Mild exercise training, cardioprotection and stress genes profile.
To improve current knowledge of the molecular mechanisms underlying exercise-induced cardioprotection in a rat model of mild exercise training, Sprague-Dawley rats were trained to run on a treadmill up to 55% of their maximal oxygen uptake for 1 h/day, 3 days/week, 14 weeks, with age-matched sedentary controls (n = 20/group). Rats were sacrificed 48 h after the last training session. Despite lack of cardiac hypertrophy, training decreased blood hemoglobin (7.94 +/- 0.21 mM vs. 8.78 +/- 0.23 mM, mean +/- SE, P = 0.01) and increased both plasma malondialdehyde (0.139 +/- 0.005 mM vs. 0.085 +/- 0.009 mM, P = 0.05) and the activity of Mn-superoxide dismutase (11.6 +/- 0.6 vs. 16.5 +/- 1.6 mU/microg, P = 0.01), whereas total superoxide dismutase activity was unaffected. When subjected to 30-min ischemia followed by 90-min reperfusion, hearts from trained rats (n = 5) displayed reduced infarct size as compared to controls (37.26 +/- 0.92% vs. 49.09 +/- 2.11% of risk area, P = 0.04). The biochemical analyses in the myocardium, which included gene expression profiles, real-time PCR, Western blot and determination of enzymatic activity, showed training-induced upregulation of the following mRNAs and/or proteins: growth-arrest and DNA-damage induced 153 (GADD153/CHOP), heme-oxygenase-1 (HO-1), cyclooxygenase-2 (Cox-2), heat-shock protein 70/72 (HSP70/72), whereas heat-shock protein 60 (HSP60) and glucose-regulated protein 75 (GRP75) were decreased. As a whole, these data indicate that mild exercise training activates a second window of myocardial protection against ischemia/reperfusion by upregulating a number of protective genes, thereby warranting further investigation in man.
Marini
Marina
M
Department of Histology, Embryology, and Applied Biology, University of Bologna, Via Belmeloro, 8, 40126, Bologna, Italy. marina.marini@unibo.it
Lapalombella
Rosa
R
Margonato
Vittoria
V
Ronchi
Raffaella
R
Samaja
Michele
M
Scapin
Cristina
C
Gorza
Luisa
L
Maraldi
Tullia
T
Carinci
Paolo
P
Ventura
Carlo
C
Veicsteinas
Arsenio
A
D000818:Animals; D015153:Blotting, Western; D002318:Cardiovascular Diseases / Q000235:genetics / Q000378:metabolism / Q000517:prevention & control*; D051546:Cyclooxygenase 2 / Q000235:genetics / Q000378:metabolism; D015870:Gene Expression; D020869:Gene Expression Profiling; D018840:HSP70 Heat-Shock Proteins / Q000235:genetics / Q000378:metabolism; D006419:Heme Oxygenase (Decyclizing) / Q000235:genetics / Q000378:metabolism; D006454:Hemoglobins / Q000378:metabolism; D008297:Male; D008315:Malondialdehyde / Q000097:blood; D008565:Membrane Proteins / Q000235:genetics / Q000378:metabolism; D023421:Models, Animal; D009203:Myocardial Infarction / Q000235:genetics / Q000517:prevention & control; D015428:Myocardial Reperfusion Injury / Q000235:genetics / Q000517:prevention & control; D009206:Myocardium / Q000378:metabolism; D020411:Oligonucleotide Array Sequence Analysis; D018384:Oxidative Stress / Q000235:genetics*; D010805:Physical Conditioning, Animal; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D015203:Reproducibility of Results; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013482:Superoxide Dismutase / Q000378:metabolism; D013997:Time Factors; D051742:Transcription Factor CHOP / Q000235:genetics / Q000378:metabolism
C497251:Ddit3 protein, rat; D018840:HSP70 Heat-Shock Proteins; D006454:Hemoglobins; D008565:Membrane Proteins; D012333:RNA, Messenger; C018551:glucose-regulated proteins; D051742:Transcription Factor CHOP; D008315:Malondialdehyde; D006419:Heme Oxygenase (Decyclizing); C491523:Hmox1 protein, rat; D051546:Cyclooxygenase 2; C489691:Ptgs2 protein, rat; D013482:Superoxide Dismutase