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Nathan Goodyear

Effect of a low-carbohydrate diet on appetite... [Ann Intern Med. 2005] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...15767618

low carb low carbohydrate diet low carbohydrate glucose insulin type II diabetes diabetes DM

shared by Nathan Goodyear on 08 Feb 13 - Cached
  • Nathan Goodyear on 08 Feb 13
     
    low carbohydrate diet found to improve glucose and insulin function in those obese with type II diabetes
Nathan Goodyear

Weight Loss with a Low-Carbohydrate, Mediterranean, or Low-Fat Diet - NEJM - 0 views

www.nejm.org/...NEJMoa0708681

obesity overweight low carb diet low carbohydrate diet mediterranean diet weight weight loss DIRECT study

shared by Nathan Goodyear on 13 Jun 12 - No Cached
  • Nathan Goodyear on 13 Jun 12
     
    Nice study, the DIRECT study, found a better weight loss and longer maintenance of weight loss in low carbohydrate diet compared to low fat diet and mediterranean diet.  
Nathan Goodyear

A Randomized Pilot Trial of a Moderate Carbohydrate Diet Compared to a Very Low Carbohy... - 0 views

www.ncbi.nlm.nih.gov/...PMC3981696

diabetes ketogenic diet nutrition diet obesity

shared by Nathan Goodyear on 09 Feb 16 - No Cached
  • Nathan Goodyear on 09 Feb 16
     
    low carb ketogenic diet, high in fat worked better in glycemic control versus DA low fat, medium carbohydrate, calorie restricted diet.
Nathan Goodyear

Effect of 6-month adherence to a very low carbohydrate diet program - 0 views

www.amjmed.com/...abstract

low carb low carbohydrate weight loss overweight obesity low carbohydrate

shared by Nathan Goodyear on 08 Feb 13 - No Cached
  • Nathan Goodyear on 08 Feb 13
     
    low carb diet resulted in 6 month weight loss.
Nathan Goodyear

JAMA Network | JAMA: The Journal of the American Medical Association | Effects of Prote... - 0 views

jama.jamanetwork.com/article.aspx

monosaturated fats low carb diet low diet triglycerides hypertension high blood pressure elevated pressure HDL CVD protein fat carbohydrate intake

shared by Nathan Goodyear on 13 Jun 12 - No Cached
  • Nathan Goodyear on 13 Jun 12
     
    In this study, a high carbohydrate diet was replaced with a diet higher in monosaturated fats.  The result was: a lower carb diet with resultant increase in monosaturated fats resulted in a reduction in triglycerides, reduction in systolic B/P, increase in HDL, and resultant decrease in CVD risk
Nathan Goodyear

Nutritional Modulation of Insulin Resistance - 0 views

www.hindawi.com/...424780

macronutrient macronutrients nutrition insulin resistance glucose protein carbohydrates metabolism fats

shared by Nathan Goodyear on 21 Oct 13 - No Cached
  • Five branched chain and aromatic amino acids (isoleucine, leucine, valine, tyrosine, and phenylalanine) showed significant associations with future diabetes
  • there is increasing evidence that longer term high-protein intake may have detrimental effects on insulin resistance [68, 117–123], diabetes risk [69], and the risk of developing cardiovascular disease
  • high-protein and the high GI diets significantly increased markers of low-grade inflammation
  • ...5 more annotations...
  • significant and clinically relevant worsening of insulin sensitivity with an isoenergetic plant-based high-protein diet
  • healthy humans that are exposed to amino acid infusions rapidly develop insulin resistance
  • longer term high-protein intake has been shown to result in whole-body insulin resistance [68, 118], associated with upregulation of factors involved in the mammalian target of rapamycin (mTOR)/S6K1 signalling pathway [68], increased stimulation of glucagon and insulin within the endocrine pancreas, high glycogen turnover [118] and stimulation of gluconeogenesis [68, 118].
  • it was recently shown in a large prospective cohort with 10 years followup that consuming 5% of energy from both animal and total protein at the expense of carbohydrates or fat increases diabetes risk by as much as 30% [69]. This reinforces the theory that high-protein diets can have adverse effects on glucose metabolism.
  • Another recent study showed that low-carbohydrate high-protein diets, used on a regular basis and without consideration of the nature of carbohydrates or the source of proteins, are also associated with increased risk of cardiovascular disease [70], thereby indicating a potential link between high-protein Western diets, T2DM, and cardiovascular risk.
  • Nathan Goodyear on 21 Oct 13
     
    macronutrient intake and effect on glucose regulation and thus metabolism.
Nathan Goodyear

JAMA Network | JAMA: The Journal of the American Medical Association | Effects of Dieta... - 0 views

jama.jamanetwork.com/article.aspx

low carb low carbohydrate diet calories overweight obesity weight-loss energy

shared by Nathan Goodyear on 27 Jun 12 - No Cached
  • Nathan Goodyear on 27 Jun 12
     
    small study shows that low carb results in greater calories burned in weight loss.  The least calories burned goes to low fat diet.  Many, many studies have show the negative benefits of a low fat diet.
Nathan Goodyear

A Review of Very Low Carbohydrate Diets for Weight Loss - 0 views

www.turner-white.com/...jcom_jul99_lowcarb.pdf

low carb low carbohydrates diet weight loss overweight obesity

shared by Nathan Goodyear on 08 Feb 13 - No Cached
  • Nathan Goodyear on 08 Feb 13
     
    Low carb diets result in significant weight loss. This is a meta-analysis.
Nathan Goodyear

Low carbohydrate diets improve atherogenic dyslipidemia even in the absence of weight loss - 0 views

www.ncbi.nlm.nih.gov/...PMC1488852

ketogenic diet low carbohydrate diet diet nutrition atherosclerosis cholesterol HDL LDL Triglycerides

shared by Nathan Goodyear on 09 Feb 18 - No Cached
mamdouh_hfz liked it
  • Nathan Goodyear on 09 Feb 18
     
    low carb diet found to benefit atherosclerosis and lipid abnormalities (Triglycerides, HDL, and LDL particle size).  Interesting enough, no significant weight loss was seen.
Nathan Goodyear

Nutrition & Metabolism | Full text | Fructose, insulin resistance, and metabolic dyslip... - 0 views

www.nutritionandmetabolism.com/...5

fructose metabolic syndrome metabolic syndrome insulin resistance obesity nutrition metabolism

shared by Nathan Goodyear on 16 Sep 13 - Cached
  • For thousands of years humans consumed fructose amounting to 16–20 grams per day
  • daily consumptions amounting to 85–100 grams of fructose per day
  • Of key importance is the ability of fructose to by-pass the main regulatory step of glycolysis, the conversion of glucose-6-phosphate to fructose 1,6-bisphosphate, controlled by phosphofructokinase
  • ...29 more annotations...
  • Thus, while glucose metabolism is negatively regulated by phosphofructokinase, fructose can continuously enter the glycolytic pathway. Therefore, fructose can uncontrollably produce glucose, glycogen, lactate, and pyruvate, providing both the glycerol and acyl portions of acyl-glycerol molecules. These particular substrates, and the resultant excess energy flux due to unregulated fructose metabolism, will promote the over-production of TG (reviewed in [53]).
  • Glycemic excursions and insulin responses were reduced by 66% and 65%, respectively, in the fructose-consuming subjects
  • reduction in circulating leptin both in the short and long-term as well as a 30% reduction in ghrelin (an orexigenic gastroenteric hormone) in the fructose group compared to the glucose group.
  • A prolonged elevation of TG was also seen in the high fructose subjects
  • Both fat and fructose consumption usually results in low leptin concentrations which, in turn, leads to overeating in populations consuming energy from these particular macronutrients
  • Chronic fructose consumption reduces adiponectin responses, contributing to insulin resistance
  • A definite relationship has also been found between metabolic syndrome and hyperhomocysteinemia
  • the liver takes up dietary fructose rapidly where it can be converted to glycerol-3-phosphate. This substrate favours esterification of unbound FFA to form the TG
  • Fructose stimulates TG production, but impairs removal, creating the known dyslipidemic profile
  • the effects of fructose in promoting TG synthesis are independent of insulinemia
  • Although fructose does not appear to acutely increase insulin levels, chronic exposure seems to indirectly cause hyperinsulinemia and obesity through other mechanisms. One proposed mechanism involves GLUT5
  • If FFA are not removed from tissues, as occurs in fructose fed insulin resistant models, there is an increased energy and FFA flux that leads to the increased secretion of TG
  • In these scenarios, where there is excess hepatic fatty acid uptake, synthesis and secretion, 'input' of fats in the liver exceed 'outputs', and hepatic steatosis occurs
  • Carbohydrate induced hypertriglycerolemia results from a combination of both TG overproduction, and inadequate TG clearance
  • fructose-induced metabolic dyslipidemia is usually accompanied by whole body insulin resistance [100] and reduced hepatic insulin sensitivity
  • Excess VLDL secretion has been shown to deliver increased fatty acids and TG to muscle and other tissues, further inducing insulin resistance
  • the metabolic effects of fructose occur through rapid utilization in the liver due to the bypassing of the regulatory phosphofructokinase step in glycolysis. This in turn causes activation of pyruvate dehydrogenase, and subsequent modifications favoring esterification of fatty acids, again leading to increased VLDL secretion
  • High fructose diets can have a hypertriglyceridemic and pro-oxidant effect
  • Oxidative stress has often been implicated in the pathology of insulin resistance induced by fructose feeding
  • Administration of alpha-lipoic acid (LA) has been shown to prevent these changes, and improve insulin sensitivity
  • LA treatment also prevents several deleterious effects of fructose feeding: the increases in cholesterol, TG, activity of lipogenic enzymes, and VLDL secretion
  • Fructose has also been implicated in reducing PPARα levels
  • PPARα is a ligand activated nuclear hormone receptor that is responsible for inducing mitochondrial and peroxisomal β-oxidation
  • decreased PPARα expression can result in reduced oxidation, leading to cellular lipid accumulation
  • fructose diets altered the structure and function of VLDL particles causing and increase in the TG: protein ratio
  • LDL particle size has been found to be inversely related to TG concentration
  • therefore the higher TG results in a smaller, denser, more atherogenic LDL particle, which contributes to the morbidity of the metabolic disorders associated with insulin resistance
  • High fructose, which stimulates VLDL secretion, may initiate the cycle that results in metabolic syndrome long before type 2 diabetes and obesity develop
  • A high flux of fructose to the liver, the main organ capable of metabolizing this simple carbohydrate, disturbs normal hepatic carbohydrate metabolism leading to two major consequences (Figure 2): perturbations in glucose metabolism and glucose uptake pathways, and a significantly enhanced rate of de novo lipogenesis and TG synthesis, driven by the high flux of glycerol and acyl portions of TG molecules coming from fructose catabolism
  • Nathan Goodyear on 16 Sep 13
     
    Fructose and metabolic syndrome.  Good discussion of the impact of high fructose intake and metabolic dysfunction.  This study also does a great job of highlighting the historical change of fructose intake.
Nathan Goodyear

Effect of low-calorie versus low-carbohydrate ketogenic diet in type 2 diabetes. - PubM... - 0 views

www.ncbi.nlm.nih.gov/...22673594

diabetes diet nutrition ketogenic diet ketogenic

shared by Nathan Goodyear on 09 Feb 16 - No Cached
  • Nathan Goodyear on 09 Feb 16
     
    low carb, high fat, ketogenic diet outperformed low calorie diet in people with type II diabetes
Nathan Goodyear

The effect of a low-carbohydrate, ketogenic diet versus a low-glycemic index diet on gl... - 0 views

www.ncbi.nlm.nih.gov/...PMC2633336

ketogenic diet ketogenic nutrition diabetes lifestyle diet glycemic index

shared by Nathan Goodyear on 26 Feb 16 - No Cached
  • Nathan Goodyear on 26 Feb 16
     
    low carb ketogenic diet outperforms low glycemic index in diabetes.
Nathan Goodyear

Weight Loss with a Low-Carbohydrate, Mediterranean, or Low-Fat Diet - NEJM - 0 views

www.nejm.org/...NEJMoa0708681

weight weight loss mediterranean loss diet overweight obesity

shared by Nathan Goodyear on 20 Dec 11 - No Cached
  • Nathan Goodyear on 20 Dec 11
     
    mediterranean and low-carb diets are effective diets to aid weight loss
Nathan Goodyear

Influence of high-carbohydrate mixed meals with different glycemic indexes on substrate... - 0 views

www.ajcn.org/...354.abstract

obesity overweight weight-loss low-glycemic exercise adipose fat

shared by Nathan Goodyear on 20 Dec 11 - No Cached
  • Nathan Goodyear on 20 Dec 11
     
    low-glycemic index diet aids in mobilization of adipose tissue in exercise.  In this study, exercise after a low-glycemic meal resulted in a greater mobilization of adipose tissue for energy production than a high glycemic meal.  This will help  in weight loss
Nathan Goodyear

Carbohydrates for training and competition. - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...21660838

carbohydrates training competition athletes

shared by Nathan Goodyear on 10 Feb 16 - No Cached
  • Nathan Goodyear on 10 Feb 16
     
    Only abstract available here.  Article looked at the evidence of daily carb intake for levels of training: low training-3-5 g/kg; moderate training (1h)-5-7 g/kg; endurance training (1-3h)-6-10 g/kg; extreme endurance (>4-5h)-8-12 g/kg   
Nathan Goodyear

Dietary Macronutrient Content Alters Cortisol Metabolism Independently of Body Weight C... - 0 views

jcem.endojournals.org/...4480.long

cortisol 11-betaHSD1 low carb diet low carb carbohydrates metabolism macronutrients

shared by Nathan Goodyear on 07 Oct 13 - No Cached
  • Nathan Goodyear on 07 Oct 13
     
    Extra-adrenal cortisol production is increased by 11-Beta-HSD1 via low Carb diet.  This is counter to that seen in mice studies.  The fat content of the diet could explain this.  This study looked at men.
Nathan Goodyear

A Lower-Carbohydrate, Higher-Fat Diet Reduces Abdominal and Intermuscular Fat and Incre... - 0 views

jn.nutrition.org/...177S.abstract

nutrition diet high fat diet low carb diet fats carbohydrates weight fat fat mass insulin resistance obesity diabetes TNF-alpha insulin sensitivity

shared by Nathan Goodyear on 23 Mar 15 - No Cached
  • Nathan Goodyear on 23 Mar 15
     
    Diet higher in fats and lower in carbs associated with a reduction in weight, fat mass, improved insulin sensitivity, lowered fasting glucose, and a reduction in TNF-alpha
Nathan Goodyear

Inflammatory cause of metabolic syndrome via brain stress and NF-κB - 0 views

www.ncbi.nlm.nih.gov/...PMC3314172

metabolic syndrome TLR cytokines hypothalamus brain neurology metabolic syndrome NF-kappaB DIO diet induced obesity over nutrition nutrition inflammation

shared by Nathan Goodyear on 09 Jul 13 - No Cached
  • Mechanistic studies further showed that such metabolic inflammation is related to the induction of various intracellular stresses such as mitochondrial oxidative stress, endoplasmic reticulum (ER) stress, and autophagy defect under prolonged nutritional excess
  • intracellular stress-inflammation process for metabolic syndrome has been established in the central nervous system (CNS) and particularly in the hypothalamus
  • the CNS and the comprised hypothalamus are known to govern various metabolic activities of the body including appetite control, energy expenditure, carbohydrate and lipid metabolism, and blood pressure homeostasis
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  • Reactive oxygen species (ROS) refer to a class of radical or non-radical oxygen-containing molecules that have high oxidative reactivity with lipids, proteins, and nucleic acids
  • a large measure of intracellular ROS comes from the leakage of mitochondrial electron transport chain (ETC)
  • Another major source of intracellular ROS is the intentional generation of superoxides by nicotinamide adenine dinucleotide phosphate (NADPH) oxidase
  • there are other ROS-producing enzymes such as cyclooxygenases, lipoxygenases, xanthine oxidase, and cytochrome p450 enzymes, which are involved with specific metabolic processes
  • To counteract the toxic effects of molecular oxidation by ROS, cells are equipped with a battery of antioxidant enzymes such as superoxide dismutases, catalase, peroxiredoxins, sulfiredoxin, and aldehyde dehydrogenases
  • intracellular oxidative stress has been indicated to contribute to metabolic syndrome and related diseases, including T2D [72; 73], CVDs [74-76], neurodegenerative diseases [69; 77-80], and cancers
  • intracellular oxidative stress is highly associated with the development of neurodegenerative diseases [69] and brain aging
  • dietary obesity was found to induce NADPH oxidase-associated oxidative stress in rat brain
  • mitochondrial dysfunction in hypothalamic proopiomelanocortin (POMC) neurons causes central glucose sensing impairment
  • Endoplasmic reticulum (ER) is the cellular organelle responsible for protein synthesis, maturation, and trafficking to secretory pathways
  • unfolded protein response (UPR) machinery
  • ER stress has been associated to obesity, insulin resistance, T2D, CVDs, cancers, and neurodegenerative diseases
  • brain ER stress underlies neurodegenerative diseases
  • under environmental stress such as nutrient deprivation or hypoxia, autophagy is strongly induced to breakdown macromolecules into reusable amino acids and fatty acids for survival
  • intact autophagy function is required for the hypothalamus to properly control metabolic and energy homeostasis, while hypothalamic autophagy defect leads to the development of metabolic syndrome such as obesity and insulin resistance
  • prolonged oxidative stress or ER stress has been shown to impair autophagy function in disease milieu of cancer or aging
  • TLRs are an important class of membrane-bound pattern recognition receptors in classical innate immune defense
  • Most hypothalamic cell types including neurons and glia cells express TLRs
  • overnutrition constitutes an environmental stimulus that can activate TLR pathways to mediate the development of metabolic syndrome related disorders such as obesity, insulin resistance, T2D, and atherosclerotic CVDs
  • Isoforms TLR1, 2, 4, and 6 may be particularly pertinent to pathogenic signaling induced by lipid overnutrition
  • hypothalamic TLR4 and downstream inflammatory signaling are activated in response to central lipid excess via direct intra-brain lipid administration or HFD-feeding
  • overnutrition-induced metabolic derangements such as central leptin resistance, systemic insulin resistance, and weight gain
  • these evidences based on brain TLR signaling further support the notion that CNS is the primary site for overnutrition to cause the development of metabolic syndrome.
  • circulating cytokines can limitedly travel to the hypothalamus through the leaky blood-brain barrier around the mediobasal hypothalamus to activate hypothalamic cytokine receptors
  • significant evidences have been recently documented demonstrating the role of cytokine receptor pathways in the development of metabolic syndrome components
  • entral administration of TNF-α at low doses faithfully replicated the effects of central metabolic inflammation in enhancing eating, decreasing energy expenditure [158;159], and causing obesity-related hypertension
  • Resistin, an adipocyte-derived proinflammatory cytokine, has been found to promote hepatic insulin resistance through its central actions
  • both TLR pathways and cytokine receptor pathways are involved in central inflammatory mechanism of metabolic syndrome and related diseases.
  • In quiescent state, NF-κB resides in the cytoplasm in an inactive form due to inhibitory binding by IκBα protein
  • IKKβ activation via receptor-mediated pathway, leading to IκBα phosphorylation and degradation and subsequent release of NF-κB activity
  • Research in the past decade has found that activation of IKKβ/NF-κB proinflammatory pathway in metabolic tissues is a prominent feature of various metabolic disorders related to overnutrition
  • it happens in metabolic tissues, it is mainly associated with overnutrition-induced metabolic derangements, and most importantly, it is relatively low-grade and chronic
  • this paradigm of IKKβ/NF-κB-mediated metabolic inflammation has been identified in the CNS – particularly the comprised hypothalamus, which primarily accounts for to the development of overnutrition-induced metabolic syndrome and related disorders such as obesity, insulin resistance, T2D, and obesity-related hypertension
  • evidences have pointed to intracellular oxidative stress and mitochondrial dysfunction as upstream events that mediate hypothalamic NF-κB activation in a receptor-independent manner under overnutrition
  • In the context of metabolic syndrome, oxidative stress-related NF-κB activation in metabolic tissues or vascular systems has been implicated in a broad range of metabolic syndrome-related diseases, such as diabetes, atherosclerosis, cardiac infarct, stroke, cancer, and aging
  • intracellular oxidative stress seems to be a likely pathogenic link that bridges overnutrition with NF-κB activation leading to central metabolic dysregulation
  • overnutrition is an environmental inducer for intracellular oxidative stress regardless of tissues involved
  • excessive nutrients, when transported into cells, directly increase mitochondrial oxidative workload, which causes increased production of ROS by mitochondrial ETC
  • oxidative stress has been shown to activate NF-κB pathway in neurons or glial cells in several types of metabolic syndrome-related neural diseases, such as stroke [185], neurodegenerative diseases [186-188], and brain aging
  • central nutrient excess (e.g., glucose or lipids) has been shown to activate NF-κB in the hypothalamus [34-37] to account for overnutrition-induced central metabolic dysregulations
  • overnutrition can present the cell with a metabolic overload that exceeds the physiological adaptive range of UPR, resulting in the development of ER stress and systemic metabolic disorders
  • chronic ER stress in peripheral metabolic tissues such as adipocytes, liver, muscle, and pancreatic cells is a salient feature of overnutrition-related diseases
  • recent literature supports a model that brain ER stress and NF-κB activation reciprocally promote each other in the development of central metabolic dysregulations
  • when intracellular stresses remain unresolved, prolonged autophagy upregulation progresses into autophagy defect
  • autophagy defect can induce NF-κB-mediated inflammation in association with the development of cancer or inflammatory diseases (e.g., Crohn's disease)
  • The connection between autophagy defect and proinflammatory activation of NF-κB pathway can also be inferred in metabolic syndrome, since both autophagy defect [126-133;200] and NF-κB activation [20-33] are implicated in the development of overnutrition-related metabolic diseases
  • Both TLR pathway and cytokine receptor pathways are closely related to IKKβ/NF-κB signaling in the central pathogenesis of metabolic syndrome
  • Overnutrition, especially in the form of HFD feeding, was shown to activate TLR4 signaling and downstream IKKβ/NF-κB pathway
  • TLR4 activation leads to MyD88-dependent NF-κB activation in early phase and MyD88-indepdnent MAPK/JNK pathway in late phase
  • these studies point to NF-κB as an immediate signaling effector for TLR4 activation in central inflammatory response
  • TLR4 activation has been shown to induce intracellular ER stress to indirectly cause metabolic inflammation in the hypothalamus
  • central TLR4-NF-κB pathway may represent one of the early receptor-mediated events in overnutrition-induced central inflammation.
  • cytokines and their receptors are both upstream activating components and downstream transcriptional targets of NF-κB activation
  • central administration of TNF-α at low dose can mimic the effect of obesity-related inflammatory milieu to activate IKKβ/NF-κB proinflammatory pathways, furthering the development of overeating, energy expenditure decrease, and weight gain
  • the physiological effects of IKKβ/NF-κB activation seem to be cell type-dependent, i.e., IKKβ/NF-κB activation in hypothalamic agouti-related protein (AGRP) neurons primarily leads to the development of energy imbalance and obesity [34]; while in hypothalamic POMC neurons, it primarily results in the development of hypertension and glucose intolerance
  • the hypothalamus, is the central regulator of energy and body weight balance [
  • Nathan Goodyear on 09 Jul 13
     
    Great article chronicles the biochemistry of "over nutrition" and inflammation through NF-kappaB activation and its impact on the brain.
Nathan Goodyear

Anticonvulsant Mechanisms of the Ketogenic Diet - Bough - 2007 - Epilepsia - Wiley Onli... - 0 views

onlinelibrary.wiley.com/...full

ketogenic ketogenic diet seizures nutrition diet glucose mitochondria insulin ROS oxidative stress

shared by Nathan Goodyear on 16 Nov 16 - No Cached
  • The ketogenic diet (KD) is a high-fat, low-protein, low-carbohydrate diet that has been employed as a treatment for medically refractory epilepsy for 86 years
  • The hallmark feature of KD treatment is the production of ketone bodies by the liver
  • almost any diet that produces ketonemia and/or diminished blood glucose levels can induce an anticonvulsant effect.
  • Nathan Goodyear on 16 Nov 16
     
    ketogenic diet reduces seizures.  Proposed mechanisms: reduced insulin, reduced ROS, reduces oxidative stress, reduced inflammation, increased GABA/Gluatamate ratio.  In the end, it reduces inflammation and increases mitochondrial efficiency.
Nathan Goodyear

Metabolic characteristics of keto-adapted ultra-endurance runners - Metabolism - Clinic... - 0 views

www.metabolismjournal.com/...abstract

endurance athletes endurance sports exercise carbohydrates ketogenic diet

shared by Nathan Goodyear on 20 Apr 16 - No Cached
  • Nathan Goodyear on 20 Apr 16
     
    For endurance athletes, low carb and high fat diet utilizes the high fat oxidation in these athletes compared to a high carb diet.  Glycogen stores did not differ between the two groups.  
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