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Protein kinase (PK) and hormone-sensitive lipase (HSL) were measured at rest in adipose tissue of untrained male rats and in that of animals subjected to a strenuous program of treadmill running. Total amounts of PK activity (decreased from 860 +/- 104 to 474 +/- 53 pmol.min-1. (10(6) cells)-1 (P less than 0.01) as a result of exercise training. At the same time, binding capacity for adenosine 3',5'-cyclic monophosphate (cAMP) was elevated in the runners. These data suggest a functional loss in catalytic activity without a loss in binding capacity. In addition, the results provide evidence that the capacity of PK to activate HSL is reduced in adipocytes of physically trained rats. HSL activity was measured in both adipose tissue slices and isolated adipocytes. The results show that the levels of activity of HSL did not increase as a result of the running program. These results provide evidence that the lipolytic capacity of adipocytes of normal untrained male rats is sufficiently large to meet the increased demand for free fatty acids imposed by the exercise program without the need for an adaptive increase in HSL activity.

A strenuous program of treadmill running increased endogenous lipoprotein lipase (LPL) activity 2.7-fold in the soleus and 2.8-fold in fast-red fibers of the quadriceps. Under these conditions, intracellular triacylglycerols (TG) decreased 25% in the soleus and 44% in fast-red muscle fibers. Free fatty acids (FFA) increased 2.1-fold (soleus) and 2.7-fold (fast-red). In the heart, a 2-h bout of swimming in untrained rats increased intracellular LPL activity 64% measured 24 h after work. The magnitude of the increase in endogenous LPL activity in heart was dependent on the intensity of the exercise. With elevated levels of intracellular LPL activity in the myocardium, TG was reduced 49% and FFA increased 3.4-fold. These results provide evidence that exercise may result in an increased capacity to hydrolyze intramuscular TG. Further, they suggest that LPL may be the enzyme responsible for intracellular TG hydrolysis in heart and skeletal muscle.