Tissue hyperoxygenation promotes oxidative metabolism in motor unit.
Some mutant hemoglobin (Hb) variants are found with lowered O2 affinity. Low oxygen affinity is reported to increase the O2 availability in peripheral tissues (Kunert et al. [1996] Microvasc. Res. 52:58-68). In the present study, we used a mouse model carrying two low-affinity Hb variants, Titusville and Presbyterian, to evaluate the chronic in vivo influence of lowered oxygen affinity on the neuromuscular system. Our model mice showed an increased voluntary running ability compared with wild-type littermates. In the tibialis anterior (TA) muscle of mutant mice, the glycolytic fibers were converted to oxidative ones in where the activity of the mitochondrial marker enzyme succinate dehydrogenase (SDH) was up-regulated. We report that the spinal ventral horn motoneurons innervating TA skeletal fibers also showed higher mitochondrial oxidative enzyme activity. This phenomenon was evidenced by increased SDH activity and electron microscopic (EM) mitochondrial electronic density in these motoneurons. Our data suggest that, as the result of adaptation to the tissue hyperoxygenation, energy metabolism in the neuron-muscle motor unit is augmented and thus function of the motor unit is promoted.
Huang
Fei
F
Department of Molecular Gerontology, Tokyo Metropolitan Institute of Gerontology, Itabashi-ku, Tokyo, Japan.
Shimizu
Takahiko
T
Ishihara
Akihiko
A
Yuasa
Shigeki
S
Nishimura
Kinya
K
Kugimiya
Toyoki
T
Shirasawa
Takuji
T
D000251:Adenosine Triphosphatases / Q000378:metabolism; D000818:Animals; D000831:Animals, Newborn; D001522:Behavior, Animal; D002772:Cholera Toxin / Q000378:metabolism; D002851:Chromatography, High Pressure Liquid / Q000379:methods; D015180:Electrophoresis, Gel, Two-Dimensional / Q000379:methods; D005914:Globins / Q000378:metabolism; D006454:Hemoglobins / Q000235:genetics / Q000378:metabolism; D006735:Horseradish Peroxidase / Q000378:metabolism; D051379:Mice; D008817:Mice, Mutant Strains; D008854:Microscopy, Electron / Q000379:methods; D008931:Mitochondria, Muscle / Q000201:enzymology / Q000648:ultrastructure; D009046:Motor Neurons / Q000201:enzymology / Q000502:physiology* / Q000648:ultrastructure; D018482:Muscle, Skeletal / Q000201:enzymology / Q000294:innervation / Q000502:physiology*; D009154:Mutation; D010100:Oxygen / Q000378:metabolism*; D010805:Physical Conditioning, Animal / Q000502:physiology*; D012333:RNA, Messenger / Q000096:biosynthesis; D020133:Reverse Transcriptase Polymerase Chain Reaction / Q000379:methods; D013126:Spinal Nerve Roots / Q000166:cytology* / Q000201:enzymology; D013385:Succinate Dehydrogenase / Q000378:metabolism; D013997:Time Factors
D006454:Hemoglobins; D012333:RNA, Messenger; C052635:cholera toxin, B subunit-horseradish peroxidase; D005914:Globins; D002772:Cholera Toxin; D006735:Horseradish Peroxidase; D013385:Succinate Dehydrogenase; D000251:Adenosine Triphosphatases; D010100:Oxygen