Background: The relationship among sleep duration, subjective well-being, and injury risk in athletes is poorly defined. Purpose: To evaluate the independent effects of sleep duration, sleep quality, and subjective well-being on in-season injuries in collegiate female volleyball athletes. Study Design: Cohort study; Level of evidence, 2. Methods: During a 9-month competitive season, 17 female National Collegiate Athletic Association (NCAA) Division I volleyball players reported mood, fatigue, stress, soreness, sleep duration (hours), and sleep quality every morning. Well-being measures were recorded from 0 (worst) to 5 (best), and all time-loss injuries were recorded by the team athletic trainer. Separate mixed-effects logistic regression models were used to evaluate the effects of sleep and subjective well-being on in-season injury. Each well-being variable was also included in a separate mixed-effects logistic regression model with sleep duration as a covariate. Results: A total of 54 injuries were recorded during the study period. Compared with days without an injury, mood, fatigue, stress, soreness, sleep quality, and sleep duration were significantly worse the day before an injury occurred. In the separate prediction models, in-season injury was significantly predicted by fatigue (odds ratio [OR], 0.56 [95% CI, 0.36-0.86]; P = .008), mood (OR, 0.52 [95% CI, 0.35-0.78]; P = .002), stress (OR, 0.63 [95% CI, 0.42-0.94]; P = .023), soreness (OR, 0.54 [95% CI, 0.38-0.79]; P = .001), sleep quality (OR, 0.49 [95% CI, 0.34-0.7]; P < .001), and sleep duration (OR, 0.69 [95% CI, 0.55-0.87]; P = .001). In the multivariable models, sleep duration remained a significant independent predictor in each of the subsequent multivariable models (OR, 0.72-0.74; P < .05 for all), as did mood (OR, 0.55 [95% CI, 0.36-0.83); P = .005) and soreness (OR, 0.57 [95% CI, 0.39-0.83]; P = .003), while fatigue (OR, 0.65 [95% CI, 0.42-1]; P = .054) and stress (OR, 0.68 [95% CI, 0.45-1]; P = .061) no longer reached statistical significance. Conclusion: Increased sleep duration, mood, and decreased soreness were independently associated with a reduced risk of in-season injury in this cohort of female NCAA volleyball players.

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Ischemic heart disease is the leading cause of death in both males and females worldwide, with myocardial infarction due to ischemia‐reperfusion (IR) injury being the most common manifestation. Exercise is known to protect the myocardium against IR injury, but the volume of exercise sufficient to confer cardioprotection is not well understood. A single bout of exercise has been shown to confer protection against IR injury, but it is not known whether longer term exercise training (weeks) adds additional cardioprotective benefit. In addition, it is unclear to what extent sex differences contribute to cardioprotection. To address these questions, we studied female and male Sprague‐Dawley rats (3 mo of age) randomly assigned to a 5 day exercise training (EX5d) group (n=20), an 8 week exercise training (EX8w) group (n=20), or a sedentary (Sed) control group (n=10). EX5d rats ran for 5 consecutive days, while EX8w animals ran 5 days a week for 8 weeks. The speed was gradually increased until animals were running 21–23 m/min for 60 min. Maximal running capacity improved in all groups as a result of training. EX5d animals improved maximal distance run by 31.9 ± 9% (pre vs post) while EX8w animals improved by 118.5 ± 15.6% (p<0.01, EX5d vs EX8w). At least 24 h after the last training session, animals were anesthetized and the left anterior descending coronary artery was occluded via suture to induce regional ischemia for 45 min, followed by 24 h of reperfusion. After 24 hours, occlusion was reestablished and 0.5% Evans blue dye was injected into the aorta and perfused through the heart. Hearts were then sectioned, placed in a 0.1% triphenyltetrazolium chloride solution and incubated at 37° C for 10 minutes, then flash frozen in OCT. Infarct areas were quantified using ImageJ software, and infarct values calculated as a percentage of the zone at risk (ZAR). Exercise training led to a significant reduction in infarct size, with Sed, 5d, and 8w animals having infarct sizes of 37.2 ± 3, 27.5 ± 2, and 21.4 ± 1% of the ZAR, respectively (p<0.01, Sed vs EX5d and Sed vs EX8w). Hearts from Sed females had significantly smaller infarcts than those of Sed males (41.8 ± 3 and 32.6 ± 1% of the ZAR, respectively). This sex difference persisted in response to exercise training, with females exhibiting smaller infarct sizes following 5 days of exercise training compared to males (25.1 ± 1 and 29.9 ± 1% of the ZAR, in females and males respectively (p<0.05)), as well as 8 weeks of training (19.4 ± 1 and 23.5 ± 1% of the ZAR, respectively (p<0.05)). When comparing within‐sex differences in cardioprotection, 8 weeks of exercise did not lead to significant infarct size reduction compared to 5 days of exercise in males (23.5 vs 29.9% of the ZAR). However, hearts from EX8w females had significantly smaller infarct sizes when compared to EX5d females (19.4 vs 25.1% of the ZAR, respectively; p<0.01). These results show that 1) long‐term exercise training can augment infarct sparing against IR injury when compared to short duration exercise, and 2) this effect is sex‐dependent.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

e13536 Background: Diffuse Large B Cell Lymphoma (DLBCL) is the most common and increasingly prevalent subtype of Non-Hodgkin lymphoma in both immunocompromised and immunocompetent patients. Its pathogenesis is thought to represent rearrangements, translocations, and transformations of both the immunoglobulin heavy and light chain genes along with somatic mutations of the variable regions of these same genes. A 66-year old Caucasian male with a past medical history of smoking presented to the hospital due to concerns of mental status change, flat affect, and fronto-orbital headache for one-week duration. The patient denied any drug or substance abuse. Physical exam was diffusely normal with the exception of flat affect. Methods: Magnetic resonance spectroscopy is a noninvasive, non-ionizing diagnostic analytical technique that has been used to measure metabolic changes in brain lesions. Results: Lhermitte’s sign was negative and NIH stroke scale was calculated to be 0. CT demonstrated a 17mm frontal lobe lesion. Follow up with MRI showed three bilateral enhancing brain lesions, but no metastasis or primary tumor was seen via CT of chest, abdomen, and pelvis. Initial differential diagnosis included: Tumefactive Multiple Sclerosis, Acute Demyelinating Encephalomyelitis or CNS lymphoma. EEG did not highlight any focal or epileptiform abnormalities and lumbar puncture was negative for Creutzfeld Jacob Disease and Multiple Sclerosis. The patient was discharged with a course of intravenous steroids only to present a few weeks later with no improvement of symptoms. The patient then had proton magnetic resonance spectroscopy (MRS). MRS pattern spikes and chemical profile suggested lymphoma, which was confirmed by a brain biopsy. The patient was subsequently transferred to the University of Pennsylvania for treatment and further management. Conclusions: This case illustrates the beneficial use of MRS, as data patterns it provides compliments the clinician’s knowledge to proceed with appropriate treatment.

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Context Movement of the human body is essential for the interaction of an individual within their environment and contributes to both physical and emotional quality of life. Movement system disorders (MSDs) are kinesiopathologic conditions that result from either altered movement patterns, trauma, or pathology. A screening tool may facilitate earlier diagnosis and treatment of acute MSDs. This tool could prevent progression to chronic conditions, leading to better patient outcomes and quality of life. Objectives Our study evaluated whether a screening tool would be able to accurately screen individuals for MSDs, explore comorbidities that may predict the prevalence of MSDs, and identify why people do not discuss these problems with their primary care provider (PCP). Methods A multisite, observational study in a primary care setting. Data were analyzed to determine the psychometric properties of the screening question. Logistic regression was performed to explore the relationship of comorbidities with MSDs. Thematic analysis was performed to explore why patients do not discuss these issues with their PCP. Results The point prevalence of MSDs was determined to be 78%. The sensitivity of the screening question was determined to be good (70%). Arthritis, obesity, sleep disorders, and gastroesophageal reflux disease (GERD) were significant predictors for an MSD. Thematic analysis regarding why patients do not discuss the MSD with their physician revealed: (1) the perceived lack of importance of the problem; (2) the lack of access to healthcare, and (3) the acuity of the problem. Conclusions Screening for an MSD and associated comorbidities could prevent the transition of acute conditions to chronic conditions. If PCPs can identify predictors and factors associated with an MSD, they may be able to screen for MSDs more effectively. Earlier identification of MSDs may facilitate earlier treatment and prevent costs associated with resulting chronic disorders and persistent pain and disability.

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Coronary artery disease (CAD) remains the leading cause of death worldwide. The most common manifestation of CAD is myocardial infarction (MI), a result of ischemia and/or reperfusion (IR) injury of the myocardium. It is well established that exercise training improves myocardial tolerance to IR, a phenomenon known as exercise‐induced cardioprotection, but the cellular adaptations resulting in cardioprotection against IR injury are not well understood. Recent work has linked IR injury to the activation of the matrix metalloproteinase‐2 (MMP‐2). MMPs are known to be involved in the degradation of the extracellular matrix, and play a key role in scar formation following MI. While this extracellular role of MMP‐2 in MI has been well established, recent studies suggest an additional, intracellular, role of MMP activation in IR injury. MMP‐2 has been shown to have intracellular proteolytic targets in cardiomyocytes, which could contribute to the cell death seen following IR. Tissue inhibitor of metalloproteinases (TIMPs) are inhibitors of the MMPs, and TIMPs have been found in cardiomyocytes. It is thus possible that exercise provides cardioprotection against IR injury through 1) decreasing MMP‐2 protein levels, or 2) inhibiting MMP‐activation by increasing the protein levels of the TIMPs. However, no study to date has investigated the effect of exercise training on the protein levels of MMP‐2 and TIMP‐2 following IR injury. Therefore, the specific aims of this study were to determine the effects of exercise training on MMP‐2 and TIMP‐2 protein expression, and to identify regional differences in the levels of these proteins. To address these questions, we studied 3‐month old Sprague‐Dawley rats randomly assigned to sedentary (SED) or exercise (EX) groups (n=10/group). EX rats were run on a treadmill for 60 min/day, 5 days/week, for 8 weeks. IR was induced by occluding the LAD for 45 min, followed by 24 hr of reperfusion. Hearts were excised and sectioned and stained to delineate the zone at risk (ZAR) from the unaffected area (UA). Infarct size was expressed as a percentage of the ZAR. Hearts from EX rats exhibited smaller infarcts compared to SED rats (21.4% vs. 37.2%; P < 0.05). MMP‐2 and TIMP‐2 levels in ventricular homogenates were determined by Western blot. MMP‐2 protein content was increased in the ZAR compared to the UA in both EX and SED rats (P < 0.05). There was no difference in MMP‐2 protein levels between EX or SED rats. TIMP‐2 protein levels were increased in the hearts from EX rats compared to SED rats (P < 0.05). There was no difference in TIMP‐2 levels between the ZAR and UA in EX or SED rats. These results show that 1) MMP‐2 levels were significantly higher in the ZAR compared to the UA, suggesting an intracellular role of MMP‐2 in IR injury, and 2) exercise training leads to an increase in myocardial TIMP‐2 protein levels, suggesting elevated TIMP‐2 inhibition of MMP‐2 as a potential mechanism of exercise‐induced cardioprotection.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.