Alterations in liver mitochondrial function as a result of fasting and exhaustive exercise.
The effect of exercise upon liver mitochondria structure and function was examined in fasted and fed rats, following a single run to exhaustion on a motor-driven treadmill. Exercise alone and exercise coupled with fasting both produced a significant decrease in the amount of hexokinase bound to the mitochondria, as well as reduction in the ADP/O ratio and acceptor control index measured in the presence of succinate. The mitochondria of the exercised animals, when exposed to freeze-fracture analysis while in state 3, displayed fewer deflections in the fracture plane between the inner and outer membrane than those isolated from control animals. This suggests that fewer contacts existed between the two membranes. Measurements based upon the binding of 8-anilinonaphthalene 1-sulphonate indicated that there was an increase in the net negative charge on the surface of the mitochondrial membranes of the exercised animals. All of these effects could be mimicked by incubation of mitochondria from control animals with free fatty acids. This fact, coupled with the observation that washing of the mitochondria with a solution comprising 5% (w/v) albumin could reverse all of the consequences of exercise, suggests that these alterations in mitochondrial structure and function may be the result of the increase in plasma free fatty acids that accompanies long-term exercise. Furthermore, the observation that the exercise-induced changes are dynamic and readily reversible indicates that the mitochondria were not necessarily damaged, but rather that the coupling of oxidative phosphorylation may be subject to physiological regulation.