阻力训练、骨骼肌肥大和葡萄糖稳态:它们之间有多大关系?系统回顾与元分析》。

J Paquin, R Tremblay, H Islam, E Riesco, A Marcotte-Chénard, I J Dionne
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引用次数: 0

摘要

阻力训练(RT)可促进骨骼肌(Skm)肥大、增强肌肉力量并改善代谢健康。尽管对阻力训练对健康和运动表现的益处进行了大量研究,但无脂质量(FFM,肌肉肥大的替代标志物)的变化是否会缓和阻力训练引起的葡萄糖稳态改善尚未确定。本荟萃分析旨在研究 RT 诱导的 Skm 肥大是否会促进葡萄糖代谢的改善,并探讨生物性别和训练参数等混杂因素。采用方差随机效应进行随机效应荟萃分析。根据异质性(I2)对混杂因素进行元回归。对 33 项干预研究进行的分析表明,研究内 FFM 显著增加,效应大小适中(研究内:(效应大小;ES = 0.24 [0.10; 0.39];p = 0.002;I2 = 56%),与对照组相比有显著性趋势(ES = 0.42 [-0.04-0.88]; p = 0.07)。在研究范围内,葡萄糖耐量显著增加(2 小时葡萄糖:ES = -0.3 [-0.50; -0.11]; p I2 = 43%; 葡萄糖曲线下面积 (AUC): -0.40 [-0.66; -0.13] I2 = 76.1%; p I2 = 53.0%; p
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Resistance training, skeletal muscle hypertrophy, and glucose homeostasis: how related are they? A Systematic review and Meta-analysis.

Resistance training (RT) promotes skeletal muscle (Skm) hypertrophy, increases muscular strength, and improves metabolic health. Whether changes in fat-free mass (FFM; a surrogate marker of muscle hypertrophy) moderate RT-induced improvements in glucose homeostasis has not been determined, despite extensive research on the benefits of RT for health and performance. The aim of this meta-analysis is to examine whether RT-induced Skm hypertrophy drives improvements in glucose metabolism and to explore confounders, such as biological sex and training parameters. Random-effects meta-analyses were performed using variance random effects. Meta-regressions were performed for confounding factors depending on the heterogeneity (I2). Analyses from 33 intervention studies revealed significant within-study increases in FFM with a moderate effect size (within-studies: (effect size; ES = 0.24 [0.10; 0.39]; p = 0.002; I= 56%) and a tendency for significance when compared with control groups (ES = 0.42 [-0.04-0.88]; p = 0.07). Within-study significant increases in glucose tolerance (2 h glucose: ES = -0.3 [-0.50; -0.11]; p < 0.01; I= 43%; glucose area under the curve (AUC): -0.40 [-0.66; -0.13] I= 76.1%; p < 0.01) and insulin sensitivity (ES = 0.38 [0.13; 0.62]; I= 53.0%; p < 0.01) were also apparent with RT. When compared to control groups, there was no significant difference in 2 h glucose, nor in glucose AUC from baseline in RT intervention groups. Meta-regression analyses failed to consistently reveal increases in FFM as a moderator of glucose homeostasis. Other mixed-effect models were also unsuccessful to unveil biological sex or training parameters as moderators of FFM increases and glucose homeostasis changes. Although Skm hypertrophy and improvements in glycemic control occur concurrently during RT, changes in these variables were not always related. Well-controlled trials including detailed description of training parameters are needed to inform RT guidelines for improving metabolic health. Registration and protocol number (Prospero): CRD42023397362.

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