Pesta 2011 Am J Physiol Regul Integr Comp Physiol

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Pesta D, Hoppel F, Macek C, Messner H, Faulhaber M, Kobel C, Parson W, Burtscher M, Schocke M, Gnaiger E (2011) Similar qualitative and quantitative changes of mitochondrial respiration following strength and endurance training in normoxia and hypoxia in sedentary humans. Am J Physiol Regul Integr Comp Physiol 301:R1078–87.

» PMID: 21775647 Open Access

Pesta D, Hoppel F, Macek C, Messner H, Faulhaber M, Kobel C, Parson W, Burtscher M, Schocke M, Gnaiger E (2011) Am J Physiol Regul Integr Comp Physiol

Abstract: Endurance and strength training are established as distinct exercise modalities, increasing either mitochondrial density or myofibrillar units. Recent research, however, suggests that mitochondrial biogenesis is stimulated by both training modalities. To test the training-"specificity" hypothesis, mitochondrial respiration was studied in permeabilized muscle fibers from 25 sedentary adults after endurance (ET) or strength training (ST) in normoxia or hypoxia (F(iO2)=21% or 13.5%). Biopsies were taken from the m. vastus lateralis and cycle-ergometric incremental V(O2max) exercise tests were performed under normoxia, before and after the 10-week training program. The main finding was a significant increase (P<0.05) of tissue-specific fatty acid oxidation capacity, after endurance and strength training under normoxia (2.6- and 2.4-fold for ET(N) and ST(N); N=8 and 3) and hypoxia (2.0-fold for ET(H) and ST(H); N=7 and 7), and higher coupling control of oxidative phosphorylation. The enhanced lipid OXPHOS capacity was mainly (87%) due to qualitative mitochondrial changes increasing the relative capacity for fatty acid oxidation (P<0.01). Mitochondrial tissue-density contributed to a smaller extent (13%), reflected by the gain in tissue-specific respiratory capacity with a physiological substrate cocktail (glutamate, malate, succinate, octanoylcarnitine). No significant increase was observed in mtDNA content. Physiological OXPHOS capacity increased significantly in ET(N) (P<0.01), with the same trend in ET(H) and ST(H) (P<0.1). The limitation of flux by the phosphorylation system was diminished after training. Importantly, key mitochondrial adaptations were similar after endurance and strength training, regardless of normoxic or hypoxic exercise. The transition from a sedentary to an active life style induced muscular changes of mitochondrial quality representative of mitochondrial health.

Keywords: Mitochondrial respiration, Endurance training, Strength training, Human skeletal muscle, Permeabilized fibers, OXPHOS capacity, Coupling control, Fatty acid oxidation

O2k-Network Lab: AT Innsbruck Gnaiger E, AT Innsbruck Burtscher M, AT Innsbruck MitoCom

Labels: MiParea: Respiration, mt-Biogenesis;mt-density, Exercise physiology;nutrition;life style  Pathology: Obesity  Stress:Ischemia-reperfusion  Organism: Human  Tissue;cell: Skeletal muscle  Preparation: Permeabilized tissue 

Regulation: Coupling efficiency;uncoupling, Fatty acid  Coupling state: LEAK, OXPHOS, ET  Pathway: F, N, S, NS  HRR: Oxygraph-2k 

Ergometry, BMI, VO2max, 1OctM;2D;3G;4S;5U;6Rot-, SUIT-017 


SUIT protocol


Tab. 2: For N=25, some average values need to be corrected:
Js: ETFL (OctM) correct value: 7.1 +- 1.6 (instead of 6.0 +- 2.0)
Js: CI+IIP (GMSOct) correct value: 99.4 +- 20.9 (instead of 86.3 +- 17.9)

Fig. 4 C and D: The correct caption of the Y-axis is: ET capacity (CI+IIE).
Methods (p. R1081): FCCP was titrated at 0.25-µM steps (not 0.025 µM-steps).