Effect of high-intensity interval training on mitochondrial autophagy in leukocyte after rush entry into plateau
LIU Jing1, ZHANG Hongying2, DUAN Fuqiang3, PENG Peng4, QIN Yongsheng4, and BO Hai4
1. Department of Pathology, Affiliated Hospital of Logistics University, Chinese People’s Armed Police Forces, Tianjin 300162, China; 2. Department of Quality Management, General Hospital of Chinese People’s Armed Police Forces, Beijing 100039, China; 3. Department of Health, Xizang Autonomous Regional Corps Hospital, Chinese People’s Armed Police Forces, Lasa 850000, China; 4. Department of Military Training Medicines, Logistics University of Chinese People’s Armed Police Forces, Tianjin 300309, China
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.
刘静,张红英,段富强,彭朋,秦永生,薄海. 高强度间歇运动训练对急进高原淋巴细胞线粒体自噬的影响[J]. 武警医学, 2014, 25(12): 1228-1231.
LIU Jing, ZHANG Hongying, DUAN Fuqiang, PENG Peng, QIN Yongsheng, and BO Hai. Effect of high-intensity interval training on mitochondrial autophagy in leukocyte after rush entry into plateau. Med. J. Chin. Peop. Armed Poli. Forc., 2014, 25(12): 1228-1231.
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.
[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.
[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.
[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.
[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.
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.
[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.
[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.
[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.
[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.
[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.
[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.
[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.
[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.
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.