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Low Carb Diet , Glycogen Level, Performance,metabolic Rate

Discussion in 'Articles & Scientific Studies' started by paymanz, Sep 18, 2017.

  1. paymanz

    paymanz Member

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    Low carbohydrate diet induces metabolic depression: a possible mechanism to conserve glycogen. - PubMed - NCBI

    Long-term studies have found low carbohydrate diets are more effective for weight loss than calorie restricted diets in the short-term, but equally or only marginally more effective in the long-term. Low carbohydrate diets have been linked to reduced glycogen stores and increased feelings of fatigue. We propose that reduced physical activity in response to lowered glycogen explains the diminishing weight loss advantage of low carbohydrate compared to low calorie diets over longer time scales. We explored this possibility by feeding adult Drosophila melanogaster either a standard or low carbohydrate diet for nine days and measured changes in metabolic rate, glycogen stores, activity, and body mass. We hypothesized that a low carbohydrate diet would cause a reduction in glycogen stores that recovers over time, reduced physical activity, and an increase in resting metabolic rate. The low carbohydrate diet was found to reduce glycogen stores, which recovered over time. Activity was unaffected by diet but the low carbohydrate group experienced a reduction in metabolic rate. We conclude that metabolic depression could explain the decreased effectiveness of low carbohydrate diets over time and recommend further investigation of long-term metabolic effects of dietary interventions and a greater focus on physiological plasticity within the study of human nutrition.

    Influence of high- and low-carbohydrate diet following glycogen-depleting exercise on heart rate variability and plasma catecholamines. - PubMed - NCBI

    Abstract
    The effects of simple-carbohydrate (CHO)- and complex-CHO-rich diets on skeletal muscle glycogen content were compared. Twenty male marathon runners were divided into four equal groups with reference to dietary consumption: depletion/simple, depletion/complex, nondepletion/simple, and nondepletion/complex. Subjects consumed either a low-CHO (15% energy [E] intake), or a mixed diet (50% CHO) for 3 days, immediately followed by a high-CHO diet (70% E intake) predominant in either simple-CHO or in complex-CHO (85% of total CHO intake) for another 3 days. Skeletal muscle biopsies and venous blood samples were obtained one day prior to the start of the low-CHO diet or mixed diet (PRE), and then again one day after the completion of the high-CHO diet (POST). The samples were analysed for skeletal muscle glycogen, serum free fatty acids (FFA), insulin, and lactate and blood glucose. Skeletal muscle glycogen content increased significantly (p less than 0.05) only in the nondepletion/simple group. When groups were combined, according to the type of CHO ingested and/or utilization of a depletion diet, significant increases were observed in glycogen content. Serum FFA decreased significantly (p less than 0.05) for the nondepletion/complex group only, while serum insulin, blood glucose, and serum lactate were not altered. It is concluded that significant increases in skeletal muscle glycogen content can be achieved with a diet high in simple-CHO or complex-CHO, with or without initial consumption of a low-CHO diet
     
  2. Nebukadnezar

    Nebukadnezar New Member

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    Hate to say that, but those studies are worthless, due to the low duration, which gives no indication of what happens after the typical low carb adaptation time.
     
  3. DaveFoster

    DaveFoster Member

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    Ketogenic adaptation takes several weeks for appreciable normalcy, and several months for complete adaptation. Over time, the body increasingly spares protein, which allows for the efficient conversion of excess protein into glucose, stored in the muscle as glycogen.

    Many who eat "ketogenic diets" eat 35%, 30%, or even 25% of their calories as protein, but, absent hypocaloric (low-calorie) intakes, even a 25% protein intake as percent of total calories interferes with the use of ketones as fuel, and the conversion stresses the kidneys. People who only consume 1500 or 2000 calories initially can subsist on a 35% protein intake, but it becomes problematic with a normal caloric intake.

    Exercise in a fasted or ketogenic state becomes significantly more stressful, accompanied with increases in circulating levels of fatty acids and more lipid peroxidative processes (indicative of inflammation.) Similar oxidative stress appears in a combination of higher dosages of caffeine (9 mg/kg) with exhausting exercise. Exercise in ketogenesis could have the effect of reducing the levels of the stored and easily oxidized PUFA, but the diet's high dietary intake of fat would more than offset this effect.

    It's possible to maintain high amounts of lean mass and build muscle on the ketogenic, particularly with a moderate protein intake, as in 20-25%, rather than a lower 10-20%, and even further more easily after several months of adaptation.

    Ketogenesis induces hypothyroidism, where it lowers T3 levels and increases circulating reverse T3. The initial stage of ketogenic adaptations results in a depression of the basal body temperature and then activates the sympathetic nervous system to elevate the temperature, which leads to many reported problems on the diet, such as poor sleep regulation, premature aging of the skin, malaise during exhaustive periods (following intense bursts of energy,) lack of tolerance for intense exertion, loss of libido and so on.

    Here's an interesting article:

    https://blog.virtahealth.com/keto-adapted/

    "Compared to highly trained ultra-endurance athletes consuming an HC diet, long-term keto-adaptation results in extraordinarily high rates of fat oxidation, whereas muscle glycogen utilization and repletion patterns during and after a 3 hour run are similar."​

    Reference: Metabolic characteristics of keto-adapted ultra-endurance runners - ScienceDirect

    Cold-inducible RNA-binding protein (CIRBP) induced by cold stress modulates the molecular circadian clock in vitro. The present study examines the effect of a ketogenic diet (KD) and fasting on Cirbp expression in the mouse liver. Chronic KD administration induced time-dependent Cirbp expression with hypothermia in mice. The circadian expression of clock genes such as Bmal1 and Clock was phase-advanced and augmented in the liver of mice fed with a KD. Transient food deprivation also induced time-dependent Cirbp expression with hypothermia in mice. These findings suggest that hypothermia is involved in the increased expression of Cirbp under ketogenic or fasting conditions.​

    Reference: Ketogenic diet and fasting induce the expression of cold-inducible RNA-binding protein with time-dependent hypothermia in the mouse liver
     
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