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1 Department of Movement Sciences, Maastricht University, Maastricht, The Netherlands; Department of Human Biology, Maastricht University, Maastricht, The Netherlands
2 School of Life Sciences, University of Dundee, Dundee, United Kingdom
3 School of Biomedical Sciences, University of Nottingham, Nottingham, United Kingdom
4 Department of Human Biology, Maastricht University, Maastricht, The Netherlands
5 Department of Movement Sciences, Maastricht University, Maastricht, The Netherlands
6 School of Sport and Exercise Sciences, University of Birmingham, Birmingham, United Kingdom
* To whom correspondence should be addressed. E-mail: L.vanLoon{at}HB.unimaas.nl.
This study investigates the consequences of inhibition of adipose tissue lipolysis on skeletal muscle substrate use. Ten subjects were studied at rest, during exercise and subsequent recovery under normal, fasting conditions (control trial: CON) and following administration of a nicotinic acid analogue (low plasma free fatty acid trial: LFA). Continuous [U-13C]palmitate and [6,6-2H2] glucose infusions were applied to quantify plasma free fatty acid (FFA) and glucose oxidation rates, and to estimate intramuscular triacylglycerol (IMTG) and glycogen use. Muscle biopsies were collected to measure 1) fibre type specific IMTG content; 2) allosteric regulators of hormone sensitive lipase (HSL), glycogen phosphorylase, and pyruvate dehydrogenase and 3) the phosphorylation status of HSL at serine563 and serine565. Administration of a nicotinic acid analogue (Acipimox) substantially reduced plasma FFA rate of appearance and subsequent plasma FFA concentrations (P<0.0001). At rest, this substantially reduced plasma FFA oxidation rates, which was compensated by an increase in the estimated IMTG use (P<0.05). During exercise, the progressive increase in FFA rate of appearance, uptake and oxidation was prevented in the LFA trial, and matched by greater IMTG and glycogen use. Differential phosphorylation of HSL or relief of its allosteric inhibition by long-chain fatty acyl-CoA could not explain the increase in muscle TG use, but there was evidence to support the contention that regulation may reside at the level of the glucose-FA cycle. This study confirms the hypothesis that plasma FFA availability regulates both intramuscular lipid and glycogen use in vivo in humans.
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