Lactate supplementation modulates molecular and functional responses during chronic neuromuscular electrical stimulation in male rats.
Level 5 - mechanism / opinion, no new human data
Animal research (preclinical rodent model)
PubMed 41781170 · doi:10.14814/phy2.70790
What was done
Male Wistar rats were given oral L-sodium lactate or water before either a single session (acute) or 2 weeks of repeated sessions (chronic) of neuromuscular electrical stimulation (NMES). Investigators measured muscle weight, strength, myonuclear-associated protein expression (PCM1), protein synthesis (puromycin incorporation), mTOR pathway markers (c-Myc, rpS6), mitochondrial proteins (PGC-1α, OXPHOS, citrate synthase), and lactate transporters/receptors (MCT1, MCT4, GPR81) in the oxidative soleus and glycolytic plantaris muscles.
What was found
The abstract reports directional findings without providing numerical data, baseline values, or effect sizes. Oral lactate supplementation with chronic NMES was associated with greater increases in muscle mass and torque, particularly in the soleus. PCM1 abundance and myofibrillar puromycin incorporation were higher with lactate supplementation. PGC-1α expression increased specifically in the plantaris muscle. No significant changes were detected in c-Myc, rpS6, GPR81, MCT1, or MCT4 expression.
Why it matters
This study provides mechanistic evidence that oral lactate can act as a signaling molecule to augment muscle mass and force adaptations during electrical stimulation in a muscle-type-dependent manner.
Limits
The study was conducted exclusively in a rodent model (male Wistar rats) over a short 2-week duration, limiting generalizability to humans. The abstract omits sample sizes, lactate dosages, and specific numerical results.
Cited by
- supports Lactate from vigorous exercise signals the activation of PGC-1alpha to promote mitochondrial biogenesis in muscle cells.