The
blood O(2)-
carrying capacity is maintained by the O(2)-regulated
production of
erythropoietin (Epo), which stimulates the proliferation and
survival of
red blood cell progenitors. Epo has been
thought to act exclusively on
erythroid progenitor cells. However, recent studies have identified the
erythropoietin receptor (EpoR) in other
cells, such as
neurons,
astrocytes,
microglia,
heart,
cancer cell lines, and
skeletal muscle provides evidence for a potential
role of Epo in other
tissues. In this study we aimed to determine the effect of recombinant
human erythropoietin (rHuEpo) on
skeletal muscle adaptations such as
mitochondrial biogenesis,
myogenesis, and
angiogenesis in different
muscle fibre types. Fourteen
male Wistar rats were randomly divided into two experimental groups, and saline or rHuEpo (300 IU) was administered subcutaneously three times a week for 3 weeks. We evaluated the
protein expression of intermediates involved in the
mitochondrial biogenesis cascade, the myogenic cascade, and in
angiogenesis in the oxidative
soleus muscle and in the glycolytic
gastrocnemius muscle. Contrary to our
expectations, rHuEpo significantly hampered the
mitochondrial biogenesis pathway in
gastrocnemius muscle (PGC-1Alpha, mTFA and
cytochrome c). We did not find any effect of the
treatment on cellular signals of
myogenesis (MyoD and Myf5) or
angiogenesis (
VEGF) in either soleus or gastrocnemius
muscles. Finally, we found no significant effect on the maximal aerobic velocity at the end of the experiment in the rHuEpo-treated
animals. Our findings suggest that 3 weeks of rHuEpo
treatment, which generates an increase of
oxygen carrying capacity, can
affect mitochondrial biogenesis in a
muscle fibre-specific dependent manner