Institute of Sport, Exercise and Active Living (ISEAL), Victoria University, Melbourne, Vic., Australia.
Department of Biochemistry and Genetics, La Trobe Institute for Molecular Science, La Trobe University, Melbourne, Vic., Australia.
Acta Physiol (Oxf). 2018 Jun;223(2):e13045. doi: 10.1111/apha.13045. Epub 2018 Feb 27.
This study explored the effects of blood flow restriction (BFR) on mRNA responses of PGC-1α (total, 1α1, and 1α4) and Na ,K -ATPase isoforms (NKA; α , β , and FXYD1) to an interval running session and determined whether these effects were related to increased oxidative stress, hypoxia, and fibre type-specific AMPK and CaMKII signalling, in human skeletal muscle.
In a randomized, crossover fashion, 8 healthy men (26 ± 5 year and 57.4 ± 6.3 mL kg min ) completed 3 exercise sessions: without (CON) or with blood flow restriction (BFR), or in systemic hypoxia (HYP, ~3250 m). A muscle sample was collected before (Pre) and after exercise (+0 hour, +3 hours) to quantify mRNA, indicators of oxidative stress (HSP27 protein in type I and II fibres, and catalase and HSP70 mRNA), metabolites, and α-AMPK Thr /α-AMPK, ACC Ser /ACC, CaMKII Thr /CaMKII, and PLBSer /PLB ratios in type I and II fibres.
Muscle hypoxia (assessed by near-infrared spectroscopy) was matched between BFR and HYP, which was higher than CON (~90% vs ~70%; P < .05). The mRNA levels of FXYD1 and PGC-1α isoforms (1α1 and 1α4) increased in BFR only (P < .05) and were associated with increases in indicators of oxidative stress and type I fibre ACC Ser /ACC ratio, but dissociated from muscle hypoxia, lactate, and CaMKII signalling.
Blood flow restriction augmented exercise-induced increases in muscle FXYD1 and PGC-1α mRNA in men. This effect was related to increased oxidative stress and fibre type-dependent AMPK signalling, but unrelated to the severity of muscle hypoxia, lactate accumulation, and modulation of fibre type-specific CaMKII signalling.
本研究旨在探讨血流限制(BFR)对 PGC-1α(总、1α1 和 1α4)和 Na +,K + -ATP 酶同工型(NKA;α、β 和 FXYD1)mRNA 对间歇跑运动反应的影响,并确定这些影响是否与增加的氧化应激、缺氧以及纤维类型特异性 AMPK 和 CaMKII 信号有关,在人体骨骼肌中。
在一项随机交叉研究中,8 名健康男性(26±5 岁,57.4±6.3 mL·kg-1·min-1)完成了 3 项运动实验:无血流限制(CON)或血流限制(BFR)或全身缺氧(HYP,~3250 m)。在运动前(Pre)和运动后(+0 小时、+3 小时)采集肌肉样本,以定量测量 mRNA、氧化应激标志物(I 型和 II 型纤维中的 HSP27 蛋白,以及过氧化氢酶和 HSP70 mRNA)、代谢物以及 I 型和 II 型纤维中α-AMPK Thr/α-AMPK、ACC Ser/ACC、CaMKII Thr/CaMKII 和 PLBSer/PLB 的比值。
BFR 和 HYP 时肌肉缺氧(通过近红外光谱评估)相匹配,高于 CON(90%比70%;P<.05)。仅在 BFR 中 FXYD1 和 PGC-1α 同工型(1α1 和 1α4)的 mRNA 水平增加(P<.05),并与氧化应激标志物和 I 型纤维 ACC Ser/ACC 比值的增加相关,但与肌肉缺氧、乳酸和 CaMKII 信号无关。
血流限制增强了男性运动诱导的肌肉 FXYD1 和 PGC-1α mRNA 的增加。这种效应与增加的氧化应激和纤维类型依赖性 AMPK 信号有关,但与肌肉缺氧的严重程度、乳酸积累以及纤维类型特异性 CaMKII 信号的调节无关。