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{"project":"2_test","denotations":[{"id":"24622769-14625449-95790399","span":{"begin":749,"end":752},"obj":"14625449"},{"id":"24622769-22029953-95790400","span":{"begin":770,"end":773},"obj":"22029953"},{"id":"24622769-22101870-95790401","span":{"begin":1210,"end":1213},"obj":"22101870"},{"id":"24622769-22442371-95790402","span":{"begin":2129,"end":2132},"obj":"22442371"},{"id":"24622769-22442371-95790403","span":{"begin":2961,"end":2964},"obj":"22442371"},{"id":"24622769-22990628-95790404","span":{"begin":2968,"end":2971},"obj":"22990628"}],"text":"Exercise\nRodent studies have shown that exercise modulates the eCB system (Table 3). The results of these studies show a critical difference between short-term, voluntary exercises (e.g., wheel running) and long-term, coerced exercise (forced swimming, treadmills). Although both types of exercise regimens increased eCB ligand concentrations, only long-term-forced exercise led to sustained elevations of eCBs, and predictable CB1 downregulation.\n10.1371/journal.pone.0089566.t003 Table 3 Effects of exercise upon the eCB system in rodent studies. In humans, serum AEA levels doubled over baseline in male subjects after ≥30 min running, and increased significantly in male subjects after biking. Serum 2-AG levels did not significantly increase [237]. Heyman et al. [238] reported similar findings in male cyclists—serum AEA levels increased significantly during exercise, whereas 2-AG concentrations remained stable. AEA levels increased incrementally at 55% maximum work output, at 75% Wmax, and during a 15 min recovery period. Beta-endorphin levels exhibited a different trajectory—they did not increase until the 75% Wmax stage, and dropped significantly during the recovery period.\nFeuerecker et al. [239] measured the effects of physical exercise in aerobically-trained male subjects. Strenuous hiking at high altitudes (up to 3196 m) significantly increased serum AEA levels over baseline. Strenuous hiking at low altitudes also increased AEA level, but to a lesser extent. In a small cadre of overweight or obese middle-aged women, 20 weeks of moderate-intensity aerobic exercise (CRM) or vigorous-intensity aerobic exercise (CRV) did not change CB1 or FAAH gene expression [235]. However, combining data from the two groups (CRM+CRV) showed a decrease in FAAH mRNA in abdominal adipose tissue, compared to a control group that participated solely in caloric restriction. The CRM and CRV groups showed a slight increase in CB1 mRNA expression in gluteal adipose tissue over baseline, whereas the control group that only participated in caloric restriction showed a significant decrease in CB1 mRNA.\nRaichlen et al., [240] measured circulating eCBs in humans and dogs (cursorial mammals) and ferrets (a non-cursorial mammal) before and after treadmill exercise to test the hypothesis that neurobiological rewards are linked to high-intensity exercise in cursorial mammals. The authors showed that humans and dogs share significantly increased exercise-induced eCB signaling following high-intensity endurance running, whereas eCB signaling did not significantly increase following low-intensity walking, nor did it increase in the non-cursorial ferrets following exercise at any intensity. The same research group showed that serum AEA levels in male and female runners significantly increased after 30 minutes of moderately intense treadmill running (70–80% age-adjusted maximum heart rate), and not after very high or very low intensity exercises [240], [241].\nIn summary, medium- to high-intensity voluntary exercise in cursorial mammals, including humans, increases eCB signaling, via increased serum AEA levels (but not 2-AG), and possibly increased CB1 expression. “Runner's high” may be an eCB-induced reward for exercise."}

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PMC:3951193 / 61130-64370 JSON TXT