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Disadvantaged communities provide adverse psychosocial exposures that have been linked to high levels of stress, and this may provide one explanatory pathway linking socioeconomic disadvantage to obesity. This study used hair cortisol analysis to quantify associations between stress and body mass index (BMI), and between hair cortisol and perceived psychological stress levels, in women and children living in socioeconomically disadvantaged neighborhoods. Participants were a volunteer sample of 70 women from the Resilience for Eating and Activity Despite Inequality study, including 30 maternal-child pairs. Women self-reported body weight, height and perceived psychological stress using the Perceived Stress Scale (PSS), and provided hair samples for themselves and their child. Children's body weight and height were measured. Following extraction, hair cortisol levels were measured using enzyme-linked immunosorbent assay. Multiple linear regression models examined associations between stress and BMI, and between hair cortisol and perceived stress levels in women and children. Women's hair cortisol levels were not associated with their BMI or PSS scores. Women's PSS scores were positively associated with their BMI (p = 0.015). Within maternal-child pairs, mothers and children's hair cortisol levels were strongly positively associated (p = 0.006). Maternal hair cortisol levels and PSS scores were unrelated to their child's zBMI. Children's hair cortisol levels were not associated with their zBMI or with their mother's PSS score. Findings suggest that cortisol-based and perceived psychological measures of stress may be distinct among women and children living in disadvantaged neighborhoods. Perceived psychological measures may be more important predictors of weight-related risk.

Allsopp, GL, Hoffmann, SM, Feros, SA, Pasco, JA, Russell, AP, and Wright, CR. The effect of normobaric hypoxia on resistance training adaptations in older adults. J Strength Cond Res 36(8): 2306–2312, 2022—The effect of normobaric hypoxia on strength, body composition, and cardiovascular fitness was investigated after a resistance training intervention in older adults. A single-blinded, randomized control trial recruited 20 healthy adults aged 60–75 years for an 8-week resistance training intervention in normoxia (n = 10) or normobaric hypoxia (14.4% O2; n = 10). Subjects performed 2 sessions per week of upper-body and lower-body exercises at 70% of 1 repetition maximum (1RM). Pretraining and post-training, maximal oxygen uptake (V̇O2max), muscular endurance (30 maximal knee flexions/extensions), and 5RM were assessed, with 5RM used to calculate 1RM. Subjects underwent whole-body dual-energy x-ray absorptiometry (DXA) at pretraining and post-training for fat and lean mass quantification. Significance was set at p < 0.05. Subjects in both groups substantially improved their calculated 1RM strength for leg extension, pectoral fly, row, and squat (normoxia; 30, 38, 27, and 29%, hypoxia; 43, 50, 28, and 64%, respectively); however, hypoxia did not augment this response. Hypoxia did not enhance V̇O2max or muscular endurance responses after the training intervention, with no improvements seen in either group. Fat mass and lean mass remained unchanged in both groups after the intervention. In summary, 8 weeks of resistance training in hypoxia was well tolerated in healthy older adults and increased upper-body and lower-body strength. However, the magnitude of strength and lean muscle improvements in hypoxia was no greater than normoxia; therefore, there is currently no evidence to support the use of hypoxic resistance training in older adults.

Chronic metabolic stress leads to cellular dysfunction, characterized by excessive reactive oxygen species, endoplasmic reticulum (ER) stress and inflammation, which has been implicated in the pathogenesis of obesity, type 2 diabetes and cardiovascular disease. The ER is gaining recognition as a key organelle in integrating cellular stress responses. ER homeostasis is tightly regulated by a complex antioxidant system, which includes the seven ER-resident selenoproteins - 15 kDa selenoprotein, type 2 iodothyronine deiodinase and selenoproteins S, N, K, M and T. Here, the findings from biochemical, cell-based and mouse studies investigating the function of ER-resident selenoproteins are reviewed. Human experimental and genetic studies are drawn upon to highlight the relevance of these selenoproteins to the pathogenesis of metabolic disease. ER-resident selenoproteins have discrete roles in the regulation of oxidative, ER and inflammatory stress responses, as well as intracellular calcium homeostasis. To date, only two of these ER-resident selenoproteins, selenoproteins S and N have been implicated in human disease. Nonetheless, the potential of all seven ER-resident selenoproteins to ameliorate metabolic dysfunction warrants further investigation.