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Aim: The present study aimed to investigate the effects of a single bout of resistance exercise on mitophagy in human skeletal muscle (SkM). Methods: Eight healthy men were recruited to complete an acute bout of one‐leg resistance exercise. SkM biopsies were obtained one hour after exercise in the resting leg (Rest‐leg) and the contracting leg (Ex‐leg). Mitophagy was assessed using protein‐related abundance, transmission electron microscopy (TEM), and fluorescence microscopy. Results: Our results show that acute resistance exercise increased pro‐fission protein phosphorylation (DRP1Ser616) and decreased mitophagy markers such as PARKIN and BNIP3L/NIX protein abundance in the Ex‐leg. Additionally, mitochondrial complex IV decreased in the Ex‐leg when compared to the Rest‐leg. In the Ex‐leg, TEM and immunofluorescence images showed mitochondrial cristae abnormalities, a mitochondrial fission phenotype, and increased mitophagosome‐like structures in both subsarcolemmal and intermyofibrillar mitochondria. We also observed increased mitophagosome‐like structures on the subsarcolemmal cleft and mitochondria in the extracellular space of SkM in the Ex‐leg. We stimulated human primary myotubes with CCCP, which mimics mitophagy induction in the Ex‐leg, and found that BNIP3L/NIX protein abundance decreased independently of lysosomal degradation. Finally, in another human cohort, we found a negative association between BNIP3L/NIX protein abundance with both mitophagosome‐like structures and mitochondrial cristae density in the SkM. Conclusion: The findings suggest that a single bout of resistance exercise can initiate mitophagy, potentially involving mitochondrial ejection, in human skeletal muscle. BNIP3L/NIX is proposed as a sensitive marker for assessing mitophagy flux in SkM. [ABSTRACT FROM AUTHOR]

Dyslipidaemia occurs in pregnancy to secure foetal development. The mother shows a physiological increase in plasma total cholesterol and Triglycerides (TG) as pregnancy progresses (i.e. maternal physiological dyslipidaemia in pregnancy). However, in some women pregnancy-associated dyslipidaemia exceeds this physiological adaptation. The consequences of this condition on the developing fetus include endothelial dysfunction of the foetoplacental vasculature and development of foetal aortic atherosclerosis. Gestational Diabetes Mellitus (GDM) associates with abnormal function of the foetoplacental vasculature due to foetal hyperglycaemia and hyperinsulinaemia, and associates with development of cardiovascular disease in adulthood. Supraphysiological dyslipidaemia is also detected in GDM pregnancies. Although there are several studies showing the alteration in the maternal and neonatal lipid profile in GDM pregnancies, there are no studies addressing the effect of dyslipidaemia in the maternal and foetal vasculature. The literature reviewed suggests that dyslipidaemia in GDM pregnancy should be an additional factor contributing to worsen GDM-associated endothelial dysfunction by altering signalling pathways involving nitric oxide bioavailability and neonatal lipoproteins., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.org.)