Cigarette smoking is a risk factor for many diseases. It could be associated with sarcopenia. The aim of this meta-analysis was to determine whether smoking is an isolated risk factor for sarcopenia. We searched PubMed, Web of Science, EBSCO, and Science Direct for articles addressing the relationship between cigarette smoking and sarcopenia. A total of 12 studies containing information on 22,515 participants were included in this meta-analysis. Odds ratio (OR) was calculated for each study group and for all studies together. An OR was also calculated separately for each sex. We used a fixed-effect model in overall estimation and in males, because results of small studies were significantly different from the results of large studies in those cases and in females where the estimation showed only moderate heterogeneity we used a random-effect model. According to proposes of the Cochrane Handbook for Systematic Reviews. The resulting OR in the fixed-effect model was 1.12 (95 % CI 1.03-1.21), OR for each sex was in the fixed-effect model 1.20 (95 % CI 1.06-1.35) in males and in the random-effect model 1.21 (95 % CI 0.92-1.59) in females. The results of this meta-analysis indicate that cigarette smoking as an isolated factor may contribute to the development of sarcopenia. However, the results of the individual studies were largely inconsistent due to different approaches of measuring the main variables which affected the results.
BackgroundSarcopenia, a loss of muscle strength and mass, has serious implications for older adults. Some risk factors for sarcopenia are well established. The role of other factors such as alcohol consumption is less certain. The main aim of this study was to explore the relationship between sarcopenia and alcohol consumption in people over 65 years old.MethodsFour electronic databases were searched to identify potentially relevant papers. Demographics and information on sarcopenia and alcohol consumption were extracted from relevant papers. The relationship between sarcopenia and alcohol consumption was described using odds ratios (ORs).ResultsOf 214 papers identified as potentially relevant, 13 were ultimately included in the meta-analyses. The papers provided data from 13,155 participants. The OR (95 % CI) for sarcopenia among alcohol drinkers was 0.67 (0.54–0.83) for males, 0.89 (0.73–1.08) for females, and 0.77 (0.67–0.88) for the overall population.ConclusionsThe results of this meta-analysis do not support alcohol consumption as a risk factor for sarcopenia.
To date, polymorphisms in several genes have been associated with a strength/power performance including alpha 3 actinin, ciliary neurotrophic factor, vitamin D receptor, or angiotensin I converting enzyme, underlining the importance of genetic component of the multifactorial strength/power-related phenotypes. The single nucleotide variation in peroxisome proliferator-activated receptor alpha gene (PPARA) intron 7 G/C (rs4253778; g.46630634G>C) has been repeatedly found to play a significant role in response to different types of physical activity. We investigated the effect of PPARA intron 7 G/C polymorphism specifically on anaerobic power output in a group of 77 elite male Czech ice hockey players (18–36 y). We determined the relative peak power per body weight (Pmax.kg−1) and relative peak power per fat free mass (W.kg−1 FFM) during the 30-second Wingate Test (WT30) on bicycle ergometer (Monark 894E Peak bike, MONARK, Sweden). All WT30s were performed during the hockey season. Overall genotype frequencies were 50.6% GG homozygotes, 40.3% CG heterozygotes, and 9.1% CC homozygotes. We found statistically significant differences in Pmax.kg−1 and marginally significant differences in Pmax.kg−1 FFM values in WT30 between carriers and non-carriers for C allele (14.6±0.2 vs. 13.9±0.3 W.kg−1 and 15.8±0.2 vs. 15.2±0.3 W.kg−1 FFM, P = 0.036 and 0.12, respectively). Furthermore, Pmax.kg−1 FFM strongly positively correlated with the body weight only in individuals with GG genotypes (R = 0.55; p<0.001). Our results indicate that PPARA 7C carriers exhibited higher speed strength measures in WT30. We hypothesize that C allele carriers within the cohort of trained individuals may possess a metabolic advantage towards anaerobic metabolism.
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