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(Hypertension. 2009;54:e15.)
© 2009 American Heart Association, Inc.

Letters to the Editor

Response to Exercise Generates Lactate and Fluid Intake: Effects on Mitochondrial Function in Heart and Vascular Smooth Muscle

Department of Pathophysiology Laboratory Sciences, Nagoya University Graduate School of Medicine, Nagoya, Japan

Kohzo Nagata

Department of Medical Technology, Nagoya University School of Health Sciences, Nagoya, Japan

An extract of the first 250 words of the full text is provided, because this article has no abstract.

We thank Thornton and Hess¹ for their comments on our article² and its editorial commentary.³ We understand the possible effects of lactate on mitochondrial function. Indeed, recent data place lactate as an active metabolite capable of moving between cells, tissues, and organs, where it may be oxidized as a fuel or reconverted to form pyruvate or glucose. Lactate is also capable of entering cells via the monocarboxylate transporter protein shuttle system. However, our concern is that data on mitochondrial dysfunction acquired in patients with end-stage heart failure do not help us in understanding the involvement of mitochondria in the disease process.

Endurance exercise increases the size and number of mitochondria and increases monocarboxylate transporter 1 density in skeletal muscle. Increased monocarboxylate transporter 1 content with exercise is likely to increase cellular and mitochondrial lactate influx, but it remains unclear whether this lactate influx enhances mitochondrial function in patients with heart failure. A single bout of exercise is shown to induce a rapid increase in mitochondrial biogenesis that is mediated by activation and increased expression of a transcription coactivator, peroxisome proliferator-activated receptor- coactivator 1. A recent study reported that mammalian target of rapamycin (mTOR), a kinase that regulates cell growth, size, and survival, is necessary for the maintenance of mitochondrial oxidative function.⁴ Computational genomics identified the transcription factor yin-yang 1 as a common target of mTOR and peroxisome proliferator-activated receptor- coactivator 1. It is, thus, possible that exercise-induced activation of phosphatidylinositol 3-kinase (p110)-Akt-mTOR signaling may have upregulated mitochondrial . . . [Full Text of this Article]