Mitochondrial Physiology Network 10.9: 99-100 (2005) - download pdf

Does endurance training limit rat heart mitochondrial dysfunction induced by in vitro anoxia-reoxygenation?

António Ascensão¹, J Magalhães¹, JMC Soares¹, R Ferreira¹, MJ Neuparth¹, F Marques^3,4, PJ Oliveira^5,6, JA Duarte^1,2

¹Dept. Sport Biology; ²Center Research in Physical Activity and Leisure, Fac. Sport Sciences; ³Dept. Biochemistry Clinical Analysis, Fac. Pharmacy; ⁴Inst. Molecular Cell Biology;University of Porto; ⁵Dept. Zoology; ⁶Centre Neurosciences Cell Biology, University of Coimbra, Portugal. - aascensao@fcdef.up.pt

    Mitochondria are clearly involved in the physiopathology of many cardiac dysfunctions [3] and endurance training is known to improve the tolerance of the heart and specifically of heart mitochondria to in vivo oxidative-based insults [1,2]. However, the effect of endurance training on heart mitochondrial function submitted to in vitro anoxia-reoxygenation (A-R) is poorly understood. The present work intended to analyse the effect of moderate endurance treadmill training (14-wk) against rat heart mitochondrial dysfunction induced by in vitro A-R.

    The respiratory parameters state 3, state 4, ADP/O and respiratory control ratio- RCR, as well as biochemical markers of protein oxidation (carbonyl groups) and lipid peroxidation (malondialdehyde) were determined in isolated mitochondria before and after 1 min anoxia followed by 4 min reoxygenation. Basal levels of heat shock protein 60 kDa (HSP60) and 70 kDa (HSP70) were measured in mitochondria and whole muscle homogenate, respectively.

    A-R significantly impaired the rate of state 3 and state 4 respiration, as well as the RCR and ADP/O in the sedentary group. Nevertheless, mitochondrial state 3 respiration was significantly higher in trained than in the non-trained group both before and after A-R. The impairments in RCR, ADP/O ratio and state 4 induced by A-R in non-trained group were significantly attenuated in endurance-trained group. Oxidative modifications of mitochondrial proteins and phospholipids were found in sedentary group after A-R, although limited in trained group. Increased levels of mitochondrial HSP60 and tissue HSP70 accompanied the lower decrease in the respiratory function after A-R observed in trained group.

    It is concluded that previous 14-wk endurance training limited the impairments on rat heart mitochondria caused by in vitro A-R.

1.  Ascensao A, Magalhaes J, Soares J, Ferreira R, Neuparth MJ, Appell HJ, Duarte J (2005) Cardiac mitochondrial respiratory function and oxidative stress: the role of exercise. Int. J. Sports Med. 26: 258-267.

2.  Ascensao A, Magalhaes J, Soares J, Ferreira R, Neuparth MJ, Marques F, Oliveira PJ, Duarte J (2005) Moderate endurance training prevents doxorubicin-induced in vivo mitochondriopathy and reduces the development of cardiac apoptosis. Am. J. Physiol. Heart Circ. Physiol. (in press).

3.  Jassem W, Fuggle SV, Rela M, Koo DD, Heaton ND (2002) The role of mitochondria in ischemia/reperfusion injury. Transplantation 73: 493-499.