MiP2005: Session 1 - Young Investigator Presentation
Mitochondrial Physiology Network 10.9: 18-19 (2005) - download pdf
Cycling efficiency is related to type I fibre content and inversely to UCP3 protein but not to mitochondrial efficiency determined in vitro.
Martin Mogensen1, M Bagger1, PK Pedersen1, M Fernström2, K Sahlin1,2
1Inst. Sports Science Clinical Biomechanics, University of Southern Denmark, Odense, Denmark; 2Stockholm University College of Physical Education and Sports, Stockholm, Sweden. - firstname.lastname@example.org
The biochemical efficiency of the mitochondrion (P/O ratio) is an important determinant for the overall efficiency of the cell. Numerous factors have an influence on the mitochondrial efficiency such as the choice of substrate and the structural and biochemical composition of the inner mitochondrial membrane. There are some data from animal and cell culture studies, which indicate that the P/O ratio is influenced by muscle fibre type composition and content of UCP3 proteins [1,2]. Previous studies have shown a negative correlation between the efficiency during cycling and UCP3 expression and a positive correlation between cycling efficiency and % type I fibres [3,4]. These studies indicate, that individual differences in cycling efficiency could be related to the mitochondrial efficiency. Training is known to decrease the UCP3 protein content and may also to some extent alter the fibre type distribution (increased oxidative fibres). These training induced changes should in theory increase the cycling efficiency of trained subjects. However, previous studies have shown contradicting results. The purpose of this study was to investigate the hypothesis that individual variations in cycling efficiency is related to mitochondrial efficiency. Furthermore we wanted to test the hypothesis that trained subjects have a higher cycling efficiency compared with untrained subjects.
On minimum two occasions trained (n = 9) and untrained (n = 9) subjects completed a submaximal cycle test at 40, 80 and 120 W. Based on the oxygen consumption the energy expenditure (EE) was calculated for assessment of individual cycling efficiency (gross-efficiency, GE; work-efficiency, WE; and delta-efficiency, DE). GE and WE were determined at all intensities. DE was calculated as the slope of the linear relationship between the EE and the work loads accomplished by the subject. GE, WE and DE were determined as the percentage conservation of energy in external work. Biopsies were taken on a separate day and used for determination of the mitochondrial respiratory efficiency, UCP3 protein content and fibre type distribution. Mitochondrial efficiency was determined during state 3 and submaximal respiration (constant rate of ADP infusion) with pyruvate+malate (Pyr) or palmitoyl-L-carnitine+malate (PC) as substrates. The relationship between the submaximal mitochondrial respiration and the resulting P/O ratio was fitted to a logarithmic function. Significance was considered at P<0.05.
Trained subjects had a higher maximal mitochondrial respiration when the respiration was expressed per kg wet weight. The relationship between the mitochondrial P/O ratio and the absolute respiration showed that the P/O ratio increased with increasing respiration. There was no significant difference between trained and untrained subjects in their mitochondrial efficiency. Untrained subjects had a significantly higher amount of UCP3 protein compared to trained individuals, but there was no difference in the fibre type distribution. UCP3 protein was negatively correlated with DE (r = -0.48), WE at 80 W (r = -0.49) and WE at 120 W (r = -0.56). Furthermore, WE was positively correlated to the % type I fibres at 80 W (r = 0.57) and at 120 W (r = 0.53). However, GE, WE and DE were not correlated to the mitochondrial efficiency determined during submaximal or maximal respiratory rates. Furthermore, there were no differences in GE, WE or DE between trained and untrained subjects.
It is concluded that cycling efficiency is correlated to the mitochondrial UCP3 protein and fibre type distribution. However, these correlations could be caused by fibre type differences in the content of UCP3 protein . It is also concluded that mitochondrial efficiency is lower at low rates of respiration. This may be explained by an increased membrane potential, which triggers an increased proton leak. Individual cycling efficiency was not correlated to mitochondrial efficiency determined in vitro and there was no difference between trained and untrained subjects in their cycling efficiency. The results indicate that cycling efficiency in vivo is not influenced by the mitochondrial efficiency as determined in vitro.
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