1 Energy Cost of Physical Activity
The 24-h energy expenditure can be broken down into several components, including resting metabolic rate (RMR), the thermic effect of feeding, and the energy cost of physical activity. Less than 20% of the RMR is attributed to skeletal muscle (1). Nonetheless, the factor that can cause the most dramatic effect on metabolic rate is strenuous exercise. During strenuous exercise, the total energy expenditure of the body may increase 15-25 times above resting levels (1). This enormous elevation in the body's metabolic rate is the result of a 200-fold increase in the energy requirement of exercising muscles (1). In terms of measurement, the resting energy expenditure of a 70-kg human is approximately 1.2 kcal/min (5.0 kJ), whereas the energy cost during strenuous exercise can be 18-30 kcal/min (75-125 kJ) (1). At first glance, these numbers look promising for weight loss; in that the energy cost of a 60-min exercise bout would be from 1080 to 1800 kcal (4518-7531 kJ). This translates into an exercise-induced weight loss of about one-third to one-half pound a day.
However, theoretical estimates of energy expenditure during exercise, such as those previously described, are not realistic for the overweight or obese individual for several reasons. For example, an intense exercise bout lasting 60 min is beyond the reach of most overweight people (2), since the functional capacity of the overweight person is generally much less than that of the normal-weight individual. Overweight people who have a history of inactivity generally can only increase their total energy expenditure by about eightfold during maximal exercise exertion (2,3), and most of these people find it very difficult to sustain an exercise intensity of 75% maximal effort for 20 min (2). Therefore, the best initial expectation for the overweight person would be to exercise for 20 min at an intensity that is six times the RMR (6 METS, or 6 metabolic equivalents). Under these conditions (20 min at 6 METS), the predicted energy expenditure of the exercise session would only be ~150 kcal (628 kJ).
As we have shown above, some of the failure for exercise programs to produce expected outcomes in the obese may be attributed to the inappropriate application of data derived from normal weight or athletic populations to the obese (3). Accordingly, practitioners are cautioned against using prediction equations and metabolic estimates for obese individuals until the predictors have been validated for the obese (2,3). (More on the use of prediction equations for energy expenditure in the obese is given later in this chapter; see Sec. II.C.)
Although it may seem that the absolute contribution of the energy cost of activity to offset the daily energy balance during weight loss treatment is small, the relative contribution of exercise to the 24-h energy expenditure is important. Even the 20-min exercise bout described above may account for 10% or more of the daily energy expenditure for an obese person. Furthermore, exercise may have a metabolic effect beyond that which is accounted for during the actual exercise session itself.
The RMR accounts for ~60-75% of the total energy expenditure. Therefore, anything that alters the RMR has the potential to significantly impact body weight. The association between obesity and an impaired RMR has received considerable attention, as have how diet and exercise affect RMR (4,5). It is well known that caloric restriction produces a rapid reduction in RMR
of up to 20%. This reduction in RMR may account for some of the plateau in weight loss observed even when energy intake is held at a reduced level. On the contrary, it is also well known that exercise increases the RMR, but the magnitude and duration of the increase post exercise are not well understood. Furthermore, it is not clear how the exercise prescription can be optimized to enhance RMR and offset any metabolic decline produced by restrictive dieting.
Early work revealed that daily aerobic exercise at 60% of VO2max, initiated 2 weeks after a very low calorie diet (500 kcal/d, 2092 kJ/d), normalized the diet-induced depression in RMR and attenuated the diet-induced loss in lean body mass (4). A later study found that when aerobic exercise was initiated simultaneously with a severely restricted diet, RMR was maintained, but the diet-induced loss in lean tissue was not safeguarded (5). Other studies, in which diet and exercise were initiated simultaneously, have shown that exercise neither minimized the loss of lean tissue nor maintained RMR (6,7). Although the data are not consistently clear, the American College of Sports Medicine attests that exercise helps maintain the RMR and slows the rate of fat-free tissue loss that occurs when a person loses weight by severe caloric restriction (1). Whether exercise completely offsets the diet-induced reduction or only partially offsets the diet-induced reduction in RMR may depend on the severity and duration of the diet restrictions; type, duration, and intensity of exercise; and the magnitude of changes in body composition.
The most extensive review of the effect of exercise on RMR was performed several years ago by Ballor and Poehlman (8). This meta-analytical review pooled together data from 33 reports, which included 60 group means from weight loss studies using either diet only or diet plus aerobic exercise interventions. The analysis revealed that there were no significant exercise or gender effects on RMR during weight loss. When diet-induced reductions in RMR were corrected for changes in body weight, RMR was reduced by less than 2% (P < .05). These meta-analytical data indicate that exercise training does not differentially affect RMR during weight loss, or enhance RMR during weight loss, and that reductions in RMR normally seen during weight loss are proportional to the loss of the metabolically active tissue (8). More recent investigations infer that aerobic exercise training does not automatically increase RMR significantly. For example, Wilmore et al. (9) showed that RMR remained unchanged following 20 weeks of aerobic exercise training in men and women of all ages, in spite of a large increase of 18% in VO2max. However, subjects in this study were not necessarily overweight, nor were they attempting to lose weight during the exercise intervention.
Nonetheless, aerobic exercise may prevent the common age-related decline in RMR (10). Endurance-trained, middle-aged and older women presented a 10% higher RMR than sedentary women, when RMR was adjusted for body composition. Although descriptive in nature, these data suggest that exercise may help prevent the age-related weight gain seen in sedentary women, and that the protective mechanism may be an altered RMR.
Since it is well accepted that strength training can increase muscle mass, and that muscle mass is very active metabolically, Byrne and Wilmore (11) have recently examined how strength training may differentially affect RMR in comparison to aerobic exercise training. This cross-sectional study found that there was no significant difference in RMR among strength-trained, aerobically trained, and untrained women. In a randomized controlled clinical trial, moderately obese men and women were assigned to one of three groups; diet plus strength training, diet plus aerobic training, or diet only (12). The exercise protocols were designed to be isoenergetic. The mean weight loss among groups did not differ significantly after 8 weeks, but the strength-trained group lost less lean tissue mass than the other two groups. The RMR declined significantly in each group, with no difference among groups. These data indicate that neither strength training nor aerobic exercise training prevents the decline in RMR caused by restrictive dieting (12).
The relationship among diet, exercise, and metabolism is complex. Diet and exercise do affect metabolic rate, but for how long and by how much remains unclear. Severely restrictive diets generally result in a transient decrease in metabolic rate, but whether this decrease is sustained has not been clearly shown. It may be that the variability in the metabolic response to diet restriction and exercise among individuals is influenced by the type of obesity (gluteal-femoral or abdominal), the cellular expression of obesity (hypertrophic or hyperplastic), and/or the genotype of obesity (8). Some of the variation in the literature with respect to the effects of exercise training on RMR may also be related to the length of time between the last exercise training session and measurement of RMR. Herring et al. (13) reported that RMR was elevated immediately following an exercise session, but that within 39 hr of the cessation of exercise the RMR had dropped 8%. It may be that in order to demonstrate a true exercise-induced elevation in RMR, which would enhance weight control success, the exercise stimulus must be repeated daily or several times per week. Accordingly, the incremental effects of the energy cost of exercise itself combined with the incremental effects of the temporary postexercise elevations in metabolic rate may act synergistically to enhance weight loss success and long-term reduced weight maintenance.
It is well established that metabolic rate (measured as oxygen consumption) remains elevated for some period of time following exercise (14-20). This phenomenon has been termed excess postexercise oxygen consumption (EPOC). Studies have shown that the magnitude of EPOC is linearly related to the duration and intensity of exercise (14,15,17,19), and that EPOC following a moderate intensity exercise bout (70% VO2max) accounts for ~15% of the total energy cost of the exercise (15). The time for metabolism to return to baseline following an acute exercise session can vary from as little as 20 min to 12 hr, depending on both the duration and intensity of exercise (15,16,18,19). Thus, one can see that over a period of months or more, increments of EPOC may play a contributing role in weight loss or reduced weight maintenance for the person struggling with body weight.
Gaesser and Brooks have identified several factors as contributing to EPOC (20). Intermediary substrates, such as lactate and free fatty acids, continue to be oxidized at an elevated rate following an exercise bout. The cost of replenishing glycogen stores also adds to the EPOC. Circulatory levels of catecholamines and other hormones, which stimulate metabolism, remain elevated post exercise. Increased respiration and elevated heart rate also add to the metabolic rate following exercise. Body temperature can remain elevated for as long as 2 hr after exercise, and this thermic response will raise energy expenditure slightly.
Although several studies have examined the possibility of a metabolic defect in RMR, 24-hr energy expenditure, or the thermic effect of food for obese compared to lean people, only a few studies have evaluated EPOC in the obese. Broeder et al. (21) examined five borderline obese men (23.5 ± 1.3% body fat) and five lean men (<15% body fat) for their metabolic response to exercise. Each group performed two exercise bouts, one at 30% of VO2max and another exercise bout at 60% of VO2max. Energy expenditure during each exercise session was 720 kcal (3.1 MJ), while oxygen consumption was measured for 180 minutes post exercise. The low-intensity exercise session did not elicit any EPOC compared to preexercise RMR for either group, but the moderate-intensity exercise elicited an EPOC that was 13.5% above RMR, for each group. The authors attributed the failure to show significant differences in EPOC between lean and borderline obese groups to a small sample number.
Although Segal et al. (22) did not study EPOC directly, they did study the postprandial thermogenesis in the obese compared to the lean at rest, during exercise, and postexercise. Eight lean men (10 ± 1% body fat) and eight obese men (30 ± 2% body fat) exercised for 30 min on a cycle ergometer at their ventilatory threshold (borderline anaerobiosis). Results showed that the 3-hr thermic effect of food was significantly higher for the lean than the obese men during rest (44 ± 7 vs. 28 ± 4 kcal, 184 ± 29 vs. 117 ± 17 kJ), during exercise (19 ± 3 vs. 6 ± 3 kcal, 79 ± 13 vs. 25 ± 12 kJ), and postexercise (44 ± 7 vs. 16 ± 5 kcal, 184 ± 29 vs. 67 ± 21 kJ). Even though the EPOC measurements in this study were confounded with diet-induced thermo-genesis, the data showed obese men to have lower metabolic rates postexercise than the lean men.
In another study, 10 lean women (BMI <25) and 10 obese women (BMI 30-45) performed exercise at 6065% of VO2max on a cycle ergometer for 13 min (23). EPOC effects lasted for 30 min postexercise for both groups, but there was no significant difference in EPOC or postexercise respiratory exchange ratio between groups.
Although the data on EPOC in overweight people are sparse, findings seem to indicate that the EPOC effect for lean and overweight individuals is similar. Therefore, one would not expect that a defect in EPOC would hinder weight control efforts for the obese. Furthermore, the beneficial effects of EPOC in the overall energy expenditure for the obese should encourage the use of exercise as a tool in weight management.
Exercise professionals often prescribe different exercise protocols for the obese person compared to the normal weight individual based on two assumptions: (1) that the obese person is less fit than the normal weight individual, so the metabolic substrate response during exercise is different from the normal weight person; and (2) that low- to moderate-intensity aerobic exercise will allow the body to use more fat as an energy source, thus hastening the loss of body fat in the obese individual (24-26). Despite several research efforts, no significant relationship between body fatness and substrate utilization in response to the same relative exercise intensity (% VO2max) has been found
(2,27). Therefore, if substrate utilization is a concern in exercise programming for previously sedentary individuals, exercise protocols need not be differentiated on the basis of the severity of obesity (2).
The second assumption is supported by data demonstrating that fat oxidation during exercise at 65% VO2max is greater than at 85% VO2max (28), while fat oxidation at 33% VO2max is even greater than at 65% VO2max (29). Furthermore, even with a higher total energy expenditure during a 15-min exercise bout at 75% VO2max, more total fat-derived energy was expended during 15 min of exercise at 50% VO2max (2). The assumption is also supported by data showing that peripheral lipolysis is maximally stimulated at low exercise intensities (28).
Most obese individuals find it difficult to sustain an exercise session for 15 min when the intensity is >70% of VO2max (2). Thus, it may be unrealistic to expect obese men and women in weight loss treatment to exercise at a high intensity for 20-60 min. The most feasible application of the data would be an exercise prescription calling for low to moderate intensity.
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