The effect of exercise intensity on ischemia/reperfusion injury and myokine profile in diabetic cardiomyopathy
äºComparative Exercise PhysiologySearch for other papers by F. Akat in
Current site
Google Scholar
Search for other papers by Y. Tatar in
Current site
Google Scholar
Search for other papers by H. Çelik in
Current site
Google Scholar
Search for other papers by H. Fıçıcılar in
Current site
Google Scholar
Search for other papers by A.D. Dursun in
Current site
Google Scholar
Search for other papers by M. BaştugÌ in
Current site
Google Scholar
Abstract
Diabetes is a metabolic disorder characterised by hyperglycaemia. The diabetic heart becomes more susceptible to ischemic injury. Although exercise induces a cardioprotective phenotype, the determination of accurate protocol is crucial. We compared two different exercise intensities in the diabetes model and evaluated the role of myokines in exercise-induced cardioprotection. Male, adult, Wistar albino rats were used (n = 20 each). First, animals were divided into two groups: Non-Diabetic (ND), Diabetic (DM); then groups were further divided into subgroups: Sedentary (S), Training-1 (T1 = 10 m/min, 0° inclination), and Training-2 (T2 = 20 m/min, 10° inclination). Diabetes was induced by streptozotocin (60 mg/kg; i.p.). Animals exercised on a treadmill 5 days/a week for 6 weeks. Then, hearts were attached to the Langendorff apparatus and baseline functional parameters were measured. After 30â/120âI/R protocol, infarct size was evaluated with tetrazolium chloride staining. Interleukin-6, FNDC5, and myonectin levels were measured both in the soleus and the left ventricle. We observed cardiac hypertrophy and impaired baseline LV function in diabetes. Infarct size was significantly larger in diabetics and only T1 decreased the infarct size whereas T2 further aggravated it. Moreover, post-ischemic recovery was worst in diabetic-T2 group. Irisin and myonectin levels were decreased in the soleus muscle of diabetic animals. T1 increased the myonectin levels in the left ventricle of non-diabetics, and this effect was blunted in diabetic-T1 animals. As a conclusion, light-intensity exercise is a better approach to prevent ischemic damage in diabetes besides moderate intensity may be hazardous in diabetic population.
Purchase
Buy instant access (PDF download and unlimited online access):
Institutional Login
Log in with Open Athens, Shibboleth, or your institutional credentials
Personal login
Log in with your brill.com account
-
Akat, F., Fıçıcılar, H., Durak, A., Tuncay, E., Dursun, A.D., Topal Çelikkan, F., SabuncuogÌlu, B., Turan, B. and BaştugÌ, M., 2018. Intermittent hypoxia induces beneficial cardiovascular remodeling in left ventricular function of type 1 diabetic rat. Anatolian Journal of Cardiology 19: 259-266. https://doi.org/10.14744/AnatolJCardiol.2018.00236
-
Anderson, E. and Durstine, J.L., 2019. Physical activity, exercise, and chronic diseases: A brief review. Sports Medicine and Health Science 1: 3-10.
-
Beckman, J.A., Creager, M.A. and Libby, P., 2002. Diabetes and atherosclerosis: epidemiology, pathophysiology, and management. JAMA 287: 2570-2581. https://doi.org/10.1001/jama.287.19.2570
-
Bi, F., Xu, Y., Chen, G. and Wang, P., 2020. Anti-inflammatory and anti-endoplasmic reticulum stress effects of catalpol against myocardial ischemia-reperfusion injury in streptozotocin-induced diabetic rats. Anais da Academia Brasileira de CieÌncias 92: e20191148. https://doi.org/10.1590/0001-3765202020191148
-
Boström, P., Wu, J., Jedrychowski, M.P., Korde, A., Ye, L., Lo, J.C., Rasbach, K.A., Boström, E.A., Choi, J.H. and Long, J.Z., 2012. A PGC1-α-dependent myokine that drives brown-fat-like development of white fat and thermogenesis. Nature 481: 463-468.
-
Brawner, C.A., Churilla, J.R. and Keteyian, S.J., 2016. Prevalence of physical activity is lower among individuals with chronic disease. Medicine and Science in Sports and Exercise 48: 1062-1067. https://doi.org/10.1249/mss.0000000000000861
-
Breisch, E.A., White, F.C., Nimmo, L.E., McKirnan, M.D. and Bloor, C.M., 1986. Exercise-induced cardiac hypertrophy: a correlation of blood flow and microvasculature. Journal of Applied Physiology 60: 1259-1267. https://doi.org/10.1152/jappl.1986.60.4.1259
-
Cao, J., Vecoli, C., Neglia, D., Tavazzi, B., Lazzarino, G., Novelli, M., Masiello, P., Wang, Y.T., Puri, N., Paolocci, N., LâAbbate, A. and Abraham, N.G., 2012. Cobalt-protoporphyrin improves heart function by blunting oxidative stress and restoring NO synthase equilibrium in an animal model of experimental diabetes. Frontiers in Physiology 3: 160. https://doi.org/10.3389/fphys.2012.00160
-
Crisafulli, A., Pagliaro, P., Roberto, S., Cugusi, L., Mercuro, G., Lazou, A., Beauloye, C., Bertrand, L., Hausenloy, D.J., Aragno, M. and Penna, C., 2020. Diabetic cardiomyopathy and ischemic heart disease: prevention and therapy by exercise and conditioning. International Journal of Molecular Sciences 21: 2896. https://doi.org/10.3390/ijms21082896
-
Daskalopoulou, S.S., Cooke, A.B., Gomez, Y.H., Mutter, A.F., Filippaios, A., Mesfum, E.T. and Mantzoros, C.S., 2014. Plasma irisin levels progressively increase in response to increasing exercise workloads in young, healthy, active subjects. European Journal of Endocrinology 171: 343-352. https://doi.org/10.1530/eje-14-0204
-
Dawn, B., Xuan, Y.T., Guo, Y., Rezazadeh, A., Stein, A.B., Hunt, G., Wu, W.J., Tan, W. and Bolli, R., 2004. IL-6 plays an obligatory role in late preconditioning via JAK-STAT signaling and upregulation of iNOS and COX-2. Cardiovascular Research 64: 61-71. https://doi.org/10.1016/j.cardiores.2004.05.011
-
Demirel, H.A., Powers, S.K., Zergeroglu, M.A., Shanely, R.A., Hamilton, K., Coombes, J. and Naito, H., 2001. Short-term exercise improves myocardial tolerance to in vivo ischemia-reperfusion in the rat. Journal of Applied Physiology 91: 2205-2212. https://doi.org/10.1152/jappl.2001.91.5.2205
-
Devereux, R.B., Roman, M.J., Paranicas, M., OâGrady, M.J., Lee, E.T., Welty, T.K., Fabsitz, R.R., Robbins, D., Rhoades, E.R. and Howard, B.V., 2000. Impact of diabetes on cardiac structure and function: the strong heart study. Circulation 101: 2271-2276. https://doi.org/10.1161/01.cir.101.19.2271
-
Durrer, C., Francois, M., Neudorf, H. and Little, J.P., 2017. Acute high-intensity interval exercise reduces human monocyte Toll-like receptor 2 expression in type 2 diabetes. American Journal of Physiology â Regulatory, Integrative and Comparative Physiology 312: R529-R538. https://doi.org/10.1152/ajpregu.00348.2016
-
Eckel, J., 2019. Myokines in metabolic homeostasis and diabetes. Diabetologia 62: 1523-1528. https://doi.org/10.1007/s00125-019-4927-9
-
Erickson, H.P., 2013. Irisin and FNDC5 in retrospect: An exercise hormone or a transmembrane receptor? Adipocyte 2: 289-293. https://doi.org/10.4161/adip.26082
-
Farrell, P.A., Joyner, M.J. and Caiozzo, V., 2011. ACSMâs advanced exercise physiology. Wolters Kluwer Health Adis (ESP), Philadelphia, PA, USA.
-
Febbraio, M.A., Hiscock, N., Sacchetti, M., Fischer, C.P. and Pedersen, B.K., 2004. Interleukin-6 is a novel factor mediating glucose homeostasis during skeletal muscle contraction. Diabetes 53: 1643-1648. https://doi.org/10.2337/diabetes.53.7.1643
-
Ferrer-MartıÌnez, A., Ruiz-Lozano, P. and Chien, K.R., 2002. Mouse PeP: a novel peroxisomal protein linked to myoblast differentiation and development. Developmental Dynamics 224: 154-167.
-
Han, Q., Liu, Q., Zhang, H., Lu, M., Wang, H., Tang, F. and Zhang, Y., 2019. Simvastatin improves cardiac hypertrophy in diabetic rats by attenuation of oxidative stress and inflammation induced by calpain-1-mediated activation of nuclear factor-κB (NF-κB). Medical Science Monitor 25: 1232-1241. https://doi.org/10.12659/msm.913244
-
Hart, G., 2003. Exercise-induced cardiac hypertrophy: a substrate for sudden death in athletes? Experimental Physiology 88: 639-644. https://doi.org/10.1113/eph8802619
-
Hou, Z., Qin, X., Hu, Y., Zhang, X., Li, G., Wu, J., Li, J., Sha, J., Chen, J., Xia, J., Wang, L. and Gao, F., 2019. Longterm exercise-derived exosomal miR-342-5p: a novel exerkine for cardioprotection. Circulation Research 124: 1386-1400. https://doi.org/10.1161/circresaha.118.314635
-
Hu, W., Wang, R., Li, J., Zhang, J. and Wang, W., 2016. Association of irisin concentrations with the presence of diabetic nephropathy and retinopathy. Annals of Clinical Biochemistry 53: 67-74.
-
Kannel, W.B., Hjortland, M. and Castelli, W.P., 1974. Role of diabetes in congestive heart failure: the Framingham study. American Journal of Cardiology 34: 29-34. https://doi.org/10.1016/0002-9149(74)90089-7
-
Kerner, W. and Brückel, J., 2014. Definition, classification and diagnosis of diabetes mellitus. Experimental and Clinical Endocrinology and Diabetes 122: 384-386. https://doi.org/10.1055/s-0034-1366278
-
Lahaye Sle, D., Gratas-Delamarche, A., MalardeÌ, L., Vincent, S., Zguira, M.S., Morel, S.L., Delamarche, P., Zouhal, H., CarreÌ, F. and Bekono, F.R., 2010. Intense exercise training induces adaptation in expression and responsiveness of cardiac β-adrenoceptors in diabetic rats. Cardiovascular Diabetology 9: 72. https://doi.org/10.1186/1475-2840-9-72
-
Lee, J.H. and Jun, H.S., 2019. Role of myokines in regulating skeletal muscle mass and function. Frontiers in Physiology 10: 42. https://doi.org/10.3389/fphys.2019.00042
-
LegaÌrd, G.E. and Pedersen, B.K., 2019. Muscle as an endocrine organ. In: Zoladz, J.A. (ed.) Muscle and exercise physiology. Academic Press, Cambridge, MA, USA, pp. 285-307. https://doi.org/10.1016/B978-0-12-814593-7.00013-X
-
Li, H., Yao, W., Irwin, M.G., Wang, T., Wang, S., Zhang, L. and Xia, Z., 2015. Adiponectin ameliorates hyperglycemia-induced cardiac hypertrophy and dysfunction by concomitantly activating Nrf2 and Brg1. Free Radical Biology and Medicine 84: 311-321. https://doi.org/10.1016/j.freeradbiomed.2015.03.007
-
Liao, Q., Qu, S., Tang, L.X., Li, L.P., He, D.F., Zeng, C.Y. and Wang, W.E., 2019. Irisin exerts a therapeutic effect against myocardial infarction via promoting angiogenesis. Acta Pharmacologica Sinica 40: 1314-1321. https://doi.org/10.1038/s41401-019-0230-z
-
McGinnis, G.R., Ballmann, C., Peters, B., Nanayakkara, G., Roberts, M., Amin, R. and Quindry, J.C., 2015. Interleukin-6 mediates exercise preconditioning against myocardial ischemia reperfusion injury. American Journal of Physiology â Heart and Circulatory Physiology 308: H1423-H1433.
-
Miki, T., Itoh, T., Sunaga, D. and Miura, T., 2012. Effects of diabetes on myocardial infarct size and cardioprotection by preconditioning and postconditioning. Cardiovascular Diabetology 11: 67. https://doi.org/10.1186/1475-2840-11-67
-
Otaka, N., Shibata, R., Ohashi, K., Uemura, Y., Kambara, T., Enomoto, T., Ogawa, H., Ito, M., Kawanishi, H., Maruyama, S., Joki, Y., Fujikawa, Y., Narita, S., Unno, K., Kawamoto, Y., Murate, T., Murohara, T. and Ouchi, N., 2018. Myonectin is an exercise-induced myokine that protects the heart from ischemia-reperfusion injury. Circulation Research 123: 1326-1338. https://doi.org/10.1161/circresaha.118.313777
-
Ouchi, N. and Walsh, K., 2012. Cardiovascular and metabolic regulation by the Adiponectin/C1q/tumor necrosis factor â related protein family of proteins. Circulation 125: 3066-3068.
-
Ãzçatal, Y., Akat, F., Tatar, Y., Fıçıcılar, H., SerdarogÌlu, B., Topal Çelikkan, F. and BaştugÌ, M., 2023. Effects of high-intensity interval training (HIIT) on skeletal muscle atrophy, function, and myokine profile in diabetic myopathy. Cytokine 169: 156279. https://doi.org/10.1016/j.cyto.2023.156279
-
Qiu, Z., Lei, S., Zhao, B., Wu, Y., Su, W., Liu, M., Meng, Q., Zhou, B., Leng, Y. and Xia, Z.Y., 2017. NLRP3 Inflammasome activation-mediated pyroptosis aggravates myocardial ischemia/reperfusion injury in diabetic rats. Oxidative Medicine and Cellular Longevity 2017: 9743280. https://doi.org/10.1155/2017/9743280
-
Riegel, B., Moser, D.K., Buck, H.G., Dickson, V.V., Dunbar, S.B., Lee, C.S., Lennie, T.A., Lindenfeld, J., Mitchell, J.E., Treat-Jacobson, D.J. and Webber, D.E., 2017. Self-care for the prevention and management of cardiovascular disease and stroke: a scientific statement for healthcare professionals from the American Heart Association. Journal of the American Heart Association 6. https://doi.org/10.1161/jaha.117.006997
-
Seldin, M.M., Peterson, J.M., Byerly, M.S., Wei, Z. and Wong, G.W., 2012. Myonectin (CTRP15), a novel myokine that links skeletal muscle to systemic lipid homeostasis. Journal of Biological Chemistry 287: 11968-11980. https://doi.org/10.1074/jbc.M111.336834
-
Severinsen, M.C.K. and Pedersen, B.K., 2020. Muscle-organ crosstalk: the emerging roles of myokines. Endocrine Reviews 41: 594-609. https://doi.org/10.1210/endrev/bnaa016
-
Smart, N., Mojet, M.H., Latchman, D.S., Marber, M.S., Duchen, M.R. and Heads, R.J., 2006. IL-6 induces PI 3-kinase and nitric oxide-dependent protection and preserves mitochondrial function in cardiomyocytes. Cardiovascular Research 69: 164-177.
-
Wang, H., Zhao, Y.T., Zhang, S., Dubielecka, P.M., Du, J., Yano, N., Chin, Y.E., Zhuang, S., Qin, G. and Zhao, T.C., 2017. Irisin plays a pivotal role to protect the heart against ischemia and reperfusion injury. Journal of Cellular Physiology 232: 3775-3785.
-
Wang, Z., Chen, K., Han, Y., Zhu, H., Zhou, X., Tan, T., Zeng, J., Zhang, J., Liu, Y. and Li, Y., 2018. Irisin protects heart against ischemia-reperfusion injury through a SOD2-dependent mitochondria mechanism. Journal of Cardiovascular Pharmacology 72: 259.
-
Whittington, H.J., Babu, G.G., Mocanu, M.M., Yellon, D.M. and Hausenloy, D.J., 2012. The diabetic heart: too sweet for its own good? Cardiology Research and Practice 2012: 845698. https://doi.org/10.1155/2012/845698
-
Yu, L.M., Dong, X., Xue, X.D., Xu, S., Zhang, X., Xu, Y.L., Wang, Z.S., Wang, Y., Gao, H., Liang, Y.X., Yang, Y. and Wang, H.S., 2021. Melatonin attenuates diabetic cardiomyopathy and reduces myocardial vulnerability to ischemia-reperfusion injury by improving mitochondrial quality control: Role of SIRT6. Journal of Pineal Research 70: e12698. https://doi.org/10.1111/jpi.12698
-
Zhang, B., Zhai, M., Li, B., Liu, Z., Li, K., Jiang, L., Zhang, M., Yi, W., Yang, J., Yi, D., Liang, H., Jin, Z., Duan, W. and Yu, S., 2018. Honokiol ameliorates myocardial ischemia/reperfusion injury in type 1 diabetic rats by reducing oxidative stress and apoptosis through activating the SIRT1-Nrf2 signaling pathway. Oxidative Medicine and Cellular Longevity 2018: 3159801. https://doi.org/10.1155/2018/3159801
| å ¨é¨æé´ | è¿å»ä¸å¹´ | è¿å»30天 | |
|---|---|---|---|
| æè¦æµè§æ¬¡æ° | 386 | 75 | 12 |
| å ¨ææµè§æ¬¡æ° | 12 | 1 | 0 |
| PDFä¸è½½æ¬¡æ° | 53 | 2 | 0 |
The effect of exercise intensity on ischemia/reperfusion injury and myokine profile in diabetic cardiomyopathy
äºComparative Exercise PhysiologySearch for other papers by F. Akat in
Current site
Google Scholar
PubMed
Search for other papers by Y. Tatar in
Current site
Google Scholar
PubMed
Search for other papers by H. Çelik in
Current site
Google Scholar
PubMed
Search for other papers by H. Fıçıcılar in
Current site
Google Scholar
PubMed
Search for other papers by A.D. Dursun in
Current site
Google Scholar
PubMed
Search for other papers by M. BaştugÌ in
Current site
Google Scholar
PubMed
Abstract
Diabetes is a metabolic disorder characterised by hyperglycaemia. The diabetic heart becomes more susceptible to ischemic injury. Although exercise induces a cardioprotective phenotype, the determination of accurate protocol is crucial. We compared two different exercise intensities in the diabetes model and evaluated the role of myokines in exercise-induced cardioprotection. Male, adult, Wistar albino rats were used (n = 20 each). First, animals were divided into two groups: Non-Diabetic (ND), Diabetic (DM); then groups were further divided into subgroups: Sedentary (S), Training-1 (T1 = 10 m/min, 0° inclination), and Training-2 (T2 = 20 m/min, 10° inclination). Diabetes was induced by streptozotocin (60 mg/kg; i.p.). Animals exercised on a treadmill 5 days/a week for 6 weeks. Then, hearts were attached to the Langendorff apparatus and baseline functional parameters were measured. After 30â/120âI/R protocol, infarct size was evaluated with tetrazolium chloride staining. Interleukin-6, FNDC5, and myonectin levels were measured both in the soleus and the left ventricle. We observed cardiac hypertrophy and impaired baseline LV function in diabetes. Infarct size was significantly larger in diabetics and only T1 decreased the infarct size whereas T2 further aggravated it. Moreover, post-ischemic recovery was worst in diabetic-T2 group. Irisin and myonectin levels were decreased in the soleus muscle of diabetic animals. T1 increased the myonectin levels in the left ventricle of non-diabetics, and this effect was blunted in diabetic-T1 animals. As a conclusion, light-intensity exercise is a better approach to prevent ischemic damage in diabetes besides moderate intensity may be hazardous in diabetic population.
| å ¨é¨æé´ | è¿å»ä¸å¹´ | è¿å»30天 | |
|---|---|---|---|
| æè¦æµè§æ¬¡æ° | 386 | 75 | 12 |
| å ¨ææµè§æ¬¡æ° | 12 | 1 | 0 |
| PDFä¸è½½æ¬¡æ° | 53 | 2 | 0 |
