Nutrition & Metabolism - Most accessed articles

Ingesting a pre-workout supplement containing caffeine, B-vitamins, amino acids, creatine, and beta-alanine before exercise delays fatigue while improving reaction time and muscular endurance

Brandon Spradley — 2012-03-30T00:00:00Z

Background: The purpose of this study was to determine the effects of the pre-workout supplement AssaultTM (MusclePharm, Denver, CO, USA) on upper and lower body muscular endurance, aerobic and anaerobic capacity, and choice reaction time in recreationally-trained males. Subjective feelings of energy, fatigue, alertness, and focus were measured to examine associations between psychological factors and human performance. Methods: Twelve recreationally-trained males participated in a 3-week investigation (mean +/ SD, age: 28 +/ 5 y, height: 178 +/ 9 cm, weight: 79.2 +/ 15.7 kg, VO2max: 45.7 +/ 7.6 ml/kg/min). Subjects reported to the human performance laboratory on three separate occasions. All participants completed a baseline/familiarization day of testing that included a maximal graded exercise test for the determination of aerobic capacity (VO2max), one-rep maximum (1-RM) for bench and leg press to determine 75% of 1-RM, choice reaction tests, and intermittent critical velocity familiarization. Choice reaction tests included the following: single-step audio and visual, one-tower stationary protocol, two-tower lateral protocol, three-tower multi-directional protocol, and three-tower multi-directional protocol with martial arts sticks. Subjects were randomly assigned to ingest either the supplement (SUP) or the placebo (PL) during Visit 2. Subjects were provided with the cross-over treatment on the last testing visit. Testing occurred 20 min following ingestion of both treatments. Results: Significant (p < 0.05) main effects for the SUP were observed for leg press (SUP: 13 +/- 6 reps, PL: 11 +/- 3 reps), perceived energy (SUP: 3.4 +/- 0.9, PL: 3.1 +/- 0.8), alertness (SUP: 4.0 +/- 0.7, PL: 3.5 +/-0.8), focus (SUP: 4.1 +/- 0.6, PL: 3.5 +/- 0.8), choice reaction audio single-step (SUP: 0.92 +/- 0.10 s, PL: 0.97 +/- 0.11 s), choice reaction multi-direction 15 s (SUP: 1.07 +/- 0.12 s, PL: 1.13 +/- 0.14 s), and multi-direction for 30 s (SUP: 1.10 +/- 0.11 s, PL: 1.14 +/- 0.13 s). Conclusions: Ingesting the SUP before exercise significantly improved agility choice reaction performance and lower body muscular endurance, while increasing perceived energy and reducing subjective fatigue. These findings suggest that the SUP may delay fatigue during strenuous exercise.

Ketogenic diets and physical performance

Stephen Phinney — 2004-08-17T00:00:00Z

Impaired physical performance is a common but not obligate result of a low carbohydrate diet. Lessons from traditional Inuit culture indicate that time for adaptation, optimized sodium and potassium nutriture, and constraint of protein to 15–25 % of daily energy expenditure allow unimpaired endurance performance despite nutritional ketosis.

Chronic inflammatory diseases are stimulated by current lifestyle: how diet, stress levels and medication prevent our body from recovering

Margarethe Bosma-den Boer — 2012-04-17T00:00:00Z

Serhan and colleagues introduced the term "Resoleomics" in 1996 as the process of inflammation resolution. The major discovery of Serhan's work is that onset to conclusion of an inflammation is a controlled process of the immune system (IS) and not simply the consequence of an extinguished or "exhausted" immune reaction. Resoleomics can be considered as the evolutionary mechanism of restoring homeostatic balances after injury, inflammation and infection. Under normal circumstances, Resoleomics should be able to conclude inflammatory responses. Considering the modern pandemic increase of chronic medical and psychiatric illnesses involving chronic inflammation, it has become apparent that Resoleomics is not fulfilling its potential resolving capacity. We suggest that recent drastic changes in lifestyle, including diet and psycho-emotional stress, are responsible for inflammation and for disturbances in Resoleomics. In addition, current interventions, like chronic use of anti-inflammatory medication, suppress Resoleomics. These new lifestyle factors, including the use of medication, should be considered health hazards, as they are capable of long-term or chronic activation of the central stress axes. The IS is designed to produce solutions for fast, intensive hazards, not to cope with long-term, chronic stimulation. The never-ending stress factors of recent lifestyle changes have pushed the IS and the central stress system into a constant state of activity, leading to chronically unresolved inflammation and increased vulnerability for chronic disease. Our hypothesis is that modern diet, increased psycho-emotional stress and chronic use of anti-inflammatory medication disrupt the natural process of inflammation resolution ie Resoleomics.

Dietary protein intake and renal function

William Martin — 2005-09-20T00:00:00Z

Recent trends in weight loss diets have led to a substantial increase in protein intake by individuals. As a result, the safety of habitually consuming dietary protein in excess of recommended intakes has been questioned. In particular, there is concern that high protein intake may promote renal damage by chronically increasing glomerular pressure and hyperfiltration. There is, however, a serious question as to whether there is significant evidence to support this relationship in healthy individuals. In fact, some studies suggest that hyperfiltration, the purported mechanism for renal damage, is a normal adaptative mechanism that occurs in response to several physiological conditions. This paper reviews the available evidence that increased dietary protein intake is a health concern in terms of the potential to initiate or promote renal disease. While protein restriction may be appropriate for treatment of existing kidney disease, we find no significant evidence for a detrimental effect of high protein intakes on kidney function in healthy persons after centuries of a high protein Western diet.

A low-carbohydrate, ketogenic diet to treat type 2 diabetes

William Yancy — 2005-12-01T00:00:00Z

Background: The low-carbohydrate, ketogenic diet (LCKD) may be effective for improving glycemia and reducing medications in patients with type 2 diabetes. Methods: From an outpatient clinic, we recruited 28 overweight participants with type 2 diabetes for a 16-week single-arm pilot diet intervention trial. We provided LCKD counseling, with an initial goal of <20 g carbohydrate/day, while reducing diabetes medication dosages at diet initiation. Participants returned every other week for measurements, counseling, and further medication adjustment. The primary outcome was hemoglobin A1c. Results: Twenty-one of the 28 participants who were enrolled completed the study. Twenty participants were men; 13 were White, 8 were African-American. The mean [± SD] age was 56.0 ± 7.9 years and BMI was 42.2 ± 5.8 kg/m2. Hemoglobin A1c decreased by 16% from 7.5 ± 1.4% to 6.3 ± 1.0% (p < 0.001) from baseline to week 16. Diabetes medications were discontinued in 7 participants, reduced in 10 participants, and unchanged in 4 participants. The mean body weight decreased by 6.6% from 131.4 ± 18.3 kg to 122.7 ± 18.9 kg (p < 0.001). In linear regression analyses, weight change at 16 weeks did not predict change in hemoglobin A1c. Fasting serum triglyceride decreased 42% from 2.69 ± 2.87 mmol/L to 1.57 ± 1.38 mmol/L (p = 0.001) while other serum lipid measurements did not change significantly. Conclusion: The LCKD improved glycemic control in patients with type 2 diabetes such that diabetes medications were discontinued or reduced in most participants. Because the LCKD can be very effective at lowering blood glucose, patients on diabetes medication who use this diet should be under close medical supervision or capable of adjusting their medication.

Fructose, insulin resistance, and metabolic dyslipidemia

Heather Basciano — 2005-02-21T00:00:00Z

Obesity and type 2 diabetes are occurring at epidemic rates in the United States and many parts of the world. The "obesity epidemic" appears to have emerged largely from changes in our diet and reduced physical activity. An important but not well-appreciated dietary change has been the substantial increase in the amount of dietary fructose consumption from high intake of sucrose and high fructose corn syrup, a common sweetener used in the food industry. A high flux of fructose to the liver, the main organ capable of metabolizing this simple carbohydrate, perturbs glucose metabolism and glucose uptake pathways, and leads to a significantly enhanced rate of de novo lipogenesis and triglyceride (TG) synthesis, driven by the high flux of glycerol and acyl portions of TG molecules from fructose catabolism. These metabolic disturbances appear to underlie the induction of insulin resistance commonly observed with high fructose feeding in both humans and animal models. Fructose-induced insulin resistant states are commonly characterized by a profound metabolic dyslipidemia, which appears to result from hepatic and intestinal overproduction of atherogenic lipoprotein particles. Thus, emerging evidence from recent epidemiological and biochemical studies clearly suggests that the high dietary intake of fructose has rapidly become an important causative factor in the development of the metabolic syndrome. There is an urgent need for increased public awareness of the risks associated with high fructose consumption and greater efforts should be made to curb the supplementation of packaged foods with high fructose additives. The present review will discuss the trends in fructose consumption, the metabolic consequences of increased fructose intake, and the molecular mechanisms leading to fructose-induced lipogenesis, insulin resistance and metabolic dyslipidemia.

The potential role of the antioxidant and detoxification properties of glutathione in autism spectrum disorders: a systematic review and meta-analysis

Penelope Main — 2012-04-24T00:00:00Z

Background: Glutathione has a wide range of functions; it is an endogenous anti-oxidant and plays a key role in the maintenance of intracellular redox balance and detoxification of xenobiotics. Several studies have indicated that children with autism spectrum disorders may have altered glutathione metabolism which could play a key role in the condition. Methods: A systematic literature review and meta-analysis was conducted of studies examining metabolites, interventions and/or genes of the glutathione metabolism pathways i.e. the gamma-glutamyl cycle and trans-sulphuration pathway in autism spectrum disorders. Results: Thirty nine studies were included in the review comprising an in vitro study, thirty two metabolite and/or co-factor studies, six intervention studies and six studies with genetic data as well as eight studies examining enzyme activity. Conclusions: The review found evidence for the involvement of the gamma-glutamyl cycle and trans-sulphuration pathway in autistic disorder is sufficiently consistent, particularly with respect to the glutathione redox ratio, to warrant further investigation to determine the significance in relation to clinical outcomes. Large, well designed intervention studies that link metabolites, cofactors and genes of the gamma-glutamyl cycle and trans-sulphuration pathway with objective behavioural outcomes in children with autism spectrum disorders are required. Future risk factor analysis should include consideration of multiple nutritional status and metabolite biomarkers of pathways linked with the gamma-glutamyl cycle and the interaction of genotype in relation to these factors.

Exploring metabolic dysfunction in chronic kidney disease

Adrian Slee — 2012-04-26T00:00:00Z

Impaired kidney function and chronic kidney disease (CKD) leading to kidney failure andend-stage renal disease (ESRD) is a serious medical condition associated with increasedmorbidity, mortality, and in particular cardiovascular disease (CVD) risk. CKD is associatedwith multiple physiological and metabolic disturbances, including hypertension, dyslipidemiaand the anorexia-cachexia syndrome which are linked to poor outcomes. Specific hormonal,inflammatory, and nutritional-metabolic factors may play key roles in CKD development andpathogenesis. These include raised proinflammatory cytokines, such as interleukin-1 and 6,tumor necrosis factor, altered hepatic acute phase proteins, including reduced albumin,increased C-reactive protein, and perturbations in normal anabolic hormone responses withreduced growth hormone-insulin-like growth factor-1 axis activity. Others includehyperactivation of the renin-angiotensin aldosterone system (RAAS), with angiotensin II andaldosterone implicated in hypertension and the promotion of insulin resistance, andsubsequent pharmacological blockade shown to improve blood pressure, metabolic controland offer reno-protective effects. Abnormal adipocytokine levels including leptin andadiponectin may further promote the insulin resistant, and proinflammatory state in CKD.Ghrelin may be also implicated and controversial studies suggest activities may be reduced inhuman CKD, and may provide a rationale for administration of acyl-ghrelin. Poor vitamin Dstatus has also been associated with patient outcome and CVD risk and may indicate a rolefor supplementation. Glucocorticoid activities traditionally known for their involvement inthe pathogenesis of a number of disease states are increased and may be implicated in CKDassociatedhypertension, insulin resistance, diabetes risk and cachexia, both directly andindirectly through effects on other systems including activation of the mineralcorticoidreceptor. Insight into the multiple factors altered in CKD may provide useful information ondisease pathogenesis, clinical assessment and treatment rationale such as potentialpharmacological, nutritional and exercise therapies.

Effects of beta-hydroxy-beta-methylbutyrate (HMB) on exercise performance and body composition across varying levels of age, sex, and training experience: A review

Gabriel Wilson — 2008-01-03T00:00:00Z

The leucine metabolite beta-hydroxy-beta-methylbutyrate (HMB) has been extensively used as an ergogenic aid; particularly among bodybuilders and strength/power athletes, who use it to promote exercise performance and skeletal muscle hypertrophy. While numerous studies have supported the efficacy of HMB in exercise and clinical conditions, there have been a number of conflicting results. Therefore, the first purpose of this paper will be to provide an in depth and objective analysis of HMB research. Special care is taken to present critical details of each study in an attempt to both examine the effectiveness of HMB as well as explain possible reasons for conflicting results seen in the literature. Within this analysis, moderator variables such as age, training experience, various states of muscle catabolism, and optimal dosages of HMB are discussed. The validity of dependent measurements, clustering of data, and a conflict of interest bias will also be analyzed. A second purpose of this paper is to provide a comprehensive discussion on possible mechanisms, which HMB may operate through. Currently, the most readily discussed mechanism has been attributed to HMB as a precursor to the rate limiting enzyme to cholesterol synthesis HMG-coenzyme A reductase. However, an increase in research has been directed towards possible proteolytic pathways HMB may operate through. Evidence from cachectic cancer studies suggests that HMB may inhibit the ubiquitin-proteasome proteolytic pathway responsible for the specific degradation of intracellular proteins. HMB may also directly stimulate protein synthesis, through an mTOR dependent mechanism. Finally, special care has been taken to provide future research implications.

Diet induced thermogenesis

Klaas Westerterp — 2004-08-18T00:00:00Z

ObjectiveDaily energy expenditure consists of three components: basal metabolic rate, diet-induced thermogenesis and the energy cost of physical activity. Here, data on diet-induced thermogenesis are reviewed in relation to measuring conditions and characteristics of the diet. Methods: Measuring conditions include nutritional status of the subject, physical activity and duration of the observation. Diet characteristics are energy content and macronutrient composition. Results: Most studies measure diet-induced thermogenesis as the increase in energy expenditure above basal metabolic rate. Generally, the hierarchy in macronutrient oxidation in the postprandial state is reflected similarly in diet-induced thermogenesis, with the sequence alcohol, protein, carbohydrate, and fat. A mixed diet consumed at energy balance results in a diet induced energy expenditure of 5 to 15 % of daily energy expenditure. Values are higher at a relatively high protein and alcohol consumption and lower at a high fat consumption. Protein induced thermogenesis has an important effect on satiety.In conclusion, the main determinants of diet-induced thermogenesis are the energy content and the protein- and alcohol fraction of the diet. Protein plays a key role in body weight regulation through satiety related to diet-induced thermogenesis.