (Nm/BW) (P = 0.026). The males were stronger than the females for flexion peak torque (Nm) (P = 0.006), average flexion torque (Nm) (P = 0.003), and average flexion torque normalized to body weight (Nm/BW) (P = 0.043). Post hoc analysis adjusting for age was performed on JMP 8.0 software. Knee extension and flexion torque measurements, with age as a covariate, were compared between those individuals serum 25(OH)D levels of C40 ng/dL (n = 12) versus those with 25(OH)D levels of \32 ng/dL (n = 19). The C40 ng/dL group had a
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Table 2 Serum 25-hydroxyvitamin D levels and neuromuscular variables in Crohn’s disease patients and controls Variables Serum 25(OH)D (ng/mL) Extension peak torque (Nm) Extension peak torque normalized to bodyweight (Nm/kg) Extension average torque (Nm) Extension average torque normalized to bodyweight (Nm/kg) Flexion peak torque (Nm) Flexion peak torque normalized to bodyweight (Nm/kg) Flexion average torque (Nm) Flexion average torque normalized to bodyweight (Nm/kg)
Crohn’s disease group
Control group
P value 0.317
32.0 (9.1)
35.3 (11.1)
n = 19
n = 19
75.24 (45.39)
105.55 (40.66)
n = 19
n = 19
0.059 (0.031)
0.070 (0.028)
n = 19
n = 19
55.91 (35.55)
76.68 (30.58)
n = 19
n = 19
0.044 (0.023)
0.057 (0.019)
0.013 0.039 0.023 0.052
n = 19
n = 19
27.23 (10.66) n = 19
53.71 (27.27) n = 19
0.001 0.022
0.023 (0.010)
0.039 (0.019)
n = 19
n = 19
19.61 (8.06)
39.26 (20.29)
n = 19
n = 19
0.16 (0.01) n = 19
0.03 (0.01)
0.001 0.063
n = 19 Rectus femoris fatigue rate (Hz/s)
-0.069 (0.06)
-0.142 (0.09)
n = 14
n = 18
Vastus lateralis fatigue rate (Hz/s)
-0.028 (0.042)
-0.027 (0.085)
n = 16
n = 19
Nerve latency (ms) Nerve amplitude (Log mV)
4.28 (1.75)
4.81 (1.61)
n = 13
n = 14
0.216 (0.360)
0.441 (0.186)
n = 13
n = 14
0.015 0.969 0.555 0.067
25(OH)D Serum 25-hydroxyvitamin D Data are presented as the mean, with the standard deviation (SD) in parenthesis
significantly greater extension peak torque (P = 0.045), a significantly greater extension peak torque normalized to body weight (P = 0.043), and a significantly greater extension average torque normalized to body weight (P = 0.014), than those with low serum 25(OH)D. The adjusted means for the post hoc analysis are presented in Table 3.
Discussion The aim of our study was to examine whether CD patients have decreased neuromuscular function and strength compared to healthy controls. Our results indicate a decrease in muscle strength among our CD patients compared to the healthy controls. This decreased muscle strength of the CD patients is indicative of a decreased neuromuscular function. When torque was normalized to the subject’s body weight, the CD patients still experienced a decrease in muscle strength. Wiroth et al. [7] reported
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similar findings using a leg press, and other researchers have used hand grip strength [8, 9]. The comparison of lower limb muscle strength is a more reliable estimate of overall body strength because about 70–80 % of the total body mass is estimated to come from the muscles of the lower body, and decreases due to aging seem to affect the legs, while arm strength is preserved [7, 25]. Silva et al. [26] tested knee isometric muscle strength at the same 45° angle as tested in our study and found the average extension peak torque to be 105.9 [standard deviation (SD) 35.2] Nm and flexion peak torque to be 63.9 (SD 32.8) Nm in healthy young and older controls. The average knee extension torque for the CD patients in our study was 75.2 (SD 45.4) Nm, and average flexion peak torque was 27.23 (SD 10.7) Nm. In another study, community dwelling healthy older individuals aged 65–70 years, tested with the same equipment used in our study, had an average of extension peak torque of 94.0 (SD 28.1) Nm and an average flexion peak torque of 37.0 (SD 17.8) Nm [27].
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We also examined 25(OH)D levels, but did not find 25(OH)D to be deficient in the CD patients according to current standards compared to controls. To our knowledge, no studies have investigated the effects 25(OH)D on neuromuscular function in patients with CD, but the prevalence of 25(OH)D deficiency in patients with CD in clinical remission has been established [1, 11, 16, 17, 22, 28–33]. We found that low levels (but not considered to be deficient) of 25(OH)D were a common finding in our study, which is in agreement with previous studies. Several cross-sectional studies have shown the 1,25hydroxyvitamin D level and low 25(OH)D level are related to lower muscle strength [11, 17, 34]. Other researchers have reported that CD patients have decreased muscle function, especially in their lower limbs [7]. Wiroth et al. [7] concluded that CD patients in clinical remission experience a decrease in skeletal muscle strength and endurance. Developing peak strength requires optimizing the neural drive to activate the maximum number of motor units. Few subjects in our study cohort experienced low serum 25(OH)D levels. According to Grant and Holick [19], serum 25(OH)D levels of \20 ng/mL (50 nmol/L) can be considered to be deficient, 20–32 ng/mL (50–80 nmol/L) insufficient, and between 32 and 100 ng/mL (80–250 nmol/L) sufficient. The criteria for serum 25(OH)D concentrations were set according to the breakpoints of physiological response as a means to help explain the response. According to these criteria, only 10.5 % of the CD patients tested in our study were deficient in terms of 25(OH)D, while 36.8 % of the CD patients tested were insufficient. Vitamin D deficiency is classified as a level at which osteomalacia occurs; insufficient vitamin D ranges are those at which there begins an inadequate absorption of calcium to maintain the necessary levels of circulating calcium [19]. While patients with CD exhibited lower strength than the control group, they did not exhibit lower serum 25(OH)D levels. Therefore, the lower maximum muscle strength for the CD patients was not reflective of a lower 25(OH)D level, which is contrary to our hypotheses. Thus, the mechanism responsible for this lower strength remains unknown and was not detected in our study. Visser et al. [17] observed that subjects with 25(OH)D levels of 50–74.9 nmol/L (20–32 ng/L) were twofold more likely to experience a decreased grip strength compared to those individuals with levels of [75 nmol/L. BischoffFerrari et al. [13] stated that the serum 25(OH)D level should be at least 40 nmol/L, but that the most advantageous concentrations are between 90 and 100 nmol/L (40 ng/dL). Because this level is difficult for some to achieve, the target level is 75 nmol/L (32 ng/dL). The controversy over the significance of vitamin D levels in relation to various pathologies is considered to be a current
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limitation of vitamin D research. In addition, because normal aging independently attenuates nutrient absorption rates, it may be important to covariate age in studies aimed at determining the neuromuscular effects of CD. Therefore, in our post hoc analysis we used age as a covariate. When we compared knee extension and flexion torque between individuals with a serum 25(OH)D level of C40 ng/dL and those with a serum 25(OH)D level of \32 ng/dL, the C40 ng/dL group had a 43 % higher extension peak torque, a 53 % greater extension peak torque normalized to body weight, and a 46 % higher extension average torque normalized to body weight than those with low serum 25(OH)D. Table 3 shows the adjusted means. Those individuals with serum 25(OH)D levels between 32 and 40 ng/dL were not included in the post hoc analysis with age as a covariate, based on set criteria [13, 17]. We found CD patients to exhibit less fatigue of the RF than the control subjects, which was contrary to our original hypothesis. The CD patients in our study did exhibit significantly less knee extension strength than the controls. Therefore, the fatigue rate of the patients tested may not have been as high because a CD subject in this study would have not exerted as much raw force to hold a percentage of 60 % of their maximum strength. When we compared the CD patients to controls for leg extension and flexion peak torque normalized to body weight as covariates, the fatigue difference between the groups only approached significance (P = 0.06). Corresponding with this finding was the fact that we found the peroneal nerve amplitude signal was 51 % greater in the controls than in the CD patient group (P = 0.067). This suggests that attenuation in neuromuscular nerve function may have contributed to our findings that CD patients had reduced peak and average torque values compared to controls. These findings are similar to those reported earlier, based on which the respective authors concluded that poor peripheral nerve function was associated with a decrease in muscle strength of the lower body in ambulatory community-dwelling older adults [35] and with autonomic neuropathy found in CD subjects [36, 37]. Vitamin D deficiency is thought to be multifactorial and may involve insufficient vitamin D intake, inadequate sun exposure, malabsorption of vitamin D, depletion of bile acids, faulty conversion of the active forms of vitamin D, and excessive loss of vitamin D [2, 33]. It is possible that we were unable to show a significant difference in the incidence of 25(OH)D deficiency between the CD patients and the controls because of the small sample size of the study. The number of subjects in our study was low, which is a limitation of the study. A number of confounding variables of the disease, such as dietary intake of vitamin D, length of the small bowel resection and, in some cases,
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Table 3 Age neuromuscular variables for the adjusted means for those subjects with low and high 25(OH)D Variables
High 25(OH)D (n = 12)
Low 25(OH)D (n = 19)
P value
Serum 25(OH)D (ng/mL)
45.43 (1.38)
25.31 (1.09)
0.001
Extension peak torque (Nm)
113.97 (12.73)
79.67 (10.09)
0.045
Extension peak torque normalized to body weight (Nm/kg)
0.088 (0.007)
0.057 (0.006)
0.045
Extension average torque (Nm)
81.70 (10.10)
59.67 (8.00)
0.100
Extension average torque normalized to body weight (Nm/kg)
0.064 (0.006)
0.043 (0.004)
0.014
Flexion peak torque (Nm)
46.49 (7.35)
40.73 (5.83)
0.545
Flexion peak torque normalized to body weight (Nm/kg)
0.036 (0.004)
0.031 (0.003)
0.400
Flexion average torque (Nm)
33.67 (5.52)
29.44 (4.38)
0.554
Flexion average torque normalized to body weight (Nm/kg)
0.03 (0.00)
0.02 (0.00)
0.414
Rectus femoris fatigue rate (Hz/s)
-0.125 (0.023)
-0.092 (0.020)
0.277
Vastus lateralis fatigue rate (Hz/s)
n = 11 -0.020 (0.023)
n = 15 -0.028 (0.020)
0.799
n = 11
n = 15
2.36 (10.10)
-9.19 (8.06)
n=9
n = 14
0.59 (0.08)
0.24 (0.07)
n=9
n = 14
Nerve latency (ms) Nerve amplitude (Log mV)
0.386 0.004
Data are presented as the mean, with the SD in parenthesis
medication use, which could not be controlled are another limitation of the study. CD is a multifactorial disease in itself, and the unique lifestyle of each patient makes a comparison to healthy controls almost impossible. Although we could not show a significant difference between CD patients and controls with regard to 25(OH)D deficiency, vitamin D deficiency is thought to be an important complication in patients with CD [11, 17, 22, 28, 29, 34, 38]. All of the CD patients were considered to be in clinical remission, having the disease for at least 5 years, and having at least one small bowel resection. Future studies need to be conducted to determine the exact mechanism responsible for the lower muscle strength in patients with CD disease. In conclusion, the CD patients participating in our study showed reduced skeletal muscle strength, greater muscle endurance in the RF muscle group, and less endurance in the VL than the control subjects. Vitamin D concentrations cannot be held responsible for the observed differences in neuromuscular performances between CD patients and controls. The multifactorial nature of the disease, which is associated with the use of glucocorticoids, immunosuppressive drugs, and length of small bowel resections, among others, may affect the differences in the neuromuscular performance of these patients. Further research is needed to identify the exact mechanisms of action for lower muscular strength. Nevertheless, understanding the etiology of the reduced strength in CD patients is important to enhancing their quality of life.
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Acknowledgments The authors received grant support from University of Pittsburgh’s Department of Health and Physical Activity Graduate Student Research Award: $1,500.00. Conflict of interest
None.
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