Dietary LA impacts mitochondrial respiration in muscles in preclinical rodent models of mitochondria dysfunction.[40, 55] In a recent study, dietary LA partially restored LA4CL and muscle contractile force phenotype in skeletal muscle of mice deficient of tafazzin.[67] In rats with heart failure, the reduction of LA4CL and mitochondrial respiration was prevented when fed a diet with LA.[40] In humans, exercise, and weight loss both increase LA4CL in muscle tissues. The gene discussed is TAFAZZIN; the disease is heart failure.