Therefore, the energetic characteristics of ATP production can explain why pharmacological stimulation of the α1-AR-PPARδ-AMPK-PGC-1α pathway prevents cardiac failure and pathologic hypertrophy, and our results suggest that the mitochondrial oxidative energetic process that was increased in cardiac muscle by midodrine increases cardiac contractility and prevents hypertrophy. The gene discussed is PPARGC1A; the disease is cardiac hypertrophy.