Pesta 2011Abstract Mitochondrial Medicine-Training
|Pesta D, Hoppel F, Macek C, Messner H, Faulhaber M, Kobel C, Parson W, Burtscher M, Schocke M, Gnaiger E (2011) Mitochondrial improvements after strength, endurance, and intermittend hypoxic training in sedentary humans. A respiratory study on permeabilized muscle fibres. Abstract Mitochondrial Medicine Chicago.|
Link: UMDF 2011
The main finding was a significant increase (P<0.05) of lipid oxidation capacity in all groups, after normoxic (255% ETN, N=8 and 238% STN, N=3), and hypoxic endurance and strength training (198% ET, N=7 and 198% ST, N=7).
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
Coupling state: LEAK, OXPHOS, ET Pathway: F, N, S, NS, ROX HRR: Oxygraph-2k
Endurance and strength training are established as two distinct training modalities, increasing either mitochondrial density or extension of myofibrillar units. Recent research, however, suggests that mitochondrial biogenesis can be induced by both strength and conventional endurance training.
In order to test the training-specific hypothesis, mitochondrial respiratory function was studied by high-resolution respirometry in response to a 10-weeks training program using human permeablized muscle fibers from 26 sedentary volunteers undergoing either endurance or strength training in normoxia (ETN, STN; FiO2=21%) or hypoxia (ETH, STH; FiO2=13.5%). Biopsies were taken from the m. vastus lateralis and all volunteers performed a cycle-ergometric incremental exercise test under normoxia to determine their VO2,max before and after training.
The main finding was a significant increase (P<0.05) of lipid oxidation capacity in all groups, after normoxic (255% ETN, N=8 and 238% STN, N=3), and hypoxic endurance and strength training (198% ET, N=7 and 198% ST, N=7). This increase was related mainly to a change in mitochondrial density, reflected by the tissue-specific respiratory capacity with Complex I- and Complex II-related substrates. Although this index of mitochondrial density increased significantly in the ETN group only (P<0.05), the trend was identical in all groups, without significant increases in mtDNA contents. Qualitative mitochondrial changes, however, were significant (P<0.01) in all training regimes, indicated by the increased relative capacity for lipid oxidation and increased coupling of oxidative phosphorylation.
Exercise training leads to several alterations of mitochondrial function regardless of normoxic or hypoxic exposure. Unexpectedly, key mitochondrial adaptations were similar in the endurance and strength training group, which reflects a different response to training in sedentary versus athletic subjects. Beyond these novel results on specific training regimes, the present study on sports science establishes a data base on healthy but sedentary subjects, as valuable controls for evaluation of functional mitochondrial defects in patients.
Supported by OeNB Jubilaeumsfond Austria, project 13476. Contribution to MitoCom_O2k-Fluorometer Network Tyrol.