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(Hypertension. 2009;54:e14.)
© 2009 American Heart Association, Inc.

Letters to the Editor

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

Institut National de la Santé et de la Recherche Médicale, U 961, Vandoeuvre les Nancy, Nancy, France, Université Henri Poincaré, Nancy Université, Nancy, France

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

To the Editor:

We were very interested to read the 2 editorials and 3 articles^1–3 published in a recent issue of Hypertension concerning exercise training and cardiovascular disease. Taking, eg, the article by Garciarena et al,¹ we were encouraged to see that the concepts of a Letter to the Editor published recently⁴ could apply equally well here. The main topic discussed is what is happening in exercise and why this improves symptoms of cardiovascular disease. We suggested for diabetes mellitus and ageing that the problem was one of lowered substrate supply for metabolic function, thus creating mitochondrial dysfunction. In many cardiovascular-related problems, dysfunction of mitochondrial metabolism has been observed both in the heart and throughout the circulatory system.^5,6 Thus, as we suggest, exercise increases the availability of the monocarboxylate family of lactate transporters and lactate production in skeletal muscles. The lactate passes into the blood and becomes a substrate that penetrates easily into cells via the monocarboxylates and improves mitochondrial biogenesis and possible function in cardiac and vascular smooth muscle cells. Although this is just a hypothesis, it would not appear to be difficult to confirm.

There is, however, another aspect of the physiology presented in the articles in this volume of Hypertension that is completely overlooked, and that is fluid ingestion. No measures of water intake are given; however, exercise, or physical activity, is associated with fluid loss and, thus, cellular and extracellular dehydration. This condition stimulates the release of renin forming angiotensin II, which is also a risk . . . [Full Text of this Article]

This article has been cited by other articles:

				M. Miyachi and K. Nagata Response to Exercise Generates Lactate and Fluid Intake: Effects on Mitochondrial Function in Heart and Vascular Smooth Muscle Hypertension, August 1, 2009; 54(2): e15 - e15. [Full Text] [PDF]

				W. P. Abhayaratna, S. Sakuragi, and R. D. Telford Response to Exercise Generates Lactate and Fluid Intake: Effects on Mitochondrial Function in Heart and Vascular Smooth Muscle Hypertension, August 1, 2009; 54(2): e16 - e16. [Full Text] [PDF]