Determining the amount of physical activity needed for long-term weight control

Wier, Larry T.; Ayers, G. W.; Jackson, Andrew S.; Rossum, Alfred C.; Poston, Walker S. Carlos; Foreyt, John P.

doi:10.1038/sj.ijo.0801586

Cited by 54 publications

(45 citation statements)

References 29 publications

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“…Post hoc analysis with Fisher's PLSD at 7.5 hours post-dose showed that recovery after heavy exercise remained lower than after rest (p Ͻ 0.05). The [d 3 ]acetate values could not be extrapolated to infinity because of the minimal datacollection time points, but could be corrected for an assumed water turnover of 3% (98.1%, 94.0%, 93.2%, and 88.3%, for rest, light, moderate, and heavy, respectively).…”

Section: Recovery Of [1-13 C]acetate and [D 3 ]Acetate Post-exercisementioning

confidence: 99%

Prior Exercise Increases Dietary Oleate, but Not Palmitate Oxidation

2003

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VOTRUBA, SUSANNE B., RICHARD L. ATKINSON, AND DALE A. SCHOELLER. Prior exercise increases dietary oleate, but not palmitate oxidation. Obes Res. 2003; 11:1509 -1518. Objective: Higher levels of physical activity have been associated with body weight maintenance, but previous work in our laboratory suggests that this is not purely related to energy balance. We hypothesize that this may be related to the partitioning of dietary fat between oxidation and storage. Research Methods and Procedures: Healthy women (age 24 Ϯ 1 years, BMI ϭ 21.2 Ϯ 0.4 kg/m 2 ) were recruited to participate in rest (n ϭ 10) or exercise sessions of light (n ϭ 11), moderate (n ϭ 10), and heavy (n ϭ 7) exercise. All exercises (1250 kJ above rest) were performed on a stationary cycle inside of a whole-body calorimeter. Results: Cumulative oxidation of [1-13 C]oleate was significantly greater after light (45 Ϯ 3%), moderate (54 Ϯ 4%), and heavy (51 Ϯ 4%) exercise than that with rest (33 Ϯ 3%) (p ϭ 0.0008). Cumulative oxidation of [d 31 ]palmitate did not differ among trials (12 Ϯ 2%, 14 Ϯ 1%, 17 Ϯ 2%, and 14 Ϯ 2% for rest, light, moderate, and heavy, respectively; p ϭ 0.30). Discussion: Exercise standardized for energy expenditure increases monounsaturated fat oxidation more than saturated fat oxidation and that the increase occurs regardless of intensity. Recommendations for physical activity for the purposes of weight control may be specific for dietary fat composition.

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Section: Recovery Of [1-13 C]acetate and [D 3 ]Acetate Post-exercisementioning

confidence: 99%

Prior Exercise Increases Dietary Oleate, but Not Palmitate Oxidation

2003

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“…Although the primary treatment for obesity historically has been caloric restriction, a more promising treatment may consist of increased physical activity in addition to controlling energy intake. Physical exercise rapidly increases energy expenditure and has been associated with improved weight control (Brook et al, 1995;King et al, 2001;Wier et al, 2001). Exercise also causes a preferential utilization of fat, resulting in less fat in active individuals compared with sedentary controls.…”

Section: Introductionmentioning

confidence: 99%

Swim training improves leptin receptor deficiency-induced obesity and lipid disorder by activating uncoupling proteins

Kim²,

Yoon³

et al. 2007

Exp Mol Med

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Leptin receptor deficiency causes morbid obesity and hyperlipidemia in mice. Since physical exercise enhances energy expenditure, it is an important part of successful weight-control regimens. We investigated the mechanism by which swim training regulates leptin receptor deficiency-induced obesity and lipid disorder in a mouse model of obesity (obese db/db mouse). Swim training for 6 weeks significantly decreased body weight gain and adipose tissue mass in both sexes of obese and lean mice, compared to their respective sedentary controls. These effects were particularly evident in obese mice. Swim training also caused significant decreases in serum levels of triglycerides, free fatty acids and total cholesterol in both obese and lean mice. In obese mice, swim training increased the levels of mRNAs and proteins encoding uncoupling protein 1 (UCP1), UCP2 and UCP3 in brown adipose tissue, white adipose tissue and skeletal muscle, respectively. In conclusion, these findings suggest that, in mice, swim training can effectively prevent body weight gain, adiposity and lipid disorders caused by leptin receptor deficiency, in part through activation of UCPs in adipose tissue and skeletal muscle, which may contribute to alleviating metabolic syndromes, such as obesity, hyperlipidemia and type 2 diabetes.

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“…17 The 2 H was measured in urinary water samples collected every 4 h while in the chamber, as previously described and validated for measurement of fatty acid oxidation. 18 After being decolorized with carbon black, urine samples were analyzed for deuterium content as a ratio of 2 19 For the measurement of 18 O, 1 ml of urine was equilibrated with CO 2 at 251C for 48 h. The 18 O concentration was measured by continuous flow IRMS and the body water was calculated by dilution. 20,21 Urinary nitrogen concentration was determined using the Antek 9000N Chemiluminescent Nitrogen analyzer (Antek Instruments, Inc., Houston, TX, USA).…”

Section: Sample Collection and Analysismentioning

confidence: 99%

“…For example, a recent cross-sectional study has found that individuals with higher daily levels of physical activity were leaner than their sedentary counterparts, 1 and a prospective study demonstrated that baseline activity levels were associated with lower body weights after B5 y at follow-up. 2 Furthermore, exercise has been shown to have a protective effect against weight regain in several populations of post-obese women such that those women with a physical activity level of greater than 1.75 are more successful in weight maintenance over a one year period than women who are more sedentary. 3 The mechanism for this effect is not entirely clear, but may be related to the effects of exercise on fat metabolism.…”

Section: Introductionmentioning

confidence: 99%

“…Interestingly, the increase in dietary fat oxidation following exercise appears to be fatty acid type dependent. The monounsaturated fatty acid, [1][2][3][4][5][6][7][8][9][10][11][12][13] C]oleate, showed increased oxidation when ingested shortly after an exercise bout compared to rest, while oxidation of the saturated fatty acid, [d 31 ]palmitate did not. 5,6 In contrast, Gill et al 7 did observe an increase in palmitate oxidation when it was administered in a breakfast meal following a large volume of exercise performed the previous day.…”

Section: Introductionmentioning

confidence: 99%

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Sustained increase in dietary oleic acid oxidation following morning exercise

Votruba

Atkinson²,

Schoeller

2004

Int J Obes

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OBJECTIVE:We have previously reported that prior exercise increases the oxidation of dietary monounsaturated fat in comparison to rest when the fat is given in a mixed meal 30 min following the completion of exercise. In this study, we determined whether the increase in dietary fat oxidation after exercise persisted when the time between exercise and fatty acid administration was lengthened. DESIGN: Six female subjects (age ¼ 2470.1 y, BMI ¼ 2171 kg/m 2 ) were recruited for a total of six visits each. During three visits, a stationary cycle exercise session (1250 kJ) was performed at 65% VO 2 peak in a whole-body calorimeter; while during three other visits, exercise was replaced with rest. Subjects received [1-13 C]oleate and [d 31 ]palmitate with a different meal at each visit: breakfast, lunch, and dinner. RESULTS: Dietary oleate oxidation following prior rest did not differ between dose times and was 3673, 4275, and 4273% for the 13 h following breakfast, lunch, and dinner. Prior exercise resulted in greater oleate oxidation following all dose times than prior rest (Po0.01) being 5274, 6473, and 5373% for the breakfast, lunch, and dinner dose. The oxidation was significantly greater following lunch than the other dose times (Po0.05). Prior exercise (1250 kJ) did not result in greater oxidation of palmitate; however, oxidation following prior exercise increased with later dose times (1372, 2372, and 2373% for breakfast, lunch, and dinner; Po0.05) and following rest (1872, 2272, and 2772% for breakfast, lunch, and dinner; Po0.005). CONCLUSIONS: The increase in oleate oxidation when administered after early morning exercise was found to persist for all three meals of the day, with the greatest effect occurring for the lunch meal. Palmitate oxidation, while apparently resistant to the effects of 1250 kJ of prior exercise, increases when administered later in the day, suggesting a diurnal variation in the oxidation of dietary fatty acids. These results demonstrate that prior exercise selectively alters the partitioning of dietary fatty acids. Furthermore, these findings demonstrate additional benefits of substituting monounsaturated for saturated fatty acids in the diet.

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Determining the amount of physical activity needed for long-term weight control

Cited by 54 publications

References 29 publications

Prior Exercise Increases Dietary Oleate, but Not Palmitate Oxidation

Prior Exercise Increases Dietary Oleate, but Not Palmitate Oxidation

Swim training improves leptin receptor deficiency-induced obesity and lipid disorder by activating uncoupling proteins

Sustained increase in dietary oleic acid oxidation following morning exercise

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