Context Athletes are often exposed to pain due to injury and competition. Using preliminary evidence, researchers have shown that cardiovascular measures could be an objective measure of pain, but the cardiovascular response can be influenced by psychological factors, such as catastrophizing. Objective To use a painful cold-pressor test (CPT) to measure the relationship among catastrophizing, pain, and cardiovascular variables in athletes. Design Cohort study. Setting Laboratory. Patients or Other Participants A total of 36 male rugby athletes (age = 24.0 ± 4.6 years, height = 180.0 ± 6.1 cm, mass = 90.5 ± 13.8 kg). Main Outcome Measure(s) We measured catastrophizing using the Pain Catastrophizing Scale and pain using a numeric pain rating scale. Cardiovascular measures were heart rate, systolic and diastolic blood pressure, and heart rate variability. Results During the CPT, participants experienced increases in pain (from 0 to 4.1 ± 2.2), systolic blood pressure (from 126.7 ± 16.5 to 149.7 ± 23.4 mm Hg), diastolic blood pressure (from 76.9 ± 8.3 to 91.9 ± 11.5 mm Hg), and heart rate variability (from 0.0164 ± 0.0121 to 0.0400 ± 0.0323 milliseconds; all P values < .001). In addition, we observed a decrease in heart rate after the CPT (P = .04). We found a correlation between athletes' pain catastrophizing and both pain intensity and change in heart rate during the CPT (P = .02 and P = .003, respectively). Linear regression indicated that pain and catastrophizing explained 29% of the variance in the change in heart rate (P = .003). Conclusions Athletes who had catastrophizing thoughts were more likely to experience higher levels of pain and a greater cardiovascular response during a painful stimulus. The change in cardiovascular variables may be a good objective measure of pain in athletes in the future.
Context: Athletes are often exposed to pain due to injury and competition. There is preliminary evidence that cardiovascular measures could be an objective measure of pain, but the cardiovascular response can be influenced by psychological factors such as catastrophizing. Objectives: The purpose of our study was to use a painful cold pressor test to measure the relationship between catastrophizing, pain, and cardiovascular variables in athletes. Design: Pre-post test. Setting: We completed all measures in a laboratory setting. Participants: Thirty-six male rugby athletes participated in the study. Main outcome measures: We measured catastrophizing with the Pain Catastrophizing Scale and pain with a Numeric Pain Rating Scale. Cardiovascular measures included heart rate, systolic, and diastolic blood pressure, and heart rate variability. Results: During the cold pressor test, participants experienced a significant increase in pain (0 to 4.1±2.2), systolic blood pressure (126.7±16.5mm Hg to 149.7±23.4mm Hg), diastolic blood pressure (76.9±8.3mm Hg to 91.9±11.5mm Hg) and heart rate variability (from 0.0164ms±0.0121 to 0.0400ms±0.0323) (all p<.001). In addition, there was a significant decrease in heart rate after the cold pressor test (p=0.04). There was a significant correlation between athlete's pain catastrophizing to both pain intensity and change in heart rate during the cold pressor test (p=.017 and p=.003 respectively). A significant linear regression indicated pain and catastrophizing explained 29% of the variance of the change in heart rate (p=.003). Conclusion: Athletes who have catastrophizing thoughts are more likely to experience higher levels of pain and a greater cardiovascular response during a painful stimulus. The change in cardiovascular variables may be a good alternative for an objective measure of pain in athletes in the future.
<abstract><sec> <title>Background</title> <p>Upon activation, helper T (Th) cells produce cytokines such as IL-17A and IFNγ, which may exacerbate inflammatory disease and disorders. Adrenergic drugs are emerging as immunomodulatory agents to treat pro-inflammatory diseases, but their function is not completely understood. Th Cells express the β2-adrenergic receptor (β2AR) that is encoded by <italic>ADRB2</italic>. Agonists of the β2AR decrease IFNγ but can increase IL-17A from Th cells. We compared a β2AR agonist to an inverse-agonist, and assessed the influence of <italic>ADRB2</italic> polymorphisms on IL-17A and IFNγ responses.</p> </sec><sec> <title>Methods</title> <p>Peripheral blood mononuclear cells (PBMCs) from venous blood of healthy human participants were cultured with T cell activators anti-CD3 and anti-CD28 antibodies. Terbutaline, a β2AR agonist or nebivolol, a β1AR antagonist and β2AR inverse-agonist, were added <italic>in vitro</italic>. Cytokines IL-17A and IFNγ were measured using enzyme-linked immunosorbent assay. Genomic <italic>ADRB2</italic> and its immediate upstream region were sequenced using Sanger's method. Cytokine response to drug was analyzed based on <italic>ADRB2</italic> polymorphisms.</p> </sec><sec> <title>Results</title> <p>Terbutaline consistently inhibited IFNγ from activated PBMC samples. In contrast, it increased IL-17A in PBMC homozygous for Gly16 codon of <italic>ADRB2</italic>. Nebivolol inhibited IL-17A and IFNγ from activated Th cells. When applied to activated-PBMCs, nebivolol inhibited IL-17A but did not significantly inhibit IFNγ although a trend was observed. The ability of nebivolol to inhibit IL-17A was attenuated by a β2AR-specific antagonist. Cellular proliferation and viability was not significantly changed by nebivolol. Nebivolol suppressed IL-17A in all of the samples regardless of <italic>ADRB2</italic> polymorphisms.</p> </sec><sec> <title>Conclusions</title> <p>This data demonstrates that terbutaline inhibited IFNγ, however, it increased IL-17A in samples with the common Gly16 polymorphism of <italic>ADRB2</italic>. Nebivolol inhibited IL-17A regardless of <italic>ADRB2</italic> polymorphisms. Thus, nebivolol is a strong candidate for treating inflammatory diseases or disorders where IL-17A exacerbates symptoms.</p> </sec></abstract>
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