Additive effects of training and high-fat diet on energy metabolism during exercise

Simi, Barbara; Semporé, B.; Mayet, M. H.; Favier, R.

doi:10.1152/jappl.1991.71.1.197

Cited by 96 publications

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“…Both exercise training and high-fat diet consumption induce an increase in mitochondrial biogenesis in skeletal muscle (1,(5)(6)(7). Increased muscle mitochondria induced by endurance exercise training were previously thought to develop through a slow process.…”

Section: Discussionmentioning

confidence: 99%

Time Course of Decrease in Skeletal Muscle Mitochondrial Biogenesis after Discontinuation of High-Fat Diet

Higashida

Kawamura

et al. 2018

J Nutr Sci Vitaminol

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SummaryIt is known that a high-fat diet induces an increase in mitochondrial biogenesis in skeletal muscle. To examine the time course of decrease in mitochondrial biogenesis in skeletal muscle after discontinuing a high-fat diet feeding, C57BL/6 mice were fed a high-fat diet for 4 wk and then switched to the control diet for another 3 or 7 d. During the high-fat diet withdrawal period, the protein content of the mitochondrial respiratory chain decreased faster than the fatty acid oxidation enzymes. The mitochondrial DNA copy number remained high for at least 1 wk after withdrawing the high-fat diet. These results suggested that after switching to the control diet following a period of high-fat diet, the increased mitochondrial biogenesis levels are maintained for a few days, and the rate of decline is divergent between the different mitochondrial components. Key Words high-fat diet, mitochondrial biogenesis, skeletal muscle Endurance exercise training induces an increase in the number and size of mitochondria in the skeletal muscles that are recruited during exercise (1, 2). The increase in mitochondria in skeletal muscle minimizes the disruption of homeostasis during exercise, as evidenced by a smaller decrease in muscle glycogen (3). Since muscle glycogen content prior to exercise is associated with endurance performance (4), these biochemical adaptations in skeletal muscle are responsible for the improvement of exercise capacity after exercise training.Similar biochemical adaptations are observed in highfat diet-adapted skeletal muscle. The enzyme activities involved in citrate cycle and b-oxidation were increased after high-fat diet consumption (5). Turner et al. also demonstrated that feeding a high-fat diet for 5 or 20 wk significantly increased the content of mitochondrial respiratory chain complex proteins (6). These high-fat diet-induced adaptations of skeletal muscle contribute to endurance exercise performance (5, 7).Although it is generally accepted that the endurance exercise performance is directly related to the muscle glycogen content before starting exercise (8), Miller et al. reported that endurance running capacity is enhanced by consuming a high-fat diet for 5 wk, in spite of having lower than normal muscle glycogen stores (5). These results led us to consider that further enhancement of endurance capacity might be possible if a control diet, rich in carbohydrates, was fed to high-fat diet-adapted animals. However, the time course of changes in the increased mitochondrial oxidative capacity after discontinuance of a high-fat diet is not known. Since the highfat diet-induced increase in plasma free fatty acids (FFA) concentration seemed to be involved in mitochondrial biogenesis in skeletal muscle (9, 10), switching to a control diet might rapidly decrease the elevated mitochondrial proteins. The purpose of the present study was to determine the time course of the reversal of high-fat diet-induced changes in mitochondrial biogenesis after switching to a control diet. MethodsAnimals and experi...

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Section: Discussionmentioning

confidence: 99%

Time Course of Decrease in Skeletal Muscle Mitochondrial Biogenesis after Discontinuation of High-Fat Diet

Higashida

Kawamura

et al. 2018

J Nutr Sci Vitaminol

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“…However, a number of earlier studies provided evidence that high-fat diets result in an increase in mitochondrial enzymes in muscle (11)(12)(13)(14), and we have shown that large increases in FFA induce an increase in mitochondrial biogenesis (16). Furthermore, Turner et al (15) recently reported that, as in the present study, feeding rats a high-fat diet resulted in increases in mitochondrial enzyme activities, mitochondrial respiratory chain subunit protein levels, and fat oxidation capacity in skeletal muscle.…”

Section: Discussionmentioning

confidence: 99%

“…In support of this concept, recent studies have reported that raising serum free fatty acids (FFA) by a high-fat diet in humans (8), or by feeding mice or rats high-fat diets (8)(9)(10), results in decreases in skeletal muscle peroxisome proliferator-activated receptor ␥ coactivator-1␣ (PGC-1␣) mRNA (8)(9)(10) and the mRNA levels of various mitochondrial constituents (8). In contrast, a number of earlier studies provided evidence that high-fat diets induce increases in mitochondrial marker enzymes (11)(12)(13)(14), and Turner et al (15) recently reported that a high-fat diet resulted in increases in mitochondrial biogenesis and fatty acid oxidative capacity in skeletal muscle of mice.…”

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confidence: 99%

High-fat diets cause insulin resistance despite an increase in muscle mitochondria

Hancock

Han

Chen

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

473

405

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It has been hypothesized that insulin resistance is mediated by a deficiency of mitochondria in skeletal muscle. In keeping with this hypothesis, high-fat diets that cause insulin resistance have been reported to result in a decrease in muscle mitochondria. In contrast, we found that feeding rats high-fat diets that cause muscle insulin resistance results in a concomitant gradual increase in muscle mitochondria. This adaptation appears to be mediated by activation of peroxisome proliferator-activated receptor (PPAR)␦ by fatty acids, which results in a gradual, posttranscriptionally regulated increase in PPAR ␥ coactivator 1␣ (PGC-1␣) protein expression. Similarly, overexpression of PPAR␦ results in a large increase in PGC-1␣ protein in the absence of any increase in PGC-1␣ mRNA. We interpret our findings as evidence that raising free fatty acids results in an increase in mitochondria by activating PPAR␦, which mediates a posttranscriptional increase in PGC-1␣. Our findings argue against the concept that insulin resistance is mediated by a deficiency of muscle mitochondria.I t has been hypothesized that insulin resistance in patients with impaired or diabetic glucose tolerance is mediated by a deficiency of mitochondria in skeletal muscle (1, 2). The mechanism by which a decrease in mitochondria is proposed to cause insulin resistance is accumulation of intramyocellular lipids caused by a decrease in the capacity to oxidize fat (2). This hypothesis is based on the finding that type 2 diabetics and insulin-resistant individuals with impaired glucose tolerance have Ϸ30% less mitochondria in their muscles than insulinsensitive control subjects (3-7). In support of this concept, recent studies have reported that raising serum free fatty acids (FFA) by a high-fat diet in humans (8), or by feeding mice or rats high-fat diets (8-10), results in decreases in skeletal muscle peroxisome proliferator-activated receptor ␥ coactivator-1␣ (PGC-1␣) mRNA (8-10) and the mRNA levels of various mitochondrial constituents (8). In contrast, a number of earlier studies provided evidence that high-fat diets induce increases in mitochondrial marker enzymes (11-14), and Turner et al. (15) recently reported that a high-fat diet resulted in increases in mitochondrial biogenesis and fatty acid oxidative capacity in skeletal muscle of mice.We have found that raising serum FFA in rats by feeding them a high-fat diet and giving them daily heparin injections results in an increase in muscle mitochondria (16). The initial purpose of the present study was to determine whether the more modest increase in FFA induced by a high-fat diet also results in increased mitochondrial biogenesis with an increase in the capacity of muscle to oxidize fat. We found that a high-fat diet does induce an increase in muscle mitochondria. This finding made it possible to evaluate whether a high-fat diet causes muscle insulin resistance despite increases in mitochondria and fat oxidative capacity.Overexpression of peroxisome proliferator-activated receptor (PPAR)␦ i...

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“…The alteration in the rate of use or balance of carbohydrates and lipids, often through training or diet, can lead to increased performance. For instance, Simi et al 18 found high-fat diet acts in an additive manner with endurance training, leading to increased VO 2max and submaximal endurance in rats. High-fat diet can serve to increase the duration of moderate physical activity by sparing glycogen, the depletion of which is considered to be a cause of fatigue.…”

Section: Discussionmentioning

confidence: 99%

“…16 In untrained human beings, half the energy used to exercise at 65% of maximal oxygen consumption (VO 2 max) comes from lipids in the form of both free fatty acids and muscle triglycerides. 16 In the context of enhancing endurance performance, ingesting carbohydrates during exercise is often emphasized, but diets rich in lipids can also lead to increased performance at low or moderate intensities in rodents [17][18][19] and in humans, 20,21 although not always. 22 Recent evidence has shown that HR mice do not deplete liver or gastrocnemius muscle glycogen stores any more than controls during nightly wheel running, nor do they have elevated glycogen synthase activity.…”

Section: Introductionmentioning

confidence: 99%

Western diet increases wheel running in mice selectively bred for high voluntary wheel running

2010

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Objective: Mice from a long-term selective breeding experiment for high voluntary wheel running offer a unique model to examine the contributions of genetic and environmental factors in determining the aspects of behavior and metabolism relevant to body-weight regulation and obesity. Starting with generation 16 and continuing through to generation 52, mice from the four replicate high runner (HR) lines have run 2.5-3-fold more revolutions per day as compared with four non-selected control (C) lines, but the nature of this apparent selection limit is not understood. We hypothesized that it might involve the availability of dietary lipids. Methods: Wheel running, food consumption (Teklad Rodent Diet (W) 8604, 14% kJ from fat; or Harlan Teklad TD.88137 Western Diet (WD), 42% kJ from fat) and body mass were measured over 1-2-week intervals in 100 males for 2 months starting 3 days after weaning. Results: WD was obesogenic for both HR and C, significantly increasing both body mass and retroperitoneal fat pad mass, the latter even when controlling statistically for wheel-running distance and caloric intake. The HR mice had significantly less fat than C mice, explainable statistically by their greater running distance. On adjusting for body mass, HR mice showed higher caloric intake than C mice, also explainable by their higher running. Accounting for body mass and running, WD initially caused increased caloric intake in both HR and C, but this effect was reversed during the last four weeks of the study. Western diet had little or no effect on wheel running in C mice, but increased revolutions per day by as much as 75% in HR mice, mainly through increased time spent running. Conclusion: The remarkable stimulation of wheel running by WD in HR mice may involve fuel usage during prolonged endurance exercise and/or direct behavioral effects on motivation. Their unique behavioral responses to WD may render HR mice an important model for understanding the control of voluntary activity levels.

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Additive effects of training and high-fat diet on energy metabolism during exercise

Cited by 96 publications

References 0 publications

Time Course of Decrease in Skeletal Muscle Mitochondrial Biogenesis after Discontinuation of High-Fat Diet

Time Course of Decrease in Skeletal Muscle Mitochondrial Biogenesis after Discontinuation of High-Fat Diet

High-fat diets cause insulin resistance despite an increase in muscle mitochondria

Western diet increases wheel running in mice selectively bred for high voluntary wheel running

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