Premium
Functionnal properties of skeletal muscles are preserved in erythropoietin deficient mice exposed to hypoxia
Author(s) -
LAUNAY Thierry,
Hagstrom Luciana,
Ca Francis,
Agbulut Onnik,
Serrurier Bernard,
Marchant Dominique,
Richalet JeanPaul,
Bigard Xavier,
Beaudry Michèle
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.801.17
Subject(s) - erythropoietin , hypoxia (environmental) , endocrinology , medicine , skeletal muscle , myosin , fast twitch muscle , chemistry , extensor digitorum muscle , angiogenesis , isometric exercise , soleus muscle , biochemistry , oxygen , organic chemistry
Epo‐induced polycythemia is the main factor of adaptation to hypoxia. In this study we analyzed the effects of Epo‐deficiency on intrinsic functional properties of slow and fast‐twitch muscles in a model of erythropoietin deficient mice (Epo‐TAg h ) exposed to hypoxia. We hypothesized that Epo‐deficiency would be deleterious for skeletal muscle development, angiogenesis and maintenance of its structure when exposed to ambient hypoxia. Wild‐type (WT) and Epo‐TAg h mice were left in hypobaric chamber at 420 mmHg pressure for 14 days. Soleus (SOL) and extensor digitorum longus (EDL) were analyzed in vitro by mechanical measurements, immuno‐histological and biochemical analyses. The results were compared to those obtained in corresponding muscles of aged matched normoxic groups. Our data did not show any difference between the groups whatever the Epo‐deficiency and/or hypoxic conditions for twitch force, tetanic force, fatigue, typology and myosin heavy chain composition. Normoxic Epo‐TAg h mice exhibit improved capillary‐to‐fibre ratio compared to WT mice in both SOL and EDL whereas no angiogenic effects of hypoxia or combined Epo‐deficency/hypoxia were observed. These results suggest that skeletal muscles possess a great capacity of adaptation to Epo‐deficiency. Then Epo‐deficiency is not a sufficient factor to induce muscle deconditioning observed in patients suffering from severe renal failure