Pesta 2011Abstract ACSM

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Pesta D, Jacobs R, Macek C, Hoppel F, Faulhaber M, Lundby C, Burtscher M, Gnaiger E, Schocke M (2011) Investigation of muscle metabolism of the quadriceps via high-resolution respirometry and 31P MRS in connection with a 10 week endurance training. Medicine & Science in Sports & Exercise 43: 71

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Pesta D, Jacobs R, Macek C, Hoppel F, Faulhaber M, Lundby C, Burtscher M, Gnaiger E, Schocke M (2011)

Event: 58th American College of Sports Medicine Meeting 2011

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β€’ O2k-Network Lab: AT Innsbruck Burtscher M, DK Copenhagen Lundby C, US CO Colorado Springs Jacobs RA

Labels: MiParea: Respiration, Exercise physiology;nutrition;life style 

Organism: Human  Tissue;cell: Skeletal muscle  Preparation: Permeabilized cells 

Coupling state: OXPHOS 

HRR: Oxygraph-2k 

skeletal muscle, endurance training, oxidative capacity 

Skeletal muscle is a highly adaptable tissue that can adjust to different stimuli. In the present study we investigated the impact of endurance training on muscle oxidative capacity with high resolution respirometry and 31P magnetic resonance spectroscopy (31P MRS).

40 healthy untrained subjects (UG) who performed an endurance training program 3 times a week lasting for 10 weeks were included in the study. 17 highly trained athletes (AG) were studied for comparison. Spatially-resolved dynamic 31P MRS measurements were obtained from the upper leg and biopsy samples were taken from the vastus lateralis to assess mitochondrial capacity with high-resolution respirometry. Subsequently, endurance and strength capacities of the subjects were determined via motor performance tests. After 10 weeks, the initial tests and muscle biopsies were repeated.

We observed a significant increase in mass specific OXPHOS flux with training in the UG from 78.97 Β± 16.05 to 101.39 Β± 19.19 (p<0.01). Flux between the UG and AG, both before and after training, respectively, was significantly different (AG: 120 Β± 32.79, UG see above, p<0.01). The capacity of the mitochondria to oxidize MCFA was significantly increased with training, observed as an increase in absolute flux (from 12.79 Β± 4.67 pre-training to 29.58 Β± 7.25 post-training, p<0.01) and in the flux control ratio (FCR=fraction of a given flux relative to the maximal flux) of octanoyl-carnitine (0.14 Β± 0.05 pre-trainig to 0.28 Β± 0.04 post-training, p<0.01). However, no difference in the FCR of MCFA oxidation was found between UG after training and the AG (0.28 Β± 0.04 post-training vs 0.26 Β± 0.06). The FCR of Oxphos was increased after training (0.95 Β± 0.09, p<0.01) but was not different between UG before training and AG (0.86 Β± 0.09 pre-training vs. 0.86 Β± 0.11). To date, analysis of the 31P MRS was still in progress.

In conclusion, mitochondria seem to adapt to endurance training in a quantitative and qualitative way. The qualitative adaptations can most prominently be observed in the capacity of MCFA oxidation, which is increased due to training. The limitation of the OXPHOS system seems to be decreased temporarily in untrained subjects exposed to exercise training. Yet, this reversed decreased limitation in athletic subjects is unknown.

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