1) How does high fat diet-induced lipid accumulation in skeletal muscle (IMTG) cause myocyte insulin resistance?

1) How does high fat diet-induced lipid accumulation in skeletal muscle (IMTG) cause myocyte insulin resistance? Why does this same IMTG in runners seem to have the opposite effect?

2) Many nutritional supplements which are advertised in body building/weight lifting magazines contain carnitine. The advertisements claim that carnitine will enhance muscle definition. Is this claim justified? What would you hypothesize would be the biggest benefit (if any) derived from carnitine supplementation? Would it alter vascular function, metabolic function, both, or neither? (be sure to defend your answer).

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3) Suppose that while you are lecturing an advanced exercise physiology class on fat metabolism, a student asks the following question: “I understand that after endurance training, a person uses more fat and less glycogen for any given sub-maximal work load, but I do not understand why. What are the vascular and metabolic alterations which occur that ensure that more fat and less glycogen is used?” Provide me with the answer you would give the student (Assume that you have unlimited time to explain it to the student.)