Endurance training limits the functional alterations of heart rat mitochondria submitted to in vitro anoxia-reoxygenation

• Type: Article in International Scientific Journal
• Date: 2006

Authors

Ascensao, A (Author) FADEUP; Magalhaes, J (Author) FADEUP; Soares, JMC (Author) Other; Ferreira, R (Author) Other; Neuparth, MJ (Author) Other; Marques, F (Author) FFUP; Oliveira, PJ (Author) Other; Duarte, JA (Author) FADEUP

Journal

Title: International Journal of Cardiology

Vol. 109 No. 2

Pages: 169-178

ISSN: 0167-5273

Publisher: Elsevier

Indexing

ISI Web of Knowledge - 36 Citations

Scopus - 40 Citations

Scientific classification

FOS: Medical and Health sciences > Clinical medicine

Other information

Authenticus ID: P-004-KSQ

DOI: 10.1016/j.ijcard.2005.06.003

Abstract (EN): Background: Studies analysing the effect of endurance training on heart mitochondrial function submitted to in vitro anoxia-reoxygenation (A-R) are missing. The present study aimed to investigate the effect of moderate endurance treadmill training (14 weeks) against rat heart mitochondrial dysfunction induced by in vitro A-R. Methods. Respiratory parameters (state 3, state 4, ADP/O and respiratory control ratio-RCR) and oxidative damage markers (carbonyl groups and malondialdehyde) were determined in isolated mitochondria before and after 1 min anoxia followed by 4 min reoxygenation. Levels of heat shock protein 60 kDa (HSP60) and 70 kDa (HSP70) were measured before A-R in mitochondria and whole muscle homogenate, respectively. Results: 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. However, mitochondrial state 3 respiration was significantly higher in trained than in the sedentary group both before and after A-R. The impairments in RCR, ADP/O ratio and state 4 induced by A-R in sedentary group were significantly attenuated in endurance-trained group. The inhibition of state 4 induced by GDP was significantly higher in trained than in sedentary 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. Conclusion: We therefore concluded that endurance training limited the impairments on rat heart mitochondria caused by the oxidant insult inflicted by in vitro A-R.

Language: English

Type (Professor's evaluation): Scientific

No. of pages: 10