Endurance Exercise and Fat Oxidation
By: Derek Charlebois B.S. CPT

      A study done by Romolo and Rhodea (1998) showed that the highest rate of plasma FFA turnover was seen at an exercise intensity of 35% VO2max. At this intensity, plasma FFA turnover rate was 4-5 times the resting rate after 30 minutes of exercise. Interestingly, plasma catecholamine levels increased by only 50-60% above resting levels, which would not explain the 400-500% increase in plasma FFA turnover. At an exercise intensity of 65%-85% VO2max, plasma FFA turnover was lower than that at 25% VO2max, but catecholamine concentrations were 3-6 times higher at 65% VO2max and 17-19 times higher at 85% VO2max than at rest. While catecholamines concentrations are directly related to the rate of lipolysis at rest (Romolo & Rhodea 1998), during exercise other factors clearly play a large role. 

     The increase in fat oxidation seen during exercise is due to an increase in FFA availability and a decrease in the re-esterification of FFA. Wolfe et al (1990) found that FFA re-esterfication dropped from 70% at rest to 25% during low to moderate intensity exercise. This decrease in the re-esterification of FFA means more FFA will be available for oxidation.

     High intensity exercise (>70% VO2max) causes a decrease in the release of fatty acids from adipose tissue. Data suggest that this decrease in circulating fatty acids is due to decreased blood flow and removal of the fatty acids from adipose tissue to the circulation (Horowitz and Klein 2000). An increase in muscle glycogen usage is also believed to play a role in the decreased oxidation of fatty acids during high-intensity exercise. Glycogenolysis elevates acetyl-CoA (derived from glycogen) concentrations that in turn elevate malonyl-CoA concentrations (Horowitz and Klein 2000). Malonyl-CoA inhibits CPT-I, which is the rate-limiting step for fatty acid (specifically long-chain fatty acids) entry in mitochondria. Interestingly, the skeletal muscle of trained individuals is more sensitive to malonyl-CoA than the skeletal muscle of untrained individuals (Starritt et al 2000). It is believed that decreased CPT-I activity is the main cause of decreased fat oxidation at high exercise intensities. During moderate to high-intensity exercise, half of the total energy used is acquired from fat sources and the other half from carbohydrate sources (Achten & Jeukendrup, 2004).

     Endurance exercise training leads to an increase in FFA oxidation during submaximal exercise, due to a decrease in CHO oxidation. Achten and Jeukendrup (2003) found that at an exercise intensity of 62% VO2max moderately trained cyclist oxidized fat at a rate of 0.48 g/min while highly-trained cyclist oxidized fat at a rate of 0.56 g/min. Endurance training causes an increase in mitochondria density and CPT-I gene expression, which would create a greater capacity to oxidize fat. Tunstall et al. (2002) found that nine days of endurance training caused a 57% increase in CPT-I gene expression at rest and after exercise. Endurance training as increases capillarization of skeletal muscle. Because transport to FFA from adipose tissue to skeletal muscle is a limited factor in fat oxidation, such adaptation should increase the rate of fat oxidation during exercise.

     From the above research, it appears that low-moderate intensity endurance exercise is ideal for fat oxidation. On the Cut Diet, we recommend performing low-intensity cardio post workout in order to burn additional fatty acids and promote recovery.

     Derek “The Beast” Charlebois is an ACE certified personal trainer, competitive bodybuilder, and holds a Bachelor’s degree in Exercise Science from The University of Michigan. Derek is the Promotions Coordinator/R&D at Scivation/Primaforce and is involved in coordinating promotions, research and development, advertising, and marketing. Derek is an accomplished author with articles on such websites as Bodybuilding.com, Bulknutrition.com, the online magazine StrengthAndScience.com, and contributed to the book Game Over: The Final Showtime Cut Diet You’ll Ever Need! Derek is available for online personal training. His website is www.beastpersonaltraining.com.

References:

Achten, J. Jeukendrup, AE. Optimizing Fat Oxidation through exercise and diet. Nutrition 2004;20:716 –727.

Horowitz, JF. Klein, S. Lipid metabolism during endurance exercise. Am J Clin Nutr. 2000 Aug;72(2 Suppl):558S-63S.

Horowitz, JF. Fatty acid mobilization from adipose tissue during exercise.
Trends Endocrinol Metab. 2003 Oct;14(8):386-92.

Klein S, Peters EJ, Holland OB, Wolfe RR. Effect of short- and long-term beta-adrenergic blockade on lipolysis during fasting in humans. Am J Physiol. 1989 Jul;257(1 Pt 1):E65-73.

McGarry, JD. Malonyl-CoA and carnitine palmitoyltransferase I: an expanding partnership. Biochem Soc Trans. 1995 Aug;23(3):481-5.

Ranallo RF, Rhodes EC. Lipid metabolism during exercise. Sports Med. 1998 Jul;26(1):29-42.

Starritt EC, Howlett RA, Heigenhauser GJ, Spriet LL. Sensitivity of CPT I to malonyl-CoA in trained and untrained human skeletal muscle. Am J Physiol Endocrinol Metab. 2000 Mar;278(3):E462-8.

Tunstall RJ, Mehan KA, Wadley GD, Collier GR, Bonen A, Hargreaves M, Cameron-Smith D. Exercise training increases lipid metabolism gene expression in human skeletal muscle. Am J Physiol Endocrinol Metab. 2002 Jul;283(1):E66-72.

Wolfe RR, Klein S, Carraro F, Weber JM. Role of triglyceride-fatty acid cycle in controlling fat metabolism in humans during and after exercise. Am J Physiol 1990;258:E382

> Epinepherine & Norepinepherine
        By: Derek Charlebois B.S. CPT

> Train Like A Beast - Muscle
   Specific Hypertrophy Workouts
        By: Derek Charlebois B.S. CPT

> Representin' The Repetition
        By: Layne Norton BS Biochemistry

> Beast Q & A

> Endurance Exercise And Fat    Oxidation
        By: Derek Charlebois B.S. CPT

> Power XL Issue #3
        By: Coach XXX