Thursday, 22 December 2011

40 Things You Should Know – The Science (part 4)

Point 26

Greater weight loss and hormonal changes after 6 months diet with carbohydrates eaten mostly at dinner.


This study was designed to investigate the effect of a low-calorie diet with carbohydrates eaten mostly at dinner on anthropometric, hunger/satiety, biochemical, and inflammatory parameters. Hormonal secretions were also evaluated. Seventy-eight police officers (BMI >30) were randomly assigned to experimental (carbohydrates eaten mostly at dinner) or control weight loss diets for 6 months. On day 0, 7, 90, and 180 blood samples and hunger scores were collected every 4 h from 0800 to 2000 hours. Anthropometric measurements were collected throughout the study. Greater weight loss, abdominal circumference, and body fat mass reductions were observed in the experimental diet in comparison to controls. Hunger scores were lower and greater improvements in fasting glucose, average daily insulin concentrations, and homeostasis model assessment for insulin resistance (HOMA(IR)), T-cholesterol, low-density lipoprotein (LDL) cholesterol, high-density lipoprotein (HDL) cholesterol, C-reactive protein (CRP), tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) levels were observed in comparison to controls. The experimental diet modified daily leptin and adiponectin concentrations compared to those observed at baseline and to a control diet. A simple dietary manipulation of carbohydrate distribution appears to have additional benefits when compared to a conventional weight loss diet in individuals suffering from obesity. It might also be beneficial for individuals suffering from insulin resistance and the metabolic syndrome. Further research is required to confirm and clarify the mechanisms by which this relatively simple diet approach enhances satiety, leads to better anthropometric outcomes, and achieves improved metabolic response, compared to a more conventional dietary approach.

Point 27

Reduced glycemic index and glycemic load diets do not increase the effects of energy restriction on weight loss and insulin sensitivity in obese men and women.


Reducing the dietary glycemic load and the glycemic index was proposed as a novel approach to weight reduction. A parallel-design, randomized 12-wk controlled feeding trial with a 24-wk follow-up phase was conducted to test the hypothesis that a hypocaloric diet designed to reduce the glycemic load and the glycemic index would result in greater sustained weight loss than other hypocaloric diets. Obese subjects (n = 29) were randomly assigned to 1 of 3 diets providing 3138 kJ less than estimated energy needs: high glycemic index (HGI), low glycemic index (LGI), or high fat (HF). For the first 12 wk, all food was provided to subjects (feeding phase). Subjects (n = 22) were instructed to follow the assigned diet for 24 additional weeks (free-living phase). Total body weight was obtained and body composition was assessed by skinfold measurements. Insulin sensitivity was assessed by the homeostasis model (HOMA). At 12 wk, weight changes from baseline were significant in all groups but not different among groups (-9.3 +/- 1.3 kg for the HGI diet, -9.9 +/- 1.4 kg for the LGI diet, and -8.4 +/- 1.5 kg for the HF diet). All groups improved in insulin sensitivity at the end of the feeding phase of the study. During the free-living phase, all groups maintained their initial weight loss and their improved insulin sensitivity. Weight loss and improved insulin sensitivity scores were independent of diet composition. In summary, lowering the glycemic load and glycemic index of weight reduction diets does not provide any added benefit to energy restriction in promoting weight loss in obese subjects.

Glycaemic index, glycaemic load and exercise performance.


The concept of the glycaemic index (GI) was first introduced in the early 1980s as a method of functionally ranking carbohydrate foods based on their actual postprandial blood glucose response compared with a reference food (either glucose or white bread). Although the GI is a debatable topic among many exercise and health professionals, nutritional recommendations to improve exercise performance and enhance exercise capacity are regularly based on information related to the GI. Studies focusing on the consumption of a pre-exercise GI meal have provided evidence that a benefit exists in relation to endurance performance and substrate utilization when a low GI meal is compared with a high GI meal. However, other investigations have shown that when nutritional strategies incorporating GI are applied to multiple meals, there is no clear advantage to the athlete in terms of exercise performance and capacity. It has been suggested that carbohydrate ingestion during endurance exercise negates the effect of the consumption of pre-exercise GI meals. The glycaemic load (GL) is a relatively novel concept in the area of sports nutrition, and has not been widely investigated. Its premise is that the effect, if any, on exercise performance is determined by the overall glycaemic effect of a diet and not by the amount of carbohydrate alone. The claims for GL have been disputed by a number of sports nutrition specialists, and have gone largely unrecognized by professional and scientific bodies. Research on the effect of the GL on exercise performance and capacity is still at an early stage, but recent studies have shown that the concept may have some merit as far as sports nutrition is concerned. It has been suggested that the GL may be a better predictor of glycaemic responses than the GI alone.

Glycaemic index effects on fuel partitioning in humans.


The purpose of this review was to examine the role of glycaemic index in fuel partitioning and body composition with emphasis on fat oxidation/storage in humans. This relationship is based on the hypothesis postulating that a higher serum glucose and insulin response induced by high-glycaemic carbohydrates promotes lower fat oxidation and higher fat storage in comparison with low-glycaemic carbohydrates. Thus, high-glycaemic index meals could contribute to the maintenance of excess weight in obese individuals and/or predispose obesity-prone subjects to weight gain. Several studies comparing the effects of meals with contrasting glycaemic carbohydrates for hours, days or weeks have failed to demonstrate any differential effect on fuel partitioning when either substrate oxidation or body composition measurements were performed. Apparently, the glycaemic index-induced serum insulin differences are not sufficient in magnitude and/or duration to modify fuel oxidation.

Elements Challenging the Glycemic Index    

By Alan Aragon

GI & Obesity - Slim Chance For Correlation

A systematic review of human intervention studies comparing the effects of high and low-GI foods or diets arrived at the following results [13]:
•  In a total of 31 short-term studies, low-GI foods were associated with greater satiety or reduced hunger in 15 studies, whereas reduced satiety or no differences were seen in 16 other studies.
•  Low-GI foods reduced ad libitum food intake in 7 studies, but not in 8 other studies. In 20 longer-term studies (<6 months), weight loss on a low-GI diet was seen in 4 and on a high-GI diet in 2, with no difference recorded in 14 studies.
•  An exhaustive assessment of these human intervention trials found no significant difference in the average weight loss between low & high GI diets. in conclusion, the current body of research evidence does not indicate that low-GI foods are superior to high-GI foods in regard to treating obesity.

More recently, Raatz & colleagues conducted a parallel-design, randomized 12-week controlled feeding trial, testing the effect of GI and GL on weight loss [14]. The controlled period was followed by a 24-week "free living" phase, in which subjects were instructed to continue their respective dietary treatments outside of lab-supervised conditions. Manipulation of GI & GL failed to make a dent in both experimental phases. As a result of the 36-week trial, the researchers conclude: "In summary, lowering the glycemic load and glycemic index of weight reduction diets does not provide any added benefit to energy restriction in promoting weight loss in obese subjects."

Conclusions (For Now) 
GI gives us clues to the behavior of certain foods, but that's exactly the main point of this article. Clues; mere hints are all we get from our current knowledge of GI. Successful application of GI is most consistent when we use higher GI sources to enhance the speed of postworkout glycogenesis, and that's about it. Carb foods are better judged on the basis of degree processing, refinement, or alteration/removal of micronutrition -- NOT on the basis of GI, or even GL. This is as good a time as any to crush the folly of what I call "food discrimination". A prime example of this is cutting out potatoes on the basis of GI. This happens all the time, & the dieter takes pride in thinking he/she is being prudent. Well, the critical thing to realize here is that all food species in nature have unique nutrient profiles. Therefore, unique nutritional benefit can be derived from each species. The natural matrix of plant &/or animal tissue cannot be duplicated in the lab, & hence there are many unidentified beneficial agents in, say, the humble potato. As a matter of trivia, it surpasses bananas in potassium & vitamin C concentration. Not to mention, it provides default hydration, and of course is a great whole-food source of starch. The list goes on & on.
Satiety, micronutrient density, insulin response, & surrounding factors altering glucose kinetics are all much like a roll of the dice in terms of bottom-line certainty & reliability of GI. Like all things in science - especially the deep bubbly cauldron that is applied nutritional science - it ain't all that simple. All avenues in this area are winding & complex.

Point 20

Enhanced amino acid sensitivity of myofibrillar protein synthesis persists for up to 24 h after resistance exercise in young men.


We aimed to determine whether an exercise-mediated enhancement of muscle protein synthesis to feeding persisted 24 h after resistance exercise. We also determined the impact of different exercise intensities (90% or 30% maximal strength) or contraction volume (work-matched or to failure) on the response at 24 h of recovery. Fifteen men (21 ± 1 y, BMI = 24.1 ± 0.8 kg · m(-2)) received a primed, constant infusion of l-[ring-(13)C(6)]phenylalanine to measure muscle protein synthesis after protein feeding at rest (FED; 15 g whey protein) and 24 h after resistance exercise (EX-FED). Participants performed unilateral leg exercises: 1) 4 sets at 90% of maximal strength to failure (90FAIL); 2) 30% work-matched to 90FAIL (30WM); or 3) 30% to failure (30FAIL). Regardless of condition, rates of mixed muscle protein and sarcoplasmic protein synthesis were similarly stimulated at FED and EX-FED. In contrast, protein ingestion stimulated rates of myofibrillar protein synthesis above fasting rates by 0.016 ± 0.002%/h and the response was enhanced 24 h after resistance exercise, but only in the 90FAIL and 30FAIL conditions, by 0.038 ± 0.012 and 0.041 ± 0.010, respectively. Phosphorylation of protein kinase B on Ser473 was greater than FED at EX-FED only in 90FAIL, whereas phosphorylation of mammalian target of rapamycin on Ser2448 was significantly increased at EX-FED above FED only in the 30FAIL condition. Our results suggest that resistance exercise performed until failure confers a sensitizing effect on human skeletal muscle for at least 24 h that is specific to the myofibrillar protein fraction.

Acute resistance exercise augments integrative myofibrillar protein synthesis.


The purpose of this study was to determine whether an acute bout of high-intensity resistance exercise (RE) would augment integrative mixed muscle and myofibrillar protein fractional synthesis rates (FSRs) when total energy and macronutrient intake was controlled. Twelve healthy young men were studied over 24 hours and performed an acute bout of exhaustive (5 sets until volitional failure of their 85% 1-repetition maximum) unilateral leg press and knee extension exercise, such that one leg was exercised (EX) and the other served as a control (CON). (2)H(2)O (70%) was provided to measure mixed muscle and myofibrillar FSR, and muscle biopsies (vastus lateralis) were collected from the EX and CON legs 16 hours following the RE session. (2)H-labeling of body water over the course of the experiment was 0.32 ± 0.01 mole percent excess. Interestingly, integrative mixed muscle FSR (percent per hour) was similar between the CON (0.76% ± 0.08%) and EX (0.69% ± 0.06%) legs. In contrast, upon determination of myofibrillar FSR, there was an RE effect (EX, 0.94% ± 0.16% vs CON, 0.75% ± 0.08%; P < .05). High-intensity RE without prior training impacts integrative myofibrillar 24-hour FSR, perhaps without altering total responses.

Mixed muscle protein synthesis and breakdown after resistance exercise in humans.


Mixed muscle protein fractional synthesis rate (FSR) and fractional breakdown rate (FBR) were examined after an isolated bout of either concentric or eccentric resistance exercise. Subjects were eight untrained volunteers (4 males, 4 females). Mixed muscle protein FSR and FBR were determined using primed constant infusions of [2H5]phenylalanine and 15N-phenylalanine, respectively. Subjects were studied in the fasted state on four occasions: at rest and 3, 24, and 48 h after a resistance exercise bout. Exercise was eight sets of eight concentric or eccentric repetitions at 80% of each subject's concentric 1 repetition maximum. There was no significant difference between contraction types for either FSR, FBR, or net balance (FSR minus FBR). Exercise resulted in significant increases above rest in muscle FSR at all times: 3 h = 112%, 24 h = 65%, 48 h = 34% (P < 0.01). Muscle FBR was also increased by exercise at 3 h (31%; P < 0.05) and 24 h (18%; P < 0.05) postexercise but returned to resting levels by 48 h. Muscle net balance was significantly increased after exercise at all time points [(in %/h) rest = -0.0573 +/- 0.003 (SE), 3 h = -0.0298 +/- 0.003, 24 h = -0.0413 +/- 0.004, and 48 h = -0.0440 +/- 0.005], and was significantly different from zero at all time points (P < 0.05). There was also a significant correlation between FSR and FBR (r = 0.88, P < 0.001). We conclude that exercise resulted in an increase in muscle net protein balance that persisted for up to 48 h after the exercise bout and was unrelated to the type of muscle contraction performed.

Fasted-state skeletal muscle protein synthesis after resistance exercise is altered with training.


The purpose of the present investigation was to determine how fasted-state protein synthesis was affected, acutely, by resistance training. Eight men (24.8+/-1.7 years, body mass index=23.2+/-1.0 kg m-2; means+/-s.e.m.) undertook an 8 week programme of unilateral resistance exercise training (3 sessions week-1, progression from two to four sets; intensity was 80% of the subjects' single repetition maximum (1RM): knee extension and leg press). Following training, subjects underwent two primed constant infusions of l-[ring-13C6]phenylalanine to determine mixed and myofibrillar muscle protein synthesis (MPS) at rest and 12 h after an acute bout of resistance exercise at the same exercise intensity--each leg 80% of 1RM. Biopsies (vastus lateralis) were taken to measure incorporation of labelled phenylalanine into mixed and myofibrillar skeletal muscle proteins and yield fractional MPS. Training resulted in significant dynamic strength gains that were greater (P<0.001) in the trained leg. Hypertrophy of type IIa and IIx fibres (P<0.05) was observed following training. After training, resting mixed MPS rate was elevated (+48%; P<0.05). Acutely, resistance exercise stimulated mixed MPS only in the untrained leg (P<0.05). Myofibrillar MPS was unchanged at rest following training (P=0.61). Myofibrillar MPS increased after resistance exercise (P<0.05), but was not different between the trained and untrained legs (P=0.36). We observed divergent changes in resting mixed versus myofibrillar protein synthesis with training. In addition, resistance training modified the acute response of MPS to resistance exercise by dampening the increased synthesis of non-myofibrillar proteins while maintaining the synthesis of myofibrillar proteins.

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