MiP2005: Session 2
Mitochondrial Physiology Network 10.9: 30 (2005) - download pdf
Structure and function of muscle mitochondria at endurance training connected with intermittent hypoxia.
Irina Mankovskaya, Bronislav Gavenauskas, Valentina Nosar, Katherine Rozova
Department of Hypoxia, Bogomolets Institute of Physiology, Kiev, Ukraine. – email@example.com
Endurance training (ET) induces muscle mitochondrial biogenesis and adaptations of mitochondrial function . ET in hypoxia is thought to modulate these effects . Intermittent hypoxic training (IHT) has been recently shown to improve oxygen transport to and within muscle cells . But, the effects of this modality of hypoxia exposure on muscle mitochondria structure and respiration at ET are poorly understood. The aim of this study was to compare muscle mitochondrial adaptations induced by severe ET combined with IHT to those occurring with ET only at the same relative workload.
Male adult Wistar rats were subjected to swimming training for 4 weeks (30 min daily, the workload corresponded to 70-75 % VO2max). The IHT course was added in the last 2 weeks of ET; the rats underwent the IHT sessions: breathing with hypoxic mixture containing 12 % O2 for 15 min with 15-min rest intervals, 5 times daily. We found that ET+IHT induced a greater increase in the numerical density, the volume density, and size of mitochondria in the red gastrocnemius compared to the similar effects of ET. Whereas ET without IHT stimulated preferential adaptation of the subsarcolemmal mitochondria, ET+IHT affect both the subsarcolemmal and intermyofibrillar mitochondria. In case of combined action of ET+IHT, the internal structure of mitochondria in terms of compartmental spaces and membranes was well-preserved. ET+IHT led to a highly expressed increase in the values of mitochondrial respiratory control (J3/J4) and ADP/O ratio under α-ketoglutarate oxidation compared to values under succinate oxidation. The combination of ET with IHT, therefore, was found to be the most productive model for stimulating mitochondrial biogenesis and increasing of the NADH-dependent oxidation pathway role in muscle energy production.
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