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Nathan Goodyear

JISSN | Full text | International Society of Sports Nutrition position stand: creatine ... - 0 views

www.jissn.com/6

creatine sports nutrition exercise

shared by Nathan Goodyear on 27 Jan 14 - No Cached
  • the energy supplied to rephosphorylate adenosine diphosphate (ADP) to adenosine triphosphate (ATP) during and following intense exercise is largely dependent on the amount of phosphocreatine (PCr) stored in the muscle
  • Creatine is chemically known as a non-protein nitrogen
  • It is synthesized in the liver and pancreas from the amino acids arginine, glycine, and methionine
  • ...26 more annotations...
  • Approximately 95% of the body's creatine is stored in skeletal muscle
  • About two thirds of the creatine found in skeletal muscle is stored as phosphocreatine (PCr) while the remaining amount of creatine is stored as free creatine
  • The body breaks down about 1 – 2% of the creatine pool per day (about 1–2 grams/day) into creatinine in the skeletal muscle
  • The magnitude of the increase in skeletal muscle creatine content is important because studies have reported performance changes to be correlated to this increase
  • "loading" protocol. This protocol is characterized by ingesting approximately 0.3 grams/kg/day of CM for 5 – 7 days (e.g., ≃5 grams taken four times per day) and 3–5 grams/day thereafter [18,22]. Research has shown a 10–40% increase in muscle creatine and PCr stores using this protocol
  • Additional research has reported that the loading protocol may only need to be 2–3 days in length to be beneficial, particularly if the ingestion coincides with protein and/or carbohydrate
  • A few studies have reported protocols with no loading period to be sufficient for increasing muscle creatine (3 g/d for 28 days)
  • Cycling protocols involve the consumption of "loading" doses for 3–5 days every 3 to 4 weeks
  • Most of these forms of creatine have been reported to be no better than traditional CM in terms of increasing strength or performance
  • Recent studies do suggest, however, that adding β-alanine to CM may produce greater effects than CM alone
  • These investigations indicate that the combination may have greater effects on strength, lean mass, and body fat percentage; in addition to delaying neuromuscular fatigue
  • creatine phosphate has been reported to be as effective as CM at improving LBM and strength
  • Green et al. [24] reported that adding 93 g of carbohydrate to 5 g of CM increased total muscle creatine by 60%
  • Steenge et al. [23] reported that adding 47 g of carbohydrate and 50 g of protein to CM was as effective at promoting muscle retention of creatine as adding 96 g of carbohydrate.
  • It appears that combining CM with carbohydrate or carbohydrate and protein produces optimal results
  • Studies suggest that increasing skeletal muscle creatine uptake may enhance the benefits of training
  • Nearly 70% of these studies have reported a significant improvement in exercise capacity,
  • Long-term CM supplementation appears to enhance the overall quality of training, leading to 5 to 15% greater gains in strength and performance
  • Nearly all studies indicate that "proper" CM supplementation increases body mass by about 1 to 2 kg in the first week of loading
  • short-term adaptations reported from CM supplementation include increased cycling power, total work performed on the bench press and jump squat, as well as improved sport performance in sprinting, swimming, and soccer
  • Long-term adaptations when combining CM supplementation with training include increased muscle creatine and PCr content, lean body mass, strength, sprint performance, power, rate of force development, and muscle diameter
  • subjects taking CM typically gain about twice as much body mass and/or fat free mass (i.e., an extra 2 to 4 pounds of muscle mass during 4 to 12 weeks of training) than subjects taking a placebo
  • The gains in muscle mass appear to be a result of an improved ability to perform high-intensity exercise via increased PCr availability and enhanced ATP synthesis, thereby enabling an athlete to train harder
  • there is no evidence to support the notion that normal creatine intakes (< 25 g/d) in healthy adults cause renal dysfunction
  • no long-term side effects have been observed in athletes (up to 5 years),
  • One cohort of patients taking 1.5 – 3 grams/day of CM has been monitored since 1981 with no significant side effects
  • Nathan Goodyear on 27 Jan 14
     
    Nice review of the data, up to the publication date, on creatine.
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 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

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
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  • 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

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

http://jap.physiology.org/content/jap/82/1/49.full.pdf - 0 views

jap.physiology.org/...49.full.pdf

exercise Testosterone protein high protein carbohydrate nutrition diet

shared by Nathan Goodyear on 12 Feb 17 - No Cached
  • Nathan Goodyear on 12 Feb 17
     
    To much protein intake can be a bad thing.  This study found that high protein intake and high protein/carbohydrate intake lowered basal Testosterone levels.
Nathan Goodyear

Dietary glycemic index, glycemic load, and the risk of breast cancer in an Italian pros... - 0 views

ajcn.nutrition.org/...1160.full

nutrition diet glycemic index glycemic load cancer breast cancer carbohydrates sugar menopause women premenopause

shared by Nathan Goodyear on 09 Dec 14 - No Cached
  • GI is a measure of carbohydrate quality in relation to glucose availability and is independent of quantity, whereas GL is a measure of the total glycemic effect and hence is anindicator of the insulin demand of the diet. High-glycemic diets are in fact generally associated with greater insulin secretion
  • the consumption of large quantities of high-GI foods rather than the consumption of high quantities of carbohydrates is linked to the development of breast cancer.
  • Nathan Goodyear on 09 Dec 14
     
    High glycemic load and glycemic index associated with increased breast cancer risk in premenopausal women.
Nathan Goodyear

Metabolic endotoxemia: a molecular link between obesity and cardiovascular risk - 0 views

jme.endocrinology-journals.org/...R51.full

metabolic endotoxemia obesity insulin resistance cardiovascular disease LPS inflammation

shared by Nathan Goodyear on 04 Aug 14 - No Cached
  • Weight gain has been associated with a higher gut permeability
  • a high-fat diet promotes LPS absorption
  • higher concentrations of fatty acids impair intestinal barrier integrity
  • ...37 more annotations...
  • The starting point for innate immunity activation is the recognition of conserved structures of bacteria, viruses, and fungal components through pattern-recognition receptors
  • TLRs are PRRs that recognize microbe-associated molecular patterns
  • TLRs are transmembrane proteins containing extracellular domains rich in leucine repeat sequences and a cytosolic domain homologous to the IL1 receptor intracellular domain
  • The major proinflammatory mediators produced by the TLR4 activation in response to endotoxin (LPS) are TNFα, IL1β and IL6, which are also elevated in obese and insulin-resistant patients
  • Obesity, high-fat diet, diabetes, and NAFLD are associated with higher gut permeability leading to metabolic endotoxemia.
  • Probiotics, prebiotics, and antibiotic treatment can reduce LPS absorption
  • LPS promotes hepatic insulin resistance, hypertriglyceridemia, hepatic triglyceride accumulation, and secretion of pro-inflammatory cytokines promoting the progression of fatty liver disease.
  • In the endothelium, LPS induces the expression of pro-inflammatory, chemotactic, and adhesion molecules, which promotes atherosclerosis development and progression.
  • In the adipose tissue, LPS induces adipogenesis, insulin resistance, macrophage infiltration, oxidative stress, and release of pro-inflammatory cytokines and chemokines.
  • the gut microbiota has been recently proposed to be an environmental factor involved in the control of body weight and energy homeostasis by modulating plasma LPS levels
  • dietary fats alone might not be sufficient to cause overweight and obesity, suggesting that a bacterially related factor might be responsible for high-fat diet-induced obesity.
  • This was accompanied in high-fat-fed mice by a change in gut microbiota composition, with reduction in Bifidobacterium and Eubacterium spp.
  • n humans, it was also shown that meals with high-fat and high-carbohydrate content (fast-food style western diet) were able to decrease bifidobacteria levels and increase intestinal permeability and LPS concentrations
  • it was demonstrated that, more than the fat amount, its composition was a critical modulator of ME (Laugerette et al. 2012). Very recently, Mani et al. (2013) demonstrated that LPS concentration was increased by a meal rich in saturated fatty acids (SFA), while decreased after a meal rich in n-3 polyunsaturated fatty acids (n-3 PUFA).
  • this effect seems to be due to the fact that some SFA (e.g., lauric and mystiric acids) are part of the lipid-A component of LPS and also to n-3 PUFA's role on reducing LPS potency when substituting SFA in lipid-A
  • these experimental results suggest a pivotal role of CD14-mediated TLR4 activation in the development of LPS-mediated nutritional changes.
  • This suggests a link between gut microbiota, western diet, and obesity and indicates that gut microbiota manipulation can beneficially affect the host's weight and adiposity.
  • endotoxemia was independently associated with energy intake but not fat intake in a multivariate analysis
  • in vitro that endotoxemia activates pro-inflammatory cytokine/chemokine production via NFκB and MAPK signaling in preadipocytes and decreased peroxisome proliferator-activated receptor γ activity and insulin responsiveness in adipocytes.
  • T2DM patients have mean values of LPS that are 76% higher than healthy controls
  • LPS-induced release of glucagon, GH and cortisol, which inhibit glucose uptake, both peripheral and hepatic
  • LPSs also seem to induce ROS-mediated apoptosis in pancreatic cells
  • Recent evidence has been linking ME with dyslipidemia, increased intrahepatic triglycerides, development, and progression of alcoholic and nonalcoholic fatty liver disease
  • The hepatocytes, rather than hepatic macrophages, are the cells responsible for its clearance, being ultimately excreted in bile
  • All the subclasses of plasma lipoproteins can bind and neutralize the toxic effects of LPS, both in vitro (Eichbaum et al. 1991) and in vivo (Harris et al. 1990), and this phenomenon seems to be dependent on the number of phospholipids in the lipoprotein surface (Levels et al. 2001). LDL seems to be involved in LPS clearance, but this antiatherogenic effect is outweighed by its proatherogenic features
  • LPS produces hypertriglyceridemia by several mechanisms, depending on LPS concentration. In animal models, low-dose LPS increases hepatic lipoprotein (such as VLDL) synthesis, whereas high-dose LPS decreases lipoprotein catabolism
  • When a dose of LPS similar to that observed in ME was infused in humans, a 2.5-fold increase in endothelial lipase was observed, with consequent reduction in total and HDL. This mechanism may explain low HDL levels in ‘ME’ and other inflammatory conditions such as obesity and metabolic syndrome
  • It is known that the high-fat diet and the ‘ME’ increase intrahepatic triglyceride accumulation, thus synergistically contributing to the development and progression of alcoholic and NAFLD, from the initial stages characterized by intrahepatic triglyceride accumulation up to chronic inflammation (nonalcoholic steatohepatitis), fibrosis, and cirrhosis
  • On the other hand, LPS activates Kupffer cells leading to an increased production of ROS and pro-inflammatory cytokines like TNFα
  • high-fat diet mice presented with ME, which positively and significantly correlated with plasminogen activator inhibitor (PAI-1), IL1, TNFα, STAMP2, NADPHox, MCP-1, and F4/80 (a specific marker of mature macrophages) mRNAs
  • prebiotic administration reduces intestinal permeability to LPS in obese mice and is associated with decreased systemic inflammation when compared with controls
  • Cani et al. also found that high-fat diet mice presented with not only ME but also higher levels of inflammatory markers, oxidative stress, and macrophage infiltration markers
  • This suggests that important links between gut microbiota, ME, inflammation, and oxidative stress are implicated in a high-fat diet situation
  • high-fat feeding is associated with adipose tissue macrophage infiltration (F4/80-positive cells) and increased levels of chemokine MCP-1, suggesting a strong link between ME, proinflammatory status, oxidative stress, and, lately, increased CV risk
  • LPS has been shown to promote atherosclerosis
  • markers of systemic inflammation such as circulating bacterial endotoxin were elevated in patients with chronic infections and were strong predictors of increased atherosclerotic risk
  • As a TLR4 ligand, LPS has been suggested to induce atherosclerosis development and progression, via a TLR4-mediated inflammatory state.
  • Nathan Goodyear on 04 Aug 14
     
    Very nice updated review on Metabolic endotoxemia
Nathan Goodyear

Dietary glycemic index and glycemic load and breast cancer risk in the European Prospec... - 0 views

www.ajcn.org/...ajcn.111.026724.abstract

dietary glycemic index nutrition breast cancer breast cancer women postmenopausal carbohydrates high ER PR

shared by Nathan Goodyear on 11 Jul 12 - No Cached
  • Nathan Goodyear on 11 Jul 12
     
    high carbohydrate intake associated with increased risk of ER/PR negative breast cancer in Postmenopausal women.
Nathan Goodyear

The role of dietary fat in peripheral thyroid hor... [Metabolism. 1980] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...7421583

diet fat carbohydrates T3 reverse T3 metabolism HF high fat

shared by Nathan Goodyear on 16 Aug 14 - No Cached
  • Nathan Goodyear on 16 Aug 14
     
    High fat diet in this small animal study finds an increase in reverse T3 and a decrease in T3.  Higher carbohydrate diet provided no significant change.
Nathan Goodyear

PCRM | Analysis of Health Problems Associated with High-Protein, High-Fat, Carbohydrate... - 0 views

www.pcrm.org/...-problems-associated-with-high

protein diet fat obesity overweight weight loss

shared by Nathan Goodyear on 07 Aug 13 - No Cached
  • Nathan Goodyear on 07 Aug 13
     
    nice review of some of the problems associated with a high fat ,high protein diet.  These effects are seen in those utilizing long term dietary patterns of high protein and high fat intake.  
Nathan Goodyear

A High-Protein Breakfast Induces Greater Insulin and Glucose-Dependent Insulinotropic P... - 0 views

jn.nutrition.org/...452

protein diabetes breakfast diet nutrition glucose

shared by Nathan Goodyear on 04 May 15 - No Cached
  • Nathan Goodyear on 04 May 15
     
    Study finds a high protein breakfast blunts and better controls glucose levels throughout the day when compared to a high carbohydrate breakfast.  The impact was seen, not just following breakfast, but at the following meal as well.
Nathan Goodyear

High-protein and high-carbohydrate breakfasts differentially change the transcriptome o... - 0 views

ajcn.nutrition.org/...1233.full

diet nutrition high protein high carbohydrate

shared by Nathan Goodyear on 20 Jan 13 - No Cached
  • Nathan Goodyear on 20 Jan 13
     
    Diet effects genetic expression, which effects the metabolic rate and satiety.
Nathan Goodyear

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

www.metabolismjournal.com/...fulltext

ketogenic diet carbohydrates fats endurance athletes endurance exercise endurance sports exercise

shared by Nathan Goodyear on 20 Apr 16 - No Cached
  • Nathan Goodyear on 20 Apr 16
     
    full study of previous abstract: low carb and high fat diet found to maintain muscle glycogen equal to high carb diet in endurance athletes.  Endurance athletes have high fat oxidation and this probably only applies to these endurance athletes; I would suspect this high fat oxidation would not be found in other short interval sports i.e. sprinting, football....
Nathan Goodyear

Diet-hormone interactions: Protein/carbohydrate ratio alters reciprocally the plasma le... - 0 views

www.sciencedirect.com/...0024320587900865

nutrition diet carbohydrates fiber protein Testosterone men hormones male hormones cortisol

shared by Nathan Goodyear on 21 Sep 16 - No Cached
  • Nathan Goodyear on 21 Sep 16
     
    small study, but complex carbs found to increase Testosterone more than high protein diet.  That goes against most marketing.  In contrast, cortisol was the opposite.
Nathan Goodyear

Carbohydrates and fat for training and recovery. - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...14971430

carbohydrates fat training recovery exercise recovery athlete athletes

shared by Nathan Goodyear on 10 Feb 16 - No Cached
  • Nathan Goodyear on 10 Feb 16
     
    only abstract available here.  Carbs, particularly high glycemic cars are helpful in recovery.  Carbs in the recovery are ket to restoration of muscle glycogen.  Immediate supplementation aids glycogen restorations compared to > 2 hours.  At 24 hours, there is no difference between early < 2h and delayed >2h; peak glycogen occurs at 24 h in this study.
Nathan Goodyear

Short-term recovery from prolonged exercise: exploring the potential for protein ingest... - 0 views

opus.bath.ac.uk/21471

training exercise exercise recovery recovery athlete athletes carbohydrates protein

shared by Nathan Goodyear on 10 Feb 16 - No Cached
  • Nathan Goodyear on 10 Feb 16
     
    only abstract available here. early high glycemic carbs benefit fast glycogen restoration.  Adding protein at 0.3 g/kg aids glycogen restoration.
Nathan Goodyear

The Addition of Beta-hydroxy-beta-methylbutyrate and Isomaltulose to Whey Protein Impro... - 0 views

www.tandfonline.com/...07315724.2014.938790

whey protein resistance training exercise exercise recovery

shared by Nathan Goodyear on 20 Oct 15 - No Cached
  • Nathan Goodyear on 20 Oct 15
     
    Whey protein is beneficial as supplementation for resistance training recovery. This study found the addition of a leucine metabolite, beta-hydroxy-beta-methylbutyrate, and the carbohydrate Isomaltulose before, during, and after high intensity exercise further augmented recovery.
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.  
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
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