Background & Aims The impact of vitamin D supplementation in overweight and obese adults during resistance training on body composition, muscle function, and glucose tolerance was investigated. Methods Twenty-three overweight and obese (age: 26.1±4.7 y; BMI: 31.3±3.2 kg/m2; 25-hydroxyvitamin D: 19.3±7.2 ng/mL) adults were recruited for participation in a double-blind, placebo-controlled trial. Participants were randomly divided into vitamin D (VitD, 4000 IU/d; 5 female, 5 male) and placebo (PL; 7 female, 6 male) groups. Both groups completed 12 wks of resistance training. 25-hydroxyvitamin D, parathyroid hormone, body composition, and glucose tolerance were assessed at baseline and 12 wks. Muscle function (strength and power) was assessed at baseline, 4, 8, and 12 wks. Results During the intervention, 25-hydroxyvitamin D increased and parathyroid hormone decreased in the VitD group (P<0.05). Peak power was significantly increased at 4 wks in the VitD group only (P<0.05). Regression analysis revealed an inverse association between the change in 25-hydroxyvitamin D with the change in waist-to-hip ratio (R2=0.205, P=0.02). No other improvements were observed with supplementation. Conclusions Vitamin D supplementation in overweight and obese adults during resistance training induced an early improvement in peak power, and elevated vitamin D status was associated with reduced waist-to-hip ratio. Clinical trial registration number NCT01199926
Age-associated hyper-inflammation or “inflamm-aging” has been linked to the development of chronic diseases and characterized as an unavoidable aspect of aging. However, the inflamm-aging model does not adequately address the potential anti-inflammatory effects of exercise training and the potential for exercise to ameliorate several age-related diseases. In this brief review, we introduce a new paradigm—inflamm-inactivity—that describes a potent counter-measure to age-associated inflammatory illness.
Rationale: The acute effect of secondhand smoke (SHS) on lung function and the duration of system disruption remain unknown. Objectives: To assess the SHS effects and their duration on lung function and inflammatory markers. Methods: In a randomized single-blind crossover experiment data were obtained from 16 (8 women) nonsmoking adults at baseline and at 0, 1, and 3 hours after a 1-hour SHS exposure set at bar/ restaurant SHS levels. Measurements and Main Results: Serum and urine cotinine, lung function, and cytokines IL-4, IL-5, IL-6, tumor necrosis factor (TNF)-a, and IFN-g. At 0 hours most lung function parameters were significantly reduced (indicative: FEV 1 , 4.3 6 0.4 vs. 3.8 6 0.3 L; FEV 1 /FVC, 0.9 6 0.1 vs. 0.8 6 0.1; P , 0.05) but at 3 hours they were at baseline levels. In contrast, cotinine (serum, 8.9 6 3.2 vs. 35.5 6 10.2 ngÁml 21 ), IL-4 (41.3 6 5.8 vs. 44.2 6 4.5 pgÁml 21 ), IL-5 (36.1 6 3.2 vs. 60.1 6 7.0 pgÁml 21 ), IL-6 (2.5 6 0.3 vs. 7.6 6 1.4 pgÁml 21 ) and IFN-g (0.3 6 0.2 vs. 0.6 6 0.2 IUÁml 21 ) at 3 hours were higher than at baseline (P , 0.05). IL-4 and TNF-a increased only in men, whereas IL-5, IL-6, and IFN-g were different between sexes after exposure (P , 0.05). Regression analyses revealed inverse associations of FEV 1 and FEV 1 /FVC ratio with IL-5 (P , 0.05) in men and with IL-5 (P 5 0.01), IL-6 (P , 0.001), IFN-g (P 5 0.034) and serum cotinine (P , 0.001) in women. Conclusions: We conclude that 1 hour of SHS exposure at bar/ restaurant levels is accompanied by significant decrements on lung function and marked increases in inflammatory cytokines, particularly in men. More importantly, whereas most smoke-induced effects on lung function appear to recede within 60 minutes, inflammatory cytokines remain elevated for at least 3 hours after exposure to SHS. Keywords: passive smoking; cotinine; respiration; inflammatory markersIn the 10 minutes you will spend reading this article, 111 people will die somewhere in the world from tobacco-induced illnesses.* Fourteen of them have never smoked. † An overwhelming amount of evidence has emerged over the past decades on the adverse health effects of secondhand smoke (SHS) (1-5). Nevertheless, more than 126 million American and 130 million Chinese adult nonsmokers suffer daily SHS exposure, whereas global estimates include 700 million children and 50 million pregnant women (1). Latest reports show that, despite current measures, the prevalence rates of smoking are increasing (2, 3), while the tobacco industry predicts a global expansion of the tobacco epidemic in the near future (3). Moreover, arguments are being expressed that only chronic exposures to SHS represent a health risk and that there is no scientific basis for claims that brief, acute, transient SHS exposures represent a significant acute health hazard in nonsmokers (6). This is, in part, because our knowledge on the effects of SHS is based predominantly on longitudinal epidemiological studies, whereas experimental studies assessing the acute and short-term effects of SHS are sca...
The purpose of this study was to observe exercise training-induced effects on adiponectin, leptin, and ghrelin. Twenty-nine older, healthy participants were classified as physically active (comparison group: N = 15, 70.9 ± 1.2 years) or physically inactive (exercise group: N = 14, 70.5 ± 1.4 years). Exercise group participants completed 12 weeks of combined aerobic and resistance exercise training, whereas comparison group participants maintained their current level of exercise and served as a physically active comparison group. Monocyte phenotype, as well as serum ghrelin, leptin, adiponectin, and soluble tumor necrosis factor receptor II were analyzed prior to and following the 12-week period. Ghrelin and adiponectin increased 47% and 55%, respectively, in exercise group participants following exercise training. Percent change in ghrelin (post and pre) was negatively correlated with the percent change in CD14+CD16+ monocytes (post and pre) in exercise group participants. Despite no changes in body mass, these data contribute to evidence for the anti-inflammatory effects of exercise.
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