Pesta 2011 Am J Physiol Regul Integr Comp Physiol

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

SUIT protocol

- - - 1OctM;2D;3G;4S;5U;6Rot-

Correction

Tab. 2: For N=25, some average values need to be corrected:

J_s: ETF_L (OctM) correct value: 7.1 +- 1.6 (instead of 6.0 +- 2.0)

J_s: CI+II_P (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+II_E).

Methods (p. R1081): FCCP was titrated at 0.25-µM steps (not 0.025 µM-steps).

MitoEAGLE V_O2max/BME data base

Human vastus lateralis
25 males
26 years
Sedentary
H = 1.82 m
M = 84.3 kg
BME = 1.21
BMI = 25.6 kg·m^-2
V_O2max/BM = 40.8 mL·min^-1·kg^-1
Permeabilized muscle fibres; 37 °C; GMS_P; m_w
J_O2,P(NS) = 76.8 µmol·s^-1·kg^-1 wet muscle mass

Human vastus lateralis
25 males
26 years
Sedentary/10 weeks trained
H = 1.82 m
M = 81.0 kg
BME = 1.16
BMI = 24.6 kg·m^-2
V_O2max/BM = 44.0 mL·min^-1·kg^-1
Permeabilized muscle fibres; 37 °C; GMS_P; m_w
J_O2,P(NS) = 86.3 µmol·s^-1·kg^-1 wet muscle mass

O2k-Publications

References: BME and VO2max

» VO2max

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Labels: MiParea: Respiration, mt-Biogenesis;mt-density, Exercise physiology;nutrition;life style Pathology: Obesity Stress:Hypoxia 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, VO2max, 1OctM;2D;3G;4S;5U;6Rot-, SUIT-017, BMI, BME, MitoEAGLE BME