Insulin sensitivity describes the efficiency of cells to transport extracellular glucose across their cell membranes to the interior of the cell. This glucose is then used as a source of energy in respiration, or to synthesise other compounds for storage. Evidence suggest that insulin resistance is a condition by which the insulin sensitivity of the tissues decreases, particularly skeletal muscle. This raises blood levels of glucose in the fasting state, and as a result fasting insulin levels also rise. Under conditions of raised insulin levels anabolic pathways are stimulated and this increases the deposition of body fat. Results from studies suggest that insulin resistance is caused by poor dietary habits, which include the consumption of processed and refined starches and sugars. Poor diet result in nutrient overload in the liver, and this increases fatty acid production, which in turn increases the tissue levels of triglycerides. In muscle tissue the accumulation of intramuscular lipids is thought to contribute to insulin resistance.
The obese tend to have high levels of intramuscular lipids, and this is associated with the insulin resistance that obese individuals possess. Likewise, those with type 2 diabetes also have high levels of intramuscular lipids, and this is associated with the insulin resistance present in this group. Some studies have investigated the association between insulin resistance and intramuscular lipids and insulin resistance. Results from one such study1 showed that subjects who were obese or who have type 2 diabetes had significantly lower insulin sensitivity than lean subjects. Further the intramuscular lipid content of the vastus lateralis muscle was 2-fold higher in those with type 2 diabetes compared to lean subjects. This supports other studies that show that insulin sensitivity may be inversely associated with intramuscular lipid content. However, the association between intramuscular lipid content and insulin sensitivity is complex, because inclusion of endurance trained individuals changes the nature of the association.
Endurance trained athletes tend to have a high oxidative capacity in their skeletal muscle. This results from a training effect on the muscle such that it adapts to the requirements of increased energy needs, and as a result becomes more efficient at oxidising fatty acids. In the process of this adaptation, the muscle stores higher concentrations of lipids, in order to provide a substrate for this increases oxidative capacity. As a result endurance trained individuals have a higher intramuscular lipid content that lean, untrained controls. However, they do not experience a loss insulin sensitivity that is normally associated with these lipids. Therefore a paradox exists whereby the endurance trained individuals have high levels of intramuscular lipids like the obese and subjects with type 2 diabetes, but do not develop insulin resistance. This may suggest that it is the decreased capacity for oxidation that is the cause of the insulin resistance, and that the intramuscular accumulation of lipids is a result of, but not a cause of, these changes.