Development and Usability Assessment of a Connected Resistance Exercise Band Application for Strength-Monitoring.

Resistance exercise bands are a core component of any physical activity strengthening program. Strength training can mitigate the development of sarcopenia, the loss of muscle mass or strength and function with aging. Yet, the adherence of such behavioral exercise strategies in a home-based setting are fraught with issues of monitoring and compliance. Our group developed a Bluetooth-enabled resistance exercise band capable of transmitting data to an open-source platform. In this work, we developed an application to capture this information in real-time, and conducted three usability studies in two mixed-aged groups of participants (n=6 each) and a group of older adults with obesity participating in a weight-loss intervention (n=20). The system was favorable, acceptable and provided iterative information that could assist in future deployment on ubiquitous platforms. Our formative work provides the foundation to deliver home-based monitoring interventions in a high-risk, older adult population.

Impact of obesity on disability, function, and physical activity: data from the Osteoarthritis Initiative.

OBJECTIVES: Older adults with obesity are at risk for osteoarthritis (OA) and are predisposed to functional decline and disability. We examined the association between obesity and disability, physical activity, and quality of life at 6 years. METHOD: Using data from the longitudinal Osteoarthritis Initiative (OAI), we analysed older adults (age ≥ 60 years) with a body mass index (BMI) at baseline ≥ 18.5 kg/m(2) (n = 2378) using standard BMI categories. Outcomes were assessed at the 6-year follow-up and included: the Late-Life Function and Disability Index (LLDI), the 12-item Short Form Health Survey (SF-12), and the Physical Activity Scale for the Elderly (PASE). Linear regression predicted outcomes based on BMI category, adjusting for age, sex, race, education, smoking, cohort status, radiographic knee OA, co-morbidity scores, and baseline scores when available. RESULTS: Follow-up data were available for 1727 (71.9%) participants (mean age 67.9 ± 5.3 years; 61.6% female). At baseline, obese subjects compared to overweight and normal were on a greater number of medications (4.28 vs. 3.63 vs. 3.32), had lower gait speeds (1.22 vs. 1.32 vs. 1.36 m/s), higher Charlson scores (0.59 vs. 0.37 vs. 0.30), and higher Western Ontario and McMaster University OA Index (WOMAC) scores (right: 14.8 vs. 10.3 vs. 7.5; left: 14.4 vs. 9.9 vs. 7.5). SF-12 scores at 6 years were lower in obese patients than in overweight or normal [99.5 (95% CI 98.7-100.4) vs. 101.1 (95% CI 100.4-101.8) vs. 102.8 (95% CI 101.8-103.8)], as were PASE scores [115.1 (95% CI 110.3-119.8) vs. 126.2 (95% CI 122.2-130.2) vs. 131.4 (95% CI 125.8-137.0)]. The LLDI limitation component demonstrated differences in obese compared to overweight or normal [78.6 (95% CI 77.4-79.9) vs. 81.2 (95% CI 80.2-82.3) vs. 82.5 (95% CI 81.1-84.0)]. CONCLUSIONS: Obesity was associated with worse physical activity scores, lower quality of life, and higher risk of 6-year disability.

Arrestin effects on internalization of vasopressin receptors.

Arrestins have been shown to facilitate the recruitment of G protein-coupled receptors to the clathrin-coated vesicles that mediate their internalization. After (8)Arg-vasopressin-induced internalization, the human V2 vasopressin receptor failed to recycle to the cell surface, whereas the vasopressin type 1a receptor (V1a) subtype did. The possibility that the lack of recycling could identify a novel role for arrestins was investigated by examining the effect of coexpressing wild-type and dominant negative arrestins on the recycling of wild-type and mutant V2 and V1a receptors. Coexpression of the V1a or V2 receptors with the last 100 amino acids of arrestin reduced significantly their internalization, whereas coexpression of wild-type and mutant arrestins had diverse effects on internalization. Arrestin3 but not arrestin2 increased the internalization of the V1aR without altering its recycling pattern. Both nonvisual arrestins enhanced vasopressin type 2 receptor (V2R) internalization, inducing the appearance of a pool of recycling receptor in addition to the nonrecycling pool. The effect of arrestins on the internalization of the chimeric V1a/V2 receptor and its reciprocal chimera was specified by the identity of the carboxyl-terminal segment. The S363A mutation that confers recycling to the V2R did not alter its interaction with arrestins. Truncation of the carboxyl-terminal segment of the V2R impaired ligand-induced internalization that could be fully restored by wild-type arrestins. Internalization of the V2 and V1a receptors required dynamin GTPase activity.