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1 Department of Movement Sciences, Maastricht University, Maastricht, The Netherlands; Department of Human Biology, Maastricht University, Maastricht, The Netherlands
2 Department of Human Biology, Maastricht University, Maastricht, The Netherlands
3 Department of Movement Sciences, Maastricht University, Maastricht, The Netherlands
* To whom correspondence should be addressed. E-mail: L.vanLoon{at}HB.unimaas.nl.
Recent evidence suggests that intramyocellular lipid (IMCL) accretion is associated with obesity and the development of insulin resistance and/or type 2 diabetes. However, trained endurance athletes are markedly insulin sensitive, despite an elevated mixed muscle lipid content. In an effort to explain this metabolic paradox, we compared muscle fibre type specific IMCL storage between populations known to have elevated IMCL deposits. Immunofluorescence microscopy was performed on muscle biopsies obtained from 8 highly trained endurance athletes, 8 type 2 diabetes patients and 8 overweight, sedentary men following an overnight fast. Mixed muscle lipid content was substantially greater in the endurance athletes (4.0±0.4% area lipid stained) compared to the diabetes patients and the overweight men (2.3±0.4 and 2.2±0.5%, respectively). More than 40% of the greater mixed muscle lipid content was attributed to a higher proportion type I muscle fibres (62±8% versus 38±3 and 33±7%, respectively), which contained 2.8±0.3 fold more lipid than the type II fibres. The remaining difference was explained by a significantly greater IMCL content in the type I muscle fibres of the trained athletes. Differences in IMCL content between groups or fibre types were accounted for by differences in lipid droplet density, not lipid droplet size. IMCL distribution showed an exponential increase in lipid content from the central region towards the sarcolemma, which was similar between groups and fibre types. In conclusion, IMCL contents can be substantially greater in trained endurance athletes compared to overweight and/or type 2 diabetes patients. As structural characteristics and intramyocellular distribution of lipid aggregates seem to be similar between groups, we conclude that elevated IMCL deposits are unlikely to be directly responsible for inducing insulin resistance.
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