Submitted on October 18, 2006
Accepted on January 8, 2007
Reduced efficiency, but increased fat oxidation in mitochondria from human skeletal muscle after 24 hours ultra-endurance exercise
Maria Fernström1, Linda Bakkman1, Michail Tonkonogi1, Irina Shabalina1, Zinaida Rozhdestvenskaya1, C. Mikael Mattsson1, Jonas Enqvist1, Bjorn T. Ekblom2, and Kent Sahlin1*
1 GIH, Sweden
2 University College of Physical Education and Sports, Astrand Laboratory of Work Physiology, Stockholm, Sweden
* To whom correspondence should be addressed. E-mail: kent.sahlin{at}fyfa.ki.se.
The hypothesis that ultra-endurance exercise influences muscle mitochondrial function has been investigated. Athletes in ultra-endurance performance performed running, kayaking and cycling at 60% of their VO2 peak for 24 hours. Muscle biopsies were taken pre-exercise (Pre-Ex), post-exercise (Post-Ex) and after 28 h of recovery (Rec). Respiration was analysed in isolated mitochondria during state 3 (coupled to ATP synthesis) and state 4 (non-coupled respiration), with fatty acids alone (palmitoyl-carnitine; PC) or together with pyruvate (Pyr,). Electron transport chain (ETC) activity was measured with NADH in permeabilized mitochondria. State 3 respiration with PC increased Post-Ex by 39 and 41 % (P<0.05) when related to mitochondrial protein and to ETC activity, respectively. State 3 respiration with Pyr was not changed (P>0.05). State 4 respiration with PC increased Post-Ex but was lower than Pre-Ex at Rec (P<0.05, vs. Pre-Ex). Mitochondrial efficiency (P/O ratio) decreased Post-Ex by 9 and 6 % (P<0.05) with PC and PC+Pyr, respectively. P/O ratio remained reduced at Rec. Muscle uncoupling protein (UCP3), measured with Western blotting, was not changed Post-Ex but tended to decrease at Rec (P=0.07, vs. Pre-Ex). In conclusion: Extreme endurance-exercise decreases mitochondrial efficiency. This will increase oxygen demand and may partly explain the observed elevation in whole body oxygen consumption during standardized exercise (+13%). The increased mitochondrial capacity for PC oxidation indicates plasticity in substrate oxidation at the mitochondrial level, which may be of advantage during prolonged exercise.
