Characteristics of Team Physicians in the National Football League: The Road to Success and a Call for Diversity.

Background: The role of team physician (TP) in professional sports is a highly coveted position within sports medicine. There is currently limited research on the demographic characteristics of TPs within the National Football League (NFL). Purpose: To identify demographic characteristics and educational backgrounds of NFL head TPs (HTPs) and assistant TPs (ATPs). Study Design: Cross-sectional study. Methods: A list of TPs was identified through the National Football League Physicians Society (NFLPS). Variables investigated include age, gender, race, medical specialty, location and year of residency and fellowship training, leadership among medical societies and editorial boards, academic rank, and personal Scopus Hirsch index (h-index). Linear regression was performed to determine correlation, and t tests were used to assess differences in the h-index. Results: Of the 170 TPs, 21.2% were HTPs and 78.8% were ATPs. TPs were 97.6% male, 91.2% were non-Hispanic White, and 60% had attained an academic rank. The mean ages of the HTPs and ATPs were a 56.2 ± 9.6 and 52.6 ± 9.6 years, respectively (P = .047). Among orthopaedic surgeons, the most common subspecialties were sports medicine (70.5%), foot and ankle (7.6%), and spine (5.7%). Of the TPs, 48.2% and 32.9% worked for a team in the same state in which they graduated residency and fellowship, respectively. HTPs and ATPs had been in the NFLPS for a mean of 16.9 ± 10.8 and 8.8 ± 8.3 years, respectively (P < .001). Further, TPs holding an academic rank had a mean h-index of 14.0 ± 19.3, while those without an academic rank had a mean h-index of 6.2 ± 8.8 (P < .01). HTPs and ATPs had mean h-indices of 15.7 ± 15.9 and 9.6 ± 16.3 (P = .0503), respectively. Conclusion: TPs in the NFL are typically White men in their mid-50s who have trained at specific high-ranking institutions and obtained a fellowship in sports medicine. HTPs were likely to be older with longer tenures within the NFLPS and with more impactful research than their ATP counterparts.

Sex hormones regulate metainflammation in diet-induced obesity in mice.

Men have a statistically higher risk of metabolic and cardiovascular disease than premenopausal women, but the mechanisms mediating these differences are elusive. Chronic inflammation during obesity contributes to disease risk and is significantly more robust in males. Prior work demonstrated that compared with obese males, obese females have reduced proinflammatory adipose tissue macrophages (ATMs). Given the paucity of data on how sex hormones contribute to macrophage responses in obesity, we sought to understand the role of sex hormones in promoting obesity-induced myeloid inflammation. We used gonadectomy, estrogen receptor-deficient alpha chimeras, and androgen-insensitive mice to model sex hormone deficiency. These models were evaluated in diet-induced obesity conditions (high-fat diet [HFD]) and in vitro myeloid assays. We found that ovariectomy increased weight gain and adiposity. Ovariectomized females had increased ATMs and bone marrow myeloid colonies compared with sham-gonadectomized females. In addition, castrated males exposed to HFD had improved glucose tolerance, insulin sensitivity, and adiposity with fewer Ly6chi monocytes and bone marrow myeloid colonies compared with sham-gonadectomized males, although local adipose inflammation was enhanced. Similar findings were observed in androgen-insensitive mice; however, these mice had fewer CD11c+ ATMs, implying a developmental role for androgens in myelopoiesis and adipose inflammation. We concluded that gonadectomy results in convergence of metabolic and inflammatory responses to HFD between the sexes, and that myeloid estrogen receptor alpha contributes minimally to diet-induced inflammatory responses, whereas loss of androgen-receptor signaling improves metabolic and inflammatory outcomes. These studies demonstrate that sex hormones play a critical role in sex differences in obesity, metabolic dysfunction, and myeloid inflammation.

Sex Differences in Inflammatory Responses to Adipose Tissue Lipolysis in Diet-Induced Obesity.

Males are known to have profound adipose tissue macrophage (ATM) accumulation in gonadal white adipose tissue (GWAT) during obesity, whereas females are protected from such an inflammatory response even with increased adiposity. The inflammatory tone in males is linked to insulin resistance and might be the underlying cause for sex differences in metabolic disease. Factors regulating the meta-inflammatory response remain unclear but enhanced lipid storage in females may explain the reduced inflammatory response to high-fat diets. In this study, we evaluated lean and obese females with stimulated lipolysis to understand whether a stress release of free fatty acids (FFAs) could induce female ATMs. We demonstrate that in both lean and obese females, GWAT CD11c- resident ATMs accumulate with ß-3 adrenergic receptor-stimulated lipolysis. Lipolysis elevated serum FFA, triglyceride, and IL-6 levels in females that corresponded to significant phosphorylated hormone-sensitive lipase and adipose triglyceride lipase protein expression in obese female GWAT compared with males. Increased lipolytic response in obese females was associated with crown-like structures and induced Il6, Mcp1, Arg1, and Mgl1 expression in obese female GWAT, suggesting an environment of lipid clearance and adipose remodeling. With this finding we next investigated whether lipid storage and lipolytic mediators differed by sex. Diacylglycerol, ceramides, phospholipids, and certain fatty acid species associated with inflammation were elevated in male GWAT compared with obese female GWAT. Overall, our data demonstrate a role for GWAT lipid storage and lipolytic metabolites to induce inflammation in males and induce remodeling in females that might explain sex differences in overall metabolic health.