Understanding the Science behind Interval Training.. PART 2
In part I, the basics of exercise physiology were introduced to provide a framework for understanding the role of interval training in cardiovascular conditioning as well as body fat management. Part II will discuss two related concepts, the post-exercise period in terms of fuel usage and the underlying rationale for interval training along with its impact on cardiovascular training. Part III will discuss the actual mechanics of interval training and suggest specific protocols that have been proven to be effective by clinical research studies on trained athletes keeping in mind the intent of interval training as discussed below.
While fuel selection during exercise is primarily determined by the training status of the individual and the intensity of the exercise (see part I), in terms of weight management, the calories burned during exercise do not typically contribute substantially to a caloric deficit that is required for weight loss. Much of this is simply a numbers game. Mild to low-moderate intensity does not produce sufficient caloric expenditure to result in noticeable weight loss by itself.
Walking for example, typically will result in about 100 calories per mile expenditure; thus even a pace of 3.5 miles per hour (which is a brisk pace to maintain) will yield only 350 calories after one hour. Even if 100% of the calories were derived from fat, 10 hours would be necessary for 1 pound of body fat to be lost. Alternatively, higher intensities are limited by the duration that they can be sustained as well as a lower percentage of fat burned since carb burning increases with intensity (see part I).
The Post Exercise Period
Fortunately, the effect of exercise is not limited to simply the exercise period. Just as importantly is the effect of exercise on the post exercise period. This period can be examined from the standpoint of the immediate time frame after exercise to the remainder of the entire non-exercise time period. In terms of the overall impact on weight loss, the inclusion of exercise offers a clear benefit. Typically, with any caloric restriction diet to generate weight loss, over time the rate of weight loss tends to zero and weight plateaus.
This phenomena is usually due to a fall in the basal metabolic rate (resting metabolism) that is probably related to both a slight reduction in lean body mass that can accompany weight loss as well as hormonal adaptation to the lowered caloric intake.2 Exercise in this setting, even of mild intensity will promote preservation of lean body mass (assuming the calorically restricted diet is still able to supply sufficient protein taking into account increased protein required with physical activity) and prevent or reduce the fall in basal metabolic rate due to hormonal adaptation.2,19,20,22
Burn Fat For 3 Hours After Exercising?
Of more particular relevance however, to an already physically active group of individuals is the immediate post-exercise period. Studies have revealed that following aerobic exercise, there is a period of excess oxygen consumption relative to a similar period of time following rest.14 In other words, after an aerobic session, more oxygen is consumed during rest than would be if the exercise had not occurred.
Greater oxygen consumption implies that something is being burned, either fat or carb. In fact, most studies suggest that fat burning is providing the bulk of the excess oxygen consumption.12,14,15 In addition, the magnitude of the excess consumption is directly related to exercise intensity and duration.3,8,12,16-18 Thus, the higher the exercise intensity, the greater the degree of increased fat burning in the post exercise period which can extend for well over three hours following exercise.
The presumed mechanism for this effect is directly related to the fuel utilization during the exercise period. Recall that with increasing intensity from moderate to high, the percentage of energy supplied by fat burning declines (although the absolute decline is slower to trail off), while carb burning continues to increase. Also, carb sources in the body are quite limited. Depending on the exercise, one session can significantly reduce carb stores (glycogen) in the specific working muscles. Even with just rest, carb stores can be exhausted in 2 - 3 days if not replenished by food intake. Thus, following an exercise session that has depleted the muscle's glycogen content, the body will attempt to replenish these stores.
This means that carb uptake by the muscle will go to make glycogen, rather than burned for energy needs. However, even under resting conditions, the muscle still has basal metabolic energy requirements. To meet these requirements, the muscle will burn fat for fuel and this is the basis for increased fat burning in the post exercise period, since the conversion of carbs to glycogen in muscle will require some energy itself.
Clearly, following low intensity exercise, the muscle has little to do since neither intramuscular carb or fat stores have been significantly impacted. In addition, at low intensity, energy can be supplied by peripheral fat stores slowly releasing fat into the bloodstream. These fat stores are the most flexible since they can grow and contract as needed, but the rate of mobilization (or release) of fat from peripheral fat stores is limited.10 However, once moderate intensity is initiated, the situation changes dramatically.
Under moderate intensities, intramuscular fat stores must be tapped to support the level of energy generation, since the fat contribution from peripheral fat stores has reached its limit. In essence, moderate intensity can be viewed as the point where intramuscular fuel stores begin to be utilized. Carb burning will also increase linearly with intensity and the breakdown of intramuscular glycogen stores become significant during upper levels of moderate intensity.
Thus, following moderate intensity exercise, the two major intramuscular energy stores of fat (in the form of intramuscular triglyceride) and carb (in the form of glycogen) need to be replaced. Since carbs are limiting as discussed above, carbs, in the form of blood sugar, are diverted exclusively for glycogen replacement. Fat uptake is also increased and fuels energy needs as well as intramuscular triglyceride replacement. Endurance athletes develop increased intramuscular triglycerides as a part of training.9,11
This fat, both for energy needs as well as intramuscular triglyceride replacement, is derived from fat circulating fat in the bloodstream and comes from peripheral fat stores. Given that depletion of peripheral fat stores is limited in their rate of release of fat (the speed at which they can be depleted) continuing peripheral fat store depletion following exercise offers an attractive method to enhance bodyfat management. Desirable weight loss and bodyfat loss implies depletion of peripheral body fat stores.
The Intensity Of Exercise And How It Will Affect You
In summary, the intensity of exercise, regardless of the amount of fat burned during the exercise directly influences the amount of fat burned in the post exercise period. Since this fat is derived from peripheral fat stores, the higher the intensity and longer the duration that can be sustained, the greater the post-exercise fat burn that can be achieved. In essence, the combination of intensity and duration generate a carb and fat depleted state in the working muscle that shifts fuel metabolism towards fat burning to allow the muscle to return to its baseline levels of glycogen and intramuscular fat stores, ready for another round of exercise.
Sustained moderate intensity (in the range of 8 - 15 calories per minute) exercise can create this condition, but we will now turn our attention to another training modality, namely interval training, that will achieve this same effect within a shorter time period, and also contribute an added benefit from a cardiovascular training standpoint.
Interval training arose as means for endurance athletes to improve their performance capability. We have seen how VO2max measures the level of aerobic fitness; however, maintenance of an intensity at 100% VO2max can only be sustained for a few minutes because of the accumulation of lactic acid. Lactic acid, derived from carb burning, will gradually accumulate in the blood as a result of increased production in working muscle as intensity is increased.1
Calculate Your VO2max, Click Here!
This lactic acid must be cleared from the bloodstream to avoid high levels that upset the pH balance and cause the biochemical steps that generate energy from being disrupted because these steps function in a narrow pH range. Once in the blood, lactic acid can be removed a number of ways: 1) working muscles can buffer themselves against the drop in pH as a result of the acid load, 2) the liver can remove lactic acid from the blood and convert it back into glucose (since lactic acid is produced as a result of glucose breakdown, high levels of lactic acid imply that muscles are using a lot of glucose in the first place), 3) non-working muscles can take up lactic acid and burn it for fuel, conserving glucose for working muscles, and 4) the heart, which must always operate under aerobic condition can utilize lactic acid for fuel.
Lactic Acid
Lactic acid is produced during any exercise to some extent, but increases with intensity. Lactic acid accumulates in the blood, but remains relatively steady until a specific intensity (specific to the individual) is reached, at which time lactic acid levels rise uncontrollably resulting in muscle failure. This threshold level is referred to as the lactic acid threshold. Prior to the threshold level, the body's ability to remove lactic acid from the blood allows it to balance lactic acid production with removal. Above the threshold, the removal system has maxed out and can no longer keep pace with production.
The key for endurance performance lasting greater than a 45 - 60 minute time frame is to operate at an intensity that is below the lactic acid threshold5. Lactic acid threshold is somewhat individual, but has been shown to be a better predictor of athletic performance than overall aerobic fitness (VO2max).4,6,7 For example, athlete A with a lactic acid threshold at 71% VO2max could maintain a 60 minute intensity at 70% VO2max, while athlete B with a lactic acid threshold of 81% VO2max could maintain 80% VO2max during the same period. If their VO2max levels were equal (and they were the same size), athlete B would win a competition lasting an hour since he could sustain a greater intensity over the time period of the event.
How Do You Raise Your Lactic Acid Threshold?
The question then becomes how to train or raise your lactic acid threshold. This is the intent behind interval training. While performance at events lasting 60 minutes or longer may not be everyone's goal, the adaptations that occur with interval training are valuable beyond the improvement in athletic performance and contribute to body fat management in a productive manner. In addition, interval training can result in aerobic fitness improvements and maintenance with far less time investment than the more traditional increasing volume (meaning more time) work.
The essence of interval training is to work at an intensity level above one's lactic acid threshold, thus causing an increase of lactic acid that would result in muscle failure. This intensity is sustained for a duration that is somewhat less than the maximum possible time (that is, before failure occurs), typically on the order of several minutes. This is followed by a rest period or extremely light exercise to allow the body's systems to clear the lactic acid from the blood. The cycle is then repeated.
Thus, the body is exposed to a long cumulative total duration (longer than could be produced from continuous exercise) of elevated lactic acid and will learn to adapt to improving its ability to clear lactic acid from the blood. Cycling is typically repeated 8 - 15 times. If conditions are chosen appropriately, lactic acid levels will slowly climb and each cycle will become progressively more difficult. With this general type of protocol, the lactic acid threshold can be increased so that a higher intensity can be maintained for long periods (60 minutes or longer) without failure due to lactic acid levels.
For an endurance athlete, the value of lactic training is clear. With any program of aerobic training, there is typically an increase in VO2max of about 25% relative to sedentary levels. Greater gains can only be achieved with reductions in body weight (since VO2max is measured in terms of liters of oxygen consumed per minute per kilogram of body weight). After this initial gain which occurs over 3 - 5 months of aerobic training, further increases in training volume (that is longer training sessions), do not lead to further gains. To increase performance further, interval training allows for a higher level of intensity to be maintained under conditions relevant for athletic competition. While most sporting events do not operate at 100% VO2max, athletes typically perform at or just slightly above their lactic acid threshold.
Even for those interested in non-endurance activities, interval training can achieve several goals. First, interval training is relatively time efficient in terms of producing aerobic benefits.13 Second, interval training, along with other vigorous activities of comparable intensity have been associated with reductions in body fat, specifically in terms of a reduction in skinfold thickness.21
While the physiologic basis for this effect has not been identified, the likely effect is a combination of post exercise fat burning as discussed above, along with secretion of growth hormone that occurs during intense physical activity.23 Growth hormone besides its obvious effects on muscle mass is also known to produce a lipolytic effect that would promote a loss of fat.
Conclusion
Finally, interval training can improve and raise the lactic acid threshold which permits a higher intensity of sustained aerobic activity for longer periods of time. Thus, for a specific time period allocated for aerobic exercise, a higher intensity level can be utilized for greater caloric expenditure.
Part II has discussed the importance of the post-exercise period in terms of bodyfat management and its relation to exercise intensity. The concept of interval training was introduced and detailed to highlight the value in an overall aerobic conditioning program. Finally, the confluence of several factors suggests that the addition of interval training provides special benefits with regards to bodyfat management because of the intensity level and the post-exercise period.
Part III will discuss various interval training protocols that can be utilized under a wide variety of conditions. Given the intensity of this type of training, some protocols are simply not suitable for all training regiments and care must taken to identify appropriate protocols. A wide range of protocols will be presented to offer options for nearly everyone.
Reference List
1. Antonutto, G. and P. E. Di Prampero. 1995. The concept of lactate threshold. A short review. J. Sports Med. Phys. Fitness 35:6-12.
2. Astrup, A., P. C. Gotzsche, W. K. van de, C. Ranneries, S. Toubro, A. Raben, and B. Buemann. 1999. Meta-analysis of resting metabolic rate in formerly obese subjects. Am. J. Clin. Nutr. 69:1117-1122.
3. Bahr, R. 1992. Excess postexercise oxygen consumption--magnitude, mechanisms and practical implications. Acta Physiol Scand. Suppl 605:1-70.
4. Bassett, D. R., Jr. and E. T. Howley. 2000. Limiting factors for maximum oxygen uptake and determinants of endurance performance. Med. Sci. Sports Exerc. 32:70-84.
5. Billat, L. V. 1996. Use of blood lactate measurements for prediction of exercise performance and for control of training. Recommendations for long-distance running. Sports Med. 22:157-175.
6. Billat, L. V. and J. P. Koralsztein. 1996. Significance of the velocity at VO2max and time to exhaustion at this velocity. Sports Med. 22:90-108.
7. Coyle, E. F. 1999. Physiological determinants of endurance exercise performance. J. Sci. Med. Sport 2:181-189.
8. Gore, C. J. and R. T. Withers. 1990. Effect of exercise intensity and duration on postexercise metabolism. J. Appl. Physiol 68:2362-2368.
9. Hardman, A. E. 1998. The influence of exercise on postprandial triacylglycerol metabolism. Atherosclerosis 141 Suppl 1:S93-100.
10. Hodgetts, V., S. W. Coppack, K. N. Frayn, and T. D. Hockaday. 1991. Factors controlling fat mobilization from human subcutaneous adipose tissue during exercise. J. Appl. Physiol 71:445-451.
11. Klein, S., E. F. Coyle, and R. R. Wolfe. 1994. Fat metabolism during low-intensity exercise in endurance-trained and untrained men. Am. J. Physiol 267:E934-E940.
12. Laforgia, J., R. T. Withers, N. J. Shipp, and C. J. Gore. 1997. Comparison of energy expenditure elevations after submaximal and supramaximal running. J. Appl. Physiol 82:661-666.
13. Laursen, P. B. and D. G. Jenkins. 2002. The scientific basis for high-intensity interval training: optimising training programmes and maximising performance in highly trained endurance athletes. Sports Med. 32:53-73.
14. Maehlum, S., M. Grandmontagne, E. A. Newsholme, and O. M. Sejersted. 1986. Magnitude and duration of excess postexercise oxygen consumption in healthy young subjects. Metabolism 35:425-429.
15. Medbo, J. I. and E. Jebens. 2002. Leg gas exchange, release of glycerol, and uptake of fats after two minutes bicycling to exhaustion. Scand. J. Clin. Lab Invest 62:211-221.
16. Phelain, J. F., E. Reinke, M. A. Harris, and C. L. Melby. 1997. Postexercise energy expenditure and substrate oxidation in young women resulting from exercise bouts of different intensity. J. Am. Coll. Nutr. 16:140-146.
17. Rauch, L. H., A. N. Bosch, T. D. Noakes, S. C. Dennis, and J. A. Hawley. 1995. Fuel utilisation during prolonged low-to-moderate intensity exercise when ingesting water or carbohydrate. Pflugers Arch. 430:971-977.
18. Sedlock, D. A., J. A. Fissinger, and C. L. Melby. 1989. Effect of exercise intensity and duration on postexercise energy expenditure. Med. Sci. Sports Exerc. 21:662-666.
19. Stefanick, M. L. 1993. Exercise and weight control. Exerc. Sport Sci. Rev. 21:363-396.
20. Thompson, J. L., M. M. Manore, and J. R. Thomas. 1996. Effects of diet and diet-plus-exercise programs on resting metabolic rate: a meta-analysis. Int. J. Sport Nutr. 6:41-61.
21. Tremblay, A., J. A. Simoneau, and C. Bouchard. 1994. Impact of exercise intensity on body fatness and skeletal muscle metabolism. Metabolism 43:814-818.
22. van Dale, D. and W. H. Saris. 1989. Repetitive weight loss and weight regain: effects on weight reduction, resting metabolic rate, and lipolytic activity before and after exercise and/or diet treatment. Am. J. Clin. Nutr. 49:409-416.
23. Wideman, L., J. Y. Weltman, M. L. Hartman, J. D. Veldhuis, and A. Weltman. 2002. Growth hormone release during acute and chronic aerobic and resistance exercise: recent findings. Sports Med. 32:987-1004.
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If you act sanctimonious I will just list out your logical fallacies until you get pissed off and spew blasphemous remarks.
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