Just some food for thought.
Low cardio shows a preference for using FFA's for fuel rather than glucose. High intensity exercise OTOH is heavily dependent on glucose.
Also
by Tom McCullough MEd., MSS
"What happens when the intensity of the exercise is increased ->70& VO2 max-? Sure the oxidation rate of FFA increased but lactate production also increases. Lactate decreases the FFA mobilization rate and increases FFA reesterification rate. Carbohydrates then become an increasingly important source of fuel. However, during prolonged sub maximal exercise blood lactate levels are very low, thus not affecting FFA mobilization significantly. Thus, carbohydrates are used much less as a fuel and oxidated fats become the most abundant source of energy"
Bottom line is keep the workouts to less then or equal to 45% VO2 Max for the best fat burning results that wont destroy muscle mass.
Balance of carbohydrate and lipid utilization during exercise: the "crossover" concept
G. A. Brooks and J. Mercier
Department of Human Biodynamics, University of California, Berkeley 94720.
The "crossover" concept represents a theoretical means by which one can understand the effects of exercise intensity and prior endurance training on the balance of carbohydrate (CHO) and lipid ****bolism during sustained exercise. According to the crossover concept, endurance training results in muscular biochemical adaptations that enhance lipid oxidation as well as decrease the sympathetic nervous system responses to given submaximal exercise stresses. These adaptations promote lipid oxidation during mild- to moderate-intensity exercise. In contrast, increases in exercise intensity are conceived to increase contraction-induced muscle glycogenolysis, alter the pattern of fiber type recruitment, and increase sympathetic nervous system activity. Therefore the pattern of substrate utilization in an individual at any point in time depends on the interaction between exercise intensity-induced responses (which increase CHO utilization) and endurance training-induced responses (which promote lipid oxidation). The crossover point is the power output at which energy from CHO-derived fuels predominates over energy from lipids, with further increases in power eliciting a relative increment in CHO utilization and a decrement in lipid oxidation. The contemporary literature contains data indicating that, after endurance training, exercise at low intensities (< or = 45% maximal O2 uptake) is accomplished with lipid as the main substrate. In contrast, the literature also contains reports that are interpreted to indicate that during hard-intensity exercise (approximately 75% maximal O2 uptake) CHO is the predominant substrate. Seen within the context of the crossover concept these apparently divergent results are, in fact, consistent.(ABSTRACT TRUNCATED AT 250 WORDS)
Fatty acid oxidation is directly regulated by carbohydrate ****bolism during exercise
E. F. Coyle, A. E. Jeukendrup, A. J. Wagenmakers and W. H. Saris
Department of Human Biology, University of Limburg, Maastricht, The Netherlands.
We determined whether increased glycolytic flux from hyperglycemia and hyperinsulinemia directly reduces fatty acid oxidation during exercise. Fatty acid oxidation rates were measured during constant-rate intravenous infusion of trace amounts of a long-chain fatty acid ([1-13C]palmitate; Pal) vs. a medium-chain fatty acid ([1-13C]octanoate; Oct). Six endurance-trained men cycled for 40 min at 50% of maximal O2 uptake 1) after an overnight fast ("fasting") and 2) after ingestion of 1.4 g/kg of glucose at 60 min and again 10 min before exercise (Glc). Glc caused hyperinsulinemia, a preexercise blood glucose of 6 mM, and a 34% reduction in total fat oxidation during exercise due to an approximately equal reduction in oxidation of plasma-free fatty acids (FFA) and intramuscular triglycerides (all P < 0.05). Oxidation of Pal was significantly reduced during Glc compared with fast (i.e., 70.0 +/- 4.1 vs. 86.0 +/- 1.9% of tracer infusion rate; P < 0.05). However, Glc had no effect on Oct oxidation, which is apparently not limited by mitochondrial transport. Furthermore, Glc reduced plasma FFA appearance 36% (P < 0.05), indicating a coordination of effects on adipose tissue and muscle. In summary, substrate oxidation during exercise can be regulated by increased glycolytic flux that is accompanied by a direct inhibition of long-chain fatty acid oxidation. These observations indicate that carbohydrate availability can directly regulate fat oxidation during exercise.
Carry on