目的 观察平原短期高强度间歇运动训练(high-intensity interval training, HIT)对青年男性急进高原淋巴细胞线粒体自噬的影响。方法 30名世居平原青年男性随机分为无运动训练组(NT组,n=15)和HIT组(n=15)。HIT组受试者进行HIT训练,以90%~95%心率贮备强度快跑3 min,间歇以45%~50%心率贮备强度慢跑3 min,重复6个循环,1次/d,共2周。NT组除日常活动外不进行任何形式运动训练。训练后所有受试者同批次急进高原,在移居高原24 h检测淋巴细胞线粒体复合体活性,以及PINK1、淋巴细胞线粒体自噬蛋白Bnip3和Beclin-1蛋白表达。结果 与NT组比较,HIT组Bnip3(100±18 vs 136±32)和Beclin-1(100±19 vs 119±26)表达明显升高(P均＜0.05),线粒体复合体Ⅰ、Ⅱ、Ⅳ和ATP合成酶活性也明显升高(P＜0.05),PINK1蛋白表达明显降低(P＜0.01)。结论 平原阶段短期HIT可通过上调线粒体自噬阈,从而减少高原低氧环境下淋巴细胞线粒体损伤,提高线粒体能量代谢水平。
Abstract
Objective To explore the effect of short-term high-intensity interval training (HIT) in plain on mitochondrial autophagy in leukocyte after rush entry into plateau. Methods Thirty male lowlanders were randomly divided into two groups: untrained group (NT, n=15) and HIT group (n=15). Participants in the HIT group run at a high training intensity, 90%-95% heart rate reserve (HRR) for 3 min, with active pauses of 3 min of walking at 45%-50% of HRR. Participants in the HIT group underwent six sessions of HIT for 36 min/d, 7 days per week for 2 weeks. After training, participants in both HIT and NT groups traveled into plateau in the same batch. Activities of mitochondrial complex, PINK1, Bnip3 and Beclin-1 protein expression in leukocyte were measured in plateau at 24 h after entry. Results As compared with NT group, in HIT group, mitochondrial autophagy proteins Bnip3 (100±18 vs 136±32) and Beclin-1(100±19 vs 119±26) expression were significantly elevated(P<0.05). Furthermore, mitochondrial complex Ⅰ, Ⅱ, Ⅳ and ATP synthase activities were significantly elevated (P<0.05), whereas PINK1 protein expression was significantly decreased (P<0.01). Conclusions Short-term HIT in plain can blunt high altitude hypoxia induced mitochondrial impariment and elevated mitochondrial energy metabolism through upregulation of mitochondrial autophagy.
关键词
高强度间歇运动训练 /
高原低氧 /
淋巴细胞 /
线粒体自噬 /
能量代谢
Key words
high-intensity interval training /
high altitude hypoxia /
leukocyte /
mitochondrial autophagy /
energy metabolism
{{custom_sec.title}}
{{custom_sec.title}}
{{custom_sec.content}}
参考文献
[1] Oliveira B R, Slama F A, Deslandes A C, et al. Continuous and high-intensity interval training: which promotes higher pleasure?[J]. PLoS One,2013,8(11):e79965.
[2] Gibala M J, Jones A M. Physiological and performance adaptations to high-intensity interval training [J]. Nestle Nutr Inst Workshop Ser, 2013, 76: 51-60.
[3] 薄 海,彭 朋,段富强,等.高原习服进程中淋巴细胞线粒体生物合成和自噬的变化规律[J]. 武警后勤学院学报(医学版), 2014, 23(7): 553-560.
[4] 薄 海, 果风春, 段富强, 等. 高原习服过程淋巴细胞线粒体DNA含量及氧化损伤变化规律[J]. 武警医学, 2014, 25(8): 11-14.
[5] Bo H, Wang Y H, Li H Y, et al. Endurance training attenuates the bioenergetics alterations of rat skeletal muscle mitochondria submitted to acute hypoxia: Role of ROS and UCP3[J]. Sheng Li Xue Bao, 2008, 60(6): 767-776.
[6] Weng T P, Huang S C, Chuang Y F, et al. Effects of interval and continuous exercise training on CD4 lymphocyte apoptotic and autophagic responses to hypoxic stress in sedentary men[J].PLoS One, 2013,8(11):e80248.
[7] Shinde S, Pasupathy K. Respiratory-chain enzyme activities in isolated mitochondria of lymphocytes from patients with Parkinson’s disease: preliminary study [J]. Neurol India, 2006, 54(4): 390-393.
[8] Freyssin C, Verkindt C, Prieur F, et al. Cardiac rehabilitation in chronic heart failure: effect of an 8-week, high-intensity interval training versus continuous training [J]. Arch Phys Med Rehabil, 2012, 93(8): 1359-1364.
[9] Wang L, Sahlin K. The effect of continuous and interval exercise on PGC-1alpha and PDK4 mRNA in type I and type II fibres of human skeletal muscle [J]. Acta Physiol (Oxf), 2012, 204(4): 525-532.
[10] 薄 海, 李 玲, 段富强, 等. 低氧复合运动抑制低氧诱导的骨骼肌线粒体DNA氧化损伤[J]. 生理学报, 2014, 66(5): 597-604.
[11] Siddall H K, Yellon D M, Ong S B, et al. Loss of PINK1 increases the heart's vulnerability to ischemia-reperfusion injury [J]. PLoS One,2014,8(4):e62400.
[12] Zhu J, Wang K Z, Chu C T. After the banquet: Mitochondrial biogenesis, mitophagy and cell survival [J]. Autophagy, 2013, 9(11): 1356-1362.
[13] Zhang H, Bosch-marce M, Shimoda L A, et al. Mitochondrial autophagy is an HIF-1-dependent adaptive metabolic response to hypoxia [J]. J Biol Chem, 2008, 283(16): 10892-10903.
[14] He C, Bassik M C, Moresi V, et al. Exercise-induced BCL2-regulated autophagy is required for muscle glucose homeostasis[J].Nature, 2012,481(7382):511-515.
[15] Kim Y A, Kim Y S, Oh S L, et al. Autophagic response to exercise training in skeletal muscle with age [J]. J Physiol Biochem, 2013, 69(4): 697-705.
基金
国家自然科学基金青年基金(31200894);天津市应用基础及前沿技术研究计划青年基金(12JCQNJC07900)
PDF(846 KB)
