Myths Under The Microscope Part 1: The Low Intensity Fat Burning Zone

By Alan Aragon  © 2006

 


The “Fat Burning Zone” On Trial

Origin of the myth

Dietary variables aside, the body’s proportional use of fat for fuel during exercise is dependent upon training intensity. The lower the intensity, the greater the proportion of stored fat is used for fuel. The higher the intensity, the greater proportional use of glycogen and/or the phosphagen system. But this is where the misunderstanding begins. Although I’m burning a greater proportion of stored fat typing this sentence, getting up and sprinting would have a greater impact on fat reduction despite its lesser proportional use of fat to power the increased intensity. Alas, sufficient investigation of the intensity threshold of maximal net fat oxidation has been done. In what’s perhaps the best designed trial of its kind, Achten & Jeukendrup found peak fat oxidation to occur during exercise at 63% VO2 max. This peak level got progressively less beyond that point, and was minimal at 82% VO2 max, near the lactate threshold of 87% [1].

Misunderstanding is perpetuated in fitness circles

It has been widely misconstrued that a greater net amount of fat is burned through lower to moderate intensity work, regardless of study duration and endpoints assessed. In addition the confusion of net fat oxidation with proportional fat oxidation, the postexercise period is critically overlooked. No distinction is ever made between during-exercise fat oxidation, recovery period fat oxidation, total fat oxidation by the end of a 24-hr period, and most importantly, a longer term of several weeks.. Thus, the superiority of lower intensity cardio continues to be touted over the more rigorous stuff that takes half the time to do. Fortunately, we have enough research data to gain a clear understanding. Let’s dig in.


Dissecting The Research

Mixed study protocols + mixed results = plenty of mixed-up trainees

As with all research involving applied physiology, the highly mixed set of results is due to a wide variation of study designs in terms subject profile, dietary manipulation, energetic balance, and actual intensities used. Nevertheless, the body of exercise-induced fat oxidation research can be easily deciphered by stratifying it into 3 subgroups: Acute effect (during exercise & immediately after), 24-hr effect, & chronic effect (results over several weeks).

Acute effects spawn ideas for further research

In addition to measuring fat oxidation during exercise, most acute effect trials look at fat oxidation at the 3 to 6 hr mark postexercise [2]. Fat oxidation during exercise tends to be higher in low-intensity treatments, but postexercise fat oxidation tends to be higher in high-intensity treatments. For example, Phelain’s team compared fat oxidation in at 3hrs postexercise of 75% VO2 max versus the same kcals burned at 50% [3]. Fat oxidation was insignificantly higher during exercise for the 50% group, but was significantly higher for the 75% group 3 hours postexercise. Lee’s team compared, in college males, the thermogenic and lipolytic effects of exercise pre-fueled with milk + glucose on high versus low-intensity training [4]. Predictably, pre-exercise intake of the milk/glucose solution increased excess postexercise oxygen consumption (EPOC, aka residual thermogenesis) significantly more than the fasted control group in both cases. The high-intensity treatment had more fat oxidation during the recovery period than the low intensity treatment. This implicates pre-fueled high-intensity training’s potential role in optimizing fat reduction while simultaneously setting the stage for quicker recovery.

24-hr effects come closer to reality

You can call it Murphy’s Law, but the promise of greater fat oxidation seen during and in the early postexercise periods of lower intensity cardio disappears when the effects are measured over 24 hours. Melanson’s research team was perhaps the first to break the redundancy of studies that only compared effects within a few hours postexercise [5]. In a design involving an even mix of lean, healthy men & women aged 20-45, identical caloric expenditures of 40% VO2 max was compared
with 70% VO2 max. Result? No difference in net fat oxidation between the low & high-intensity groups at the 24 hr mark.

Saris & Schrauwen conducted a similar study on obese males using a high-intensity interval protocol versus a low-intensity linear one [6]. There was no difference in fat oxidation between high & low intensity treatments at 24 hrs. In addition, the high-intensity group actually maintained a lower respiratory quotient in postexercise. This means that their fat oxidation was higher than the low-intensity group the rest of the day following the training bout, thus the evening out the end results at 24 hrs.

Chronic effects come even closer

Long-term/Chronic effect studies are the true tests of whatever hints and clues we might get from acute studies. The results of trials carried out over several weeks have obvious advantages over shorter ones. They also afford the opportunity to measure changes in body composition, versus mere substrate use proximal to exercise. The common thread running through these trials is that when caloric expenditure during exercise is matched, negligible fat loss differences are seen. The fact relevant to bodybuilding is that high-intensity groups either gain or maintain LBM, whereas the low-intensity groups tend to lose lean mass, hence the high intensity groups experience less net losses in weight [7-9].

The body of research strongly favors high-intensity interval training (HIIT) for both fat loss and lean mass gain/maintenance, even across a broad range of study populations [9-12]. A memorable example of this is work by Tremblay’s team, observing the effect of 20 weeks of HIIT versus endurance training (ET) on young adults [9]. When energy expenditure between groups was corrected, HIIT group showed a whopping 9 times the fat loss as the ET group. In the HIIT group, biopsies showed an increase of glycolytic enzymes, as well as an increase of 3-hydroxyacyl coenzyme A dehydrogenase (HADH) activity, a marker of fat oxidation. Researchers concluded that the metabolic adaptations in muscle in response to HIIT favor the process of fat oxidation. The mechanisms for these results are still under investigation, but they’re centered around residual thermic and lipolytic effects mediated by enzymatic, morphologic, and beta-adrenergic adaptations in muscle. Linear/steady state comparisons of the 2 types tends to find no difference, except for better cardiovascular fitness gains in the high-intensity groups [13].

Summing Up the Research Findings

• In acute trials, fat oxidation during exercise tends to be higher in low-intensity treatments, but postexercise fat oxidation and/or energy expenditure tends to be higher in high-intensity treatments.
• Fed subjects consistently experience a greater thermic effect postexercise in both intensity ranges.
• In 24-hr trials, there is no difference in fat oxidation between the 2 types, pointing to a delayed rise in fat oxidation in the high-intensity groups which evens out the field.
• In long-term studies, both linear high-intensity and HIIT training is superior to lower intensities on the whole for maintaining and/or increasing cardiovascular fitness & lean mass, and are at least as effective, and according to some research, far better at reducing bodyfat.

 

 

References

  1. Achten J, Jeukendrup AE. Relation between plasma lactate concentration and fat oxidation rates over a wide range of exercise intensities. Int J Sports Med. 2004 Jan;25(1):32-7.
  2. Thompson DL, et al. Substrate use during and following moderate- and low-intensity exercise: implications for weight control. Eur J Appl Physiol Occup Physiol. 1998 Jun;78(1):43-9.
  3. Phelain JF, et al. Postexercise energy expenditure and substrate oxidation in young women resulting from exercise bouts of different intensity.J Am Coll Nutr. 1997 Apr;16(2):140-6.
  4. Lee YS. Et al. The effects of various intensities and durations of exercise with and without glucose in milk ingestion on postexercise oxygen consumption. J Sports Med Phys Fitness. 1999 Dec;39(4):341-7.
  5. Melanson EL, et al. Effect of exercise intensity on 24-h energy expenditure and nutrient oxidation. J Appl Physiol. 2002 Mar;92(3):1045-52.
  6. Saris WH, Schrauwen P. Substrate oxidation differences between high- and low-intensity exercise are compensated over 24 hours in obese men. Int J Obes Relat Metab Disord. June; 28 (6): 759-65.
  7. Grediagin A, et al. Exercise intensity does not effect body composition change in untrained, moderately overfat women. J Am Diet Assoc. 1995 Jun;95(6):661-5.
  8. Mougios V, et al. Does the intensity of an exercise programme modulate body composition changes? Int J Sports Med. 2006 Mar;27(3):178-81.
  9. Okura T, et al. Effects of exercise intensity on physical fitness and risk factors for coronary heart disease. Obes Res. 2003 Sep;11(9):1131-9.
  10. Tremblay, et al. Impact of exercise intensity on body fatness and skeletal muscle metabolism. Metabolism. 1994 Jul;43(7):814-8.
  11. Yoshioka M, et al. Impact of high-intensity exercise on energy expenditure, lipid oxidation and body fatness. Int J Obes Relat Metab Disord. 2001 Mar;25(3):332-9.
  12. Broeder CE, et al. The effects of either high-intensity resistance or endurance training on resting metabolic rate. Am J Clin Nutr. 1992 Apr;55(4):802-10.
  13. Gutin B, et al. Effects of exercise intensity on cardiovascular fitness, total body composition, and visceral adiposity of obese adolescents. Am J Clin Nutr. 2002 May;75(5):818-26.

    Part 2 of this article    Part 3 of this article   

 

 

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