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Item Associations of Muscle Mass and Strength with All-Cause Mortality among US Older Adults(Lippincott, Williams & Wilkins, 2018-03) Li, Ran; Xia, Jin; Zhang, Xi; Gathirua-Mwangi, Wambui Grace; Guo, Jianjun; Li, Yufeng; McKenzie, Steve; Song, Yiqing; Epidemiology, School of Public HealthINTRODUCTION: Recent studies suggested that muscle mass and muscle strength may independently or synergistically affect aging-related health outcomes in older adults; however, prospective data on mortality in the general population are sparse. METHODS: We aimed to prospectively examine individual and joint associations of low muscle mass and low muscle strength with all-cause mortality in a nationally representative sample. This study included 4449 participants age 50 yr and older from the National Health and Nutrition Examination Survey 1999 to 2002 with public use 2011 linked mortality files. Weighted multivariable logistic regression models were adjusted for age, sex, race, body mass index (BMI), smoking, alcohol use, education, leisure time physical activity, sedentary time, and comorbid diseases. RESULTS: Overall, the prevalence of low muscle mass was 23.1% defined by appendicular lean mass (ALM) and 17.0% defined by ALM/BMI, and the prevalence of low muscle strength was 19.4%. In the joint analyses, all-cause mortality was significantly higher among individuals with low muscle strength, whether they had low muscle mass (odds ratio [OR], 2.03; 95% confidence interval [CI], 1.27-3.24 for ALM; OR, 2.53; 95% CI, 1.64-3.88 for ALM/BMI) or not (OR, 2.66; 95% CI, 1.53-4.62 for ALM; OR, 2.17; 95% CI, 1.29-3.64 for ALM/BMI). In addition, the significant associations between low muscle strength and all-cause mortality persisted across different levels of metabolic syndrome, sedentary time, and LTPA. CONCLUSIONS: Low muscle strength was independently associated with elevated risk of all-cause mortality, regardless of muscle mass, metabolic syndrome, sedentary time, or LTPA among US older adults, indicating the importance of muscle strength in predicting aging-related health outcomes in older adults.Item Excess TGF-β mediates muscle weakness associated with bone metastases in mice(SpringerNature, 2015-11) Waning, David L.; Mohammad, Khalid S.; Reiken, Steven; Xie, Wenjun; Andersson, Daniel C.; John, Sutha; Chiechi, Antonella; Wright, Laura E.; Umanskaya, Alisa; Niewolna, Maria; Trivedi, Trupti; Charkhzarrin, Sahba; Khatiwada, Pooja; Wronska, Anetta; Haynes, Ashley; Benassi, Maria Serena; Witzmann, Frank A.; Zhen, Gehua; Wang, Xiao; Cao, Xu; Roodman, G. David; Marks, Andrew R.; Guise, Theresa A.; Department of Medicine, IU School of MedicineCancer-associated muscle weakness is a poorly understood phenomenon, and there is no effective treatment. Here we find that seven different mouse models of human osteolytic bone metastases-representing breast, lung and prostate cancers, as well as multiple myeloma-exhibited impaired muscle function, implicating a role for the tumor-bone microenvironment in cancer-associated muscle weakness. We found that transforming growth factor (TGF)-β, released from the bone surface as a result of metastasis-induced bone destruction, upregulated NADPH oxidase 4 (Nox4), resulting in elevated oxidization of skeletal muscle proteins, including the ryanodine receptor and calcium (Ca(2+)) release channel (RyR1). The oxidized RyR1 channels leaked Ca(2+), resulting in lower intracellular signaling, which is required for proper muscle contraction. We found that inhibiting RyR1 leakage, TGF-β signaling, TGF-β release from bone or Nox4 activity improved muscle function in mice with MDA-MB-231 bone metastases. Humans with breast- or lung cancer-associated bone metastases also had oxidized skeletal muscle RyR1 that is not seen in normal muscle. Similarly, skeletal muscle weakness, increased Nox4 binding to RyR1 and oxidation of RyR1 were present in a mouse model of Camurati-Engelmann disease, a nonmalignant metabolic bone disorder associated with increased TGF-β activity. Thus, pathological TGF-β release from bone contributes to muscle weakness by decreasing Ca(2+)-induced muscle force production.Item Predictors of change in grip strength over 3 years in the African American health project(Sage Publications, 2010-03) Miller, Douglas K.; Malmstrom, Theodore K.; Miller, J. Philip; Andresen, Elena M.; Schootman, Mario; Wolinsky, Fredric D.; Department of Medicine, IU School of MedicineOBJECTIVE: To examine factors associated with change in grip strength. METHOD: Grip strength was measured at baseline and 3 years later. Change was divided into "decreased >/=5 kg," "increased >/=5 kg," and "no change" and analyzed using multinomial multivariable logistic regression. RESULTS: Decline in grip strength was more likely for men, those reporting having cardiovascular disease, and those with instrumental activities of daily living, lower body functional limitations, high diastolic blood pressure, higher physical activity, and greater body mass. Decline was less likely among those ever having Medicaid, those with basic activities of daily living disabilities, and those unable to see a doctor in past year due to cost. Gain in grip strength was more likely for men and those with instrumental activities of daily living disabilities, lower body functional limitations, high diastolic blood pressure, and higher physical activity; it was less likely for older participants. DISCUSSION: Results can be used to design interventions to improve strength outcomes.