Submitted on September 23, 2008
Revised on January 28, 2009
Accepted on February 12, 2009
Dietary glycemic index influences lipid oxidation but not muscle or liver glycogen oxidation during exercise
Emma Jane Stevenson1*, Peter Thelwall2, Kevin Thomas1, Fiona Smith2, Janette C Brand-Miller3, and Michael Iain Trenell4
1 Northumbria University
2 Newcastle University
3 The University of Sydney
4 Newcastle Univeristy
* To whom correspondence should be addressed. E-mail: e.stevenson{at}northumbria.ac.uk.
The glycemic index (GI) of dietary carbohydrates influences glycogen storage in skeletal muscle and circulating non-esterifed fatty acid (NEFA) concentrations. We hypothesized that diets differing only in GI would alter intramuscular lipid oxidation and glycogen usage in skeletal muscle and liver during subsequent exercise. Endurance-trained individuals (n = 9) cycled for 90 min at 70 % VO2peak and then consumed either high or low GI meals over the following 12 h. The following day after an overnight fast, the 90 min cycle was repeated. 1H and 13C magnetic resonance spectroscopy was used before and after exercise to assess intra-muscular lipid and glycogen content of the vastus muscle group and liver. Blood and expired air samples were collected at 15 min intervals throughout exercise. NEFA availability was reduced during exercise in the high compared to the low GI trial (area under curve 44.5 ± 6.0 vs. 38.4 ± 7.30 mM•h-1, P < 0•05). Exercise elicited a ~55% greater reduction in IMCL in the high vs. low GI trial (1.6 ± 0.2 vs. 1.0 ± 0.3 mmol•kg wet weight, P< 0.05). There was no difference in the exercise induced reduction of the glycogen pool in skeletal muscle (76 ± 8 vs. 68 ± 5 mM) or in liver (65 ± 8 vs. 71 ± 4 mM) between the low and high GI trials respectively. High GI recovery diets reduce NEFA availability and increase reliance on IMCL during moderate intensity exercise. Skeletal muscle and liver glycogen storage or usage are not affected by the GI of a acute recovery diet.
