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(Hypertension. 2009;54:e16.)
© 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

Academic Unit of Internal Medicine, Canberra Hospital, Canberra, Australia, College of Medicine, Biology, and Environment, Australian National University, Canberra, Australia

Satoru Sakuragi

Academic Unit of Internal Medicine, Canberra Hospital, Canberra, Australia

Richard D. Telford

College of Medicine, Biology, and Environment, Australian National University, Canberra, Australia, The Commonwealth Institute, Canberra, Australia

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 2 potential mechanisms that could account for the beneficial effects of exercise on cardiovascular structure and function. Exercise-induced effects on mitochondrial function and fluid loss/replacement have been proposed as intermediary processes.

The protective effects of mitochondrial function against diabetes mellitus and cardiovascular aging are well documented. Thornton and Hess¹ propose that exercise exerts a positive effect on mitochondrial function through the enhanced supply of substrates and lactate in particular. This mechanism is plausible. Indeed, the role of lactate has evolved from simply being a "waste" product of anaerobic metabolism into an important substrate for mitochondrial function and a gluconeogenic precursor via the lactate shuttle mechanism.² Thornton and Hess¹ further speculate that exercise may facilitate the lactate transport into the mitochondria through the increased expression of monocarboxylate transporter 1 (MCT1) membrane proteins, which are ubiquitously distributed throughout the body.³ However, we agree with previous responses to this assertion,⁴ which fails to recognize that there are other barriers to oxidative phosphorylation, including decreased mitochondrial content and a defect intrinsic to the tricarboxylic acid cycle or electron transport machinery. In addition, the proposed exercise-induced effects on increased monocarboxylate transporter 1 expression and lactate metabolism would need to occur in parallel with other mitochondrial adaptations to promote lactate oxidation in response to the increased lactate supply into the mitochondria.

To the best of our knowledge, there is little if any evidence that fluid loss/replacement has a role in promoting a tissue perfusion–related protective effect on . . . [Full Text of this Article]