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Neuropathic pain is a disease of the somatosensory system that is characterized by tingling, burning, and/or shooting pain. Medication is often the primary treatment, but it can be costly, thus there is an interest in understanding alternative low-cost treatments such as exercise. The following review includes an overview of the preclinical and clinical literature examining the influence of exercise on neuropathic pain. Preclinical studies support the hypothesis that exercise reduces hyperalgesia and allodynia in animal models of neuropathic pain. In human research, observational studies suggest that those who are more physically active have lower risk of developing neuropathic pain compared to those who are less active. Exercise studies suggest aerobic exercise training (e.g., 16 weeks); a combination of aerobic and resistance exercise training (e.g., 10–12 weeks); or high-intensity interval training (e.g., 15 weeks) reduces aspects of neuropathic pain such as worst pain over the past month, pain over the past 24 h, pain scores, or pain interference. However, not all measures of pain improve following exercise training (e.g., current pain, heat pain threshold). Potential mechanisms and future directions are also discussed to aid in the goal of understanding the role of exercise in the management of neuropathic pain. Future research using standardized methods to further understanding of the dose of exercise needed to manage neuropathic pain is warranted. [ABSTRACT FROM AUTHOR]

Objective. The purpose of this study was to examine the interaction between the endogenous opioid and endocannabinoid (eCB) systems in a pain modulatory process known as exercise-induced hypoalgesia (EIH). Design. Randomized controlled trial. Setting. Clinical research unit in a hospital. Subjects. Fifty-eight healthy men and women (mean age52163 years) participated in this study. Methods. Participants were administered (randomized, double-blind, counterbalanced procedure) an opioid antagonist (i.e., naltrexone) and a placebo prior to performing pain testing and isometric exercise. Results. Results indicated that 2-arachidonoylglycerol (2-AG) and 2-oleoylglycerol (2-OG) increased significantly (P< 0.05) following exercise in both placebo and naltrexone conditions. In comparison, N-arachidonylethanolamine (AEA) and oleoylethanolamine (OEA) increased significantly (P < 0.05) following exercise in the placebo condition but not the naltrexone condition. There were no significant (P> 0.05) differences in palmitolethanolamine (PEA) between the placebo and naltrexone conditions. Conclusions. As reductions in pain (i.e., EIH) were observed following both conditions, these results suggest that the opioid system may not be the primary system involved in exercise-induced hypoalgesia and that 2-AG and 2-OG could contribute to nonopioid exercise-induced hypoalgesia. Moreover, as exercise-induced increases in AEA and OEA were blocked by naltrexone pretreatment, this suggests that the opioid system may be involved in the increase of AEA and OEA following exercise. [ABSTRACT FROM AUTHOR]

Objective. The purpose of this study was to examine psychosocial influences on exercise-induced hypoalgesia (EIH). Design. Randomized controlled trial. Setting. Clinical research unit in a hospital. Subjects. Fifty-eight healthy men and women (mean age52163 years) participated in this study. Methods. Participants were first asked to complete a series of baseline demographic and psychological questionnaires including the Pain Catastrophizing Scale, the Fear of Pain Questionnaire, and the Family Environment Scale. Following this, they were familiarized with both temporal summation of heat pain and pressure pain testing protocols. During their next session, participants completed the Profile of Mood States, rated the intensity of heat pulses, and indicated their pressure pain thresholds and ratings before and after three minutes of submaximal, isometric exercise. Situational catastrophizing was assessed at the end of the experimental session. Results. Results indicated that experimental pain sensitivity was significantly reduced after exercise (P< 0.05). Men and women did not differ on any of the measured psychosocial variables (P> 0.05). Positive family environments predicted attenuated pain sensitivity and greater EIH, whereas negative and chronic pain-present family environments predicted worse pain and EIH outcomes. Situational catastrophizing and negative mood state also predicted worse pain and EIH outcomes and were additionally associated with increased ratings of perceived exertion and muscle pain during exercise. Conclusions. This study provides preliminary evidence that psychosocial variables, such as the family environment and mood states, can affect both pain sensitivity and the ability to modulate pain through exercise-induced hypoalgesia. [ABSTRACT FROM AUTHOR]

Objective Brain-derived neurotrophic factor (BDNF) has recently emerged as one potential mechanism with which exercise improves mood in major depressive disorder (MDD). This study examined the relationship between changes in serum total BDNF and mood following acute exercise in MDD. It was hypothesized that acute exercise would increase BDNF in an intensity-dependent manner and that changes in BDNF would be significantly related to improvement in depressed mood post-exercise. Methods Twenty-four women (age: 38.6 ± 14.0 years) with MDD exercised for 30 min on a stationary bicycle at light, moderate and hard exercise intensities and performed a quiet rest session using a within-subjects, randomized and counter-balanced design. Before, 10 and 30 min after each session, participants completed the profile of mood states (POMS). Blood was drawn before and within 10 min after completion of each session and serum total BDNF (sBDNF) was measured by enzyme-linked immunosorbent assay. Acute exercise-induced changes in POMS Depression and sBDNF were analyzed via 4 session (quiet rest, light, moderate, hard) by 2 measurement (pre, post) ANOVA. Secondary analyses examined the effects of baseline mood and antidepressant usage on sBDNF. Results Exercise resulted in an acute improvement in depressed mood that was not intensity dependent ( p > 0.05), resulting in significant acute increases in sBDNF ( p = 0.006) that were also not intensity-dependent ( p > 0.05). Acute changes in sBDNF were not significantly correlated to changes in POMS depression at 10 m (r = −0.171, p = 0.161) or 30 m (r = −0.151, p = 0.215) post-exercise. The fourteen participants taking antidepressant medications exhibited lower post-exercise sBDNF ( p = 0.015) than the participants not currently taking antidepressants, although mood responses were similar. Conclusion Acute exercise is an effective mood-enhancing stimulus, although sBDNF does not appear to play a role in this short-term response. Patients who are not currently taking antidepressant medications and those who have greater pre-exercise depression may experience a greater sBDNF response to exercise, but the clinical significance of this is currently unclear. Circulating BDNF levels are unlikely to be altered by steady-state acute exercise in a linear dose-dependent manner. This does not eliminate its potential relevance in the antidepressant response to chronic exercise training, but suggests that other mechanisms are involved in the acute affective response to exercise in depression. [ABSTRACT FROM AUTHOR]

Background: Despite cannabis being the most widely used illicit substance in the United States, individuals diagnosed with cannabis use disorder (CUD) have few well-researched, affordable treatment options available to them. Although found to be effective for improving treatment outcomes in other drug populations, exercise is an affordable and highly accessible treatment approach that has not been routinely investigated in cannabis users.Objectives: The aim of this paper is to inform the topic regarding exercise's potential as an adjunctive treatment for individuals with CUD.Methods: We reviewed the evidence surrounding cannabis use and its current treatment in the United States, explored the rationale for including exercise in the treatment of substance use disorders (SUDs), and in particular, proposed a biological mechanism (i.e., endocannabinoids (eCBs)) that should be examined when utilizing exercise for the treatment of CUD.Results: Cannabis use is widespread and increasing in the United States. Chronic, heavy cannabis use may dysregulate the endogenous cannabinoid system, which has implications for several psychobiological processes that interact with the eCB system such as reward processing and the stress response. Given that exercise is a potent activator of the eCB system, it is mechanistically plausible that exercise could be an optimal method to supplement cessation efforts by reducing psychophysical withdrawal, managing stress, and attenuating drug cravings.Conclusion: We suggest there is a strong behavioral and physiological rationale to design studies which specifically assess the efficacy of exercise, in combination with other therapies, in treating CUD. Moreover, it will be especially important to include the investigation of psychobiological mechanisms (e.g., eCBs, hippocampal volume), which have been associated with both exercise and SUDs, to examine the broader impact of exercise on behavioral and physiological responses to treatment. [ABSTRACT FROM AUTHOR]

Exercise acutely improves mood in major depressive disorder (MDD). However, it is unknown whether benefits differ depending on whether exercise intensity is self-selected or prescribed. Purpose: This study aimed to compare psychological and biological responses to preferred and prescribed steady-state exercise intensities to a patient-selected preferred intensity. Method: Female adults (N = 24, age = 38.6 ± 14.0 yr) diagnosed with MDD completed four 30-min sessions of cycling exercise at three prescribed intensities (RPE of 11, 13, and 15) and one session with a self-selected intensity (preferred). Order was randomized and counterbalanced. Depressed mood (DM) was evaluated before, 10 min, and 30 min postexercise using the Profile of Mood States. Serum brain-derived neurotrophic factor (BDNF) was measured before and within 10 min postexercise. Changes in BDNF and DM for the preferred session were compared with the following prescribed sessions: 1) performed at the most similar intensity (matched on RPE; closest) and 2) with the greatest improvement in DM (greatest). Results: Compared with the preferred session, improvement in DM was significantly larger after the greatest session (30 min postexercise: -11.8 ± 7.4 vs -3.4 ± 4.8), and the BDNF response was significantly greater after the closest session (5.4 ± 6.9 vs -1.4 ± 9.8 ng⋅mL-1). Conclusions: Permitting patients to select their own exercise intensity did not maximize improvements in mood. Further, preferred intensity exercise was also associated with a smaller BDNF response. Overall, the results suggest that exercise undertaken to improve mood should be prescribed on an individual basis in MDD and not necessarily based on the patient's preferred intensity. Clinicians, psychologists, and other practitioners should consider providing clear exercise intensity recommendations for symptom management in depression rather than allowing patients to self-select their intensity. [ABSTRACT FROM AUTHOR]

Supplemental digital content is available in the text. The endocannabinoid (eCB) system is implicated in the pathophysiology of depression and is responsive to acute exercise in healthy adults. Purpose: We aimed to describe acute changes in serum eCB across a prescribed moderate (MOD) and a self-selected/preferred (PREF) intensity exercise session in women with major depressive disorder (MDD) and determine relationships between changes in eCB and mood states. Methods: Women with MDD (n = 17) exercised in separate sessions for 20 min on a cycle ergometer at both MOD or PREF in a within-subjects design. Blood was drawn before and within 10 min after exercise. Serum concentrations of eCB (anandamide [AEA], 2-arachidonoylglycerol) and related lipids (palmitoylethanolamine, oleoylethanolamine, 2-oleoylglycerol) were quantified using stable isotope-dilution, liquid chromatography/mass spectrometry/mass spectrometry. The profile of mood states and state-trait anxiety inventory (state only) were completed before, 10 min and 30 min postexercise. Results: Significant elevations in AEA (P = 0.013) and oleoylethanolamine (P = 0.024) occurred for MOD (moderate effect sizes: Cohen's d = 0.58 and 0.41, respectively). Significant (P < 0.05) moderate negative associations existed between changes in AEA and mood states for MOD at 10 min (depression, confusion, fatigue, total mood disturbance [TMD] and state anxiety) and 30 min postexercise (confusion, TMD and state anxiety). Significant (P < 0.05) moderate negative associations existed between 2-arachidonoylglycerol and mood states at 10 min (depression and confusion) and 30 min postexercise (confusion and TMD). Changes in eCB or related lipids or eCB–mood relationships were not found for PREF. Conclusion: Given the broad, moderate–strength relationships between improvements in mood states and eCB increases after MOD, it is plausible that the eCB system contributes to the mood-enhancing effects of prescribed acute exercise in MDD. Alternative mechanisms are likely involved in the positive mood state effects of preferred exercise. [ABSTRACT FROM AUTHOR]