ELEVATED MUSCLE CITRATE DOES NOT REDUCE CARBOHYDRATE UTILIZATION DURING TETANIC STIMULATION

The purposes of this study were to determine whether enhanced free fatty acid delivery would result in increased muscle citrate levels and to establish whether the effects of this putative phosphofructokinase inhibitor would be manifested during intense stimulation demanding glycogen as a fuel. Hind-limb muscles were perfused with either no or high (0.93 +/- 0.03 mM) free fatty acids for 10 min at rest, and during 5 min of tetanic stimulation. Muscles sampled at the end of the rest perfusion or stimulation were soleus (slow oxidative), red gastrocnemius (fast oxidative glycolytic), and white gastrocnemius (fast glycolytic). Muscle citrate content was unaffected during rest perfusion with no free fatty acids, whereas high free fatty acids significantly elevated citrate above control in soleus, red gastrocnemius, and white gastrocnemius (by 0.39 +/- 0.13, 0.53 +/- 0.10, and 0.29 +/- 0.07 mu mol.g(-1) dry muscle, respectively). Following 1 min of stimulation, citrate content in soleus and red gastrocnemius was not different from control in the absence of free fatty acids but accumulated significantly with high free fatty acids (0.26 +/- 0.05 and 0.28 +/- 0.04 mu mol.g(-1) dry muscle, respectively). Following 5 min of stimulation, soleus and red gastrocnemius citrate content decreased with no free fatty acids but increased significantly with high free fatty acids (0.42 +/- 0.10 mu mol.g(-1) dry muscle) in soleus and remained unchanged in red gastrocnemius. The presence of high free fatty acids had no effect on glycogen utilization or lactate accumulation in stimulated soleus and red gastrocnemius, or stimulated white gastrocnemius citrate, glycogen, or lactate contents. In addition, no effect of elevated free fatty acids on resting or stimulated muscle glucose-6-phosphate content, glucose uptake, or lactate efflux was observed. In conclusion, the elevation of muscle citrate due to the presence of free fatty acids in the perfusate did not reduce muscle glycogenolysis when the demand for energy was great.