CLINICAL RESEARCH: HEART FAILURE/TRANSPLANTATION
Preserved response of mitochondrial function to short-term endurance training in skeletal muscle of heart transplant recipients
Joffrey Zoll, PhD*,*,
Benoit N’Guessan, BS*,
Florence Ribera, PhD*,
Eliane Lampert, MD*,
Dominique Fortin ,
Vladimir Veksler, MD, PhD,
Xavier Bigard, MD, PhD ,
Bernard Geny, MD, PhD*,
Jean Lonsdorfer, MD, PhD*,
Renée Ventura-Clapier, PhD and
Bertrand Mettauer, MD, PhD*
* Service de Physiologie Clinique et des Explorations Fonctionnelles, Département de Physiologie, Faculté de Médecine, Strasbourg, France
Cardiologie Cellulaire et Moléculaire, U-446 INSERM, Faculté de Pharmacie, Université Paris-Sud, Châtenay-Malabry, France
Unité de Bioénergétique, CRSSA, La-Tronche Cedex, France
Manuscript received January 23, 2003;
revised manuscript received March 19, 2003,
accepted March 27, 2003.
* Reprint requests and correspondence: Dr. Joffrey Zoll, Département de Physiologie, Faculté de Médecine, 11, rue Humann, 67000 Strasbourg, France.
Zolljoffrey{at}yahoo.com
OBJECTIVES: We sought to determine whether intrinsic mitochondrial function and regulation were altered in heart transplant recipients (HTRs) and to investigate the response of mitochondrial function to six-week endurance training in these patients.
BACKGROUND: Despite the normalization of central oxygen transport during exercise, HTRs are still characterized by limited exercise capacity, which is thought to result from skeletal muscle metabolic abnormalities.
METHODS: Twenty HTRs agreed to have vastus lateralis biopsies and exercise testing: before and after training for 12 of them and before and after the same control period for eight subjects unwilling to train. Mitochondrial respiration was evaluated on saponin-permeabilized muscle fibers in the absence or presence (maximum respiration rate [Vmax]) of saturating adenosine diphosphate.
RESULTS: Mitochondrial function was preserved at the level of sedentary subjects in untrained HTRs, although they showed 28 ± 5% functional aerobic impairment (FAI). After training, Vmax, citrate synthase, cytochrome c oxidase, and mitochondrial creatine kinase (CK) activities were significantly increased by 48%, 40%, 67%, and 53%, respectively (p < 0.05), whereas FAI decreased to 12 ± 5% (p < 0.01). The control of mitochondrial respiration by creatine and mitochondrial CK was also improved (p < 0.01), suggesting that phosphocreatine synthesis and transfer by the mitochondrial CK become coupled to oxidative phosphorylation, as shown in trained, healthy subjects.
CONCLUSIONS: In HTRs, the mitochondrial properties of skeletal muscle were preserved and responded well to training, reaching values of physically active, healthy subjects. This suggests that, in HTRs, immunosuppressive drugs do not alter the intrinsic muscle oxidative capacities and that the patients’ physical handicap results from nonmitochondrial mechanisms.
|
Abbreviations and Acronyms
| | ADP | | adenosine diphosphate | | CHF | | congestive heart failure | | CK | | creatine kinase | | CsA | | cyclosporin A | | FAI | | functional aerobic impairment | | HTRs | | heart transplant recipients | | MTP | | maximum tolerated power | | MyHC | | myosin heavy chain | | T | | trained subjects | | UT | | untrained subjects | | Vmax | | maximum respiration rate | | VO2 | | oxygen consumption | | VT | | ventilatory threshold |
|
This article has been cited by other articles:
|
|
|
|
 
F. N. Daussin, J. Zoll, S. P. Dufour, E. Ponsot, E. Lonsdorfer-Wolf, S. Doutreleau, B. Mettauer, F. Piquard, B. Geny, and R. Richard
Effect of interval versus continuous training on cardiorespiratory and mitochondrial functions: relationship to aerobic performance improvements in sedentary subjects
Am J Physiol Regulatory Integrative Comp Physiol,
July 1, 2008;
295(1):
R264 - R272.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
F. N. Daussin, J. Zoll, E. Ponsot, S. P. Dufour, S. Doutreleau, E. Lonsdorfer, R. Ventura-Clapier, B. Mettauer, F. Piquard, B. Geny, et al.
Training at high exercise intensity promotes qualitative adaptations of mitochondrial function in human skeletal muscle
J Appl Physiol,
May 1, 2008;
104(5):
1436 - 1441.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
R. Richard, J. Zoll, B. Mettauer, F. Piquard, and B. Geny
Counterpoint: Cardiac denervation does not play a major role in exercise limitation after heart transplantation
J Appl Physiol,
February 1, 2008;
104(2):
560 - 562.
[Full Text]
[PDF]
|
|
|
|
|
|
|
O. Rouyer, J. Zoll, F. Daussin, C. Damge, P. Helms, S. Talha, L. Rasseneur, F. Piquard, and B. Geny
Muscle: Effect of angiotensin-converting enzyme inhibition on skeletal muscle oxidative function and exercise capacity in streptozotocin-induced diabetic rats
Exp Physiol,
November 1, 2007;
92(6):
1047 - 1056.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
R. Ventura-Clapier, B. Mettauer, and X. Bigard
Beneficial effects of endurance training on cardiac and skeletal muscle energy metabolism in heart failure
Cardiovasc Res,
January 1, 2007;
73(1):
10 - 18.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
J. Zoll, L. Monassier, A. Garnier, B. N'Guessan, B. Mettauer, V. Veksler, F. Piquard, R. Ventura-Clapier, and B. Geny
ACE inhibition prevents myocardial infarction-induced skeletal muscle mitochondrial dysfunction
J Appl Physiol,
August 1, 2006;
101(2):
385 - 391.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
K. Guerrero, B. Wuyam, P. Mezin, I. Vivodtzev, M. Vendelin, J.-C. Borel, R. Hacini, O. Chavanon, S. Imbeaud, V. Saks, et al.
Functional coupling of adenine nucleotide translocase and mitochondrial creatine kinase is enhanced after exercise training in lung transplant skeletal muscle
Am J Physiol Regulatory Integrative Comp Physiol,
October 1, 2005;
289(4):
R1144 - R1154.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
