Creating a proper environment for fat loss from exercise

It has long been known that for practical purposes, the effect of exercise on energy expenditure is essentially confined to the increased energy expenditure during exercise. Exercise and training do not appear to enhance resting metabolic rate (RMR).

However many studies going back 25 years have demonstrated a post-exercise reduction of respiratory quotient (RQ) for several hours (1-6) which is more pronounced and sustained after prolonged glycogen-depleting exercise. This results from a post-exercise increase in free fatty acid (FFA) levels (from the lipolytic response to exercise), during a time of reduced glucose availability as a result of glycogen depletion.

The respiratory quotient is the ratio of the volume of carbon dioxide produced when a substance is oxidized, to the volume of oxygen used. A RQ of 1.0 means that we produce the same volume of carbon dioxide (CO2) as the volume of oxygen (O2) we take in. RQ of 0.7 means that we take in more oxygen and we produce less carbon dioxide. Carbohydrates have an RQ of 1.0 and fats have RQ of about 0.7. Research demonstrates that high carbohydrate diets have higher RQ and low carbohydrate diets have lower RQ. When our RQ is closer to 1.0 we are burning more carbohydrates as fuel and when our RQ gets closer to 0.7 we are burning more fat.

So a post-exercise reduction in respiratory quotient means we move away from using carbohydrates as an energy source in favor of fats.

Without prior glycogen depletion, aerobic exercise of at least 20 minutes duration is required to bring about a response that stimulates lipolysis (7). So the fats that we will use for energy come from lipolysis unless we make the mistake of choosing to ingest carbohydrates PWO which will have the effect of moving the RQ back toward 1.0. In that situation the body will leave more of the fatty acids alone and they will remain and redeposit. If we make the mistake of choosing to ingest fats PWO we add to the supply of fat available for use as energy. As we have less need for energy this will surely mean a deposition of fat.

If we make the correct choice and ingest nothing, then the lower RQ and the available FFAs will mean we burn the fats we liberate for energy.

The effects of aerobic exercise on fat balance come from increased fat oxidation during exercise and a temporary depression of respiratory quotient following exercise. Maximizing these events will maximize fatloss.


Exercise

The rate of fat oxidation is approximately proportional to the FFA levels in the blood. Increasing FFA levels will promote a reduced respiratory quotient (RQ) during exercise (8,9).

Intensity

The intensity and duration of exercise influences the exercise RQ (10). High intensity exercise in excess of 70% VO2 max (i.e. exceeding the "aerobic threshhold') tend to selectively increase the burning of carbohydrate. An increased proportion of fat is burned during moderate intensity exercise.

Duration

In addition, as exercise is prolonged and glycogen stores are gradually depleted, RQ tends to decline as fats must provide a higher proportion of energy needs (11).

Therefore prolonged continuous exercise (at least 35-60 min) of moderate intensity, conducted when serum FFA levels are maximal, should optimize the amount and proportion of fat burned during exercise (10).


Maximizing pre-workout FFA

To create high FFA levels, exercise should be done on an empty stomach away from meals and/or preferably during morning fasting's metabolism, when no food has been consumed for at least 8 hours. Food consumption prior to or during exercise will result in an insulin-mediated suppression of FFAs while increasing blood glucose, and this will favor carbohydrate oxidation.

Boosting FFA

Caffeine

FFA levels can be boosted further by pre-administration of an effective dose of caffeine (12,13), equivalent to one or two cups of strong coffee. For the reason that the impact of oral caffeine on FFAs is delayed, the caffeine should be taken at least 45-60 min prior to the exercise session. Caffeine consumption prior to exercise has been shown to spare glycogen and reduce the respiration quotient in exercising humans (12,14,15). Caffeine's efficacy in this regard will be higher in individuals who are not carbohydrate loaded (16), and who have not developed caffeine resistance stemming from excessive habitual use.

GHRP-2, Ipamorelin, Modified GRF(1-29) and GH Frag (176-191)

I don't need to elaborate much on this as much more detailed information is available throughout this forum. Suffice it to say that use of these items to increase GH or its lipolytic fragment will increase the amount of FFAs in circultaion.

These GH effectors should be dosed prior to exercise. They can be taken with coffee and should add to exercise induced FFA as well as post-exercise FFAs.


Increasing the liver's capacity for lipid oxidation

In short the more carntine you can have delivered to and retained in the mitochondria of muscle cells, the more oxidation of fats will occur. Insulin and it also appears Choline increase the transport and retainment of Carnitine in muscle. L-Carnitine has a slow release rate from tissue and thus will build up over time if taken daily. Oral bioavailability is lower then injection but still of substantial cumulative benefit.

L-Carnitine (in injectable or oral form) should always be ingested when you take exogenous insulin and/or when you are spiking insulin with carbohydrates throughout the week. In addition the following oral regime taken 45 minutes prior to exercise (at coffee time) should provide benefit.

1.3 - 2 grams of Choline and 1 - 1.4 grams of L-Carnitine.

Notes:
1. Bahr R, Ingnes V, Vaage O et al. Effect of duration of exercise on excess postexercise 02 consumption. J Appl Physiol 1987; 485-490.

2. Maehlum S, Grandmontagne M, Newsholme E A, Sejersted O M. Magnitude and duration of excess postexercise oxygen consumption in healthy young subjects. Metabolism 1986; 35: 425-429.

3. Bielinski R, Schutz Y, J6quier E. Energy metabolism during the postexercise recovery in man. Am J Clin Nutr 1985; 42: 69-82.

4. Flatt J P. Dietary fat, carbohydrate balance, and weight maintenance: effects of exercise. Am J Clin Nutr 1987; 45: 296-306.

5. Chad K, Quigley B. The effects of substrate utilization, manipulated by caffeine, on post-exercise oxygen consumption in untrained female subjects. Eur J Appl Physiol 1989; 49: 48-54.

6. Weststrate J A, Weys P, Poortvliet E et al. Lack of a systematic sustained effect of prolonged exercise bouts on resting metabolic rate in fasting subjects. Eur J Clin Nutr 1990; 44: 91-97.

7. Carlson L A, Edelund L G, Oro L. Studies on blood lipids during exercise. J Lab Clin Med 1963; 61: 724--729.

8. Costill D L, Coyle E, Dalsky Get al. Effects of elevated plasma FFA and insulin on muscle glycogen usage during exercise. J Appl Physiol 1977; 43: 695--699.

9. Hickson R C, Rennie M J, Conlee R K et al. Effects of increased plasma fatty acids on glycogen utilisation and endurance. J Appl Physiol 1977; 43: 829-833.

10. Andrews J F. Exercise for slimming. Proc Nutr Soc 1991; 50: 459-471.

11. Flatt J P. Dietary fat, carbohydrate balance, and weight maintenance: effects of exercise. Am J Clin Nutr 1987; 45: 296-306.

12. Chad K, Quigley B. The effects of substrate utilization, manipulated by caffeine, on post-exercise oxygen consumption in untrained female subjects. Eur J Appl Physiol 1989; 49: 48-54.

13. Bellet S, Kershbaum A, Finck E. Response of free fatty acids to coffee and caffeine. Metabolism 1968; 17: 702-707.

14. Costill D L, Dalsky G P, Fink W J. Effects of caffeine ingestion on metabolism and exercise performance. Med Sci Sports 1978; 10: 155-158.

15. Essig D, Costill D L, Van Handel P J. Effects of caffeine ingestion on utilization of muscle glycogen and lipid during leg ergometer cycling. Int J Sports Med 1980; 1: 86-90.

16. Weir J, Noakes T D, Myburgh K, Adams B. A high carbohydrate carbohydrate diet negates the metabolic effects of caffeine during exercise. Med Sci Sports Exerc 1987; 19: 100-105.