To examine the impact of prolonged hypoxia exposure on mitochondrial function, we followed respiratory functions of mitochondria isolated from the thoraxes of AF flies by monitoring oxygen consumption while providing them with NAD+-linked substrates in the presence of ADP (state 3) or while inhibiting F1-F0-ATPase by oligomycin (State 4-oligo). Here, ATP5F1E is linked to atrial fibrillation.