The journal of pain : official journal of the American Pain Society
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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. ⋯ Lower 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.
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While it is generally accepted that women have lower pain thresholds for diverse forms of noxious stimuli, the mechanistic basis for this sexual dimorphism in nociceptive pain remains to be elucidated. We confirmed, in the rat, that females have lower cutaneous mechanical nociceptive thresholds and established a similar sexual dimorphism in muscle. To determine if a peripheral mechanism underlies this sexual dimorphism in pain threshold, we compared biophysical properties of cultured dorsal root ganglion (DRG) neurons that innervated the gastrocnemius muscle in female and male rats. DRG neurons from female rats, which innervated the gastrocnemius muscle, had a more hyperpolarized resting membrane potential. To determine if this was associated with a higher mechanical nociceptive threshold, in contradiction to our working hypothesis, we compared the function, in vivo, of nociceptive afferents innervating the gastrocnemius muscle in male and female rats. C-fiber nociceptors innervating muscle in female rats had higher mechanical thresholds than those in males. Other response characteristics of these nociceptors were not significantly different. Thus, both in vitro and in vivo electrophysiology experiments support the idea that lower mechanical nociceptive threshold in females may be due to sexual dimorphism in central nervous system mechanisms, a difference large enough to overcome an opposing difference in peripheral pain mechanisms. ⋯ This article unifies in vivo and in vitro electrophysiology with behavioral data examining the differences in mechanical nociceptive threshold between male and female rats. The data provide a novel perspective on the peripheral and behavioral outcomes of noxious mechanical stimulation.
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Review Meta Analysis
A meta-analytic review of the hypoalgesic effects of exercise.
The purpose of this article was to examine the effects of acute exercise on pain perception in healthy adults and adults with chronic pain using meta-analytic techniques. Specifically, studies using a repeated measures design to examine the effect of acute isometric, aerobic, or dynamic resistance exercise on pain threshold and pain intensity measures were included in this meta-analysis. The results suggest that all 3 types of exercise reduce perception of experimentally induced pain in healthy participants, with effects ranging from small to large depending on pain induction method and exercise protocol. In healthy participants, the mean effect size for aerobic exercise was moderate (d(thr) = .41, d(int) = .59), while the mean effect sizes for isometric exercise (d(thr) = 1.02, d(int) = .72) and dynamic resistance exercise (d(thr) = .83, d(int) = .75) were large. In chronic pain populations, the magnitude and direction of the effect sizes were highly variable for aerobic and isometric exercise and appeared to depend on the chronic pain condition being studied as well as the intensity of the exercise. While trends could be identified, the optimal dose of exercise that is needed to produce hypoalgesia could not be systematically determined with the amount of data available. ⋯ This article presents a quantitative review of the exercise-induced hypoalgesia literature. This review raises several important questions that need to be addressed while also demonstrating that acute exercise has a hypoalgesic effect on experimentally induced pain in healthy adults, and both a hypoalgesic and hyperalgesic effect in adults with chronic pain.
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Randomized Controlled Trial
Effects of nicotine on spinal cord injury pain vary among subtypes of pain and smoking status: results from a randomized, controlled experiment.
Smoking has been associated with increased pain severity in general chronic pain populations. Less is known about the effects of smoking and nicotine on the multifaceted and often complex subtypes of pain that frequently occur following spinal cord injury (SCI). The purpose of this study was to examine the effects of nicotine on self-reported pain among individuals with SCI and to determine if the effect of nicotine varied by pain subtype. A randomized, placebo-controlled crossover design was used to determine the effect of nicotine exposure on subtypes of SCI-related pain among smokers and nonsmokers. A complex relationship emerged, such that the degree of reported pain with exposure to 2 mg of nicotine compared to placebo varied according to pain type and smoking status of the subject. Pain sites that had characteristics of both neuropathic and musculoskeletal symptoms (deemed complex neuropathic pain sites) exhibited pain reduction after nicotine exposure in nonsmokers. In sharp contrast, smokers with this form of pain exhibited an increase in pain severity. Data were also examined descriptively to determine potentially unique factors associated with complex neuropathic pain that may explain trends associated with clinically relevant changes following nicotine exposure. In sum, smoking or tobacco use history may determine the analgesic (or enhanced pain perception) effect of nicotine on post-SCI pain. ⋯ Pain characterized by both neuropathic and musculoskeletal symptoms decreased in severity after nicotine exposure in nonsmokers with SCI but increased in severity among smokers with SCI. The analgesic (or enhanced nociceptive) effect of nicotine may depend on tobacco use history.
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Previous studies have associated depression and temporomandibular joint disorders (TMDs). The temporality, however, remains to be clarified. Most patient studies have selected subjects from treatment facilities, whereas in epidemiological studies a clinical examination has not been performed. In this study the 5-year follow-up data of the population-based Study of Health in Pomerania (SHIP) were analyzed. To estimate the effect of symptoms of depression and those of anxiety on the risk of TMD pain, the Composite International Diagnostic-Screener (CID-S) and a clinical functional examination with palpation of the temporomandibular joint and the masticatory muscles were used. After exclusion of subjects having joint pain at baseline, a sample of 3,006 Caucasian participants with a mean age of 49 years resulted. Of those, 122 participants had signs of TMD joint pain upon palpation. Subjects with symptoms of depression had an increased risk of TMD joint pain upon palpation (rate ratio: 2.1; 95% confidence interval: 1.5-3.0; P < .001). Anxiety symptoms were associated with joint and with muscle pain. The diagnosis, prevention, and therapy of TMD pain should also consider symptoms of depression and those of anxiety, and appropriate therapies if necessary. ⋯ Depressive and anxiety symptoms should be considered as risk factors for TMD pain. Depressive symptoms are specific for joint pain whereas anxiety symptoms are specific for muscle pain, findings that deserve detailed examination. These findings may support decision-making in treating TMD.