Exercise can generate alterations in body composition and modulate the immune system. The objective of this study was to verify whether a circuit resistance training (CRT) protocol can increase lean body mass (LM), and reduce fat body mass (FM) and the percent of FM (%FM) of sedentary women, without inducing inflammatory responses, indicated by serum cytokine levels. The initial hypothesis was that CRT would improve body composition, without changing serum cytokine levels. The study consisted of 14 healthy, sedentary women, aged 33-45 years (mean +/- SD, 40.23 +/- 3.98 years), with a normal body mass index. They participated in 3 sessions per week of CRT, which included 2 rounds in 9 stations with 1 set of 8-12 repetition maximum at each station, for 10 weeks. During the 10-week CRT period, participants maintained their pretraining nutritional standard. Body composition was analysed with dual-energy X-ray absorptiometry both pre- and post-training. Blood samples were collected after 96 h of rest pre- and post-training, and 5 min, 24 h, and 48 h after the second and last training sessions to measure serum cytokine levels by flow cytometry. The nutritional standard was accompanied throughout the study period with 24-h dietary recall. Increases in LM (35.937 +/- 4.926 to 39.130 +/- 4.950 kg) and decreases in FM (21.911 +/- 8.150 to 17.824 +/- 4.235 kg) and %FM (37.10 +/- 10.84 to 31.19 +/- 6.06), without concurrent changes in serum cytokine levels, and in the nutritional standard (alpha = 0.05). The proposed CRT improved body composition and did not induce any changes in serum cytokine levels characteristic of the inflammatory response in women.
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http://dx.doi.org/10.1139/H09-136 | DOI Listing |
Inflammopharmacology
January 2025
Department of Pharmacology, Faculty of Pharmacy, The Islamia University of Bahawalpur, Punjab, 63100, Pakistan.
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December 2024
University of North Dakota, Grand Forks, ND, USA.
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December 2024
Georgia Institute of Technology, Atlanta, GA, USA.
Background: Mitogen activated protein kinase (MAPK) signaling is a critical regulator of microglial phenotype, including phagocytic function, cytokine expression, and motility, among others. Importantly, both canonical and non-canonical MAPK signaling is directly activated by RTKs, including Interestingly, CSF1R, is activated by two agonists, CSF1 and IL-34, which have been shown to activate the receptor in different ways that can lead to However, little is known about how the affect microglial MAPK signaling, and whether their effects are dependent on disease state/Aβ exposure. In this study, we hypothesized that IL-34 and CSF-1 elicit distinct patterns of MAPK signaling activation in microglia and MAPK activation would be dependent on whether the cells were exposed to Aβ.
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December 2024
Xuanwu Hospital of Capital Medical University, Beijing, Beijing, China.
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Alzheimers Dement
December 2024
University of Kentucky, Lexington, KY, USA.
Background: Aging microglia accumulate lipid droplets (LDs), secrete pro-inflammatory cytokines, and are defective in phagocytosis. The E4 allele of Apolipoprotein E (APOE) is the strongest genetic risk factor for late-onset Alzheimer's disease (LOAD) and is associated with increased neuroinflammation and LD accumulation. Here, we aimed to determine if the effects of aging and the E4 allele are synergistic in causing the accumulation of LDs seen in LOAD.
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