Response to letter from Professor Flatt

Sir:

The initiation and termination of feeding are complex processes that involvea large number of signals to the central nervous system. In addition, culturaland social conventions can be major determinants of food intake volume, itstiming, and composition. Eating is rarely initiated solely in response to acuteenergy deficits, rather our eating decisions take into account such things asthe presence or availability of food, the sight and smell of it, time of day,whether other people are eating, our diet goals, and our emotional state. Oncea person has started eating, the decision to stop takes into account a differentset of factors, and again energy balance is just a part of the story. Both thedistension of the stomach and the food-triggered release of hormones fromthe gastrointestinal tract send satiety signals to the brain, but these are onlysuggestions, not orders. A man served his favorite dessert may eat on well pastsatiation. A woman on a diet or in a hurry to get back to work may stop beforeher body says it’s full. While all such factors (biophysiological, environmental,behavioral) are certainly of interest in obesity treatment research, appetite andfood intake regulation are not the focus of this study.

The objective of the first experiment (the one involving a diet intervention)was to compare weight loss from a moderate level of daily exercise to theloss from dieting when both produced equivalent energy deficits. It has beendifficult to answer such questions precisely because in human experiments asin real life ‘‘. . . lack of compliance with dietary prescriptions is the ruleand situations with constant energy intakes rarely prevail.’’ Accordingly,it is useful to seek other methods for testing and experimentation. Thesimulation-based experimentation approach proposed in this article on whichProfessor Flatt has commented [System Dynamics Review 18: 431–471, 2002]provides a viable laboratory tool for such a task. In addition to permittingless costly and less time-consuming experimentation, simulation-type modelsmake ‘‘perfectly’’ controlled experimentation possible. In the model system,unlike the real systems, the effect of changing one factor (e.g. diet/exercisetreatment intervention) can be observed while all other factors (e.g., energydeficit) are held unchanged. Internally, the model provides complete controlof the system.

On the question of the increase in fat free mass (FFM), this has been observedin a number of studies:

ž American Journal of Clinical Nutrition 70: 346–352, 1999;ž American Journal of Clinical Nutrition 63(suppl): 456S–60S, 1996;

System Dynamics Review Vol. 19, No. 2, (Summer 2003): 169–170Published online in Wiley InterScience(www.interscience.wiley.com). DOI: 10.1002/sdr.270Copyright 2003 John Wiley & Sons, Ltd.

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170 System Dynamics Review Volume 19 Number 2 Summer 2003

ž Ballor DL. 1996. Exercise Training and Body Composition. In Human BodyComposition. Roche AF, Heymsfield SB, Lohman TG (eds). Human Kinetics:Champaign, IL;

ž Journal of Applied Physiology 64: 1038, 1988;ž American Journal of Clinical Nutrition 47: 19, 1988;ž American Journal of Clinical Nutrition 33: 1776, 1979ž International Journal of Obesity 15: 717–726, 1991.

Skeletal muscle adaptations to exercise are rapid, and they rapidly plateau. . . which suggests that a ‘‘ceiling’’ may exist with respect to the ability ofweekly energy expenditure to increase fat-free mass (Ballor DL. 1996. ExerciseTraining and Body Composition. In Human Body Composition. Roche AF,Heymsfield SB, Lohman TG (eds). Human Kinetics: Champaign, IL). This iscaptured in the model as a ‘‘Logistic equation’’ (i.e., S-shaped exponentialgrowth, with an eventual plateau) with a C parameter (defining the ceiling formuscle enlargement rate) of 0.15%/day (Physiological Review 71: 541–585,1991).

Finally, I do agree that the causes of muscle fatigue are multifocal and varyfrom occasion to occasion. The reasons why people are unable to continuemuscular work and why they experience fatigue depend on several generalfactors, including the nature of the activity, the training and physiologicalstatus of the individual, environmental conditions, and the depletion of keymetabolites, such as muscle creatine phosphate (CP) and ATP, muscle glycogen,liver glycogen, blood glucose, and arterial as well as muscle O2. Most of thesefactors are beyond the boundary of our model. Our results are intended todemonstrate the effects of ‘‘nutrient fatigue’’ during prolonged submaximalexercise.

Tarek Abdel-HamidNaval Postgraduate School

Monterey, CA, USA