Energy Cost Of Exercise Research Articles

Clinical evaluation of peak endocardial acceleration as a sensor for rate responsive pacing.

An innovative control parameter for rate responsive (RR) pacing that uses a sensor to measure mechanical vibrations generated by the myocardium during the isovolumetric contraction phase (peak endocardial acceleration [PEA]), has been devised by SORIN Biomedica (BEST Living System). To assess the physiological sensitivity of the pacemaker sensor along with reliability of the algorithm to supply appropriate pacing rates three different relationships were examined (linear regression analysis): (1) recorded deltaPEA exercise steps against the calculated energy cost of exercise (MET), (2) exercise pacing rates against predicted values, and (3) deltaPEA against exercise pacing rates. Fifteen patients (mean age 68 +/- 12 years) in NYHA Class I-II, implanted with the BEST Living System (Living 1 DDDR pacemaker) for advanced AVB and/or SSS, underwent one of the following maximal exercise stress protocols: bicycle (25 W, 2-minute steps) or Bruce or Chronotropic Assessment Exercise Protocol (CAEP). Pacing rates for each step were matched against those predicted by a reliable and tested custom software called Pacing Rate Profile Software (PRPS). The PRPS is based on the oxygen pulse reserve (OPR) method (OPR = VO2 reserve divided by heart rate reserve), American College of Sports Medicine (ACSM) formulas for calculating workload/metabolic requirements, and data derived from the Weber functional classes. On the basis of certain patient, data the PRPS then supplies appropriate metabolic pacing rate profiles. In all 15 patients linear regression analysis of deltaPEA against MET, as evaluated during the exercise protocol steps, showed a high correlation (r = 0.97). Likewise, a high correlation was also obtained between PRPS predicted heart rates and exercise pacing rates (r = 0.96) and PEA against exercise pacing rates (r = 0.96). The results of this study show that, through PEA dynamic monitoring, the SORIN Best Living System produces physiological pacing rates that are significantly related to metabolic needs.

Pulse rate criteria for determining the energy cost of exercise

From the pulse rate curve taken during exercise and recovery from highly qualified sportsmen performing a bicycle exercise test at a maximum workload, the work pulse sum, pulse debt, and pulse cost were calculated. Plots of these indices versus the time to exhaustion and versus the relative exercise workload were identical to the respective plots of oxygen consumption during exercise, oxygen debt, and oxygen requirement. The exercise pulse cost can serve as a criterion for quantifying physical workloads.

THE ENERGY COST OF SUBMAXIMALWALKING AND RUNNING IN MODERATELY FIT ADULTS

The relationship between heart rate and the energy cost of exercise is dependent on many factors, including fitness level. Previous research has failed to develop models for estimating energy cost based on heart rate in moderately fit and active adults. The purpose of this study was to develop a model for estimating submaximal steady-state VO2 (ml/kg/min) in moderately fit adults based on heart rate during submaximal walking and running. Subjects were 92 moderately fit and active (PAR > 3) adults, ages 20–45 years. Each subject performed a submaximal treadmill exercise test at randomly selected walking and running speeds from 2–8 mph. The sample was randomly divided into a derivation sample of 46 subjects, and a cross-validation sample of 46 subjects. The relationship between heart rate and VO2 was linear (p < .05). Additional variation in VO2 was accounted for by the interaction between HR and mode (walking = 1, running = 0) (p < .05). The restricted model is: VO2 (ml/kg/min) = 0.25(HR) ûC 0.051 (HR x walk = 1, run = 0), R = .90, SEE = 5.1 ml/kg/min. Percent fat also accounted for significant additional variation in VO2 (p < .05). The full model is: VO2 (ml/kg/min) = 0.235(HR) ûC 0.053(HR x walk = 1, run = 0) - 0.223(Percent Fat), R = .91, SEE = 4.9 ml/kg/min. Cross-validation revealed very little shrinkage in either the restricted model (R = .91, Cross-Validation Error = 5.3 ml/kg/min), or the full model (R = .93, Cross-Validation Error = 4.8 ml/kg/min). These data demonstrate that the energy cost of steady-state walking and running across a broad range of submaximal speeds can be accurately estimated from heart rate in moderately fit and active adults.

THE METABOLIC COST OF ELLIPTICAL EXERCISE VS PREDICTED VALUES

PURPOSE: To determine the actual (A) metabolic cost of elliptical exercise as compared with predicted (P) values. METHODS: 20 subjects (age = 28.9 ± 9.1 yrs. Weight 63.6 ± 13.0 kg) performed 9 randomly assigned trials at combinations of resistance (R) and elevation (E) representing low, mid and high workloads on a Precor EFX 546 Elliptical Trainer. All trials were conducted at a cadence of 125 strides per minute at different combinations of resistance (5,10,15) and elevation settings (5,10,15). Oxygen consumption was obtained by open circuit spirometry and heart rate by telemetry. RESULTS: The metabolic cost of elliptical exercise ranged from 5.3 METS or 5.7 kcal/min to 12.3 METS or 15 kcal/min. With the exception of the high resistance workloads (15), the actual metabolic cost was significantly less (P < .05) than the predicted values at all workloads. CONCLUSION: Changes in resistance settings provided significantly different energy requirements between levels, however the elevation of the elliptical trainer did not significantly alter the energy cost of exercise. The following regression formula (R = .92) was developed to accurately predict energy cost at 125 strides/min: Adelphi Elliptical Regression Equation (METS) = Resistance (.619)+ 2.367

Methods to determine aerobic endurance.

Physiological testing of elite athletes requires the correct identification and assessment of sports-specific underlying factors. It is now recognised that performance in long-distance events is determined by maximal oxygen uptake (V(2 max)), energy cost of exercise and the maximal fractional utilisation of V(2 max) in any realised performance or as a corollary a set percentage of V(2 max) that could be endured as long as possible. This later ability is defined as endurance, and more precisely aerobic endurance, since V(2 max) sets the upper limit of aerobic pathway. It should be distinguished from endurance ability or endurance performance, which are synonymous with performance in long-distance events. The present review examines methods available in the literature to assess aerobic endurance. They are numerous and can be classified into two categories, namely direct and indirect methods. Direct methods bring together all indices that allow either a complete or a partial representation of the power-duration relationship, while indirect methods revolve around the determination of the so-called anaerobic threshold (AT). With regard to direct methods, performance in a series of tests provides a more complete and presumably more valid description of the power-duration relationship than performance in a single test, even if both approaches are well correlated with each other. However, the question remains open to determine which systems model should be employed among the several available in the literature, and how to use them in the prescription of training intensities. As for indirect methods, there is quantitative accumulation of data supporting the utilisation of the AT to assess aerobic endurance and to prescribe training intensities. However, it appears that: there is no unique intensity corresponding to the AT, since criteria available in the literature provide inconsistent results; and the non-invasive determination of the AT using ventilatory and heart rate data instead of blood lactate concentration ([La(-)](b)) is not valid. Added to the fact that the AT may not represent the optimal training intensity for elite athletes, it raises doubt on the usefulness of this theory without questioning, however, the usefulness of the whole [La(-)](b)-power curve to assess aerobic endurance and predict performance in long-distance events.

The association between the val/ala-55 polymorphism of the uncoupling protein 2 gene and exercise efficiency.

Energy expenditure may partly be determined by genetic variations in uncoupling proteins. We have previously found an increased physical activity but a similar 24-h energy expenditure (EE) in subjects with the val/val-55 UCP2 genotype compared to those with the ala/ala genotype which indicates that the val-55 allele is statistically associated with a higher metabolic efficiency. EE during bicycling was determined by indirect calorimetry at three different loads (30, 40 and 60% of VO2max in eight subjects with the val/val-55 genotype (35+/-6 y weight=76.8+/-13.6 kg, VO2max=2.79+/-0.71 l/min) and eight subjects with the ala/ala-55 genotype (37+/-3 y, weight=78.3+/-16.5 kg, VO2max=2.66+/-0.41 l/min). Incremental exercise efficiency across the three different work levels was higher in the val/val (25.3%, c.i. 24.2-26.4%) than in the ala/ala (23.6%, c.i. 22.5-24.7%) genotype P<0.05. Gross exercise efficiency at 40% VO2max was higher in the val/val (15.3+/-0.6%) than in the ala/ala (13.5+/-0.4%) group. As the val/ala-55 polymorphism is located in a domain of the protein without any known function, the different exercise efficiency between the two genotypes most likely reflects a linkage disequilibrium with a functionally significant polymorphism in UCP2 or in the neighbouring UCP3 gene. The study suggests that variations in the UCP genes may affect not only basal metabolic rate but also influence energy costs of exercise.

No energy compensation at the meal following exercise indietary restrained and unrestrained women

The objective of this investigation was to compare the acute effects of exercise and diet manipulations on energy intake, between dietary restrained and unrestrained females. Comparisons of two studies using an identical 2 x 2 repeated-measures design (level of activity (rest or exercise) and lunch type (high-fat or low-fat)) including thirteen dietary unrestrained and twelve restrained females were performed. Energy expenditure during the rest session was estimated and the energy cost of exercise was measured by indirect calorimetry. Relative energy intake was calculated by subtracting the energy expenditure of the exercise session from the energy intake of the test meal. Post-meal hedonic ratings were completed after lunch. Energy intake and relative energy intake increased during high-fat conditions compared with the low-fat, independently of exercise (P < 0.001). There was a positive relationship between dietary restraint scores and energy intake or relative energy intake in the rest conditions only (r 0.54, P < 0.01). The decrease of relative energy intake between the rest and exercise conditions was higher in restrained than in unrestrained eaters (P < 0.01). These results confirm that a high-fat diet reversed the energy deficit due to exercise. There was no energy compensation in response to an acute bout of exercise during the following meal. In restrained eaters, exercise was more effective in creating an energy deficit than in unrestrained eaters. Exercise may help restrained eaters to maintain control over appetite.

Energy cost calculations for exercise prescription: an update.

Recent research has resulted in a number of recommended changes in how fitness professionals should prescribe target workloads and calculate the energy cost of exercise. The principal changes are in the use of oxygen consumption reserve (VO2R) as an alternative to percentage of maximal oxygen consumption (VO2max) for prescribing exercise intensity, the use of net VO2 rather than gross VO2 for the calculation of caloric expenditure during exercise, and a modification of the American College of Sports Medicine (ACSM) equation for calculating the oxygen cost of leg cycle ergometry. The VO2R method of prescribing exercise workloads is similar to the heart rate reserve (HRR) method of prescribing target heart rates, i.e. the target workload is established at a given percentage of the difference between maximal and resting VO2. Several recent studies have shown that there is a discrepancy between the exercise intensity at given percentages of HRR and VO2max, but that HRR and VO2R yield equivalent exercise intensities. The use of VO2R in exercise prescription provides more accurate target workloads, especially for individuals with a low fitness level. Net VO2 during exercise is that amount above resting VO2 due to the exercise itself. A recent recommendation is to employ net VO2 in the calculation of the caloric expenditure during exercise, so as not to overestimate potential bodyweight loss. Several recent studies of leg cycling ergometry have yielded equations for the estimation of VO2 that include a term for unloaded cycling, i.e. the oxygen cost of moving the legs against zero resistance. The equations from these studies provide more accurate estimations of cycling VO2 than the existing ACSM equation, and a new standardised equation has been developed and adopted by the ACSM. The new equation is especially useful for improving the accuracy of VO2 estimates during low intensity leg cycle ergometry. The ACSM equation for bench stepping has also been modified to include a term for resting metabolism.

Influence of intense physical activity on energy balance and body fatness

The reduced contribution of physical activity to daily energy expenditure and the accessibility to high-fat foods have put an excessive burden on energy balance, resulting in an increase in the prevalence of obesity throughout the world. In this context, fat gain can be seen as a natural adaptation to deal with a fattening lifestyle, since the hormonal adaptations that accompany fat gain favour the readjustment of energy expenditure to energy intake. Intense physical activity would also seem to facilitate the regulation of energy balance, since it increases the energy cost of exercise, increases post-exercise energy expenditure and the potential of skeletal muscles to utilize lipids, and also favours a decrease in post-exercise intake. Moreover, the effects of intense exercise seem to be mediated by an activation of sympathetic nervous system activity that seems to be specific to skeletal muscle. It is also important to manipulate macronutrient composition in order to reduce fat intake, because unhealthy food habits can favour overfeeding and thus overcome the energy deficit caused by regular physical activity. Under free-living conditions, the combination of vigorous activity and healthy food practices can amount to a substantial weight loss which is comparable with that of other non-surgical approaches to treat obesity.

Reduced metabolic efficiency of skeletal muscle energetics in hyperthyroid patients evidenced quantitatively by in vivo phosphorus-31 magnetic resonance spectroscopy

Skeletal muscle energetics of seven hyperthyroid patients were investigated throughout a rest-exercise-recovery protocol using phosphorus-31 magnetic resonance spectroscopy ( 31P MRS) to quantitatively document in vivo the metabolic bases of impaired muscle performance in hyperthyroidism. The contributions of the main pathways of adenosine triphosphate (ATP) synthesis to energy production and proton efflux were measured and compared with results from normal muscle. At rest, a reduced concentration of phosphocreatine (PCr) was calculated for hyperthyroid patients when compared with controls, whereas pH and concentrations of inorganic phosphate (Pi) and phosphomonoesters (PME) were not different from controls. During exercise, the analysis of changes in pH and PCr concentration demonstrated that (1) at the onset of exercise, the magnitude of glycolysis activation is significantly larger for patients, resulting in a marked pH decrease; (2) the energy cost of exercise is higher for patients as compared with controls performing the same amount of work; and (3) both anaerobic and aerobic pathways are significantly more activated in the hyperthyroid group throughout the 3 minutes of exercise. During recovery, the rates of proton efflux and PCr resynthesis were similar in both groups, excluding any alteration in oxidative function and proton handling as a cause of initial glycolytic hyperactivation. The increased energy cost measured for patients during exercise evidences an increased need for energy, which is (1) probably linked to the existence of additional ATP-consuming mechanism(s), and (2) supported by hyperactivation of both aerobic and anaerobic pathways. These findings imply that, all things equal, a hyperthyroid muscle requires more energy to function than normal, and as a result is potentially more fatiguable.

Characteristics of energy metabolism in males with mental retardation.

To characterize the energy metabolism in individuals with mental retardation (MRs), we measured energy cost at several physical activity levels (basal, supine, sitting, standing, and walking at 30, 50 and 70 m/min), maximal oxygen consumption (Vo2max), and body composition in 23 male MRs and the same number of volunteer male controls. Both groups were individually matched for age, body height, and body weight. Energy cost was measured by the Douglas bag technique. The recently developed sulfur hexafluoride (SF6) dilution technique was employed for measuring body composition. In addition, 3-dimensional accelerometry was used for evaluating body movements, and plasma indices of macronutrients were also measured. The energy cost of MRs, when sitting, standing, and walking at 30 and 50 m/min, was significantly higher than that of controls (p < 0.05), while the basal and resting metabolic rates were similar in both groups. Vo2max was significantly lower (p < 0.05) in MRs than controls. Accelerometry demonstrated excessive movement by MRs, which may explain their higher energy cost of exercise. In contrast, no significant difference was observed in percent body fat or lean body mass. Concentrations of plasma total cholesterol, triacylglycerols and albumin were significantly lower in MRs as compared with the controls. Our findings suggest that MRs are burdened with an energy metabolism less economical than non-MRs. Limited physical activity in their daily life may be the cause. These characteristics of MRs' energy metabolism should be considered for planning their proper dietary schedules and physical activity programs.

Improved walking economy in patients with peripheral arterial occlusive disease.

The effect of exercise rehabilitation on the oxygen cost of ambulation in patients with peripheral arterial occlusive disease (PAOD) was evaluated with specific emphasis on the effects of exercise rehabilitation on the slow component of VO2. Because the slow component of VO2 represents an increase in VO2 despite constant-intensity exercise, it can profoundly affect the relative energy cost of exercise in individuals with a low functional capacity. Twenty-six patients with intermittent claudication performed treadmill walking at 2.0 mph/0% grade for 20 min or until maximal claudication pain before and after 4 months of rehabilitation. The slow component of VO2 during the treadmill test was defined as the difference between the end-exercise VO2 and the VO2 observed at minute 3. Ankle/brachial systolic pressure index (ABI) was measured before and immediately following the exercise test. Rehabilitation consisted of 3 d x wk(-1) of treadmill walking for 15-30 min at 60-70% of VO2peak. The slow component of VO2 and end-exercise VO2 at pretraining (0.75 +/- 0.90 and 11.12 +/- 2.10 mL x kg[-1] x min[-1]) were significantly reduced after 4 months of exercise rehabilitation (-0.07 +/- 1.11 and 10.07 +/- 1.80 mL x kg[-1] x min[-1]; P < 0.05). Exercise rehabilitation also significantly (P < 0.05) increased the post-exercise ABI (pre-rehabilitation = 0.36 +/- 0.26, post-rehabilitation = 0.43 +/- 0.25). These data suggest that 4 months of exercise rehabilitation: 1) improves walking economy in PAOD patients because of a decreased slow component of VO2, and 2) increases post-exercise ABI.

Impaired counterregulatory hormonal and metabolic response to exhaustive exercise in obese subjects.

A reduction of postprandial thermogenesis has been described in obesity; insulin resistance and/or decreased sympathetic nervous system activity seem to play the major role in its pathogenesis. On the other hand, a normal energy expenditure during exercise has been reported. At present, the response and the role of catecholamines in energy metabolism during exercise in obesity have not been well clarified yet. The aim of this work was to study the metabolic and hormonal changes caused by intense exercise in obesity. Nine obese subjects and ten normal weight controls were submitted to exhaustive exercise on a cycloergometer. Blood glucose, free fatty acids (FFA), glycerol, lactate, beta-OH-butyrate, insulin, glucagon, plasma growth hormone (HGH), catecholamine plasma levels were assayed before and at the end of exercise, and after a recovery period. The energy cost of exercise was evaluated by indirect calorimetry. In our experiment muscular exercise did not provoke any change in blood glucose and FFA plasma levels in either of our groups. In the obese subjects the insulin plasma levels were higher than in the controls. Glucagon plasma levels did not change. The exercise responses of norepinephrine (NE) (4.28 +/- 0.74 vs 8.81 +/- 1.35 nmol/l; P < 0.01), epinephrine (E) (234.21 +/- 64.18 vs 560.51 +/- 83.38 pmol/l; P < 0.01) and plasma growth hormone (HGH) (134.84 +/- 58.97 vs 825.92 +/- 195.25 pmol/l; P < 0.01) were significantly lower in obese subjects. At the end of exercise, the thermic effect of exercise did not differ between obese and control subjects (0.335 +/- 0.038 vs 0.425 +/- 0.040 kJ/min x kg fat-free mass. Our findings indicate that an impaired counterregulatory hormone response to exercise exists in obese subjects. The thermic effect of exercise does not seem to be affected by either the reduced catecholamine response nor insulin resistance.

Refeeding improves muscle performance without normalization of muscle mass and oxygen consumption in anorexia nervosa patients

The effect of starvation-related malnutrition on muscle performance and on the energy cost of exercise remains unknown, as does the timing of improvement by refeeding. Indeed, in most diseases that induce malnutrition, muscle dysfunction is worsened by an inflammatory process. Thus, physical performance and the energy cost of exercise were studied in 15 semistarvated malnourished anorexia nervosa (AN) patients during exercise on an ergometric bicycle (3-min steps of 30 W) before and after 8, 30, and 45 d of refeeding. Results were compared with those of 15 normal-weight healthy subjects matched for age, sex, and physical activity. Before refeeding, the workload reached during the exercise was 49% lower in AN patients than in control subjects (P < 0.01). It was correlated with body weight, fat-free mass, and leg muscle circumference (P < 0.002). The performance improved dramatically during refeeding (P < 0.03), reaching normal values after 45 d of refeeding, despite fat-free mass and leg muscle circumference values that were still 20% lower in AN patients than in control subjects (P < 0.01). At this time, the exercise-related VO2 remained unchanged, being approximately 25% lower than that of the control subjects when corrected for muscle mass differences (P < 0.03). In conclusion, in AN patients muscle performance was restored by refeeding long before the patients achieved normal nutritional status. The economic cost of physical activity for these malnourished patients allows them to maintain a relatively high level of physical activity. This relative overactivity has two goals in AN: it reinforces anorexia and contributes to the excess of energy expenditure needed for weight loss.

Endurance training with constant energy intake in identical twins: Changes over time in energy expenditure and related hormones

The effects of exercise training and of its interaction with the genotype on components of energy expenditure and related hormones were examined in young male monozygotic twins. Energy intake was maintained at the pretraining level for a 93-day training period. The estimated net energy deficit induced by training was 244 MJ and was associated with a 5-kg body weight loss that was almost entirely explained by body fat loss. Resting metabolic rate (RMR) was significantly decreased by 8% after training despite the preservation of fat-free mass (FFM). Accordingly, plasma norepinephrine (NE) concentrations, NE appearance rate, and plasma levels of triiodothyronine (T 3), free T 3, and total thyroxine (T 4) were lower after training. The energy cost of standardized exercise was also reduced after the training program. A modest to significant within—twin-pair resemblance was observed for absolute changes in the RMR, thermic effect of food, energy cost of exercise, NE clearance, and plasma concentrations of thyroid hormones. These results suggest that when exercise training is associated with a substantial negative energy balance, energy expenditure and levels of related hormones are decreased, and this effect is partly accounted for by heredity.

Energy cost of exercise in multiple sclerosis patients with low degree of disability.

In 10 patients (five females) suffering from multiple sclerosis with mild degree of disability, (EDSS ranging from 0 to 2) and in 10 age and sex matched control subjects we investigated lung function, respiratory muscles strength and cardiorespiratory response to incremental exercise in order to assess the metabolic cost of exercise. In the absence of any impairment of lung volumes and flows and in- and expiratory maximal mouth pressures, at peak of exercise oxygen consumption (VO2max = 1886 +/- 145 ml/min) and workload (Wmax = 137 +/- 9.8 watts) were slightly diminished in patients, as compared with controls (VO2max = 2246 +/- 196 ml/min and Wmax = 164 +/- 14.7 watts). These findings were associated with an increased heart rate (HR) and reduced oxygen pulse (VO2/HR) at the same workloads. During the whole exercise, however, the slope of the linear relationship between VO2 and work exhibited by the patients, amounting to 9.9 +/- 0.6 ml/min/watt, was similar to that of the controls (10.9 +/- 0.42 ml/min/watt). Incidentally, both at rest and during exercise, the patients showed a significantly greater minute ventilation (VE) due to a faster respiratory rate, associated with an augmented dead space (P < 0.05). We conclude that an increase of metabolic cost of exercise does not occur in multiple sclerosis patients with mild disability, suggesting a lack or a low degree of spasticity and/or ataxia elicited by the effort. Thus, their exertional capacity appears to be limited mainly by a poor training. The tachypnea observed in these patients at rest and during exercise was unexpected and the reason for adopting such a pattern of breathing is unclear.

Prediction of oxygen uptake and energy expenditure during exercise in obese women.

For patients concerned with weight loss, monitoring the energy balance between daily dietary intake and exercise expenditure can be useful. Formulas commonly used to estimate the energy costs of exercise were previously derived from healthy men of normal body weight. The purpose of this study was to determine the relationship between measured and predicted exercise energy expenditure for obese women. Oxygen uptake (VO2) was measured using respiratory gas analysis in 45 obese (92 +/- 16 kg; 40 +/- 7% fat) and 10 normal weight (control) (58 +/- 5 kg; 21 +/- 6% fat) women during progressive exercise on a motorized treadmill. VO2 was also calculated at matched workrates using a regression equation published by the American College of Sports Medicine. The relationship between predicted versus measured VO2 was determined using least squares regression analysis. The slope of the regression line for measured versus predicted VO2 for controls (y = 0.98x +/- 0.56; P < .001) was different than that of obese women (y = 0.75x +/- 3.06; P < .001). The slope of the regression line for controls was in close approximation to the line of identity, whereas the slope for obese was below it. Using VO2 to calculate kcal, measured energy expenditure, was significantly lower than predicted energy expenditure for obese subjects, but not for controls at several matched workrates: Stage III (213 +/- 40 versus 225 +/- 38 kcal per 30 minutes, P < .001); stage 4 (292 +/- 55 versus 340 +/- 58 kcal per 30 minutes, P < .001); and stage 5 (330 +/- 55 versus 412 +/- 70 kcal per 30 minutes, P < .001) obese measured versus obese predicted, respectively. The authors conclude that the standard prediction equation gives a better estimation of VO2 for women who have average body weight and body fat than for obese women. This may, in part, be due to the differences in weight and/or fat mass between these subjects and those used to derive this equation. These findings should be considered when estimates of VO2 and energy expenditure are used rather than direct measures for obese women.

Exercise and energy intake: Effect of substrate oxidation

The main objective of this study was to evaluate the short-term effect of exercise-induced alteration in fat oxidation on postexercise spontaneous energy and macronutrient intakes. Eleven young males were submitted to two randomly assigned sessions of 48 h each, during which they were requested to eat in the laboratory. One of these sessions was preceded by a 90-min exercise bout at an intensity of 60% VO 2max. During both sessions, subjects ate ad lib food with a fat content conforming to the recommendations of nutrition agencies with a food quotient (FQ) ⩾ 0.85. Results showed that there was no significant change in postexercise energy and macronutrient intakes in comparison with the sedentary session. However, when subjects were subdivided into two groups on the basis of the respiratory quotient (RQ) measured during exercise, men with a low RQ (high fat oxidation) were characterized by a reduced postexercise increase in energy intake relative to the energy cost of exercise (ECE), i.e., they were more predisposed to be in negative posterexercise energy balance compared to those exhibiting a high RQ. Accordingly, exercise RQ was positively associated with postexercise energy and lipid balance. These results show that postexercise energy balance partly depends on the composition of the substrate mix oxidized during exercise.

Diet composition and postexercise energy balance

This study was aimed at investigating the effect of exercise on energy balance under dietary conditions differing by the relative lipid content of foods. Nine healthy men performed a 60-min treadmill exercise followed by a 48-h observation period during which they maintained their habitual daily activities and had free access to either a low-fat, a mixed, or a high-fat diet. Energy balance, summing up the excess of energy expended during exercise and the 48-h postexercise energy balance, was -6.4, -4.5, and 0.9 MJ under low-fat, mixed, and high-fat diet conditions, respectively. These observations suggest that exercise can induce a substantial energy deficit when a low-fat diet conforming to nutritional recommendations is consumed after exercise. They also suggest that the increase in energy intake associated with a high-fat diet is sufficient to fully compensate for the energy deficit resulting from the energy cost of exercise and the increase in postexercise energy expenditure.

The thermogenic role of exercise in the treatment of morbid obesity: a critical evaluation

Exercise induces negative energy balance either directly or by enhancing meal thermogenesis, increasing resting metabolic rate, and/or decreasing food intake. A quantitative evaluation of these effects in programs of weight control led to the following conclusions: 1) energy cost of exercise per se is minimal, 2) effects on thermic of food are negligible, and 3) exercise training may be advantageous in conjunction with low-calorie diet programs because it helps to maintain resting metabolic rate and fat-free mass. However, exercise may not prevent, and may even accentuate, the fall in metabolic rate in programs of severe calorie restriction, thus hampering weight reduction. Overall, exercise should not be envisioned as a sole agent to induce negative energy balance, but it is an essential element in comprehensive programs for morbidly obese patients due to its effects on lipids, carbohydrate metabolism, and cardiovascular system.