Exercise, as the fundamental therapy for metabolic diseases, often exhibits a dose-dependent fashion. However, the adverse effects of overtraining and underlying mechanisms remain unclear. Here, we show that long-term overtraining induces hepatic fibrosis in humans and mice. Mechanistically, excessive lactate accumulation in skeletal muscle renders SH3 domain containing 3 (SORBS3) lactylation, triggering the liquid-liquid phase separation (LLPS) of SORBS3. LLPS of SORBS3 enhances the interaction with flotillin 1 (FLOT1) and selectively facilitates the sorting of F-Box Protein 2 (FBXO2) into specific exosome, named as ‘lactate body’, which induces hepatocyte apoptosis and hepatic satellite cell activation. Inhibition of the SORBS3 lactylation disrupts lactate body formation and alleviates the overtraining-triggered liver fibrosis. Of importance, serum lactate levels are positive-associated with exercise intensity and lactate body levels in mice and humans. Collectively, we identify a novel mechanism of selective loading of exosome cargos, and the inter-tissue communication between muscle and liver during overtraining.