Relationship between bread consumption, body weight, and abdominal fat distribution: evidence from epidemiological studies Inmaculada Bautista-Castaño and Lluis Serra-Majem Nutrition Reviews Vol. 70(4):218–233
A long-standing belief held by the general public is that bread fattens. This encourages many people to restrict, or even eliminate, bread from their diet. The present review was conducted to assess whether or not eating patterns that include bread are associated with overall obesity or excess abdominal adiposity, whether in the general population or in subjects undergoing obesity management. The literature search included articles published over the past 30 years that focused on dietary patterns that included bread (refined or whole-grain) and their association with ponderal status and abdominal fat distribution. A total of 38 epidemiological studies fulfilled the inclusion criteria (22 cross-sectional, 11 prospective cohort, and five intervention). The results indicate that dietary patterns that include whole-grain bread do not positively influence weight gain and may be beneficial to ponderal status. With respect to dietary patterns that include refined bread, the majority of cross-sectional studies indicate beneficial effects, while most of the well-designed cohort studies demonstrate a possible relationship with excess abdominal fat. Because differences in the study designs make it difficult to form definitive conclusions, more studies are needed that focus specifically on bread consumption, within different dietary patterns, and its influence on ponderal status.
Dairy foods comprise a range of products with varying nutritional content. The intake of dairy products (DPs) has been shown to have beneficial effects on body weight and body fat. This study aimed to examine the independent association between DP intake, body mass index (BMI), and percentage body fat (%BF) in adolescents. A cross-sectional, school-based study was conducted with 1,001 adolescents (418 boys), ages 15–18 years, from the Azorean Archipelago, Portugal. Anthropometric measurements were recorded (weight and height), and %BF was assessed using bioelectric impedance analysis. Adolescent food intake was measured using a self-administered, semiquantitative food frequency questionnaire. Data were analyzed separately for girls and boys, and separate multiple linear regression analysis was used to estimate the association between total DP, milk, yogurt, and cheese intake, BMI, and %BF, adjusting for potential confounders. For boys and girls, respectively, total DP consumption was 2.6 ± 1.9 and 2.9 ± 2.5 servings/day (P = 0.004), while milk consumption was 1.7 ± 1.4 and 2.0 ± 1.7 servings/day (P = 0.001), yogurt consumption was 0.5 ± 0.6 and 0.4 ± 0.7 servings/day (P = 0.247), and cheese consumption was 0.4 ± 0.6 and 0.5 ± 0.8 servings/day (P = 0.081). After adjusting for age, birth weight, energy intake, protein, total fat, sugar, dietary fiber, total calcium intake, low-energy reporters, parental education, pubertal stage, and physical activity, only milk intake was negatively associated with BMI and %BF in girls (respectively, girls: β = −0.167, P = 0.013; boys: β = −0.019, P = 0.824 and girls: β = −0.143, P = 0.030; boys: β = −0.051, P = 0.548). Conclusion: We found an inverse association between milk intake and both BMI and %BF only in girls.
We have reported that the acute post-exercise increases in muscle protein synthesis rates, with differing nutritional support, are predictive of longer-term training-induced muscle hypertrophy. Here, we aimed to test whether the same was true with acute exercise-mediated changes in muscle protein synthesis. Eighteen men (21±1 yr, 22.6±2.1 kg•m(-2) means±SE) had their legs randomly assigned to two of three training conditions that differed in contraction intensity (% of maximal strength [1RM]) or contraction volume (1 or 3 sets of repetitions): 30%-3, 80%-1 and, 80%-3. Subjects trained each leg with their assigned regime for a period of 10wk, 3 times/wk. We made pre- and post-training measures of strength, muscle volume by magnetic resonance (MR) scans, as well as pre- and post-training biopsies of the vastus lateralis, and a single post-exercise (1h) biopsy following the first bout of exercise, to measure signalling proteins. Training-induced increases in MR-measured muscle volume were significant (P<0.01), with no difference between groups: 30%-3 = 6.8±1.8%, 80%-1 = 3.2±0.8%, and 80%-3= 7.2±1.9%, P=0.18. Isotonic maximal strength gains were not different between 80%-1 and 80%-3, but were greater than 30% -3 (P=0.04), whereas training-induced isometric strength gains were significant but not different between conditions (P =0.92). Biopsies taken 1h following the initial resistance exercise bout showed increased phosphorylation (P<0.05) of p70S6K only in the 80%-1 and 80%-3 conditions. There was no correlation between phosphorylation of any signalling protein and hypertrophy. In accordance with our previous acute measurements of muscle protein synthetic rates a lower load lifted to failure resulted in similar hypertrophy as a heavy load lifted to failure.
Bigger weights may not beget bigger muscles: evidence from acute muscle protein synthetic responses after resistance exercise.
It is often recommended that heavier training intensities (∼70%-80% of maximal strength) be lifted to maximize muscle growth. However, we have reported that intensities as low as 30% of maximum strength, when lifted to volitional fatigue, are equally effective at stimulating muscle protein synthesis rates during resistance exercise recovery. This paper discusses the idea that high-intensity contractions are not the exclusive driver of resistance exercise-induced changes in muscle protein synthesis rates.
Supplementation of a suboptimal protein dose with leucine or essential amino acids: effects on myofibrillar protein synthesis at rest and following resistance exercise in men. J Physiol. 2012 Mar 25. [Epub ahead of print] Churchward-Venne TA, Burd NA, Mitchell CJ, West DW, Philp A, Marcotte GR, Baker SK, Baar K, Phillips SM. Leucine is a nutrient regulator of muscle protein synthesis by activating mTOR and possibly other proteins in this pathway. The purpose of this study was to examine the role of leucine in the regulation of human myofibrillar protein synthesis (MPS). Twenty-four males completed an acute bout of unilateral resistance exercise prior to consuming either: a dose (25 g) of whey protein (WHEY); 6.25 g whey protein with total leucine equivalent to WHEY (LEU); or 6.25 g whey protein with total essential amino acids (EAA) equivalent to WHEY for all EAA except leucine (EAA-LEU). Measures of MPS, signalling through mTOR, and amino acid transporter (AAT) mRNA abundance were made while fasted (FAST), and following feeding under rested (FED) and post-exercise (EX-FED) conditions. Leucinemia was equivalent between WHEY and LEU and elevated compared to EAA-LEU (P = 0.001). MPS was increased above FAST at 1-3h post-exercise in both FED (P < 0.001) and EX-FED (P < 0.001) conditions with no treatment effect. At 3-5h, only WHEY remained significantly elevated above FAST in EX-FED (WHEY 184% vs. LEU 55% and EAA-LEU 35%; P = 0.036). AAT mRNA abundance was increased above FAST after feeding and exercise with no effect of leucinemia. In summary, a low dose of whey protein supplemented with leucine or all other essential amino acids was as effective as a complete protein (WHEY) in stimulating postprandial MPS; however only WHEY was able to sustain increased rates of MPS post-exercise and may therefore be most suited to increase exercise-induced muscle protein accretion.
Strength Gains: Block Versus Daily Undulating Periodization Weight Training Among Track and Field Athletes International Journal of Sports Physiology and Performance, 2012, 7, 161-169 Keith B. Painter, Gregory G. Haff, Mike W. Ramsey, Jeff McBride, Travis Triplett, William A. Sands, Hugh S. Lamont, Margaret E. Stone, and Michael H. Stone
Recently, the comparison of “periodized” strength training methods has been a focus of both exercise and sport science. Daily undulating periodization (DUP), using daily alterations in repetitions, has been developed and touted as a superior method of training, while block forms of programming for periodization have been questioned. Therefore, the purpose of this study is to compare block to DUP in Division I track and field ath- letes. Thirty-one athletes were assigned to either a 10-wk block or DUP training group in which sex, year, and event were matched. Over the course of the study, there were 4 testing sessions, which were used to evaluate a variety of strength characteristics. Although performance trends favored the block group for strength and rate of force development, no statistically significant differences were found between the 2 training groups. However, statistically different (P ≤ .05) values were found for estimated volume of work (volume load) and the amount of improvement per volume load between block and DUP groups. Based on calculated training efficiency scores, these data indicate that a block training model is more efficient than a DUP model in pro- ducing strength gains.
Beneficial Effects of Resistance Exercise on Glycemic Control Are Not Further Improved by Protein Ingestion. Breen L, Philp A, Shaw CS, Jeukendrup AE, Baar K, et al. (2011) PLoS ONE 6(6): e20613. doi:10.1371/journal.pone.0020613 Purpose: To investigate the mechanisms underpinning modifications in glucose homeostasis and insulin sensitivity 24 h after a bout of resistance exercise (RE) with or without protein ingestion. Methods: Twenty-four healthy males were assigned to a control (CON; n = 8), exercise (EX; n = 8) or exercise plus protein condition (EX+PRO; n = 8). Muscle biopsy and blood samples were obtained at rest for all groups and immediately post-RE (75% 1RM, 8610 repetitions of leg-press and extension exercise) for EX and EX+PRO only. At 24 h post-RE (or post-resting biopsy for CON), a further muscle biopsy was obtained. Participants then consumed an oral glucose load (OGTT) containing 2 g of [U-13C] glucose during an infusion of 6, 6-[2H2] glucose. Blood samples were obtained every 10 min for 2 h to determine glucose kinetics. EX+PRO ingested an additional 25 g of intact whey protein with the OGTT. A final biopsy sample was obtained at the end of the OGTT. Results: Fasted plasma glucose and insulin were similar for all groups and were not different immediately post- and 24 h post-RE. Following RE, muscle glycogen was 2668 and 1966% lower in EX and EX+PRO, respectively. During OGTT, plasma glucose AUC was lower for EX and EX+PRO (75.162.7 and 75.362.8 mmol?L21:120 min, respectively) compared with CON (90.664.1 mmol?L21:120 min). Plasma insulin response was 1362 and 2164% lower for EX and CON, respectively, compared with EX+PRO. Glucose disappearance from the circulation was ,12% greater in EX and EX+PRO compared with CON. Basal 24 h post-RE and insulin-stimulated PAS-AS160/TBC1D4 phosphorylation was greater for EX and EX+PRO. Conclusions: Prior RE improves glycemic control and insulin sensitivity through an increase in the rate at which glucose is disposed from the circulation. However, co-ingesting protein during a high-glucose load does not augment this response at 24 h post-exercise in healthy, insulin-sensitive individuals.
Substrate utilization during submaximal exercise in children with a severely obese parent Nutrition & Metabolism 2012, 9:38 doi:10.1186/1743-7075-9-38 Audrey D Eaves
Abstract Background We have reported a reduction in fatty acid oxidation (FAO) at the whole-body level and in skeletal muscle in severely obese (BMI ≥ 40 kg/m2) individuals; this defect is retained in cell culture suggesting an inherent component. The purpose of the current study was to determine if an impairment in whole-body fatty acid oxidation (FAO) was also evident in children with a severely obese parent. Methods Substrate utilization during submaximal exercise (cycle ergometer) was determined in children ages 8–12 y with a severely obese parent (OP, n = 13) or two lean/non-obese (BMI range of 18 to 28 kg/m2) parents (LP, n = 13). A subgroup of subjects (n = 3/group) performed 4 weeks of exercise training with substrate utilization measured after the intervention. Results The children did not differ in age (LP vs. OP, respectively) (10.7 ± 0.5 vs. 10.2 ± 0.5 y), BMI percentile (65.3 ± 5.2 vs. 75.9 ± 7), Tanner Stage (1.4 ± 0.2 vs. 1.5 ± 0.2), VO2peak (40.3 ± 2.7 vs. 35.6 ± 2.6 ml/kg/min) or physical activity levels (accelerometer). At the same absolute workload of 15 W (~38% VO2peak), RER was significantly (P ≤ 0.05) lower in LP vs. OP (0.83 ± 0.02 vs. 0.87 ± 0.01) which was reflected in a reduced reliance on FAO for energy production in the OP group (58.6 ± 5.1 vs. 43.1 ± 4.0% of energy needs during exercise from FAO). At a higher exercise intensity (~65% VO2peak) there were no differences in substrate utilization between LP and OP. After exercise training RER tended to decrease (P = 0.06) at the 15 W workload, suggesting an increased reliance on FAO regardless of group. Conclusions These findings suggest that the decrement in FAO with severe obesity has an inherent component that may be overcome with exercise training.
Gluteofemoral Adipose Tissue Plays a Major Role in Production of the Lipokine Palmitoleate in Humans. Diabetes. 2012 Apr 9. [Epub ahead of print] Pinnick KE, Neville MJ, Fielding BA, Frayn KN, Karpe F, Hodson L. The expansion of lower-body adipose tissue (AT) is paradoxically associated with reduced cardiovascular disease and diabetes risk. We examined whether the beneficial metabolic properties of lower-body AT are related to the production and release of the insulin-sensitizing lipokine palmitoleate (16:1n-7). Using venoarterial difference sampling, we investigated the relative release of 16:1n-7 from lower-body (gluteofemoral) and upper-body (abdominal subcutaneous) AT depots. Paired gluteofemoral and abdominal subcutaneous AT samples were analyzed for triglyceride fatty acid composition and mRNA expression. Finally, the triglyceride fatty acid composition of isolated human preadipocytes was determined. Relative release of 16:1n-7 was markedly higher from gluteofemoral AT compared with abdominal subcutaneous AT. Stearoyl-CoA desaturase 1 (SCD1), the key enzyme involved in endogenous 16:1n-7 production, was more highly expressed in gluteofemoral AT and was associated with greater enrichment of 16:1n-7. Furthermore, isolated human preadipocytes from gluteofemoral AT displayed a higher content of SCD1-derived fatty acids. We demonstrate that human gluteofemoral AT plays a major role in determining systemic concentrations of the lipokine palmitoleate. Moreover, this appears to be an inherent feature of gluteofemoral AT. We propose that the beneficial metabolic properties of lower-body AT may be partly explained by the intrinsically greater production and release of palmitoleate.
OBJECTIVE: Gluteo-femoral, in contrast to abdominal, fat accumulation appears protective against diabetes and cardiovascular disease. Our objective was to test the hypothesis that this reflects differences in the ability of the two depots to sequester fatty acids, with gluteo-femoral fat acting as a longer-term "sink." RESEARCH DESIGN AND METHODS: A total of 12 healthy volunteers were studied after an overnight fast and after ingestion of a mixed meal. Blood samples were taken from veins draining subcutaneous femoral and abdominal fat and compared with arterialized blood samples. Stable isotope-labeled fatty acids were used to trace specific lipid fractions. In 36 subjects, adipose tissue blood flow in the two depots was monitored with (133)Xe. RESULTS: Blood flow increased in response to the meal in both depots, and these responses were correlated (r(s) = 0.44, P < 0.01). Nonesterified fatty acid (NEFA) release was suppressed after the meal in both depots; it was lower in femoral fat than in abdominal fat (P < 0.01). Plasma triacylglycerol (TG) extraction by femoral fat was also lower than that by abdominal fat (P = 0.05). Isotopic tracers showed that the difference was in chylomicron-TG extraction. VLDL-TG extraction and direct NEFA uptake were similar in the two depots. CONCLUSIONS: Femoral fat shows lower metabolic fluxes than subcutaneous abdominal fat, but differs in its relative preference for extracting fatty acids directly from the plasma NEFA and VLDL-TG pools compared with chylomicron-TG.
Since the 1968 Mexico City Olympics, Kenyan and Ethiopian runners have dominated the middle- and long- distance events in athletics and have exhibited comparable dominance in international cross-country and road- racing competition. Several factors have been proposed to explain the extraordinary success of the Kenyan and Ethiopian distance runners, including (1) genetic predisposition, (2) development of a high maximal oxygen uptake as a result of extensive walking and running at an early age, (3) relatively high hemoglobin and hematocrit, (4) development of good metabolic “economy/efficiency” based on somatotype and lower limb characteristics, (5) favorable skeletal-muscle-fiber composition and oxidative enzyme profile, (6) traditional Kenyan/Ethiopian diet, (7) living and training at altitude, and (8) motivation to achieve economic success. Some of these factors have been examined objectively in the laboratory and field, whereas others have been evaluated from an observational perspective. The purpose of this article is to present the current data relative to factors that potentially contribute to the unprecedented success of Kenyan and Ethiopian distance runners, including recent studies that examined potential links between Kenyan and Ethiopian genotype characteristics and elite running performance. In general, it appears that Kenyan and Ethiopian distance-running success is not based on a unique genetic or physiological characteristic. Rather, it appears to be the result of favorable somatotypical characteristics lending to exceptional biomechanical and metabolic economy/efficiency; chronic exposure to altitude in combination with moderate-volume, high-intensity training (live high + train high), and a strong psychological motivation to succeed
Physical activity and exercise in the regulation of human adipose tissue physiology. Physiol Rev. 2012 Jan;92(1):157-91. doi: 10.1152/physrev.00012.2011. Thompson D, Karpe F, Lafontan M, Frayn K.
Physical activity and exercise are key components of energy expenditure and therefore of energy balance. Changes in energy balance alter fat mass. It is therefore reasonable to ask: What are the links between physical activity and adipose tissue function? There are many complexities. Physical activity is a multifaceted behavior of which exercise is just one component. Physical activity influences adipose tissue both acutely and in the longer term. A single bout of exercise stimulates adipose tissue blood flow and fat mobilization, resulting in delivery of fatty acids to skeletal muscles at a rate well-matched to metabolic requirements, except perhaps in vigorous intensity exercise. The stimuli include adrenergic and other circulating factors. There is a period following an exercise bout when fatty acids are directed away from adipose tissue to other tissues such as skeletal muscle, reducing dietary fat storage in adipose. With chronic exercise (training), there are changes in adipose tissue physiology, particularly an enhanced fat mobilization during acute exercise. It is difficult, however, to distinguish chronic "structural" changes from those associated with the last exercise bout. In addition, it is difficult to distinguish between the effects of training per se and negative energy balance. Epidemiological observations support the idea that physically active people have relatively low fat mass, and intervention studies tend to show that exercise training reduces fat mass. A much-discussed effect of exercise versus calorie restriction in preferentially reducing visceral fat is not borne out by meta-analyses. We conclude that, in addition to the regulation of fat mass, physical activity may contribute to metabolic health through beneficial dynamic changes within adipose tissue in response to each activity bout.
Republished review: Triglycerides and atherogenic dyslipidaemia: extending treatment beyond statins in the high-risk cardiovascular patient. Postgrad Med J. 2011 Nov;87(1033):776-82. Watts GF, Karpe F. Although statins significantly decrease the incidence of cardiovascular disease (CVD), residual CVD risk remains high. This may partly be due to uncorrected atherogenic dyslipidaemia. The driving force behind atherogenic dyslipidaemia is hypertriglyceridaemia, which results from hepatic oversecretion and/or hypocatabolism of triglyceride-rich lipoproteins, and is typical of type 2 diabetes and metabolic syndrome. Persistent atherogenic dyslipidaemia in patients treated with a statin according to low-density lipoprotein-cholesterol goals may be corrected with niacin, fibrates or n-3 fatty acids. Clinical trial evidence to inform best practice is limited, but new data support adding fenofibrate to a statin. A consistent feature of fibrate clinical trials is the specific benefit of these agents in dyslipidaemic patients and the improvement in diabetic retinopathy with fenofibrate. Ongoing clinical trials may provide good evidence for adding niacin to a statin. Low-dose n-3 fatty acids could be used routinely after a myocardial infarction, but the value of higher doses of n-3 fatty acids in reducing CVD risk remains to be demonstrated.
Exercise, appetite and weight management: understanding the compensatory responses in eating behaviour and how they contribute to variability in exercise-induced weight loss Br J Sports Med 2012;46:315-322 doi:10.1136/bjsm.2010.082495 King, NA et al
Does exercise promote weight loss? One of the key problems with studies assessing the efficacy of exercise as a method of weight management and obesityis that mean data are presented and the individual variability in response is overlooked. Recent data have highlighted the need to demonstrate and characterise the individual variability in response to exercise. Do people who exercise compensate for the increase in energy expenditure via compensatory increases in hunger and food intake? The authors address the physiological, psychological and behavioural factors potentially involved in the relationship between exercise and appetite, and identify the research questions that remain unanswered. A negative consequence of the phenomena of individual variability and compensatory responses has been the focus on those who lose little weight in response to exercise; this has been used unreasonably as evidence to suggest that exercise is a futile method of controlling weight and managing obesity. Most of the evidence suggests that exercise is useful for improving body composition and health. For example, when exercise-induced mean weight loss is <1.0 kg, significant improvements in aerobic capacity (+6.3 ml/kg/min), systolic (−6.00 mm Hg) and diastolic (−3.9 mm Hg) blood pressure, waist circumference (−3.7 cm) and positive mood still occur. However, people will vary in their responses to exercise; understanding and characterising this variability will help tailor weight loss strategies to suit individuals.
Why, when and how should hypertriglyceridemia be treated in the high-risk cardiovascular patient? Expert Rev Cardiovasc Ther. 2011 Aug;9(8):987-97. Watts GF, Karpe F. Recent epidemiology attests that hypertriglyceridemia may be a causal risk factor for cardiovascular disease (CVD). The specific atherogenicity of hypertriglyceridemia relates to the accumulation in plasma of triglyceride-rich lipoprotein remnants. Hypertriglyceridemia also drives a 'global' atherogenic dyslipidemic profile, which is frequent in high-risk cardiovascular patients, such as Type 2 diabetics. Elevated triglyceride in fasting or nonfasting blood samples should be a trigger for assessing atherogenic components of the lipid profile, particularly HDL-cholesterol, non-HDL-cholesterol and apoB. Residual risk of CVD remains high in statin-treated diabetic patients owing to persistent atherogenic dyslipidemia, which is not fully corrected by these agents nor by the addition of ezetimibe. Hypertriglyceridemia may then be targeted with niacin, fibrates or n-3 fatty acids, after correcting aggravating factors, especially obesity and hyperglycemia. Fibrates consistently decrease coronary events in dyslipidemic patients in outcome studies. New evidence supports adding fenofibrate to a statin in Type 2 diabetics with residual hypertriglyceridemia and low HDL-cholesterol; extrapolating from a recent meta-analysis, a 15% reduction in triglycerides could translate into a further 15% reduction in coronary events. Ongoing clinical trials may provide new evidence for adding niacin to a statin. The value of higher doses of n-3 fatty acids in reducing CVD risk remains to be demonstrated. The high triglyceride/low HDL nexus is an under-recognized risk factor for CVD that merits more detailed clinical assessment and treatment, particularly in patients with Type 2 diabetes already receiving a statin.