Purpose: 

Lactate (La) has long been considered as a waste product of energy metabolism and the cause of decrease in muscle pH and hence muscle fatigue. This idea has changed massively in the past. Now it is known that La is an intermediate of glucose metabolism as well as it has been termed Lactormon for its signalling properties inducing gene expression for skeletal muscle adaptation. It has been shown to increase monocarboxylate transporters content as well as to increase mitochondrial biogenesis. Such skeletal muscle adaptation is one of the major foci in sports medicine. La, as a metabolic stimulus, has not yet been investigated extensively in this context.

Methods: 

C2C12 mouse and primary human myoblasts were constantly incubated with medium containing different lactate concentrations (10 mM, 20 mM) at 37°C and 5% CO₂ over a time period of 15 days. Cells were fixed using 4% PFA in PBS for immunocytochemical staining for Ki67, activated Caspase-3, F5D (myogenin) and Mf-20 (myosin heavy chain). Additionally, cell lysates were made for Western Blot analysis using the same markers as for immunostaining. Furthermore, we repeated the experiments with an intermittent incubation of 2 h every day to simulate a more realistic training situation.

Results: 

Densitometrical analysis of cells stained for Ki67 showed a significant decrease if treated with La in a dose-dependent manner. Controversially, apoptotic induction by activated caspase-3 was increased if treated with La. Differentiation was shown to be delayed, but not decreased if cells received the La intervention.

Conclusion: 

Lactate seems to exhibit an inhibitory effect on the proliferation and apoptotic behaviour of C2C12 and primary human myoblasts. Furthermore, differentiation seems to be delayed but not reduced in a dose-dependent manner.