ELEVATED MUSCLE CITRATE DOES NOT REDUCE CARBOHYDRATE UTILIZATION DURING TETANIC STIMULATION

The purposes of this study were to determine whether enhanced free fat ty acid delivery would result in increased muscle citrate levels and t o establish whether the effects of this putative phosphofructokinase i nhibitor would be manifested during intense stimulation demanding glyc ogen 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 per fusion 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 gastroc nemius (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 c ontent 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) dr y muscle, respectively). Following 5 min of stimulation, soleus and re d 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 gastrocn emius. The presence of high free fatty acids had no effect on glycogen utilization or lactate accumulation in stimulated soleus and red gast rocnemius, or stimulated white gastrocnemius citrate, glycogen, or lac tate contents. In addition, no effect of elevated free fatty acids on resting or stimulated muscle glucose-6-phosphate content, glucose upta ke, or lactate efflux was observed. In conclusion, the elevation of mu scle citrate due to the presence of free fatty acids in the perfusate did not reduce muscle glycogenolysis when the demand for energy was gr eat.