Research Institute for Sport and Exercise Sciences (RISES), Liverpool John Moores University, Byrom Street, Liverpool, L3 3AF, UK.
J Physiol. 2021 Jun;599(11):2823-2849. doi: 10.1113/JP281127. Epub 2021 May 3.
Muscle glycogen and intramuscular triglycerides (IMTG, stored in lipid droplets) are important energy substrates during prolonged exercise. Exercise-induced changes in lipid droplet (LD) morphology (i.e. LD size and number) have not yet been studied under nutritional conditions typically adopted by elite endurance athletes, that is, after carbohydrate (CHO) loading and CHO feeding during exercise. We report for the first time that exercise reduces IMTG content in both central and peripheral regions of type I and IIa fibres, reflective of decreased LD number in both fibre types whereas reductions in LD size were exclusive to type I fibres. Additionally, CHO feeding does not alter subcellular IMTG utilisation, LD morphology or muscle glycogen utilisation in type I or IIa/II fibres. In the absence of alterations to muscle fuel selection, CHO feeding does not attenuate cell signalling pathways with regulatory roles in mitochondrial biogenesis.
We examined the effects of carbohydrate (CHO) feeding on lipid droplet (LD) morphology, muscle glycogen utilisation and exercise-induced skeletal muscle cell signalling. After a 36 h CHO loading protocol and pre-exercise meal (12 and 2 g kg , respectively), eight trained males ingested 0, 45 or 90 g CHO h during 180 min cycling at lactate threshold followed by an exercise capacity test (150% lactate threshold). Muscle biopsies were obtained pre- and post-completion of submaximal exercise. Exercise decreased (P < 0.01) glycogen concentration to comparable levels (∼700 to 250 mmol kg DW), though utilisation was greater in type I (∼40%) versus type II fibres (∼10%) (P < 0.01). LD content decreased in type I (∼50%) and type IIa fibres (∼30%) (P < 0.01), with greater utilisation in type I fibres (P < 0.01). CHO feeding did not affect glycogen or IMTG utilisation in type I or II fibres (all P > 0.05). Exercise decreased LD number within central and peripheral regions of both type I and IIa fibres, though reduced LD size was exclusive to type I fibres. Exercise induced (all P < 0.05) comparable AMPK (∼4-fold), p53 (∼2-fold) and CaMKII phosphorylation (∼2-fold) with no effects of CHO feeding (all P > 0.05). CHO increased exercise capacity where 90 g h (233 ± 133 s) > 45 g h (156 ± 66 s; P = 0.06) > 0 g h (108 ± 54 s; P = 0.03). In conditions of high pre-exercise CHO availability, we conclude CHO feeding does not influence exercise-induced changes in LD morphology, glycogen utilisation or cell signalling pathways with regulatory roles in mitochondrial biogenesis.
在长时间运动中，肌肉糖原和肌内甘油三酯（IMTG，储存在脂滴中）是重要的能量底物。在精英耐力运动员通常采用的营养条件下，即运动过程中碳水化合物（CHO）补充和 CHO 喂养后，脂滴（LD）形态的运动诱导变化（即 LD 大小和数量）尚未得到研究。我们首次报道，运动降低了 I 型和 IIa 型纤维中央和外周区域的 IMTG 含量，反映了两种纤维类型的 LD 数量减少，而 LD 大小的减少则仅限于 I 型纤维。此外，CHO 喂养不会改变 I 型或 IIa/II 纤维的亚细胞 IMTG 利用、LD 形态或肌肉糖原利用。在没有改变肌肉燃料选择的情况下，CHO 喂养不会减弱细胞信号通路，这些信号通路在调节线粒体生物发生中具有重要作用。
我们研究了 CHO 喂养对脂滴（LD）形态、肌肉糖原利用和运动诱导的骨骼肌细胞信号的影响。在 36 小时的 CHO 加载方案和运动前餐（分别为 12 克和 2 克/公斤）后，8 名训练有素的男性在乳酸阈下进行 180 分钟的自行车运动，并在运动能力测试（150%乳酸阈）前摄入 0、45 或 90 克/小时的 CHO。在完成亚最大强度运动前和后获取肌肉活检。运动降低（P<0.01）了糖原浓度，使其达到相似的水平（约 700 至 250 毫摩尔/公斤干重），但 I 型纤维（约 40%）的利用度高于 II 型纤维（约 10%）（P<0.01）。I 型（约 50%）和 IIa 型纤维（约 30%）的 LD 含量减少（P<0.01），I 型纤维的利用度更高（P<0.01）。CHO 喂养对 I 型或 II 纤维的糖原或 IMTG 利用没有影响（均 P>0.05）。运动降低了 I 型和 IIa 型纤维中央和外周区域的 LD 数量，而减少 LD 大小仅见于 I 型纤维。运动诱导了 AMPK（约 4 倍）、p53（约 2 倍）和 CaMKII 磷酸化（约 2 倍）（均 P<0.05），而 CHO 喂养没有影响（均 P>0.05）。CHO 增加了运动能力，其中 90 克/小时（233±133 秒）>45 克/小时（156±66 秒；P=0.06）>0 克/小时（108±54 秒；P=0.03）。在高运动前 CHO 可用性的条件下，我们得出结论，CHO 喂养不会影响运动诱导的 LD 形态、糖原利用或细胞信号通路的变化，这些信号通路在调节线粒体生物发生中具有重要作用。
