Exercise-induced Muscle Pain Research Articles

Transcranial direct current stimulation improves isometric time to exhaustion of the knee extensors

Transcranial direct current stimulation (tDCS) can increase cortical excitability of a targeted brain area, which may affect endurance exercise performance. However, optimal electrode placement for tDCS remains unclear. We tested the effect of two different tDCS electrode montages for improving exercise performance. Nine subjects underwent a control (CON), placebo (SHAM) and two different tDCS montage sessions in a randomized design. In one tDCS session, the anodal electrode was placed over the left motor cortex and the cathodal on contralateral forehead (HEAD), while for the other montage the anodal electrode was placed over the left motor cortex and cathodal electrode above the shoulder (SHOULDER). tDCS was delivered for 10min at 2.0mA, after which participants performed an isometric time to exhaustion (TTE) test of the right knee extensors. Peripheral and central neuromuscular parameters were assessed at baseline, after tDCS application and after TTE. Heart rate (HR), ratings of perceived exertion (RPE), and leg muscle exercise-induced muscle pain (PAIN) were monitored during the TTE. TTE was longer and RPE lower in the SHOULDER condition (P<0.05). Central and peripheral parameters, and HR and PAIN did not present any differences between conditions after tDCS stimulation (P>0.05). In all conditions maximal voluntary contraction (MVC) significantly decreased after the TTE (P<0.05) while motor-evoked potential area (MEP) increased after TTE (P<0.05). These findings demonstrate that SHOULDER montage is more effective than HEAD montage to improve endurance performance, likely through avoiding the negative effects of the cathode on excitability.

Effects of caffeinated chewing gum on muscle pain during submaximal isometric exercise in individuals with fibromyalgia

Physical activity is important to manage symptom of fibromyalgia (FM); however, individuals with FM typically experience augmented muscle pain during exercise. This study examined the effects of caffeinated chewing gum on exercise-induced muscle pain in individuals with FM. This study was conducted with a double-blind, placebo-controlled, cross-over design. Twenty-three patients with FM completed a caffeine condition where they consumed a caffeinated chewing gum that contains 100mg of caffeine, and a placebo condition where they consumed a non-caffeinated chewing gum. They completed isometric handgrip exercise at 25% of their maximal strength for 3min, and muscle pain rating (MPR) was recorded every 30s during exercise. Clinical pain severity was assessed in each condition using a pain questionnaire. The order of the two conditions was randomly determined. MPR increased during exercise, but caffeinated chewing gum did not attenuate the increase in MPR compared to placebo gum. Clinical pain severity was generally associated with the average MPR and the caffeine effects on MPR, calculated as difference in the average MPR between the two conditions. The results suggest that more symptomatic individuals with FM may experience greater exercise-induced muscle pain, but benefit more from caffeinated chewing gum to reduce exercise-induced muscle pain.

Effects of MSM on exercise-induced muscle and joint pain: a pilot study

Background Participants in organized running commonly experience muscle and joint pain while training for and competing in distance events. Many runners report pain as a major influence on changes or breaks in training regimens, and as a common deterrent for returning to exercise after a break. Methylsulfonylmethane (MSM) is a sulfurbased nutritional supplement shown through several clinical trials to be effective in reducing pain associated with osteoarthritis, and to exhibit anti-inflammatory properties. To further investigate the role of MSM in pain management, this randomized, double-blind, placebo-controlled study evaluated the effects of MSM supplementation on exercise-induced muscle and joint pain.

Re: Sodium Valproate-Induced Myopathy in a Child.

Sir, I read with interest the letter to the editor by Ahmed published in the SQUMJ February 2015 issue.1 The patient, after a diagnosis of childhood-onset epilepsy with absence seizures, was started on 250 mg of sodium valproate in two divided doses (20 mg/kg). As response to treatment was inadequate, the dose of the drug was gradually increased over the following weeks to the maximum permissible dose of 500 mg twice daily.1 Six months later, slowly developing myopathy was observed. Based on the clinical picture, a myopathic needle electromyography pattern and low serum carnitine levels, the author attributed the myopathy to carnitine deficiency secondary to valproate therapy.1 Nakajima et al. reported that the long-term treatment of paediatric patients with sodium valproate could have an impact on specific acylcarnitines and proposed that this effect is augmented by simultaneous use of other anticonvulsants.2 However, they also noted that valproylcarnitine formation through the use of therapeutic sodium valproate seems insufficient for the development of severe carnitine deficiency.2 Hence, such biochemical changes in acylcarnitines in children are not clinically significant.2,3 I presume that the development of myopathy in the patient described by Ahmed cannot be solely attributed to valproate therapy, as the drug was prescribed at permissible doses.1 The myopathy in the studied patient may be due to a carnitine palmitoyltransferase (CPT) II deficiency. This condition leads to a disorder of long-chain fatty-acid oxidation.4 There are several clinical presentations of CPT II deficiency, including the myopathic form, which is usually mild and can manifest from infancy to adulthood. Myopathic CPT II deficiency can be associated with myoglobinuria and manifest as exercise-induced muscle pain and weakness.4 There is evidence that valproate is among the factors that trigger myopathy in CPT II-deficient patients.4 Tandem mass spectrometry are used to measure serum and plasma acylcarnitines.3 Reduced CPT enzyme activity indicate a definitive diagnosis. However, new advances in molecular genetic testing have provided an improved non-invasive diagnostic method with the presence of the carnitine palmitoyltransferase 2 gene (the only gene associated with CPT II deficiency).4 Although, to the best of my knowledge, no studies yet exist which investigate CPT II deficiency in Saudi Arabia, the high prevalence of consanguinity in this region might be a strong indicator of its potential existence.5 Consanguinity is significantly associated with various patterns of inborn errors of the metabolism.6 A myopathic form of CPT II deficiency ought to be seriously considered for this reported patient and suitable laboratory tests employed.1 However, the patient reported by Ahmed could still be included among the paediatric valproate-associated myopathy cases reported in the literature.1 Valproate is a broad-spectrum antiepileptic drug. In high-risk patients, carnitine supplementation with combined antiepileptic drug therapy, carnitine-free enteral tube feeding and the maintenance of a healthy body weight have been recently recommended to prevent epilepsy-related complications.7 However, controlled, randomised and multicentre studies are needed to investigate the therapeutic and prophylactic roles and the optimal administration of carnitine supplementation during valproate therapy.

Interleukin-10 limits intense acute swimming-induced muscle mechanical hyperalgesia in mice.

What is the central question of this study? This study investigated the role of the endogenous anti-inflammatory cytokine interleukin-10 in intense acute swimming-induced muscle mechanical hyperalgesia in mice. What is the main finding and its importance? Endogenous interleukin-10 has a key role in limiting exercise-induced muscle pain in a model presenting similarities to delayed-onset muscle soreness in mice. Interleukin-10 reduced muscle pain by diminishing leucocyte recruitment, hyperalgesic cytokine production, oxidative stress and myocyte damage. Interleukin-10 (IL-10) is an antihyperalgesic cytokine. In this study, IL-10-deficient (IL-10(-/-) ) mice were used to investigate the role of endogenous IL-10 in intense acute swimming-induced muscle mechanical hyperalgesia, which presents similarities with delayed-onset muscle soreness. An intense acute swimming session of 1 or 2h induced significant muscle mechanical hyperalgesia in a time-dependent manner in wild-type mice compared with the sham group 24h after the session, which was further increased in IL-10(-/-) mice (P˂0.05). Intraperitoneal treatment of wild-type mice with IL-10 (1-10ng) reduced muscle mechanical hyperalgesia in a dose-dependent manner and reversed the enhanced muscle hyperalgesia in IL-10(-/-) mice (P˂0.05). The 2h swimming session induced increases in tumour necrosis factor-α, interleukin-1β and IL-10 production in the soleus muscle. However, tumour necrosis factor-α and interleukin-1β production in the soleus muscle were even higher in IL-10(-/-) mice between 2 and 6h after the stimulus (P˂0.05). There was no statistical difference in the levels of the antihyperalgesic cytokines interleukin-4, interleukin-5, interleukin-13 and transforming growth factor-β between wild-type and IL-10(-/-) mice (P˃0.05). Interleukin-10 deficiency also resulted in increased myeloperoxidase activity, greater depletion of reduced glutathione levels, increased superoxide anion production and the maintenance of high plasma concentrations of creatine kinase (until 24h after the swimming session) in soleus muscle (P˂0.05). These results demonstrate that endogenous IL-10 controls intense acute swimming-induced muscle mechanical hyperalgesia by limiting oxidative stress and cytokine production.

G.P.190: Multiple deletions in mitochondrial DNA in myofibrillar myopathy and centronuclear myopathy

Multiple deletions in mitochondrial DNA (mtDNA) are associated with mutations in nuclear genes which encode proteins either directly or indirectly involved in the replication or maintenance of mtDNA. To date, mutations in twelve nuclear genes, POLG, POLG2, C10orf2, SLC25A4, RRM2B, TK2, MPV17, DGUOK, OPA1, MFN2, MGME1, and DNA2 have been identified in patients with multiple deletions in mtDNA, yet the genetic cause of multiple mtDNA deletions still remains undefined in a large number of patients. In addition to patients with a classic mitochondrial myopathy, multiple mtDNA deletions are also found in patients with myopathies such as sporadic IBM. Mitochondrial changes have also been identified in skeletal muscle from patients with myofibrillar myopathy, with histochemical changes such as rubbed out fibres observed with COX and NADH staining, and focal clustering and depletion of mitochondria. Mitochondrial pathology, including COX negative and ragged red fibres, and paracrystalline inclusions have also been described in patients with centronuclear myopathy due to mutations in DNM2, which encodes Dynamin 2, a GTPase which is involved in membrane trafficking. Here we describe our findings in two patients with multiple mtDNA deletions. In one patient, a 70 year old male who presented with a history of exercise induced muscle pain and distal myopathy we identified a novel pArg2364His mutation in the gene FLNC which encodes the actin binding protein filamin-C. In the second patient, a 40 year old male who presented at age 3 years with ataxia and later developed facial myopathy, proximal muscle weakness, and CPEO, histochemical investigation indicated centronuclear myopathy, and a p.Glu560Lys mutation in DNM2 was identified. Our findings suggest that FLNC and DNM2 should be added to the list of genes associated with multiple deletions in mtDNA.

Targeting interleukin-1β reduces intense acute swimming-induced muscle mechanical hyperalgesia in mice

The role of interleukin (IL)-1β in intense acute swimming-induced muscle mechanical hyperalgesia was investigated in mice. Untrained mice were submitted to one session of intense acute swimming for 120 min or were submitted to sham conditions (30 s exposure to water), and muscle mechanical hyperalgesia (before and 6-48 h after swimming session), IL-1β production (skeletal muscle and spinal cord), myeloperoxidase activity, reduced glutathione (GSH) levels (skeletal muscle and spinal cord), and cortisol, glucose, lactate and creatine kinase (CK) levels (plasma) were analysed. Intense acute swimming-induced muscle mechanical hyperalgesia was dose-dependently inhibited by IL-1ra treatment. IL-1β levels were increased in soleus, but not gastrocnemius muscle and spinal cord 2 and 4 h after the session, respectively. Intense acute swimming-induced increase of myeloperoxidase activity and reduced GSH levels in soleus muscle were reversed by IL-1ra treatment. In the spinal cord, exercise induced an increase of GSH levels, which was reduced by IL-1ra. Finally, IL-1ra treatment reduced plasma levels of CK, an indicator of myocyte damage. IL-1β mediates intense acute swimming-induced muscle mechanical hyperalgesia by peripheral (soleus muscle) and spinal cord integrative mechanisms and could be considered a potential target to treat exercise-induced muscle pain.

Active Wii Gaming Reduces Exercise Induced Muscle Pain

Active Wii Gaming Reduces Exercise Induced Muscle Pain

Does exercise induce hypoalgesia through conditioned pain modulation?

Pain sensitivity decreases with exercise. The mechanisms that underlie this exercise-induced hypoalgesia (EIH) are unclear. Our purpose was to investigate conditioned pain modulation (CPM) as a potential mechanism of EIH. Sixteen women completed pain testing during three sessions: painful exercise, nonpainful exercise, and quiet rest. Intensity and unpleasantness ratings to noxious heat stimuli were assessed at baseline and during and following each session. Results showed that pain sensitivity decreased significantly during both exercise sessions (p < .05), but not during quiet rest. Effect size calculations showed that the size of the hypoalgesic response was greater following painful exercise than nonpainful exercise. Our results suggest that exercise-induced muscle pain may contribute to the magnitude of EIH. However, as pain sensitivity also decreased following nonpainful exercise, CPM is not likely the primary mechanism of EIH.

Catechol-O-Methyltransferase and psychological interactions predict exercise induced muscle pain phenotypes

COMT represents one of the most frequently studied pain candidate genes. Considerable evidence demonstrates associations of COMT SNPs and haplotype’s with both clinical and experimental pain responses. Furthermore, in our previous work, COMT haplotypes interacted with catastrophizing to influence both clinical and exercise-induced shoulder pain; however, whether these interactions extend to COMT SNPs and other psychological constructs has not been explored. In this analysis our objective was to determine how COMT SNPs and haplotypes interact with pain relevant psychological factors for different exercise induced muscle pain phenotypes.

Regular physical activity prevents development of chronic pain and activation of central neurons.

Chronic musculoskeletal pain is a significant health problem and is associated with increases in pain during acute physical activity. Regular physical activity is protective against many chronic diseases; however, it is unknown if it plays a role in development of chronic pain. The current study induced physical activity by placing running wheels in home cages of mice for 5 days or 8 wk and compared these to sedentary mice without running wheels in their home cages. Chronic muscle pain was induced by repeated intramuscular injection of pH 4.0 saline, exercise-enhanced pain was induced by combining a 2-h fatiguing exercise task with a low-dose muscle inflammation (0.03% carrageenan), and acute muscle inflammation was induced by 3% carrageenan. We tested the responses of the paw (response frequency) and muscle (withdrawal threshold) to nociceptive stimuli. Because the rostral ventromedial medulla (RVM) is involved in exercise-induced analgesia and chronic muscle pain, we tested for changes in phosphorylation of the NR1 subunit of the N-methyl-D-aspartate (NMDA) receptor in the RVM. We demonstrate that regular physical activity prevents the development of chronic muscle pain and exercise-induced muscle pain by reducing phosphorylation of the NR1 subunit of the NMDA receptor in the central nervous system. However, regular physical activity has no effect on development of acute pain. Thus physical inactivity is a risk factor for development of chronic pain and may set the nervous system to respond in an exaggerated way to low-intensity muscle insults.

Sex Differences in Exercise-Induced Muscle Pain and Muscle Damage

There is uncertainty about sex differences in exercise-induced muscle pain and muscle damage due to several methodological weaknesses in the literature. This investigation tested the hypothesis that higher levels of exercise-induced muscle pain and muscle damage indicators would be found in women than men when several methodological improvements were executed in the same study. Participants (N = 33; 42% women) with an average age of 23 years (SD = 2.82) consented to participate. After a familiarization session, participants visited the laboratory before and across 4 days after eccentric exercise was completed to induce arm muscle pain and muscle damage. Our primary outcomes were arm pain ratings and pressure pain thresholds. However, we also measured the following indicators of muscle damage: arm girth; resting elbow extension; isometric elbow flexor strength; myoglobin (Mb); tumor necrosis factor (TNFa); interleukin 1beta (IL1b); and total nitric oxide (NO). Temporary induction of muscle damage was indicated by changes in all outcome measures except TNFa and IL1b. In contrast to our hypotheses, women reported moderately lower and less frequent muscle pain than men. Also, women's arm girth and Mb levels increased moderately less than men's, but the differences were not significant. Few large sex differences were detected. PerspectiveLower muscle pain among women than men was detected with corresponding, but nonsignificant sex differences in other muscle damage indicators. Methodological advances may have improved alignment of these results with the nonhuman animal findings. This line of research continues to show exceptions to the generalization that women experience greater pain than men.

Dynamic, but not static, pain sensitivity predicts exercise-induced muscle pain: Covariation of temporal sensory summation and pain intensity

Cross-section studies suggest that measures of pain sensitivity, derived from quantitative sensory testing (QST), are elevated in persons with chronic pain conditions. However, little is known about whether development of chronic pain is preceded by elevated pain sensitivity or pain sensitivity increases as a result of prolonged experience of pain. Here we used QST to test static (single suprathreshold stimuli) and dynamic (temporal sensory summation) pain processing of thermal stimuli. Muscle pain was induced using high-intensity exercise (DOMS). Multi-level modeling approaches determined the daily covariation among static and dynamic QST measures and pain intensity. Variation in responses to static pain sensitivity was not associated with pain intensity from DOMS while, in contrast, variation in dynamic pain sensitivity was positively associated with variation in pain intensity from DOMS. This finding supports the use of TSS as a marker of the central pain state and potentially as an appropriate measure for treatment monitoring.

Investigation of Central Pain Processing in Shoulder Pain: Converging Results From 2 Musculoskeletal Pain Models

Recent reports suggest deficits in conditioned pain modulation (CPM) and enhanced suprathreshold heat pain response (SHPR) potentially play a role in the development of chronic pain. The purpose of this study was to investigate whether central pain processing was altered in 2 musculoskeletal shoulder pain models. The goals of this study were to determine whether central pain processing: 1) differs between healthy subjects and patients with clinical shoulder pain; 2) changes with induction of exercise-induced muscle pain; and 3) changes 3 months after shoulder surgery. Fifty-eight patients with clinical shoulder pain and 56 age- and sex-matched healthy subjects were included in these analyses. The healthy cohort was examined before inducing EIMP, and 48 and 96 hours later. The clinical cohort was examined before shoulder surgery and 3 months later. CPM did not differ between the cohorts, however; SHPR was elevated for patients with shoulder pain compared to healthy controls. Induction of acute shoulder pain with EIMP resulted in increased shoulder pain intensity but did not change CPM or SHPR. Three months following shoulder surgery, clinical pain intensity decreased but CPM was unchanged from preoperative assessment. In contrast, SHPR was decreased and showed values comparable with healthy controls at 3 months. Therefore, the present study suggests that: 1) clinical shoulder pain is associated with measurable changes in central pain processing; 2) exercise-induced shoulder pain did not affect measures of central pain processing; and 3) elevated SHPR was normalized with shoulder surgery. Collectively our findings support neuroplastic changes in pain modulation were associated with decreases in clinical pain intensity only, and could be detected more readily with thermal stimuli. Perspective Longitudinal studies involving quantitative sensory testing are rare. In exploring 2 musculoskeletal shoulder pain models (exercise-induced muscle pain and surgical pain), conditioned pain modulation was unchanged from pre- to post-assessment in both models. Suprathreshold heat pain response decreased after shoulder surgery and was comparable to healthy controls, suggesting this measure may be sensitive to decreases in clinical pain intensity.

Genetic risk for malignant hyperthermia in non-anesthesia-induced myopathies

Malignant hyperthermia (MH) is a pharmacogenetic, autosomal dominantly inherited disorder of skeletal muscle triggered by volatile anesthetics and infrequently by extreme exertion and heat exposure. MH has variable penetrance with an incidence ranging from 1 in 5000 to 1 in 50,000–100,000 anesthesias. Mutations in the ryanodine receptor gene, RYR1, are found in 50–70% of cases. We hypothesized that a portion of patients with drug-induced muscle diseases, unrelated to anesthesia, such as severe statin myopathy, have underlying genetic liability that may include RYR1 gene mutations. DNA samples were collected from 885 patients in 4 groups: severe statin myopathy (n=197), mild statin myopathy (n=163), statin-tolerant controls (n=133), and non-drug-induced myopathies of unknown etiology characterized by exercise-induced muscle pain and weakness (n=392). Samples were screened for 105 mutations and variants in 26 genes associated with 7 categories of muscle disease including 34 mutations and variants in the RYR1 gene. Disease-causing mutations or variants in RYR1 were present in 3 severe statin myopathy cases, 1 mild statin myopathy case, 8 patients with non-drug-induced myopathy, and none in controls. These results suggest that disease-causing mutations and certain variants in the RYR1 gene may contribute to underlying genetic risk for non-anesthesia-induced myopathies and should be included in genetic susceptibility screening in patients with severe statin myopathy and in patients with non-statin-induced myopathies of unknown etiology.

Stability of behavioral estimates of activity-dependent modulation of pain

Temporal sensory summation of pain (TSSP) is a proxy measure of windup in humans and results in increased ratings of pain caused by a repetitive, low-frequency noxious stimulus. Aftersensations (ASs) are pain sensations that remain after TSSP has been induced. We examined the within-session and across-session variability in TSSP and AS estimation in healthy participants and in participants with exercise-induced muscle pain in order to determine whether the presence of pain affected the stability of TSSP and ASs. TSSP was estimated by application of 10 repetitive, low-frequency (<0.33 Hz) thermal pulses and measured by the simple slope of pain ratings between the first and fifth pulses. ASs were measured by the presence of any remaining pain sensations up to 1 minute after TSSP was induced. TSSP estimation remained moderately stable in pain-free participants and in participants with pain within a single testing session but demonstrated low stability across sessions in pain-free participants. AS estimation was stable for all groups. Estimation of TSSP and ASs using these protocols appears to be a reliable single-session outcome measure in studies of interventions for acute muscle pain and in experimental studies with healthy participants. This article evaluates the reliability of a commonly used method of estimating TSSP and ASs in both healthy participants and in a clinically relevant model of acute pain. These protocols have the potential to be used as single-session outcome measures for interventional studies and in experimental studies.

Primary Adenosine Monophosphate (AMP) Deaminase Deficiency in a Hypotonic Infant

The spectrum of the adenosine monophosphate (AMP) deaminase deficiency ranges from asymptomatic carriers to patients who manifest exercise-induced muscle pain, occasionally rhabdomyolysis, and idiopathic hyperCKemia. However, previous to the introduction of molecular techniques, rare cases with congenital weakness and hypotonia have also been reported. We report a 6-month-old girl with the association of congenital muscle weakness and hypotonia, muscle deficiency of adenosine monophosphate deaminase, and the homozygous C to T mutation at nucleotide 34 of the adenosine monophosphate deaminase-1 gene. This observation indicates the possible existence of a primary adenosine monophosphate deaminase deficiency manifested by congenital muscle weakness and hypotonia.

Acute effects of dietary ginger on muscle pain induced by eccentric exercise.

Zingiber officinale, commonly known as ginger, has analgesic and antiinflammatory properties. The acute effects of ginger on muscle pain, inflammation and dysfunction induced by eccentric exercise were examined. Twenty-seven participants performed 24 eccentric actions of the non-dominant elbow flexors. In a double-blind, cross-over design, participants ingested a 2 g dose of ginger or placebo 24 h and 48 h after exercise. Pain intensity (0-100 mm), arm volume (water displacement), range-of-motion (goniometry) and metabolic rate were assessed before and 45 min after ingestion of ginger or placebo. Eccentric exercise induced moderate arm pain (39 ± 20 mm; mean ± SD) and dysfunction (14% decrease in ROM) and an increase in volume (1.8%). Overall, ginger consumption demonstrated no effect on muscle pain, dysfunction, or metabolic rate compared with placebo. In the sub-set of participants who consumed ginger 24 h after exercise, arm pain was reduced (13%, -5.9 ± 8.8 mm) the following day, 48 h after exercise. Participants who ingested placebo 24 h post-exercise exhibited no change in pain the following day (0.0 ± 14.7 mm). In conclusion, a single 2 g dose of ginger does not attenuate eccentric exercise-induced muscle pain, inflammation or dysfunction 45 min after ingestion. However, ginger may attenuate the day-to-day progression of muscle pain.

Eccentric exercise induces chronic alterations in musculoskeletal nociception in the rat

Eccentric muscle exercise is a common cause of acute and chronic (lasting days to weeks) musculoskeletal pain. To evaluate the mechanisms involved, we have employed a model in the rat, in which eccentric hind limb exercise produces both acute mechanical hyperalgesia as well as long-term changes characterized by enhanced hyperalgesia to subsequent exposure to an inflammatory mediator. Eccentric exercise of the hind limb produced mechanical hyperalgesia, measured in the gastrocnemius muscle, which returned to baseline at 120 h post-exercise. When nociceptive thresholds had returned to baseline, intramuscular injection of prostaglandin E(2) (PGE(2) ) induced hyperalgesia that was unattenuated 240 h later, much longer than PGE(2) -induced hyperalgesia in unexercised rats (4 h). This marked prolongation of PGE(2) hyperalgesia induced by eccentric exercise was prevented by the spinal intrathecal injection of oligodeoxynucleotide antisense to protein kinase Cε, a second messenger in nociceptors implicated in the induction of chronic pain. Exercise-induced hyperalgesia and prolongation of PGE(2) hyperalgesia were inhibited by the spinal intrathecal administration of antisense for the interleukin-6 but not the tumor necrosis factor α type 1 receptor. These findings provide further insight into the mechanism underlying exercise-induced chronic muscle pain, and suggest novel approaches for the prevention and treatment of exercise- or work-related chronic musculoskeletal pain syndromes.

Vitamin D Status Is Not Associated with Outcomes of Experimentally-Induced Muscle Weakness and Pain in Young, Healthy Volunteers

Vitamin D receptors have been identified in skeletal muscle; and symptoms of vitamin D deficiency include muscle weakness and pain. Moreover, increased serum 25-hydroxyvitamin D (25(OH)D) concentrations have been associated with improved muscle function. To further clarify the importance of vitamin D to muscle, we examined the association between vitamin D status and exercise-induced muscle pain and weakness in healthy people. Muscle damage to the elbow flexors was induced with eccentric exercise (EE) in 48 individuals (22.5 ± 3.2 yrs). Muscle pain ratings following unloaded movement and peak isometric force (IF) were collected before EE and for 4 days post-EE. Linear regression was used to determine if serum 25(OH)D was a predictor of any outcome. In males, R 2-values from 0.48 to 1.00. R 2 for IF ranged from 0 to 0.02 and P-values from 0.48 to 1.00. In females, R 2 for pain ratings ranged from 0.01 to 0.11 and P-values from 0.14 to 0.59. R 2 for IF ranged from 0 to 0.04 and P-values from 0.41 to 0.90. In conclusion, vitamin D status did not predict muscle pain or strength after EE-induced muscle damage in young healthy men and women.