Plenge 2012 Front Physiol
|Plenge U, Belhage B, Guadalupe-Grau A, Andersen PR, Lundby C, Dela F, Stride N, Pott FC, Helge JW, Boushel RC (2012) Erythropoietin treatment enhances muscle mitochondrial capacity in humans. Front Physiol 3:50.|
Abstract: Erythropoietin (Epo) treatment has been shown to induce mitochondrial biogenesis in cardiac muscle along with enhanced mitochondrial capacity in mice. We hypothesized that recombinant human Epo (rhEpo) treatment enhances skeletal muscle mitochondrial oxidative phosphorylation (OXPHOS) capacity in humans. In six healthy volunteers rhEpo was administered by sub-cutaneous injection over 8 weeks with oral iron (100 mg) supplementation taken daily. Mitochondrial OXPHOS was quantified by high-resolution respirometry in saponin-permeabilized muscle fibers obtained from biopsies of the vastus lateralis before and after rhEpo treatment. OXPHOS was determined with the mitochondrial Complex I substrates malate, glutamate, pyruvate, and Complex II substrate succinate in the presence of saturating ADP concentrations, while maximal electron transport capacity (ET-pathway) was assessed by addition of an uncoupler. rhEpo treatment increased OXPHOS (from 92 ± 5 to 113 ± 7 pmol·s(-1)·mg(-1)) and ET-pathway (107 ± 4 to 143 ± 14 pmol·s(-1)·mg(-1), p < 0.05), demonstrating that Epo treatment induces an upregulation of OXPHOS and ET-pathway in human skeletal muscle.
• Keywords: Erythropoietin (Epo), oral iron supplementation, maximal electron transport capacity (ET-pathway)
Organism: Human Tissue;cell: Skeletal muscle Preparation: Permeabilized tissue Enzyme: Complex I, Complex II;succinate dehydrogenase
Coupling state: OXPHOS