Short-term intensified training temporarily impairs mitochondrial respiratory capacity in elite endurance athletes

Bidragets oversatte titel: Kortvarig intens træning forringer mitokondriers respiratoriske kapacitet hos elite udholdenhedsatleter

Daniele A Cardinale, Kasper Degn Gejl, Kristine Grøsfjeld Petersen, Joachim Nielsen, Niels Ørtenblad, Filip J Larsen

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Aim: The maintenance of healthy and functional mitochondria is the result of a complex mitochondrial turnover and herein quality-control program which includes both mitochondrial biogenesis and autophagy of mitochondria. The aim of this study was to examine the effect of an intensified training load on skeletal muscle mitochondrial quality control in relation to changes in mitochondrial oxidative capacity, maximal oxygen consumption and performance in highly trained endurance athletes.

Methods: 27 elite endurance athletes performed high intensity interval exercise followed by moderate intensity continuous exercise 3 days per week for 4 weeks in addition to their usual volume of training. Mitochondrial oxidative capacity, abundance of mitochondrial proteins, markers of autophagy and antioxidant capacity of skeletal muscle were assessed in skeletal muscle biopsies before and after the intensified training period.

Results: The intensified training period increased several autophagy markers suggesting an increased turnover of mitochondrial and cytosolic proteins. In permeabilized muscle fibers, mitochondrial respiration was ~20 % lower after training although some markers of mitochondrial density increased by 5-50%, indicative of a reduced mitochondrial quality by the intensified training intervention. The antioxidative proteins UCP3, ANT1, and SOD2 were increased after training, whereas we found an inactivation of aconitase. In agreement with the lower aconitase activity, the amount of mitochondrial LON protease that selectively degrades oxidized aconitase, was doubled.

Conclusion: Together, this suggests that mitochondrial respiratory function is impaired during the initial recovery from a period of intensified endurance training while mitochondrial quality control is slightly activated in highly trained skeletal muscle.
Bidragets oversatte titelKortvarig intens træning forringer mitokondriers respiratoriske kapacitet hos elite udholdenhedsatleter
TidsskriftJournal of Applied Physiology
Udgave nummer1
Sider (fra-til)388-400
StatusUdgivet - 1. jul. 2021

Bibliografisk note

This study was supported financially by Team Denmark, The Danish Ministry of Culture, and The Swedish Research Council for Sport Science.


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