Abstract
BackgroundEpidemiological studies showed that physical exercise, specifically moderate lifelong training, is protective against cardiovascular morbidity and mortality. Most experimental work has focused into the effects and molecular mechanisms underlying intense, rather than mild exercise, by exploring the acute effect of training. Our study aims at investigating the cardioprotective effect of mild chronic exercise training and the gene expression profile changes at 48 hrs after the exercise cessation. Rats were trained at mild intensity on a treadmill: 25 m/min, 10%incline, 1 h/day, 3 days/week, 10 weeks; about 60% of the maximum aerobic power. By Affymetrix technology, we investigated the gene expression profile induced by exercise training in the left ventricle (LV) of trained (n = 10) and control (n = 10) rats. Cardioprotection was investigated by ischemia/reperfusion experiments (n = 10 trained vs. n = 10 control rats).ResultsMild exercise did not induce cardiac hypertrophy and was cardioprotective as demonstrated by the decreased infarct size (p = 0.02) after ischemia/reperfusion experiments in trained with respect to control rats. Ten genes and 2 gene sets (two pathways) resulted altered in LV of exercised animals with respect to controls. We validated by real-time PCR the increased expression of four genes: similar to C11orf17 protein (RGD1306959), caveolin 3, enolase 3, and hypoxia inducible factor 1 alpha. Moreover, caveolin 3 protein levels were higher in exercised than control rats by immunohistochemistry and Western Blot analysis. Interestingly, the predicted gene similar to C11orf17 protein (RGD1306959) was significantly increased by exercise. This gene has a high homology with the human C11orf17 (alias: protein kinase-A interacting protein 1 or breast cancer associated gene 3). This is the first evidence that this gene is involved in the response to the exercise training.ConclusionOur data indicated that few, but significant, genes characterize the gene expression profile of the rat LV, when examined 48 hrs since the last training section and that mild exercise training determines cardioprotection without the induction of hypertrophy.
Highlights
Epidemiological studies showed that physical exercise, moderate lifelong training, is protective against cardiovascular morbidity and mortality
In order to get a greater insight into the molecular mechanisms underlying the beneficial effects of mild physical exercise, we investigated the cardioprotective effect and evaluated gene expression changes induced by mild chronic exercise training in the left ventricle (LV) of the rat
Two evidences showed that animals had been efficiently trained: i) the soleus to body weight ratio was higher in TRA than in CTR rats; and, ii) during the second and the last week of training each rat was evaluated for maximal endurance running capacity, which resulted to be in the 15–25 min range while running at 15 m/min in the second week and in 100–120 min range at 25 m/min in the last week
Summary
Epidemiological studies showed that physical exercise, moderate lifelong training, is protective against cardiovascular morbidity and mortality. Our study aims at investigating the cardioprotective effect of mild chronic exercise training and the gene expression profile changes at 48 hrs after the exercise cessation. By Affymetrix technology, we investigated the gene expression profile induced by exercise training in the left ventricle (LV) of trained (n = 10) and control (n = 10) rats. Mild chronic exercise training (14 weeks, increasing in intensity to 55% of the maximum aerobic power, VO2max), which resembles the procedure recommended for middle-aged human beings (Recommendations of the American College of Sport Medicine, http:www.acsm.org//AM/Template.cfm?Sec tion=Home_Page), was demonstrated to protect the heart against I/R [14] in a similar way to more intense training programs [9,10,11]. Reports based on the microarray approach are beginning to emerge concerning the evaluation of responses to the physical exercise of leukocytes [15], skeletal muscle [16], and left ventricle (LV) [9,17,18]
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