Jacobs, Robert A2; Díaz, Víctor3; Soldini, Lavinia7; Haider, Thomas7; Thomassen, Martin8; Nordsborg, Nikolai B8; Gassmann, Max5; Lundby, Carsten6
1 Integrated Physiology, Department of Nutrition, Exercise and Sports, Faculty of Science, Københavns Universitet2 Zurich Center for Integrative Human Physiology (ZIHP), Institute of Veterinary Physiology, Vetsuisse Faculty, and Institute of Physiology, University of Zurich, Zurich3 Department of Health and Human Performance, Universidad Politécnica de Madrid, Madrid4 University of Zurich5 Universidad Peruana Cayetano Heredia (UPCH), Lima6 Zurich Center for Integrative Human Physiology (ZIHP) and Institute of Physiology, University of Zurich, Zurich7 University of Zurich8 Integrated Physiology, Department of Nutrition, Exercise and Sports, Faculty of Science, Københavns Universitet
The etiology of mammalian senescence is suggested to involve the progressive impairment of mitochondrial function; however, direct observations of age-induced alterations in actual respiratory chain function are lacking. Accordingly, we assessed mitochondrial function via high-resolution respirometry and mitochondrial protein expression in soleus, quadricep, and lateral gastrocnemius skeletal muscles, which represent type 1 slow-twitch oxidative muscle (soleus) and type 2 fast-twitch glycolytic muscle (quadricep and gastrocnemius), respectively, in young (10-12 weeks) and mature (74-76 weeks) mice. Electron transport through mitochondrial complexes I and III increases with age in quadricep and gastrocnemius, which is not observed in soleus. Mitochondrial coupling efficiency during respiration through complex I also deteriorates with age in gastrocnemius and shows a tendency (p = .085) to worsen in quadricep. These data demonstrate actual alterations in electron transport function that occurs with age and are dependent on skeletal muscle type.
Journals of Gerontology. Series A: Biological Sciences and Medical Sciences, 2013, Vol 68, Issue 9, p. 1010-1022