Mitochondria and Metabolism Journal Club –  September 2016

Journal article presented by Michal Handzlik, PhD,  Senior Fellow in Tian Laboratory

It is well recognized that both skeletal and cardiac muscle consume more carbohydrates during increased workload (e.g. high intensity exercise or pressure overload). Although accumulation of glycolytically-derived lactate has long been considered a byproduct of anaerobic glycolysis, a controversial review by Roberts et al. questioned production of lactic acid per se highlighting performance-enhancing benefits of lactate accumulation.

In their review, Robergs et al. challenges the classical concept of muscle acidosis during high-intensity exercise. The authors analyze existing literature and highlight the main sources of protons during physical activity. It appears that it is rather ATP hydrolysis and not dissociation of lactic acid per se that is the main source of muscle acidosis during high-intensity exercise. It is also stress that lactate dehydrogenase (LDH) catalyzed reaction is central to maintaining cellular acid-base balance. Specifically, Robergs et al. demonstrate that without pyruvate to lactate conversion, accelerated acidosis would be detrimental to red blood cell function and longevity.

Excessive lactate accumulation has long been associated with impaired muscle performance. Contrary to this classical view, Robergs et al. provide further evidence that muscle lactate accumulation during physical activity is advantageous. A growing body of evidence appears to indicate that lactate accumulation preserves excitability of contracting tissue delaying fatigue.

It is well established that failing heart displays altered substrate utilization patterns with increased anaerobic glycolysis. Based on Robergs et al. review, it appears that accelerated cardiac glycolysis may be hypothesized as a protective mechanisms to preserve function and excitability. On the other hand, it is well known that increasing oxidative metabolism in the acutely and chronically failing heart improves cardiac function. Further research is warranted to fully explain the role lactate may play in the failing heart.