Response to Exercise Generates Lactate and Fluid Intake: Effects on Mitochondrial Function in Heart and Vascular Smooth Muscle
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 cardiac and vascular function. In addition, it would be difficult to assert that the intermittent and nonprolonged exercise undertaken by our young subjects in a cool-to-moderate climate could induce cellular dehydration.
Our recent findings suggest that adiposity and cardiorespiratory fitness can affect arterial stiffness in healthy children as young as 10 years of age.5 This finding is sobering in the midst of the current epidemic of childhood obesity. Given the limitations inherent to cross-sectional data, we will take the opportunity to further evaluate causal relationships between exercise and health using serial assessments in the Lifestyle of Our Children cohort.
Thornton SN, Hess K. Exercise generates lactate and fluid intake: effects on mitochondrial function in heart and vascular smooth muscle. Hypertension. 2009; 54: e14.
Lanza IR, Nair KS. Response to exercise, lactate, and mitochondrial function in aging and diabetes. Am J Clin Nutr. 2009; 89: 1476–1477.
Sakuragi S, Abhayaratna K, Gravenmaker KJ, O'Reilly C, Srikusalanukul W, Budge MM, Telford RD, Abhayaratna WP. Influence of adiposity and physical activity on arterial stiffness in healthy children: the lifestyle of our kids study. Hypertension. 2009; 53: 611–616.