Exercise training prevents skeletal muscle damage in an experimental sepsis model

Carregando...
Imagem de Miniatura
Citações na Scopus
19
Tipo de produção
article
Data de publicação
2013
Título da Revista
ISSN da Revista
Título do Volume
Editora
HOSPITAL CLINICAS, UNIV SAO PAULO
Autores
JANNIG, Paulo R.
SOUZA, Arlete B. de
FRONZA JR., Hercilio
WESTPHAL, Glauco A.
PETRONILHO, Fabricia
CONSTANTINO, Larissa
DAL-PIZZOL, Felipe
FERREIRA, Gabriela K.
STRECK, Emilio E.
Citação
CLINICS, v.68, n.1, p.107-114, 2013
Projetos de Pesquisa
Unidades Organizacionais
Fascículo
Resumo
OBJECTIVE: Oxidative stress plays an important role in skeletal muscle damage in sepsis. Aerobic exercise can decrease oxidative stress and enhance antioxidant defenses. Therefore, it was hypothesized that aerobic exercise training before a sepsis stimulus could attenuate skeletal muscle damage by modulating oxidative stress. Thus, the aim of this study was to evaluate the effects of aerobic physical preconditioning on the different mechanisms that are involved in sepsis-induced myopathy. METHODS: Male Wistar rats were randomly assigned to either the untrained or trained group. The exercise training protocol consisted of an eight-week treadmill program. After the training protocol, the animals from both groups were randomly assigned to either a sham group or a cecal ligation and perforation surgery group. Thus, the groups were as follows: sham, cecal ligation and perforation, sham trained, and cecal ligation and perforation trained. Five days after surgery, the animals were euthanized and their soleus and plantaris muscles were harvested. Fiber cross-sectional area, creatine kinase, thiobarbituric acid reactive species, carbonyl, catalase and superoxide dismutase activities were measured. RESULTS: The fiber cross-sectional area was smaller, and the creatine kinase, thiobarbituric acid reactive species and carbonyl levels were higher in both muscles in the cecal ligation and perforation group than in the sham and cecal ligation and perforation trained groups. The muscle superoxide dismutase activity was higher in the cecal ligation and perforation trained group than in the sham and cecal ligation and perforation groups. The muscle catalase activity was lower in the cecal ligation and perforation group than in the sham group. CONCLUSION: In summary, aerobic physical preconditioning prevents atrophy, lipid peroxidation and protein oxidation and improves superoxide dismutase activity in the skeletal muscles of septic rats.
Palavras-chave
CLP, Skeletal Muscle, Myopathy, Oxidative Stress, Antioxidant Enzymes, Aerobic Exercise
Referências
  1. AEBI H, 1984, METHOD ENZYMOL, V105, P121
  2. BAGBY GJ, 1994, J APPL PHYSIOL, V77, P1542
  3. BANNISTER JV, 1987, METHOD BIOCHEM ANAL, V32, P279, DOI 10.1002/9780470110539.ch5
  4. Bayir H, 2005, CRIT CARE MED, V33, pS498, DOI 10.1097/01.CCM.0000186787.64500.12
  5. Bone R C, 2009, Chest, V136, pe28
  6. Boveris A, 2008, FREE RADICAL BIO MED, V44, P224, DOI 10.1016/j.freeradbiomed.2007.08.015
  7. Brealey D, 2004, AM J PHYSIOL-REG I, V286, pR491, DOI 10.1152/ajpregu.00432.2003
  8. BROOKE MH, 1970, ARCH NEUROL-CHICAGO, V23, P369
  9. Chen HI, 2007, MED SCI SPORT EXER, V39, P435, DOI 10.1249/mss.0b013e31802d11c8
  10. Cooney RN, 1997, SHOCK, V7, P1, DOI 10.1097/00024382-199701000-00001
  11. Crouser ED, 2002, CRIT CARE MED, V30, P276, DOI 10.1097/00003246-200202000-00002
  12. Dal-Pizzol F, 2010, NEUROCHEM RES, V35, P1, DOI 10.1007/s11064-009-0043-4
  13. DEBLIEUX PMC, 1989, J APPL PHYSIOL, V66, P2805
  14. Deem S, 2006, RESPIR CARE, V51, P1042
  15. DEEM S, 2006, RESP CARE, V51, P1052
  16. De Jonghe B, 2002, JAMA-J AM MED ASSOC, V288, P2859, DOI 10.1001/jama.288.22.2859
  17. DRAPER HH, 1990, METHOD ENZYMOL, V186, P421
  18. Ferreira JCB, 2007, CLIN EXP PHARMACOL P, V34, P760, DOI 10.1111/j.1440-1681.2007.04635.x
  19. Fredriksson K, 2008, PLOS ONE, V3, DOI 10.1371/journal.pone.0003686
  20. Fredriksson K, 2006, AM J PHYSIOL-ENDOC M, V291, pE1044, DOI 10.1152/ajpendo.00218.2006
  21. Garnacho-Montero J, 2001, INTENS CARE MED, V27, P1288
  22. Gerovasili V, 2009, CRIT CARE, V13, DOI 10.1186/cc8123
  23. Hasselgren PO, 2005, INT J BIOCHEM CELL B, V37, P2156, DOI 10.1016/j.biocel.2005.01.017
  24. Hotchkiss RS, 2003, NEW ENGL J MED, V348, P138, DOI 10.1056/NEJMra021333
  25. Hund E, 2001, J NEUROL, V248, P929, DOI 10.1007/s004150170043
  26. Jackson MJ, 2008, IUBMB LIFE, V60, P497, DOI 10.1002/iub.72
  27. Kazi AA, 2011, SHOCK, V35, P117, DOI 10.1097/SHK.0b013e3181ecb57c
  28. Kozlov AV, 2003, FREE RADICAL BIO MED, V34, P1555, DOI 10.1016/S0891-5849(03)00179-5
  29. Leeuwenburgh C, 1997, AM J PHYSIOL-REG I, V272, pR363
  30. LEVINE RL, 1990, METHOD ENZYMOL, V186, P464
  31. Linares E, 2003, FREE RADICAL BIO MED, V34, P766, DOI 10.1016/S0891-5849(02)01424-7
  32. Ljubicic V, 2010, BBA-GEN SUBJECTS, V1800, P223, DOI 10.1016/j.bbagen.2009.07.031
  33. McArdle A, 2001, AM J PHYSIOL-CELL PH, V280, pC621
  34. Noble EG, 2008, APPL PHYSIOL NUTR ME, V33, P1050, DOI 10.1139/H08-069
  35. OLIVER IT, 1955, BIOCHEM J, V61, P116
  36. Pinho RA, 2006, CELL BIOL INT, V30, P848, DOI 10.1016/j.cellbi.2006.03.011
  37. Poulsen JB, 2011, CRIT CARE MED, V39, P456, DOI 10.1097/CCM.0b013e318205c7bc
  38. POWERS SK, 1994, AM J PHYSIOL, V266, pR375
  39. Powers SK, 2008, PHYSIOL REV, V88, P1243, DOI 10.1152/physrev.00031.2007
  40. Reid WD, 1998, MOL CELL BIOCHEM, V179, P63, DOI 10.1023/A:1006803703128
  41. Ritter C, 2003, INTENS CARE MED, V29, P1782, DOI 10.1007/s00134-003-1789-9
  42. Ritter C, 2004, CRIT CARE MED, V32, P342, DOI 10.1097/01.CCM.000010954.13145.CA
  43. Salvemini D, 2002, FREE RADICAL BIO MED, V33, P1173, DOI 10.1016/S0891-5849(02)00961-9
  44. Smuder AJ, 2011, J APPL PHYSIOL, V110, P935, DOI 10.1152/japplphysiol.00677.2010
  45. Starkie R, 2003, FASEB J, V17, P884, DOI 10.1096/fj.02-0670fje
  46. ZIMMERMAN JJ, 1995, CRIT CARE MED, V23, P616, DOI 10.1097/00003246-199504000-00003