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Mice lacking CHIP (CHIP\u2212\/\u2212) suffer decreased survival, enhanced myocardial injury and increased arrhythmias compared with wild\u2010type controls following challenge with cardiac ischaemia reperfusion injury. Recent evidence implicates a role for CHIP in chaperone\u2010assisted selective autophagy, a process that is associated with exercise\u2010induced cardioprotection. To determine whether CHIP is involved in cardiac autophagy, we challenged CHIP\u2212\/\u2212 mice with voluntary exercise. CHIP\u2212\/\u2212 mice respond to exercise with an enhanced autophagic response that is associated with an exaggerated cardiac hypertrophy phenotype. No impairment of function was identified in the CHIP\u2212\/\u2212 mice by serial echocardiography over the 5\u2009weeks of running, indicating that the cardiac hypertrophy was physiologic not pathologic in nature. It was further determined that CHIP plays a role in inhibiting Akt signalling and autophagy determined by autophagic flux in cardiomyocytes and in the intact heart. Taken together, cardiac CHIP appears to play a role in regulating autophagy during the development of cardiac hypertrophy, possibly by its role in supporting Akt signalling, induced by voluntary running <jats:italic>in vivo<\/jats:italic>. 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