Acute and Chronic Resistance Training, Acute Endurance Exercise, nor physiologically Plausible Lactate In Vitro Affect Skeletal Muscle Lactylation

We examined changes in skeletal muscle protein lactylation and acetylation in response to acute resistance exercise, chronic resistance training (RT), and a single endurance cycling bout. Additionally, we performed in vitro experiments to determine if different sodium lactate treatments affect myotube protein lactylation and acetylation. The acute and chronic RT study (n=12 college-aged participants) consisted of 10 weeks of unilateral leg extensor RT with vastus lateralis (VL) biopsies taken at baseline, 24-hours following the first RT bout, and the morning of the last day of the RT bout. For the acute cycling study (n=9 college-aged participants), VL biopsies were obtained before, 2 hours, and 8 hours after 60 minutes of cycling. For in vitro experiments, C2C12 myotubes were treated with varying levels of sodium lactate including LOW (1mM for 24-hours), HIGH (10mM for 24 hours), and PULSE (10mM for 30 minutes followed by 1 mM for 23.5-hours). Neither acute nor chronic RT significantly affected nuclear or cytoplasmic protein lactylation. However, cytoplasmic protein acetylation was significantly reduced following one RT bout (-15%, p=0.002) and chronic RT (-16%, p=0.006). Cycling did not acutely alter post-exercise global protein lactylation or acetylation patterns. Lastly, varying 24-hour lactate treatments did not alter nuclear or cytoplasmic protein lactylation or acetylation, cytoplasmic protein synthesis levels, or myotube diameters. These findings continue to support that exercise induces changes in skeletal muscle protein acetylation but not lactylation.