Functional coupling of adenine nucleotide translocase and mitochondrial creatine kinase is enhanced after exercise training in lung transplant skeletal muscle.
Mechanisms responsible for limitation of exercise capacity in lung transplant recipients (LR) and benefits gained by exercise training were studied. Mitochondrial respiration parameters, energy transfer, and cell structure were assessed in vastus lateralis biopsies using the permeabilized fiber technique with histochemical and morphometric measurements. Twelve male controls (C) and 12 LR performed exercise training over 12 wk. Before exercise training, there were strong correlations between exercise capacity (maximal O(2) consumption and endurance time at 70% maximal power output) and cellular events, as assessed by percentage of type I fibers and apparent K(m) for exogenous ADP. Anticalcineurins were not involved in LR exercise limitation, since there were no differences in maximal mitochondrial rate of respiration before exercise training and no abnormalities in respiratory chain complexes compared with C. Training resulted in a significant increase in physiological parameters both at the cellular (apparent K(m) for exogenous ADP and stimulating effect of creatine) and integrated (maximal O(2) consumption, power output at ventilatory threshold, maximal power output, and endurance time at 70% maximal power output) levels in LR and C. After the training period, improvements in maximal O(2) consumption and in maximal mitochondrial rate of respiration were noted, as well as changes in endurance time and percentage of type I fibers. Because there were no changes in diameters and fiber types, baseline alteration of apparent K(m) for exogenous ADP and its improvement after training might be related to changes within the intracellular energetic units. After the training period, intracellular energetic units exhibited a higher control of mitochondrial respiration by creatine linked to a more efficient functional coupling adenine nucleotide translocase-mitochondrial creatine kinase, resulting in better exercise performances in C and LR.
Guerrero
Karen
K
Laboratoire de Bioénergétique Fondamentale et Appliquée, Institut National de la Santé et de la Recherche Médicale E221, Université Joseph Fourier, Grenoble, France.
Wuyam
Bernard
B
Mezin
Paulette
P
Vivodtzev
Isabelle
I
Vendelin
Marko
M
Borel
Jean-Christian
JC
Hacini
Rachid
R
Chavanon
Olivier
O
Imbeaud
Sandrine
S
Saks
Valdur
V
Pison
Christophe
C
D000222:Adaptation, Physiological / Q000502:physiology; D000328:Adult; D000368:Aged; D003402:Creatine Kinase / Q000378:metabolism*; D052281:Creatine Kinase, Mitochondrial Form; D015444:Exercise / Q000502:physiology*; D017079:Exercise Tolerance / Q000502:physiology*; D006801:Humans; D007527:Isoenzymes / Q000378:metabolism; D016040:Lung Transplantation / Q000502:physiology*; D008297:Male; D008875:Middle Aged; D000226:Mitochondrial ADP, ATP Translocases / Q000378:metabolism*; D018482:Muscle, Skeletal / Q000502:physiology*; D010101:Oxygen Consumption / Q000502:physiology*; D005082:Physical Exertion / Q000502:physiology
D007527:Isoenzymes; D000226:Mitochondrial ADP, ATP Translocases; D003402:Creatine Kinase; D052281:Creatine Kinase, Mitochondrial Form