Adaptations to a high-fat diet that increase exercise endurance in male rats

Miller, William C.; Bryce, G. Rex; Conlee, R. K.

doi:10.1152/jappl.1984.56.1.78

Cited by 121 publications

(109 citation statements)

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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%

“…Miller et al (5) reported that feeding a high-fat diet for only 1 wk increased muscle 3-hydroxyacyl CoA dehydrogenase activity and endurance exercise capacity, without effects on other mitochondrial enzymes, such as citrate synthase. These results suggest that fatty acid b-oxidation is responsible for the high-fat diet-induced increase in endurance capacity.…”

Section: Discussionmentioning

confidence: 99%

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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%

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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“…A high-fat diet and elevated levels of plasma fatty acids lead to increases in the activity of citrate synthase, 3-hydroxyacyl-CoA dehydrogenase and carnitine palmitoyl-transferase 17,29,35,38 and induce increased biogenesis of mitochondria in skeletal muscle, 39,40 all of which would act to potentially increase fatty-acid metabolism. These effects can appear in only a matter of days, and in some cases reach their maximum levels within a week.…”

Section: Discussionmentioning

confidence: 99%

“…These effects can appear in only a matter of days, and in some cases reach their maximum levels within a week. 17,19 However, high-fat diets can also lead to higher levels of mitochondrial uncoupling protein (UCP3), which reduces the efficiency of energy production and, therefore, can impair exercise capacity. 41 Although the precise limitation(s) on endurance exercise performance depend on the intensity and/or duration of the activity, the depletion of energy substrates is a commonly considered 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%

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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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