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1 Skeletal Muscle Research Laboratory, Royal Melbourne Institute of Technology, Bundoora, Victoria, Australia
2 St. Vincent's Institute of Medical Research, Fitzroy, Victoria, Australia
* To whom correspondence should be addressed. E-mail: matthew.watt{at}rmit.edu.au.
Intramuscular triacylglycerols (IMTG) are proposed to be an important metabolic substrate for
contracting muscle, although this remains controversial. To test the hypothesis that reduced plasma
FFA availability would increase IMTG degradation during exercise, seven active men cycled for
180 min at 60% VO2 peak either without (CON) or with (NA) prior ingestion of nicotinic acid to
suppress adipose tissue lipolysis. Skeletal muscle and adipose tissue biopsy samples were obtained
before and at 90 and 180 min of exercise. NA ingestion decreased (P<0.05) plasma FFA at rest and
completely suppressed the exercise induced increase in plasma FFA (180 min: CON, 1.42 ± 0.07;
NA, 0.10 ± 0.01 mM). The decreased plasma FFA during NA was associated with decreased
(P<0.05) adipose tissue hormone sensitive lipase (HSL) activity (CON: 13.9 ± 2.5, NA: 9.1 ± 3.0
nmol.min-1.mg-1 protein). NA ingestion resulted in decreased whole body fat oxidation and
increased carbohydrate oxidation. Despite the decreased whole body fat oxidation, net IMTG
degradation was greater in NA compared with CON (net change: CON, 2.3 ± 0.8; NA, 6.3 ± 1.2
mmol.kg-1 dm). The increased IMTG degradation did not appear to be due to reduced fatty acid
esterification as glycerol-3-phosphate activity was not different between trials and was unaffected
by exercise (rest: 0.21 ± 0.07; 180 min: 0.17 ± 0.04 nmol.min.-1mg protein-1). HSL activity was not
increased from resting rates during exercise in either trial despite elevated plasma adrenaline,
decreased plasma insulin and increased ERK1/2 phosphorylation. AMPK
-1 activity was not
affected by exercise or NA, whereas AMPK-2 activity was increased (P<0.05) from rest during
exercise in NA and was greater (P<0.05) than CON at 180 min. These data suggest that plasma FFA
availability is an important mediator of net IMTG degradation, and in the absence of plasma FFA,
IMTG degradation cannot maintain total fat oxidation. These changes in IMTG degradation appear
to disassociate, however, from the activity of the key enzymes responsible for synthesis and
degradation of this substrate.
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