Hulston Carl J, Woods Rachel M, Dewhurst-Trigg Rebecca, Parry Sion A, Gagnon Stephanie, Baker Luke, James Lewis J, Markey Oonagh, Martin Neil R W, Ferguson Richard A, van Hall Gerrit
School of Sport, Exercise & Health Sciences, Loughborough University, Loughborough, Leicestershire, United Kingdom.
Clinical Metabolomics Core Facility, Department of Clinical Biochemistry, Rigshospitalet, Department of Biomedical Sciences, University of Copenhagen, Copenhagen, Denmark.
Physiol Rep. 2018 Jul;6(14):e13799. doi: 10.14814/phy2.13799.
Obese individuals exhibit a diminished muscle protein synthesis response to nutrient stimulation when compared with their lean counterparts. However, the effect of obesity on exercise-stimulated muscle protein synthesis remains unknown. Nine lean (23.5 ± 0.6 kg/m ) and 8 obese (33.6 ± 1.2 kg/m ) physically active young adults participated in a study that determined muscle protein synthesis and intracellular signaling at rest and following an acute bout of resistance exercise. Mixed muscle protein synthesis was determined by combining stable isotope tracer ([ C ]phenylalanine) infusion with serial biopsies of the vastus lateralis. A unilateral leg resistance exercise model was adopted so that resting and postexercise measurements of muscle protein synthesis could be obtained simultaneously. Obesity was associated with higher basal levels of serum insulin (P < 0.05), plasma triacylglycerol (P < 0.01), plasma cholesterol (P < 0.01), and plasma CRP (P < 0.01), as well as increased insulin resistance determined by HOMA-IR (P < 0.05). However, resting and postexercise rates of muscle protein synthesis were not significantly different between lean and obese participants (P = 0.644). Furthermore, resistance exercise stimulated muscle protein synthesis (~50% increase) in both groups (P < 0.001), with no difference between lean and obese (P = 0.809). Temporal increases in the phosphorylation of intracellular signaling proteins (AKT/4EBP1/p70S6K) were observed within the exercised leg (P < 0.05), with no differences between lean and obese. These findings suggest a normal anabolic response to muscle loading in obese young adults.
与瘦人相比,肥胖个体对营养刺激的肌肉蛋白质合成反应减弱。然而,肥胖对运动刺激的肌肉蛋白质合成的影响尚不清楚。9名瘦的(23.5±0.6kg/m²)和8名肥胖的(33.6±1.2kg/m²)身体活跃的年轻成年人参与了一项研究,该研究测定了静息状态和急性抗阻运动后肌肉蛋白质合成及细胞内信号传导情况。通过将稳定同位素示踪剂([¹³C]苯丙氨酸)输注与股外侧肌的系列活检相结合来测定混合肌肉蛋白质合成。采用单侧腿部抗阻运动模型,以便能同时获得静息和运动后肌肉蛋白质合成的测量值。肥胖与较高的基础血清胰岛素水平(P<0.05)、血浆三酰甘油(P<0.01)、血浆胆固醇(P<0.01)和血浆CRP(P<0.01)相关,同时通过HOMA-IR测定的胰岛素抵抗增加(P<0.05)。然而,瘦人和肥胖参与者之间静息和运动后的肌肉蛋白质合成速率无显著差异(P=0.644)。此外,两组抗阻运动均刺激了肌肉蛋白质合成(增加约50%)(P<0.001),瘦人和肥胖者之间无差异(P=0.809)。在运动的腿部观察到细胞内信号蛋白(AKT/4EBP1/p70S6K)磷酸化的时间性增加(P<0.05),瘦人和肥胖者之间无差异。这些发现表明肥胖年轻成年人对肌肉负荷有正常的合成代谢反应。