AUTHOR=Mattingly Madison L. , Ruple Bradley A. , Sexton Casey L. , Godwin Joshua S. , McIntosh Mason C. , Smith Morgan A. , Plotkin Daniel L. , Michel J. Max , Anglin Derick A. , Kontos Nicholas J. , Fei Shengyi , Phillips Stuart M. , Mobley C. Brooks , Vechetti Ivan , Vann Christopher G. , Roberts Michael D. TITLE=Resistance training in humans and mechanical overload in rodents do not elevate muscle protein lactylation JOURNAL=Frontiers in Physiology VOLUME=14 YEAR=2023 URL=https://www.frontiersin.org/journals/physiology/articles/10.3389/fphys.2023.1281702 DOI=10.3389/fphys.2023.1281702 ISSN=1664-042X ABSTRACT=
Although several reports have hypothesized that exercise may increase skeletal muscle protein lactylation, empirical evidence in humans is lacking. Thus, we adopted a multi-faceted approach to examine if acute and subchronic resistance training (RT) altered skeletal muscle protein lactylation levels. In mice, we also sought to examine if surgical ablation-induced plantaris hypertrophy coincided with increases in muscle protein lactylation. To examine acute responses, participants’ blood lactate concentrations were assessed before, during, and after eight sets of an exhaustive lower body RT bout (n = 10 trained college-aged men). Vastus lateralis biopsies were also taken before, 3-h post, and 6-h post-exercise to assess muscle protein lactylation. To identify training responses, another cohort of trained college-aged men (n = 14) partook in 6 weeks of lower-body RT (3x/week) and biopsies were obtained before and following the intervention. Five-month-old C57BL/6 mice were subjected to 10 days of plantaris overload (OV, n = 8) or served as age-matched sham surgery controls (Sham, n = 8). Although acute resistance training significantly increased blood lactate responses ∼7.2-fold (