Cardiac energy metabolism is a determinant of the response to hypertrophic stimuli. To investigate how it responds to physiological or pathological stimuli, we compared the energetic status in models of hypertrophy induced by physiological stimuli (pregnancy or treadmill running) and by pathological stimulus (spontaneously hypertensive rats, SHR) in 15 week-old female rats, leading to a 10% cardiac hypertrophy. Late stage of compensated hypertrophy was also studied in 25 week-old SHR (35% of hypertrophy). Markers of cardiac remodelling did not follow a unique pattern of expression: in trained rats, only ANF was increased; in gravid rats, calcineurin activation and BNP expression were reduced while beta-MHC expression was enhanced; all markers were clearly up-regulated in 25 week-old SHR. Respiration of permeabilized fibers revealed a 17% increase in oxidative capacity in trained rats only. Mitochondrial enzyme activities, expression of the master regulator PGC-1alpha and mitochondrial transcription factor A, and content of mitochondrial DNA were not consistently changed, suggesting that compensated hypertrophy does not involve alterations of mitochondrial biogenesis. Mitochondrial fatty acid utilization tended to increase in trained rats and decreased by 14% in 15 week-old SHR. Expression of markers of lipid oxidation, PPARalpha and its down-stream targets MCAD and CPTI, was up-regulated after training and tended to decrease in gravid and 15 week-old SHR rats. Taken together these results show that there is no univocal pattern of cardiac adaptation in response to physiological or pathological hypertrophic stimuli, suggesting that other factors could play a role in determining adaptation of energy metabolism to increased workload.

中文翻译：

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肥大心脏的能量代谢的刺激特异性变化。

心脏能量代谢是对肥大刺激反应的决定因素。为了研究其对生理或病理刺激的反应，我们在15周龄雌性大鼠中比较了生理刺激（妊娠或跑步机跑步）和病理刺激（自发性高血压大鼠，SHR）引起的肥大模型中的能量状态。到10％的心脏肥大。在25周大的SHR（肥大35％）中也研究了代偿性肥大的晚期。心脏重塑的标志物并没有遵循独特的表达方式：在训练有素的大鼠中，仅ANF增加；在妊娠大鼠中，钙调神经磷酸酶的活化和BNP表达降低，而β-MHC表达增强。在25周龄的SHR中，所有标记均明显上调。透化纤维的呼吸仅在训练的大鼠中显示出17％的氧化能力增加。线粒体酶活性，主调节物PGC-1alpha和线粒体转录因子A的表达以及线粒体DNA的含量并未持续变化，这表明代偿性肥大并不涉及线粒体生物发生的改变。在经过训练的大鼠中，线粒体脂肪酸的利用率趋于增加，而在15周龄的SHR中，线粒体的脂肪酸利用率却下降了14％。训练后，脂质氧化，PPARalpha及其下游靶标MCAD和CPTI的表达上调，并且在妊娠和15周龄SHR大鼠中趋于下降。综上所述，这些结果表明，对生理或病理性肥大性刺激没有明显的心脏适应模式，