Overconsumption of fructose, particularly in the form of soft drinks, is increasingly recognized as a public health concern. The acute cardiovascular responses to ingesting fructose have not, however, been well-studied in humans. In this randomized crossover study, we compared cardiovascular autonomic regulation after ingesting water and drinks containing either glucose or fructose in 15 healthy volunteers (aged 21-33 yr). The total volume of each drink was 500 ml, and the sugar content 60 g. For 30 min before and 2 h after each drink, we recorded beat-to-beat heart rate, arterial blood pressure, and cardiac output. Energy expenditure was determined on a minute-by-minute basis. Ingesting the fructose drink significantly increased blood pressure, heart rate, and cardiac output but not total peripheral resistance. Glucose ingestion resulted in a significantly greater increase in cardiac output than fructose but no change in blood pressure and a concomitant decrease in total peripheral resistance. Ingesting glucose and fructose, but not water, significantly increased blood pressure variability and decreased cardiovagal baroreflex sensitivity. Energy expenditure increased by a similar amount after glucose and fructose ingestion, but fructose elicited a significantly greater increase in respiratory quotient. These results show that ingestion of glucose and fructose drinks is characterized by specific hemodynamic responses. In particular, fructose ingestion elicits an increase in blood pressure that is probably mediated by an increase in cardiac output without compensatory peripheral vasodilatation.

PurposeEnergy drinks are beverages containing vasoactive metabolites, usually a combination of caffeine, taurine, glucuronolactone and sugars. There are concerns about the safety of energy drinks with some countries banning their sales. We determined the acute effects of a popular energy drink, Red Bull, on cardiovascular and hemodynamic variables, cerebrovascular parameters and microvascular endothelial function.MethodsTwenty-five young non-obese and healthy subjects attended two experimental sessions on separate days according to a randomized crossover study design. During each session, primary measurements included beat-to-beat blood pressure measurements, impedance cardiography and transcranial Doppler measurements for at least 20 min baseline and for 2 h following the ingestion of either 355 mL of the energy drink or 355 mL of tap water; the endothelial function test was performed before and two hours after either drink.ResultsUnlike the water control load, Red Bull consumption led to increases in both systolic and diastolic blood pressure (p < 0.005), associated with increased heart rate and cardiac output (p < 0.05), with no significant changes in total peripheral resistance and without diminished endothelial response to acetylcholine; consequently, double product (reflecting myocardial load) was increased (p < 0.005). Red Bull consumption also led to increases in cerebrovascular resistance and breathing frequency (p < 0.005), as well as to decreases in cerebral blood flow velocity (p < 0.005) and end-tidal carbon dioxide (p < 0.005).ConclusionOur results show an overall negative hemodynamic profile in response to ingestion of the energy drink Red Bull, in particular an elevated blood pressure and double product and a lower cerebral blood flow velocity.

The present study investigates whether excessive fat accumulation and hyperinsulinaemia during catch-up growth on high-fat diets are altered by n-6 and n-3 PUFA derived from oils rich in either linoleic acid (LA), a-linolenic acid (ALA), arachidonic acid (AA) or DHA. It has been shown that, compared with food-restricted rats refed a high-fat (lard) diet low in PUFA, those refed isoenergetically on diets enriched in LA or ALA, independently of the n-6:n-3 ratio, show improved insulin sensitivity, lower fat mass and higher lean mass, the magnitude of which is related to the proportion of total PUFA precursors (LA þ ALA) consumed. These relationships are best fitted by quadratic regression models (r 2 . 0·8, P,0·001), with threshold values for an impact on body composition corresponding to PUFA precursors contributing 25-30 % of energy intake. Isoenergetic refeeding on high-fat diets enriched in AA or DHA also led to improved body composition, with increases in lean mass as predicted by the quadratic model for PUFA precursors, but decreases in fat mass, which are disproportionately greater than predicted values; insulin sensitivity, however, was not improved. These findings pertaining to the impact of dietary intake of PUFA precursors (LA and ALA) and their elongated -desaturated products (AA and DHA), on body composition and insulin sensitivity, provide important insights into the search for diets aimed at counteracting the pathophysiological consequences of catch-up growth. In particular, diets enriched in essential fatty acids (LA and/or ALA) markedly improve insulin sensitivity and composition of weight regained, independently of the n-6:n-3 fatty acid ratio.Key words: Obesity: Thermogenesis: Programming and insulin sensitivity: Weight regain It has long been known from studies of nutritional rehabilitation in malnourished humans and other mammals that the recovery of body fat occurs at a disproportionately faster rate than that of lean tissue deposition (1,2) , independently of the level of dietary energy or protein supplementation (1,3,4) . This phenomenon of preferential catch-up fat, with lean tissue recovery lagging, has been demonstrated not only during weight recovery in adults who have lost weight in response to poverty and famine-related malnutrition (1 -4) , anorexia nervosa (5) and disease-related cachexia (6 -8) , but also during nutritional rehabilitation of undernourished children (9 -12) and in young adolescents recovering from anorexia nervosa (13,14) . In more recent years, there has also been a resurgence of interest into this phenomenon of preferential catch-up fat in infants and younger children, primarily because its occurrence concomitant to hyperinsulinaemia during catch-up growth (15 -19) is viewed to be of central importance in the mechanisms by which catch-up growth predisposes to obesity, type 2 diabetes and CVD later in life (20 -22) . Consequently, approaches that redirect nutrient partitioning from preferential catch-up fat to enhanced lean tissue accretion are of pote...

We have investigated whether altered hepatic mitochondrial energetics could explain the differential effects of high‐fat diets with low or high ω6 polyunsaturated fatty acid content (lard vs. safflower oil) on the efficiency of body fat recovery (catch‐up fat) during refeeding after caloric restriction. After 2 weeks of caloric restriction, rats were isocalorically refed with a low‐fat diet (LF) or high‐fat diets made from either lard or safflower oil for 1 week, and energy balance and body composition changes were assessed. Hepatic mitochondrial energetics were determined from measurements of liver mitochondrial mass, respiratory capacities, and proton leak. Compared to rats refed the LF, the groups refed high‐fat diets showed lower energy expenditure and increased efficiency of fat gain; these differences were less marked with high‐safflower oil than with high‐lard diet. The increase in efficiency of catch‐up fat by the high‐fat diets could not be attributed to differences in liver mitochondrial activity. By contrast, the lower fat gain with high‐safflower oil than with high‐lard diet is accompanied by higher mitochondrial proton leak and increased proportion of arachidonic acid in mitochondrial membranes. In conclusion, the higher efficiency for catch‐up fat on high‐lard diet than on LF cannot be explained by altered hepatic mitochondrial energetics. By contrast, the ability of the high‐safflower oil diet to produce a less pronounced increase in the efficiency of catch‐up fat may partly reside in increased incorporation of arachidonic acid in hepatic mitochondrial membranes, leading to enhanced proton leak and mitochondrial uncoupling.

Limitations of current methods: The assessment of human variability in various compartments of daily energy expenditure (EE) under standardized conditions is well defined at rest [as basal metabolic rate (BMR) and thermic effect of feeding (TEF)], and currently under validation for assessing the energy cost of low-intensity dynamic work. However, because physical activities of daily life consist of a combination of both dynamic and isometric work, there is also a need to develop standardized tests for assessing human variability in the energy cost of low-intensity isometric work.Experimental objectives: Development of an approach to study human variability in isometric thermogenesis by incorporating a protocol of intermittent leg press exercise of varying low-intensity isometric loads with measurements of EE by indirect calorimetry.Results: EE was measured in the seated position with the subject at rest or while intermittently pressing both legs against a press-platform at 5 low-intensity isometric loads (+5, +10, +15, +20, and +25 kg force), each consisting of a succession of 8 cycles of press (30 s) and rest (30 s). EE, integrated over each 8-min period of the intermittent leg press exercise, was found to increase linearly across the 5 isometric loads with a correlation coefficient (r) > 0.9 for each individual. The slope of this EE-Load relationship, which provides the energy cost of this standardized isometric exercise expressed per kg force applied intermittently (30 s in every min), was found to show good repeatability when assessed in subjects who repeated the same experimental protocol on 3 separate days: its low intra-individual coefficient of variation (CV) of ~ 10% contrasted with its much higher inter-individual CV of 35%; the latter being mass-independent but partly explained by height.Conclusion: This standardized approach to study isometric thermogenesis opens up a new avenue for research in EE phenotyping and metabolic predisposition to obesity.