Addressing mental health needs of NCAA student-athletes of colour: foundational concepts from the NCAA Summit on Diverse Student-Athlete Mental Health and Well-Being.

We sought to identify concepts that may facilitate National Collegiate Athletic Association efforts to assist member institutions in addressing the mental health needs of student-athletes of colour. A two-step process was followed to generate and refine concepts, guided by Delphi methodology. First, a scoping review was conducted, including original peer-reviewed research articles that quantified or qualitatively described determinant(s) of racial or ethnic differences in athlete mental health or mental healthcare. Next, a multiday virtual meeting was facilitated to review the results of the scoping review, discuss lived experiences and generate potential concepts. Participants included a racially and ethnically diverse group of student-athletes, medical and mental health professionals, athletics administrators, diversity, equity and inclusion experts, health educators and representatives from leading organisations involved in athlete mental health. Through the consensus process, participants identified 42 concepts that member institutions might consider implementing on their campuses. Concepts were largely focused on organisational policies and practices such as staffing diversity and inclusion, expanded options for clinical support (ie, identity-relevant support groups) and within-organisation accountability. Concepts related to specific areas for stakeholder education were also identified. Institutions have the potential to play an important role in supporting the mental well being of student-athletes of colour, and the present concepts can help inform institutional action. While concepts proposed are believed to be broadly relevant across athletics settings, they would need to be further considered and tailored to reflect setting-specific organisational structures, resources and needs.

Associations between preoperative depression and opioid use after anterior cruciate ligament reconstruction and concomitant procedures.

Objectives: To determine rates of perioperative opioid use and characterize associations between preoperative depression and chronic and cumulative opioid consumption after ACL reconstruction.Methods: Using insurance claims data, we identified 48,657 adults who underwent ACL reconstruction from 2010 to 2015, had prescription drug insurance, and had ≥1 year of continuous insurance enrollment postoperatively. Chronic opioid use was defined as filling ≥120 days' supply from 3 to 12 months postoperatively. Logistic and linear regression, controlled for age, sex, and Charlson Comorbidity Index value, were used to determine associations of preoperative depression with binary and continuous outcomes, respectively.Results: Preoperatively, 2,237 patients (4.6%) had depression and 2,387 (4.9%) were taking opioids; patients with depression had 6.5 times the odds (95% confidence interval [CI]: 5.8, 7.3) of taking opioids than patients without depression. Postoperatively, 25% of the patients filled ≥1 opioid prescription; mean duration of use was 13 ± 11 days, and 362 patients (0.7%) had chronic use. Patients with preoperative depression were less likely than patients without depression to fill an opioid prescription postoperatively (OR 0.2, 95% CI: 0.2, 0.2). Of patients who filled opioid prescriptions postoperatively, those with preoperative depression were more likely to refill that prescription at least once (OR 2.0, 95% CI: 1.9, 2.2) but did not have greater odds of chronic use (OR 0.9, 95% CI: 0.5, 1.5). Preoperative depression was not associated with greater cumulative opioid consumption from 3 to 12 months postoperatively (ß = -40, 95% CI: -226, 146).Conclusion: Although patients with preoperative depression were more likely to take opioids preoperatively and to obtain ≥1 opioid refill postoperatively, they did not have greater odds of chronic postoperative opioid use or greater cumulative opioid consumption after ACL reconstruction.

Wake up call for collegiate athlete sleep: narrative review and consensus recommendations from the NCAA Interassociation Task Force on Sleep and Wellness.

Sleep is an important determinant of collegiate athlete health, well-being and performance. However, collegiate athlete social and physical environments are often not conducive to obtaining restorative sleep. Traditionally, sleep has not been a primary focus of collegiate athletic training and is neglected due to competing academic, athletic and social demands. Collegiate athletics departments are well positioned to facilitate better sleep culture for their athletes. Recognising the lack of evidence-based or consensus-based guidelines for sleep management and restorative sleep for collegiate athletes, the National Collegiate Athletic Association hosted a sleep summit in 2017. Members of the Interassociation Task Force on Sleep and Wellness reviewed current data related to collegiate athlete sleep and aimed to develop consensus recommendations on sleep management and restorative sleep using the Delphi method. In this paper, we provide a narrative review of four topics central to collegiate athlete sleep: (1) sleep patterns and disorders among collegiate athletes; (2) sleep and optimal functioning among athletes; (3) screening, tracking and assessment of athlete sleep; and (4) interventions to improve sleep. We also present five consensus recommendations for colleges to improve their athletes' sleep.

Brain biomarkers based assessment of cognitive workload in pilots under various task demands.

Cognitive workload is an important element of cognitive-motor performance such as that exhibited during the piloting of an aircraft. Namely, an increase in task demands on the pilot can elevate cognitive information processing and, thus, the risk of human error. As such, there is a need to develop methods that reliably assess mental workload in pilots within operational settings. The present study contributes to this research goal by identifying physiological and brain biomarkers of cognitive workload and attentional reserve during a simulated aircraft piloting task under three progressive levels of challenge. A newly developed experimental method was employed by which electroencephalography (EEG) was acquired via a dry (i.e., gel-free sensors) system using few scalp sites. Self-reported responses to surveys and piloting performance indicators were analyzed. The findings revealed that as the challenge (task demands) increased, the perceived mental load increased, attentional reserve was attenuated, and task performance decreased. Such an increase in task demands was also reflected by changes in heart rate variability (HRV), as well as in the amplitude of the P300 component of event-related potentials to auditory probes, and in the spectral power of specific EEG frequency bands. This work provides a first step towards a long-term goal to develop a composite system of biomarkers for real-time cognitive workload assessment and state assessment of pilots in operational settings.

IGF-1 reduces inflammatory responses, suppresses oxidative stress, and decreases atherosclerosis progression in ApoE-deficient mice.

OBJECTIVE: Whereas growth factors, via their ability to stimulate vascular smooth muscle cell (VSMC) proliferation and migration, have been thought to play a permissive role in atherosclerosis initiation and progression, the role of insulin-like growth factor-1 (IGF-1) is unknown. Here we report for the first time that IGF-1 infusion decreased atherosclerotic plaque progression in ApoE-deficient mice on a Western diet. METHODS AND RESULTS: ApoE-null mice (8 weeks) were infused with vehicle or recombinant human IGF-1 and fed a high-fat diet for 12 weeks. Analysis of aortic sinuses revealed that IGF-1 infusion decreased atherosclerotic plaque progression and macrophage infiltration into lesions. Furthermore, IGF-1 decreased vascular expression of the proinflammatory cytokines interleukin-6 and tumor necrosis factor-alpha, reduced aortic superoxide formation and urinary 8-isoprostane levels, and increased aortic pAkt and eNOS expression and circulating endothelial progenitor cells, consistent with an antiinflammatory, antioxidant, and prorepair effect on the vasculature. CONCLUSIONS: Our data indicate that an increase in circulating IGF-1 reduces vascular inflammatory responses, systemic and vascular oxidant stress and decreases atherosclerotic plaque progression. These findings have major implications for the treatment of atherosclerosis.

ANG II induces apoptosis of human vascular smooth muscle via extrinsic pathway involving inhibition of Akt phosphorylation and increased FasL expression.

In addition to well-documented vascular growth-promoting effects, ANG II exerts proapoptotic effects that are poorly understood. IGF-1 is a potent survival factor for human vascular smooth muscle cells (hVSMC), and its antiapoptotic effects are mediated via the IGF-1 receptor (IGF-1R) through a signaling pathway involving phosphatidylinositol 3-kinase and Akt. We hypothesized that there would be cross talk between ANG II proapoptotic effects and IGF-1 survival effects in hVSMC. To investigate ANG II-induced apoptosis and the potential involvement of IGF-1, we exposed quiescent and nonquiescent hVSMC to ANG II. ANG II induced apoptosis only in nonquiescent cells but stimulated hypertrophy in quiescent cells. ANG II-induced apoptosis was characterized by marked inhibition of Akt phosphorylation and stimulation of membrane Fas ligand (FasL) expression, caspase-8 activation, and a reduction in soluble FasL expression. Adenovirally mediated overexpression of Akt rescued hVSMC from ANG II-induced apoptosis. IGF-1R activation increased Akt phosphorylation and soluble FasL expression, and these effects were completely blocked by coincubating hVSMC with ANG II. In conclusion, ANG II-induced apoptosis of hVSMC is characterized by marked inhibition of Akt phosphorylation and stimulation of an extrinsic cell death signaling pathway via upregulation of membrane FasL expression, caspase-8 activation, and a reduction in soluble FasL expression. Furthermore, ANG II antagonizes the antiapoptotic effect of IGF-1 by blocking its ability to increase Akt phosphorylation and soluble FasL. These findings provide novel insights into ANG II-induced apoptotic signaling and have significant implication for understanding ANG II-induced remodeling in hypertension and atherosclerosis.