Skeletal Muscle Mitochondrial Plasticity Is Reduced In Liver Transplant Recipients

Abstract

PURPOSE Sarcopenic obesity is a hallmark of liver transplant recipients, of which the mechanisms are not yet fully understood. Decline in mitochondrial plasticity could play a mechanistic role in muscle wasting, loss of strength, and increased adiposity via impaired energy substrate utilization. The purpose of this study is to determine if skeletal muscle mitochondrial plasticity is reduced in liver transplant (LT) recipients. METHODS In this prospective cohort study, 15 LT patients (Mean±SD; Age: 58±10 years; months since transplant: 55±81 months) and 10 age matched healthy controls (Age: 55±4 years), underwent assessment of mitochondrial oxidative capacity of the wrist flexor muscle group. Near infrared spectroscopy coupled with repeated, transient arterial occlusions, measured the recovery kinetics of oxygen consumption following a 10 second bout of hand grip exercise. Post exercise metabolic recovery rate constant was calculated and reported as an index of mitochondrial oxidative capacity. RESULTS Post exercise metabolic recovery rates were significantly greater in LT recipients (Mean±SEM; Recovery Time Constant: 72±7 s) compared to HC (51±4 s; p=0.03) indicative of diminished mitochondrial plasticity in this patient cohort (Figure 1). CONCLUSION Skeletal muscle mitochondrial plasticity is reduced in LT patients compared to matched healthy controls. Further investigations are warranted to determine the role of mitochondrial dysfunction in the development of sarcopenic obesity and frailty following LT.