Pharmacological activation of AdipoR1 (AdipoRon) and fenofibrate attenuated myosteatosis and restored exercise capacity in KAL-TG mice (p < 0.05).<h4>Conclusions</h4>Abnormal elevation of KAL drives metabolic myopathy and exercise intolerance by antagonizing the AdipoR1-AMPK axis. Here, ADIPOR1 is linked to metabolic myopathy.