Brook Matthew S, Wilkinson Daniel J, Mitchell William K, Lund Jonathan N, Phillips Bethan E, Szewczyk Nathaniel J, Greenhaff Paul L, Smith Kenneth, Atherton Philip J
MRC-ARUK Centre of Excellence for Musculoskeletal Ageing Research, Clinical, Metabolic and Molecular Physiology, University of Nottingham, Derby, UK.
Departments of Surgery, Royal Derby Hospital, Derby, UK.
J Physiol. 2016 Dec 15;594(24):7399-7417. doi: 10.1113/JP272857. Epub 2016 Nov 7.
Resistance exercise training (RET) is one of the most effective strategies for preventing declines in skeletal muscle mass and strength with age. Hypertrophic responses to RET with age are diminished compared to younger individuals. In response to 6 weeks RET, we found blunted hypertrophic responses with age are underpinned by chronic deficits in long-term muscle protein synthesis. We show this is likely to be the result of multifactorial deficits in anabolic hormones and blunted translational efficiency and capacity. These results provide great insight into age-related exercise adaptations and provide a platform on which to devise appropriate nutritional and exercise interventions on a longer term basis.
Ageing is associated with impaired hypertrophic responses to resistance exercise training (RET). Here we investigated the aetiology of 'anabolic resistance' in older humans. Twenty healthy male individuals, 10 younger (Y; 23 ± 1 years) and 10 older (O; 69 ± 3 years), performed 6 weeks unilateral RET (6 × 8 repetitions, 75% of one repetition maximum (1-RM), 3 times per week). After baseline bilateral vastus lateralis (VL) muscle biopsies, subjects consumed 150 ml D O (70 atom%; thereafter 50 ml week ), further bilateral VL muscle biopsies were taken at 3 and 6 weeks to quantify muscle protein synthesis (MPS) via gas chromatography-pyrolysis-isotope ratio mass spectrometry. After RET, 1-RM increased in Y (+35 ± 4%) and O (+25 ± 3%; P < 0.01), while MVC increased in Y (+21 ± 5%; P < 0.01) but not O (+6 ± 3%; not significant (NS)). In comparison to Y, O displayed blunted RET-induced increases in muscle thickness (at 3 and 6 weeks, respectively, Y: +8 ± 1% and +11 ± 2%, P < 0.01; O: +2.6 ± 1% and +3.5 ± 2%, NS). While 'basal' longer term MPS was identical between Y and O (∼1.35 ± 0.1% day ), MPS increased in response to RET only in Y (3 weeks, Y: 1.61 ± 0.1% day ; O: 1.49 ± 0.1% day ). Consistent with this, O exhibited inferior ribosomal biogenesis (RNA:DNA ratio and c-MYC induction: Y: +4 ± 2 fold change; O: +1.9 ± 1 fold change), translational efficiency (S6K1 phosphorylation, Y: +10 ± 4 fold change; O: +4 ± 2 fold change) and anabolic hormone milieu (testosterone, Y: 367 ± 19; O: 274 ± 19 ng dl (all P < 0.05). Anabolic resistance is thus multifactorial.
抗阻运动训练（RET）是预防骨骼肌质量和力量随年龄下降的最有效策略之一。与年轻人相比，随着年龄增长，对RET的肥大反应会减弱。在进行6周的RET后，我们发现随着年龄增长，肥大反应减弱是由长期肌肉蛋白合成的慢性缺陷所致。我们表明，这可能是合成代谢激素多因素缺陷以及翻译效率和能力减弱的结果。这些结果为与年龄相关的运动适应性提供了深刻见解，并为制定长期适当的营养和运动干预措施提供了一个平台。
衰老与抗阻运动训练（RET）引起的肥大反应受损有关。在此，我们研究了老年人“合成代谢抵抗”的病因。20名健康男性个体，10名年轻人（Y组；23±1岁）和10名老年人（O组；69±3岁），进行了6周的单侧RET（6组，每组8次重复，1次重复最大值（1-RM）的75%，每周3次）。在进行基线双侧股外侧肌（VL）肌肉活检后，受试者饮用150毫升D2O（70原子%；此后每周50毫升），在3周和6周时再次进行双侧VL肌肉活检，通过气相色谱-热解-同位素比率质谱法量化肌肉蛋白合成（MPS）。RET后，1-RM在Y组增加（+35±4%），在O组增加（+25±3%；P<0.01），而最大随意收缩（MVC）在Y组增加（+21±5%；P<0.01），在O组未增加（+6±3%；无显著性差异（NS））。与Y组相比，O组在RET诱导的肌肉厚度增加方面表现出减弱（分别在3周和6周时，Y组：+8±1%和+11±2%，P<0.01；O组：+_2.6±1%和+3.5±2%，无显著性差异）。虽然Y组和O组之间的“基础”长期MPS相同（约1.35±0.1%/天），但MPS仅在Y组对RET有反应时增加（3周时，Y组：1.61±0.1%/天；O组：1.49±0.1%/天）。与此一致的是，O组的核糖体生物合成较差（RNA:DNA比率和c-MYC诱导：Y组：+4±2倍变化；O组：+1.9±1倍变化），翻译效率（S6K1磷酸化，Y组：+10±4倍变化；O组：+4±2倍变化）和合成代谢激素环境（睾酮，Y组：367±19；O组：274±19纳克/分升（所有P<0.05）。因此，合成代谢抵抗是多因素的。
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