Sarcopenia is a major health issue associated with increased risk of falls, fractures, and insulin resistance. The undercarboxylated form of osteocalcin (ucOC) has been implicated in energy metabolism and possibly muscle function, but its role in muscle from older humans remains unclear. This study aimed to test whether ucOC improves insulin sensitivity in myotubes derived from older women and to determine whether the GPRC6A receptor mediates these effects. Associations between ucOC, metabolic and anthropometric measures, and skeletal muscle protein content were also explored. Primary human myoblasts from older women were differentiated into myotubes and cultured under normal (5 mM) and high (16 mM) glucose conditions. Insulin-stimulated glucose uptake and glycogen synthesis were assessed following treatment with ucOC. GPRC6A knockdown using siRNA was performed to examine receptor involvement. RNA sequencing from myotubes and analysis of key metabolic proteins in skeletal muscle samples were conducted in older women (n = 18, age 73.4 ± 4.9 years). UcOC (30 ng/mL) increased insulin-stimulated glucose uptake and glycogen synthesis under normal glucose conditions (24.1% and 28.3%, respectively), and at 100 ng/mL under high glucose conditions (19.1% and 25.9%). GPRC6A knockdown attenuated glycogen synthesis responses. RNA sequencing showed ucOC upregulated ribosomal and mitochondrial pathways, which were blunted with GPRC6A silencing. No significant associations were observed between circulating ucOC and skeletal muscle metabolic proteins. These findings suggest that, in muscle from older women, ucOC enhances muscle metabolism partly via GPRC6A-mediated transcriptional regulation.