| Popis: |
LPL directs the body wide distribution of fatty acids derived from circulating triglycerides. This is accomplished by tissue-specific regulation. In adipose tissue, LPLA per gram is higher than in muscle tissue. Eating increases adipose tissue LPLA and may increase blood flow. Exercise greatly increases SM blood flow and LPLA over a longer time frame as compared to the effect of eating on adipose tissue LPLA. The regulation of LPLA occurs at several levels and is better understood in adipose tissue models. In muscle, the study of regulation has been neglected. LPL expression in muscle may be more complex than in adipose tissue owing to the changes in blood flow and metabolism associated with contractile activity, as well as to other factors intrinsic to contraction, such as electrical events and cellular deformation. Sixty to 90 minutes of continuous leg exercise at 60% of VO2 max induces muscle LPL expression, increases LPL mRNA in humans with 4 hours of exercise, and raises immunoreactive mass by 8 hours post-exercise. Within 24 hours, both LPL and mRNA and mass have returned to normal levels. Increased muscle LPL mass following exercise may serve to replenish intramyofibral stores of triglyceride, which are depleted with endurance exercise and are greater in aerobically-trained individuals as compared to untrained individuals. The post-exercise increase in muscle LPL mass coincides with the post-exercise acute fall in circulating triglycerides typically observed in subjects capable of exercising for 60-90 minutes at 60% of VO2 max. The low fasting triglyceride levels often seen in highly trained individuals are due in part to their high levels of muscle LPLA. Both the physiological mediator and the molecular mediator of the exercised-induced induction of muscle LPL expression are known. Hopefully, the next decade will see careful studies aimed at better defining the molecular physiology of LPL expression in muscle. |
