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Only few data are available on the effect of training on phospholipid metabolism in skeletal muscles. The aim of the present study was to examine the effect of 6 weeks of endurance training on the content of particular phospholipid fractions and on the incorporation of blood-borne [14C]-palmitic acid into the phospholipids in different skeletal muscles (white and red sections of the gastrocnemius, the soleus and the diaphragm) of the rat. Lipids were extracted from the muscles and separated using thin-layer chromatography into the following fractions: sphingomyelin, phosphatidylcholine, phosphatidylserine, phosphatidylinositol, phosphatidylethanolamine, cardiolipin and neutral lipids (this fraction being composed mostly of triacylglycerols). It was found that training did not affect the content of any phospholipid fraction in soleus muscle. It increased the content of sphingomyelin in white gastrocnemius muscle, cardiolipin and phosphatidylethanolamine in red gastrocnemius muscle and phosphatidylinositol in white gastrocnemius muscle and diaphragm. The total phospholipid content in red gastrocnemius muscle of the trained group was higher than in the control group. Training reduced the specific activity of sphingomyelin and cardiolipin in all muscles, phosphatidylcholine in soleus, red, and white gastrocnemius muscles, phosphatidylserine in all muscles, phosphatidylinositol in all except the soleus muscle, and phosphatidylethanolamine in hindleg muscles, but not in the diaphragm compared to the corresponding values in the sedentary group. It was concluded that endurance training affects skeletal muscle phospholipid content and the rate of incorporation of the blood-borne [14C]palmitic acid into the phospholipid moieties.

The rats were made to run daily to exhaustion, for 28 days at a speed of 1,200 m.h-1 on a treadmill set at a gradient of +10 degrees. The training increased the time of running to exhaustion [184 (SD 49) and 308 (SD 28) min on the 1st and 28th day, respectively; P < 0.001]. The body mass was reduced by training [257 (SD 21) g before and 221 (SD 20) g after; P < 0.001] whereas the food intake increased [9 (SD 1) g.100 g-1 body mass before and 14 (SD 2) g after; P < 0.001]. The heart mass was not affected by training. Training increased the resting glycogen concentration in muscles composed of different fibre types (soleus, white and red vastus muscles) and in the liver, but had no effect on its concentration in the heart and diaphragm. During exercise lasting for 30 min glycogen mobilization in the red vastus and soleus muscles and the liver was more pronounced after than before training. A "sparing" effect of training on the skeletal muscles and liver glycogen was markedly apparent only after exercise to exhaustion. The trained rats, contrary to the untrained, did not develop hypoglycaemia during exercise to exhaustion. An increase in the plasma free fatty acid concentration during exercise after training was delayed and attenuated compared to that before training. The 24-h excretion of urea after exercise to exhaustion on the 28th day of training was higher than on the 1st day by 39% (P < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

In the rat, muscle glycogen is mobilized during the first stage of exercise, despite normoglycaemia. The aim of the present study was to examine if this process could be prevented or reduced by hyperglycaemia. Three experiments were carried out: in the first, rats were forced to run on a treadmill; in the second the gastrocnemius muscle group was made to contract by stimulation of the sciatic nerve and in the third adrenaline was administered subcutaneously. Each group was divided into two subgroups: control and enriched with glucose (hyperglycaemic). It was shown that hyperglycaemia has no effect on running-induced glycogen mobilization in hind-limb muscles of different fibre composition but prevented it totally in diaphragm muscle. Hyperglycaemia also did not affect the glycogen mobilization induced by stimulation of the sciatic nerve. However, it delayed and reduced markedly the glycogenolytic effect of adrenaline. It is concluded that increased glycogenolysis in muscles at the beginning of exercise may be a consequence of a delay in the activation of glucose transporting mechanisms in muscle cells.