124 resultados para Graded index (GI)

em Queensland University of Technology - ePrints Archive


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Aims: Dietary glycemic index (GI) and glycemic load (GL) have been associated with risk of chronic diseases, yet limited research exists on patterns of consumption in Australia. Our aims were to investigate glycemic carbohydrate in a population of older women, identify major contributing food sources, and determine low, moderate and high ranges. Methods: Subjects were 459 Brisbane women aged 42-81 years participating in the Longitudinal Assessment of Ageing in Women. Diet history interviews were used to assess usual diet and results were analysed into energy and macronutrients using the FoodWorks dietary analysis program combined with a customised GI database. Results: Mean±SD dietary GI was 55.6±4.4% and mean dietary GL was 115±25. A low GI in this population was ≤52.0, corresponding to the lowest quintile of dietary GI, and a low GL was ≤95. GI showed a quadratic relationship with age (P=0.01), with a slight decrease observed in women aged in their 60’s relative to younger or older women. GL decreased linearly with age (P<0.001). Bread was the main contributor to carbohydrate and dietary GL (17.1% and 20.8%, respectively), followed by fruit (15.5% and 14.2%), and dairy for carbohydrate (9.0%) or breakfast cereals for GL (8.9%). Conclusions: In this population, dietary GL decreased with increasing age, however this was likely to be a result of higher energy intakes in younger women. Focus on careful selection of lower GI items within bread and breakfast cereal food groups would be an effective strategy for decreasing dietary GL in this population of older women.

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Background: Diets with a high postprandial glycemic response may contribute to long-term development of insulin resistance and diabetes, however previous epidemiological studies are conflicting on whether glycemic index (GI) or glycemic load (GL) are dietary factors associated with the progression. Our objectives were to estimate GI and GL in a group of older women, and evaluate cross-sectional associations with insulin resistance. Subjects and Methods: Subjects were 329 Australian women aged 42-81 years participating in year three of the Longitudinal Assessment of Ageing in Women (LAW). Dietary intakes were assessed by diet history interviews and analysed using a customised GI database. Insulin resistance was defined as a homeostasis model assessment (HOMA) value of >3.99, based on fasting blood glucose and insulin concentrations. Results: GL was significantly higher in the 26 subjects who were classified as insulin resistant compared to subjects who were not (134±33 versus 114±24, P<0.001). In a logistic regression model, an increment of 15 GL units increased the odds of insulin resistance by 2.09 (95%CI 1.55, 2.80, P<0.001) independently of potential confounding variables. No significant associations were found when insulin resistance was assessed as a continuous variable. Conclusions: Results of this cross-sectional study support the concept that diets with a higher GL are associated with increased risk of insulin resistance. Further studies are required to investigate whether reducing glycemic intake, by either consuming lower GI foods and/or smaller serves of carbohydrate, can contribute to a reduction in development of insulin resistance and long-term risk of type 2 diabetes.

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BACKGROUND:Previous epidemiological investigations of associations between dietary glycemic intake and insulin resistance have used average daily measures of glycemic index (GI) and glycemic load (GL). We explored multiple and novel measures of dietary glycemic intake to determine which was most predictive of an association with insulin resistance.METHODS:Usual dietary intakes were assessed by diet history interview in women aged 42-81 years participating in the Longitudinal Assessment of Ageing in Women. Daily measures of dietary glycemic intake (n = 329) were carbohydrate, GI, GL, and GL per megacalorie (GL/Mcal), while meal based measures (n = 200) were breakfast, lunch and dinner GL; and a new measure, GL peak score, to represent meal peaks. Insulin resistant status was defined as a homeostasis model assessment (HOMA) value of >3.99; HOMA as a continuous variable was also investigated.RESULTS:GL, GL/Mcal, carbohydrate (all P < 0.01), GL peak score (P = 0.04) and lunch GL (P = 0.04) were positively and independently associated with insulin resistant status. Daily measures were more predictive than meal-based measures, with minimal difference between GL/Mcal, GL and carbohydrate. No significant associations were observed with HOMA as a continuous variable.CONCLUSION:A dietary pattern with high peaks of GL above the individual's average intake was a significant independent predictor of insulin resistance in this population, however the contribution was less than daily GL and carbohydrate variables. Accounting for energy intake slightly increased the predictive ability of GL, which is potentially important when examining disease risk in more diverse populations with wider variations in energy requirements.

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Objective: To assess the effect of graded increases in exercised-induced energy expenditure (EE) on appetite, energy intake (EI), total daily EE and body weight in men living in their normal environment and consuming their usual diets. Design: Within-subject, repeated measures design. Six men (mean (s.d.) age 31.0 (5.0) y; weight 75.1 (15.96) kg; height 1.79 (0.10) m; body mass index (BMI) 23.3(2.4) kg/m2), were each studied three times during a 9 day protocol, corresponding to prescriptions of no exercise, (control) (Nex; 0 MJ/day), medium exercise level (Mex; ~1.6 MJ/day) and high exercise level (Hex; ~3.2 MJ/day). On days 1-2 subjects were given a medium fat (MF) maintenance diet (1.6 ´ resting metabolic rate (RMR)). Measurements: On days 3-9 subjects self-recorded dietary intake using a food diary and self-weighed intake. EE was assessed by continual heart rate monitoring, using the modified FLEX method. Subjects' HR (heart rate) was individually calibrated against submaximal VO2 during incremental exercise tests at the beginning and end of each 9 day study period. Respiratory exchange was measured by indirect calorimetry. Subjects completed hourly hunger ratings during waking hours to record subjective sensations of hunger and appetite. Body weight was measured daily. Results: EE amounted to 11.7, 12.9 and 16.8 MJ/day (F(2,10)=48.26; P<0.001 (s.e.d=0.55)) on the Nex, Mex and Hex treatments, respectively. The corresponding values for EI were 11.6, 11.8 and 11.8 MJ/day (F(2,10)=0.10; P=0.910 (s.e.d.=0.10)), respectively. There were no treatment effects on hunger, appetite or body weight, but there was evidence of weight loss on the Hex treatment. Conclusion: Increasing EE did not lead to compensation of EI over 7 days. However, total daily EE tended to decrease over time on the two exercise treatments. Lean men appear able to tolerate a considerable negative energy balance, induced by exercise, over 7 days without invoking compensatory increases in EI.

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To shed light on the potential efficacy of cycling as a testing modality in the treatment of intermittent claudication (IC), this study compared physiological and symptomatic responses to graded walking and cycling tests in claudicants. Sixteen subjects with peripheral arterial disease (resting ankle: brachial index (ABI) < 0.9) and IC completed a maximal graded treadmill walking (T) and cycle (C) test after three familiarization tests on each mode. During each test, symptoms, oxygen uptake (VO2), minute ventilation (VE), respiratory exchange ratio (RER) and heart rate (HR) were measured, and for 10 min after each test the brachial and ankle systolic pressures were recorded. All but one subject experienced calf pain as the primary limiting symptom during T; whereas the symptoms were more varied during C and included thigh pain, calf pain and dyspnoea. Although maximal exercise time was significantly longer on C than T (690 +/- 67 vs. 495 +/- 57 s), peak VO2, peak VE and peak heart rate during C and T were not different; whereas peak RER was higher during C. These responses during C and T were also positively correlated (P < 0.05) with each other, with the exception of RER. The postexercise systolic pressures were also not different between C and T. However, the peak decline in ankle pressures from resting values after C and T were not correlated with each other. These data demonstrate that cycling and walking induce a similar level of metabolic and cardiovascular strain, but that the primary limiting symptoms and haemodynamic response in an individual's extremity, measured after exercise, can differ substantially between these two modes.

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