Psychological stress moderates the relationship between running volume and CD4+ T cell subpopulations.

Endurance-based exercise training can lead to alterations in components of the immune system, but it is unknown how psychological stress (another potent immunomodulator) may impact these changes. The purpose of this study was to determine the moderating role of psychological stress on exercise-induced immune changes. Twenty-nine recreational runners were recruited for this study four weeks before completing a marathon. Each subject reported: weekly training volume (miles/wk) for the week prior to the study visit; completed the Perceived Stress Scale (PSS), the state version of the State-Trait Anxiety Inventory (STAI) and the Penn State Worry Questionnaire (PSWQ); and donated blood for assessment of CD4+ T cell subpopulations and mitogen-induced cytokine production. Participants ran an average of 30 (±13.4) miles (1 mile=1.6 km) per week. Average values (SD) for immune biomarkers were: regulatory T cells (Treg), 3.2% (±1.2%); type 1 regulatory cells (Tr1), 27.1% (±8.3%); T helper 3 (Th3), 1.8% (±0.7%); interferon gamma (IFNγ), 3.1 pg/ml (±1.0); interleukin (IL)-4, 1.4 pg/ml (±1.1); IFNγ/IL-4, 8.6 (±1.2); IL-10, 512 pg/ml (±288). There was a significant relationship between running volume and both Treg cell numbers (slope of the regression line (ß)=0.05, p less than 0.001) and IL-10 production ß=-10.6, p=0.002), and there was a trending relationship between running volume and Tr1 cell numbers (ß=-0.2%, p=0.064). Perceived stress was a trending moderator of the running volume-Treg relationship, whereas worry was a significant moderator of the running volume-IFNγ and running volume-IFNγ/IL-4 relationships. These data indicate that various forms of psychological stress can impact endurance exercise-based changes in certain immune biomarkers. These changes may reflect an increased susceptibility to clinical risks in some individuals.

Increased Circulating Anti-inflammatory Cells in Marathon-trained Runners.

Exercise training can alter immune function. Marathon training has been associated with an increased susceptibility to infectious diseases and an increased activity of inflammatory-based diseases, but the precise mechanisms are unknown. The purpose of this study was to compare levels of circulating CD4+ T cell subsets in the periphery of marathon-trained runners and matched non-marathon controls. 19 recreational marathoners that were 4 weeks from running a marathon and 19 demographically-matched healthy control subjects had the percentage of CD4+ T cell subpopulations (T helper 1, T helper 2, T helper 1/T helper 2 ratio, regulatory T cells, CD4+ IL10+, and CD4+ TGFß+ (Transforming Growth Factor-beta) measured by flow cytometry. Marathon-trained runners had significantly less T helper 1 and regulatory T cells and significantly more T helper 2, CD4+ IL10+, and TGFß+ cells than the control subjects. The alterations in the percentage of T helper 1 and T helper 2 cells led to a significantly lower T helper 1/T helper 2 ratio in the marathon-trained runners. These data suggest that endurance-based training can increase the number of anti-inflammatory cells. This may be a potential mechanism for the increased incidence of both infectious and inflammatory diseases observed in endurance athletes.

PP039. The importance of intentionally considering class 1 HELLP syndrome outcomes versus all other categories of HELLP syndrome or severe preeclampsia.

INTRODUCTION: Combining HELLP syndrome patient groups in publications and presentations may obfuscate any potential differences among patient groups with regard to maternal-perinatal outcomes and rendered therapies. OBJECTIVES: We explored the prevalence of major maternal morbidity (MMM) for patients with severe preeclampsia (SPRE) and each defined group of HELLP syndrome. METHODS: Retrospective cohort study 2000-2007 of patients categorized either as class 1 HELLP syndrome (HELLP1, platelets⩽50,000, AST⩽70,LDH⩽600), class 2 (HELLP2, platelets>50,000 to ⩽100,000), class 3 (HELLP3, platelets>100,000 to ⩽150,000), or partial/incomplete (HELLP4) with only 2 of 3 diagnostic parameters present. All SPRE patients (no HELLP) of 2005-2007 were also evaluated. Total MMM for each group was determined. MMM included cardiopulmonary [cardiogenic or noncardiogenic pulmonary edema, pleural or pericardial effusion, pulmonary embolus, indicated intubation, myocardial infarction or arrest], hematologic/coagulation [DIC, transfused blood products], central nervous system/visual [stroke, cerebral edema, hypertensive encephalopathy, vision loss], hepatic [subcapsular hematoma or rupture] or renal complications [acute tubular necrosis or renal failure]. All HELLP1 and HELLP2 patients received corticosteroids, magnesium sulfate and anti-hypertensives. Comparison among groups was done using Chi-square or Fisher exact test at 95% CI. RESULTS: Four hundred and twenty patients had a form of HELLP syndrome 2000-2007; 688 patients had SPRE 2005-2007.The prevalence of MMM for each patient group was determined: HELLP1=41.5%; HELLP2=10.3%; HELLP3=20.0%; HELLP4=21.0%; and SPRE=17.7%. MMM in HELLP1 was significantly increased over all other groups (P<0.001). Combining MMM for HELLP1+HELLP2 produced a prevalence of 22.1% MMM, insignificantly different from all others including HELLP3, HELLP4 and SPRE (p=0.19), thereby obscuring the significantly elevated MMM of HELLP1 patients. CONCLUSION: Only patients with HELLP1 have significantly increased MMM compared to other HELLP groups or SPRE. Failing to separately evaluate patients with HELLP1 in studies of HELLP syndrome could lead to mistaken conclusions about the effectiveness of a treatment to reduce MMM. All publications reviewing HELLP syndrome management should address how well it functions to reduce patient development of HELLP1 and thus minimize MMM.