A single high-fat, high-carbohydrate meal (HFHC) results in elevated postprandial glucose (GLU), triglycerides (TAG) and metabolic load index (MLI; TAG (mg/dl) + GLU (mg/dl)) that contributes to chronic disease risk. While disease risk is higher in older adults (OA) compared to younger adults (YA), the acute effects of exercise on these outcomes in OA is understudied. Twelve YA (age 23.3 ± 3.9 yrs, n = 5 M/7 F) and 12 OA (age 67·7 ± 6.0 yrs, n = 8 M/4 F) visited the laboratory in random order to complete a HFHC with no exercise (NE) or acute exercise (EX) condition. EX was performed 12 hours prior to HFHC at an intensity of 65 % of maximal heart rate to expend 75 % of the kcals consumed in HFHC (Marie Callender’s Chocolate Satin Pie; 12 kcal/kgbw; 57 % fat, 37 % CHO). Blood samples were taken at 0, 30, 60, 90 minutes, and then every hour until 6 hours post-meal. TAG levels increased to a larger magnitude in OA (Δ∼61 ± 31 %) compared to YA (Δ∼37 ± 34 %, P < 0·001), which were attenuated in EX compared to NE (P < 0·05) independent of age. There was no difference in GLU between OA and YA after the HFM, however, EX had attenuated GLU independent of age (NE: Δ∼21 ± 26 %; EX: Δ∼12 ± 18 %, P = 0·027). MLI was significantly lower after EX compared to NE in OA and YA (P < 0·001). Pre-prandial EX reduced TAG, GLU and MLI post-HFHC independent of age.

Whole apples are a source of pectin and polyphenols, both of which show potential to modulate postprandial lipaemia (PPL). The present study aimed to explore the effects of whole apple consumption on PPL, as a risk factor for CVD, in generally healthy but overweight and obese adults. A randomised, crossover acute meal trial was conducted with seventeen women and nine men (mean BMI of 34·1 (sem 0·2) kg/m2). Blood samples were collected for 6 h after participants consumed an oral fat tolerance test meal that provided 1 g fat/kg body weight and 1500 mg acetaminophen per meal for estimating gastric emptying, with and without three whole raw Gala apples (approximately 200 g). Plasma TAG (with peak postprandial concentration as the primary outcome), apoB48, chylomicron-rich fraction particle size and fatty acid composition, glucose, insulin and acetaminophen were analysed. Differences between with and without apples were identified by ANCOVA. Apple consumption did not alter postprandial TAG response, chylomicron properties, glucose or acetaminophen (P > 0·05), but did lead to a higher apoB48 peak concentration and exaggerated insulin between 20 and 180 min (P < 0·05). Overall, as a complex food matrix, apples did not modulate postprandial TAG when consumed with a high-fat meal in overweight and obese adults, but did stimulate insulin secretion, potentially contributing to an increased TAG-rich lipoprotein production.

Non-fasting TAG – postprandial lipaemia (PPL) – are to a higher degree associated with cardiovascular risk compared with fasting TAG. Dietary protein, especially whey proteins (WP), may lower PPL. We hypothesised that a WP pre-meal (17·6 g protein) consumed 15 v. 30 min before a fat-rich meal reduces the PPL response in subjects with the metabolic syndrome (MetS) and that a WP pre-meal has more potent effects than casein and gluten pre-meals. A total of sixteen subjects with the MetS completed an acute, randomised, crossover trial. WP pre-meals were consumed 15 and 30 min, and casein and gluten 15 min before a fat-rich meal. Blood samples were drawn 360 min postprandially to determine metabolite and hormone responses, S-paracetamol (for assessment of gastric emptying) and amino acids. Insulin and glucagon responses were affected by both timing and protein type (for all P <0·01), with significantly higher concentrations for WP given at –15 min than WP at –30 min and higher responses compared with gluten for the first 30 min after pre-meal consumption (for all P <0·05). The PPL responses changed neither by timing nor by protein type. Glucose-dependent insulinotropic peptide but not glucagon-like peptide 1 responses differed between the three protein types. S-paracetamol concentration was higher for WP (–30 min) than for WP (–15 min) 15 min after the main meal (P = 0·028), and higher for casein and gluten than for WP at time point 30 min (for all P <0·05). In conclusion, the PPL response was not changed by ingestion of a 17·6 g protein pre-meal, whereas both timing and protein quality affected hormone secretion (insulin and glucagon).

The aim of this study was to re-examine the chronic effect (>7 d) of fructose consumption on postprandial TAG, in adolescents and adults. The research was carried out in March 2017 and used different electronic databases, such as Medline® (Pubmed®), Embase® and Cochrane. The review considered clinical trials (parallel or crossed) that evaluated the effect of fructose consumption for a period longer than 7 d, in humans. Two investigators independently performed data extraction. The outcome was the absolute delta of TAG concentration in a 4-h postprandial period. The results were presented with delta mean difference between treatments with 95 % CI. The calculations were made based on random-effect models. Statistical heterogeneity of treatment effects between studies was assessed by Cochrane’s ‘Q Test’ and ‘I2’ inconsistency test. The meta-analysis of the twelve selected interventions (n 318) showed that fructose generated larger variation (δ) of TAG concentrations during the postprandial period, compared with other carbohydrates (mean difference: 8·02 (95 % CI 0·46, 15·58) mg/dl (0·09 (95 % CI 0·01, 0·18) mmol/l); I2: 74 %). High heterogeneity was generated almost exclusively by one study, and its withdrawal did not alter the result. We concluded that chronic consumption of fructose (>7 d) has a negative role on postprandial TAG in healthy adolescents and adults, as well as in overweight/obese individuals, but not in diabetics.

CVD are the leading cause of death in women globally, with ageing associated with progressive endothelial dysfunction and increased CVD risk. Natural menopause is characterised by raised non-fasting TAG concentrations and impairment of vascular function compared with premenopausal women. However, the mechanisms underlying the increased CVD risk after women have transitioned through the menopause are unclear. Dietary fat is an important modifiable risk factor relating to both postprandial lipaemia and vascular reactivity. Meals rich in SFA and MUFA are often associated with greater postprandial TAG responses compared with those containing n-6 PUFA, but studies comparing their effects on vascular function during the postprandial phase are limited, particularly in postmenopausal women. The present review aimed to evaluate the acute effects of test meals rich in SFA, MUFA and n-6 PUFA on postprandial lipaemia, vascular reactivity and other CVD risk factors in postmenopausal women. The systematic search of the literature identified 778 publications. The impact of fat-rich meals on postprandial lipaemia was reported in seven relevant studies, of which meal fat composition was compared in one study described in three papers. An additional study determined the impact of a high-fat meal on vascular reactivity. Although moderately consistent evidence suggests detrimental effects of high-fat meals on postprandial lipaemia in postmenopausal (than premenopausal) women, there is insufficient evidence to establish the impact of meals of differing fat composition. Furthermore, there is no robust evidence to conclude the effect of meal fatty acids on vascular function or blood pressure. In conclusion, there is an urgent requirement for suitably powered robust randomised controlled trials to investigate the impact of meal fat composition on postprandial novel and established CVD risk markers in postmenopausal women, an understudied population at increased cardiometabolic risk.

TAG depleted remnants of postprandial chylomicrons are a risk factor for atherosclerosis. Recent studies have demonstrated that in the fasted state, the majority of chylomicrons are small enough for transcytosis to arterial subendothelial space and accelerate atherogenesis. However, the size distribution of chylomicrons in the absorptive state is unclear. This study explored in normolipidaemic subjects the postprandial distribution of the chylomicron marker, apoB-48, in a TAG-rich lipoprotein plasma fraction (Svedberg flotation rate (Sf>400), in partially hydrolysed remnants (Sf 20–400) and in a TAG-deplete fraction (Sf<20), following ingestion of isoenergetic meals with either palm oil (PO), rice bran or coconut oil. Results from this study show that the majority of fasting chylomicrons are within the potentially pro-atherogenic Sf<20 fraction (70–75 %). Following the ingestion of test meals, chylomicronaemia was also principally distributed within the Sf<20 fraction. However, approximately 40 % of subjects demonstrated exaggerated postprandial lipaemia specifically in response to the SFA-rich PO meal, with a transient shift to more buoyant chylomicron fractions. The latter demonstrates that heterogeneity in the magnitude and duration of hyper-remnantaemia is dependent on both the nature of the meal fatty acids ingested and possible metabolic determinants that influence chylomicron metabolism. The study findings reiterate that fasting plasma TAG is a poor indicator of atherogenic chylomicron remnant homoeostasis and emphasises the merits of considering specifically, chylomicron remnant abundance and kinetics in the context of atherogenic risk. Few studies address the latter, despite the majority of life being spent in the postprandial and absorptive state.

The ingestion of high-fat meals induces a state of endothelial dysfunction in adults. This dysfunction is attenuated by prior exercise. The response of young people to these nutritional and physiological stressors has not been established. Thus, the purpose of the present study was to investigate if a bout of moderate-intensity exercise influenced endothelial function (as indicated by flow-mediated dilation (FMD)) following the ingestion of a high-fat breakfast and lunch in adolescent boys (aged 12·6–14·3 years). Two, 2 d main trials (control and exercise) were completed by thirteen adolescent boys in a counter-balanced, cross-over design. Participants were inactive on day 1 of the control trial, but completed 60 min of walking at 60 % peak oxygen uptake in the exercise trial. On day 2, endothelial function was assessed via FMD prior to, and following, ingestion of a high-fat breakfast and lunch. There was no difference in fasting FMD between the control and exercise trial (P= 0·449). In the control trial, FMD was reduced by 32 % following consumption of the high-fat breakfast and by 24 % following lunch. In the exercise trial, the corresponding reductions were 6 and 10 %, respectively (main effect trial, P= 0·002). These results demonstrate that moderate-intensity exercise can attenuate the decline in FMD seen following the consumption of high-fat meals in adolescent boys.

Foods high in monounsaturated fat, such as olive oil, and endurance exercise are both known to independently reduce postprandial TAG concentrations. We examined the combined effects of exercise and dietary fat composition on postprandial TAG concentrations in nine healthy pre-menopausal females (age 26·8 (sd 3·3) years, BMI 22·3 (sd 2·0) kg/m2). Each participant completed four, 2 d trials in a randomised order: (1) butter–no exercise, (2) olive oil–no exercise, (3) butter–exercise, (4) olive oil–exercise. On day 1 of the exercise trials, participants walked or ran on a treadmill for 60 min. On the no-exercise trials, participants rested on day 1. On day 2 of each trial, participants rested and consumed an olive oil meal (saturated fat 15 % and unsaturated fat 85 %) or a butter meal (saturated fat 71 % and unsaturated fat 29 %) for breakfast. Venous blood samples were obtained in the fasted state and for 6 h postprandially on day 2. A significant main effect on physical activity (exercise or control) was obtained for plasma TAG concentration (three-way ANOVA, P = 0·043), and the total area under the concentration v. time curve for TAG was 26 % lower on the olive oil–exercise trial (4·40 (sd 0·40) mmol × 6 h/l) than the butter–no exercise trial (5·91 (sd 1·01) mmol × 6 h/l) (one-way ANOVA, P = 0·029). These findings suggest that the combination of exercise and a preference for monounsaturated dietary fat intake in the form of olive oil may be most beneficial for reducing postprandial TAG concentrations.

The melanocortin-4 receptor (MC4R) is an essential regulator of food intake and energy homeostasis. Previous data suggest an influence of MC4R activity on TAG levels. Thus, the aim of the present study was to determine whether the presence of the rs12970134 polymorphism near the MC4R gene could influence postprandial lipoprotein metabolism in healthy subjects. A total of eighty-eight volunteers were selected, fifty-three homozygous for the common genotype (G/G) and thirty-five carriers for the minor A-allele (G/A and A/A). They were given a fat-rich meal containing 1 g fat and 7 mg cholesterol/kg body weight and vitamin A (60 000 IU/m2 body surface). Fat accounted for 60 % of energy, and protein and carbohydrates accounted for 15 and 25 % of energy, respectively. Blood samples were taken at time 0, every 1 h until 6 h and every 2·5 h until 11 h. Total cholesterol and TAG in plasma, and cholesterol, TAG and retinyl palmitate in TAG-rich lipoproteins (TRL, large and small TRL) were separated by ultracentrifugation. Individuals carrying the G/G genotype displayed a higher postprandial response of plasma TAG (P = 0·033), total cholesterol (P = 0·019) and large TRL–TAG (P = 0·023) than did carriers of the minor A-allele. Furthermore, G/G subjects showed a greater postprandial response of small TRL–apoB48 than did carriers of the A-allele (P = 0·032). These results suggest that the rs12970134 polymorphism near the MC4R gene region may partly explain the inter-individual differences in postprandial lipoprotein response in healthy subjects.

Moderate-intensity exercise can lower the TAG response to a high-fat meal; however, the British diet is moderate in fat, and no study to date has compared the effect of such exercise on responses to high-fat and moderate-fat meals. The present work investigated the effect of brisk walking performed 13 h before intake of both high-fat and moderate-fat meals on postprandial plasma TAG concentrations. Eight inactive, overweight men completed four separate 2 d trials, i.e. rest (Con) or a 90-min treadmill walk (Ex) on the evening of day 1, followed by the ingestion of a moderate-fat (Mod) or high-fat (High) meal on the morning of day 2. High-fat meals contained 66 % of total energy as fat, while the percentage was 35 % for moderate-fat meals; both the meals were, however, isoenergetic. On day 2, venous blood was sampled in the fasted state, 30 and 60 min after ingesting the test meal and then hourly until 6 h post-meal. Exercise reduced plasma TAG concentrations significantly (P < 0·001), with no exercise × meal interaction (P = 0·459). Walking reduced the total TAG response to a high-fat meal by 29 % (relative to High Con); the same bout of exercise performed before ingesting a moderate-fat meal lowered total TAG by 26 % (compared with Mod Con). The ability of a single moderate-intensity aerobic exercise bout to lower postprandial TAG concentrations is just as great, in percentage terms, when the test meal ingested is of a moderate rather than a high fat content.

Postprandial lipaemia impairs endothelial function, possibly by changes in oxidative stress, but whether this affects cardiac output and/or systemic vascular resistance (SVR) at rest and in response to dynamic exercise remains uncertain. The present study set out to investigate the effects of a high-fat meal (HFM) v. a low-fat, high-carbohydrate meal (HCM) on cardiac output and SVR. A HFM (50 g fat) and an isoenergetic HCM (5 g fat) were randomly fed to thirty healthy adults using a crossover design. Cardiac output, heart rate and blood pressure (BP) were measured, and stroke volume and SVR were calculated over a 3 h rest following the meal, during exercise 3 h postprandially and for 45 min post-exercise. Blood samples were collected at fasting, 3 h postprandially and immediately post-exercise. Plasma TAG increased by 63·8 % 3 h following the HFM, and NEFA fell by 94·1 % 3 h after the HCM. There was a 9·8 % rise in plasma 8-isoprostane-F2α concentration following the HFM, and a 6·2 % fall following the HCM. Cardiac output increased postprandially, but the difference between meals at rest or exercise was not statistically significant. The HFM resulted in a 3·2 mmHg (95 % CI 0·7, 5·7) smaller increase in exercise mean arterial BP compared with the HCM due to a greater fall in exercise SVR. Postprandial lipaemia induced by a HFM does not affect cardiac output and/or SVR at rest, but it blunts the increase in BP during exercise.

We tested the hypothesis that 30 min of brisk walking daily would offset the increase in plasma TAG concentrations associated with substituting dietary fat for carbohydrate. Fourteen subjects (six males) aged 57 (sd 5) years underwent three 4 d trials in a counterbalanced order: (i) 4 d on a typical UK diet (40 % energy from fat, 45 % carbohydrate and 15 % protein); (ii) 4 d on an isoenergetic diet but substituting fat for carbohydrate in line with the present recommendations (30 % fat, 55 % carbohydrate and 15 % protein); (iii) 4 d on the same recommended diet with 30 min of brisk walking each day. The food provided for the first 3 d of each trial was isoenergetic with each volunteer's previously determined daily energy intake. On day 4, the subjects consumed breakfast, lunch and an early evening meal, equivalent in total to 90 % of their daily energy intake. Blood samples were collected and substrate utilisation and energy expenditure were determined in the fasted state and for 9 h postprandially. Substrate utilisation differed significantly among trials (P = 0·003); RER was higher on the recommended diet trial than during either of the other two trials (P = 0·012 and 0·021 for the UK diet and recommended diet with walking, respectively). The rise in plasma TAG concentrations over the day was steeper on the recommended diet trial than on the other two trials (trial × time interaction, P = 0·040). The increase in postprandial TAG concentrations associated with substituting dietary fat for carbohydrate was offset by 30 min of brisk walking daily.

A single bout of prolonged, moderate-intensity endurance exercise lowers fasting and postprandial TAG concentrations the next day. However, the TAG-lowering effect of exercise is dose-dependent and does not manifest after light exercise of low energy cost ( < 2 MJ). We aimed to investigate whether superimposing mild energy intake restriction to such exercise, in order to augment total energy deficit, potentiates the hypotriacylglycerolaemic effect. Eight healthy, sedentary, premenopausal women (age 27·1 (sem 1·3) years; BMI 21·8 (sem 0·9) kg/m2) performed two oral fat tolerance tests in the morning on two different occasions: once after a single bout of light exercise (100 min at 30 % of peak oxygen consumption; net energy expenditure 1·04 (sem 0·01) MJ) coupled with mild energy intake restriction (1·39 (sem 0·22) MJ) on the preceding day, and once after resting coupled with isoenergetic feeding on the preceding day (control). Fasting plasma TAG, TAG in the TAG-rich lipoproteins (TRL-TAG) and serum insulin concentrations were 18, 34 and 30 % lower, respectively, after exercise plus diet compared with the control trial (P < 0·05). Postprandial concentrations of plasma TAG and TRL-TAG were 19 and 27 % lower after exercise plus diet compared with the control condition (P < 0·01), whereas postprandial insulin concentrations were not different. It is concluded that a combination of light exercise along with mild hypoenergetic diet may be a practical and feasible intervention to attenuate fasting and postprandial triacylglycerolaemia, especially for people who cannot exercise for prolonged periods of time at moderate-to-high intensities, such as many sedentary individuals.

Most of diurnal time is spent in a postprandial state due to successive meal intakes during the day. As long as the meals contain enough fat, a transient increase in triacylglycerolaemia and a change in lipoprotein pattern occurs. The extent and kinetics of such postprandial changes are highly variable and are modulated by numerous factors. This review focuses on factors affecting postprandial lipoprotein metabolism and genes, their variability and their relationship with intermediate phenotypes and risk of CHD. Postprandial lipoprotein metabolism is modulated by background dietary pattern as well as meal composition (fat amount and type, carbohydrate, protein, fibre, alcohol) and several lifestyle conditions (physical activity, tobacco use), physiological factors (age, gender, menopausal status) and pathological conditions (obesity, insulin resistance, diabetes mellitus). The roles of many genes have been explored in order to establish the possible implications of their variability in lipid metabolism and CHD risk. The postprandial lipid response has been shown to be modified by polymorphisms within the genes for apo A-I, A-IV, A-V, E, B, C-I and C-III, lipoprotein lipase, hepatic lipase, fatty acid binding and transport proteins, microsomal triglyceride transfer protein and scavenger receptor class B type I. Overall, the variability in postprandial response is important and complex, and the interactions between nutrients or dietary or meal compositions and gene variants need further investigation. The extent of present knowledge and needs for future studies are discussed in light of ongoing developments in nutrigenetics.

Exaggerated postprandial lipaemia may increase the risk of CHD by contributing to both thrombotic and atherogenic processes. Previous research has focused on the quantity and composition of dietary fat, whereas the effect of triacylglycerol (TAG) structure on postprandial lipaemia and clotting factor VII activity has received little attention. TAG with similar fatty acid composition may have different biochemical and physical properties that are dependent on their TAG structure, and these differences may affect lipid metabolism. Recent findings suggest that differences in the physical properties of stearic acid-rich fats are associated with differences in postprandial lipaemia, and may play an important role in determining their rates of digestion and absorption.

Postprandial lipaemia (PL) is associated with the metabolic syndrome, CVD and endothelial dysfunction. Aerobic exercise has been shown to reduce PL. Although resistance exercise is recommended for the improvement of the quality of life, management of body weight and prevention of several disorders, its effect on PL has received little attention. The present study examined the effects of low-volume resistance exercise (LVRE) and high-volume resistance exercise (HVRE) on PL. Ten healthy young men performed three trials, each conducted over 2 d. On the afternoon of day 1, they either refrained from exercise (control), performed LVRE (two sets of eight exercises, twelve repetitions at twelve repetitions maximum (RM) in each set; energy expenditure 0·76 MJ), or performed HVRE (four sets of eight exercises, twelve repetitions at 12RM in each set; energy expenditure 1·40 MJ). On the morning of day 2 they consumed a meal containing 67 kJ/kg body weight, of which 65 % energy was from fat. Blood samples were obtained in the fasted state and for 6 h postprandially. The total area under the TAG curve (AUC; mmol/l × h) was lower (P < 0·05) in HVRE (8·76 (sd 3·20)) and LVRE (9·29 (sd 3·64)) compared with control (11·60 (sd 4·35)). The incremental AUC was lower in HVRE compared with control (3·07 (sd 2·53) v. 5·58 (sd 3·72)), but not different between LVRE (3·86 (sd 2·29)) and control. In conclusion, resistance exercise of 1·40 MJ (four sets – eight exercises – twelve RM) or 0·76 MJ (two sets – eight exercises – twelve RM) before a high-fat meal reduces the total postprandial lipaemic response.

There is a growing body of scientific evidence which demonstrates that plasma triacylglycerol (TAG) concentration, especially in the postprandial state, is an important risk factor in relation to the development of CHD. Postprandial hypertriacylglycerolaemia is associated with a number of adverse metabolic risk factors, including the preponderance of small dense LDL, low HDL-cholesterol concentrations and elevated factor VII activity. Traditionally, a low-fat high-carbohydrate diet was used to prevent CHD because it effectively reduces plasma cholesterol concentrations, but this dietary regimen increases plasma TAG concentrations and reduces HDL-cholesterol concentrations. There is substantial epidemiological evidence which demonstrates that high plasma TAG and low plasma HDL concentrations are associated with an increased risk of CHD. Thus, there is reason for concern that the adverse effects of low-fat high-carbohydrate diets on TAG and HDL may counteract or negate the beneficial effect of reducing LDL-cholesterol concentrations. Although there have been no prospective studies to investigate whether reduced fat intake has an adverse effect on CHD, there is strong epidemiological evidence that reducing total fat intake is not protective against CHD. On the other hand, high-fat diets predispose to obesity, and central obesity adversely affects TAG metabolism. There is substantial evidence that in free-living situations low-fat high-carbohydrate diets lead to weight loss, which in turn will correct insulin resistance and plasma TAG metabolism. Clearly there is a need for prospective studies to resolve the issue as to whether low-fat high-carbohydrate diets play an adverse or beneficial role in relation to the development of CHD.

The aim of the study was to determine the effect of consuming meals with different fatty acid compositions on the postprandial changes over 6h in plasma triacylglycerol, NEFA, total cholesterol, glucose and insulin concentrations in middle-aged men and women. Men (n 11; 58 (5) years) and women (n 11; 56 (4) years) consumed four test meals with a similar macronutrient energy content in random order: a reference meal based on the habitual pattern of fatty acid intake in the UK, a meal with an increased (155%) linoleic acid (LA) to α-linolenic acid (αLNA) ratio (high LA:αLNA), a meal with increased (23%) MUFA content (high MUFA) and a meal with increased (583%) EPA and DHA content (high EPA+DHA). The high-LA:αLNA and high-EPA+DHA meals selectively increased the ratio of LA to αLNA (men 341%; women 310%) and the EPA+DHA (men 414%; women 438%) concentration in plasma triacylglycerol. The high-MUFA meal did not alter the change in MUFA content of the plasma. Plasma triacylglycerol, NEFA, glucose and insulin, but not total cholesterol, concentrations changed significantly after each meal. There was no significant effect of meal fatty acid composition or gender on maximum change in concentration, time to maximum concentration or area under the curve of any of the metabolites measured in the blood. These results suggest that differences in meal fatty acid composition exert little or no effect on postprandial changes in plasma lipids, glucose and insulin concentrations.

Exercise prior to eating has repeatedly been shown to reduce postprandial lipaemia. The aim of the present study was to investigate whether this effect was manifest in the presence of two factors that independently mitigate postprandial lipaemia: eumenorrhoea and moderate fat intake. Eight healthy eumenorrhoeic rowers consumed a meal of moderate fat content (35% total energy, 0·66g/kg body mass) 14h after having either rowed at 55% of maximal aerobic power (81% of maximal heart rate) for 80min or rested. Both trials were performed during the luteal phase. Blood samples were drawn before the meal and for 8h postprandially for the measurement of individual fatty acids in the triacylglycerol and NEFA fractions, as well as of glucose, insulin and oestradiol. Plasma oestradiol concentrations were not significantly different in the two trials. The postprandial lipaemic response, expressed as either plasma triacylglycerol concentration or area under the triacylglycerol–time curve, was 35% lower (P<0·05) after exercise. The postprandial glycaemic and insulinaemic responses were also lower, indicating increased insulin sensitivity, whereas the NEFA response was higher, suggesting a lower entrapment of dietary fatty acids in adipose tissue after exercise. Finally, exercise increased the proportion of unsaturated:saturated NEFA during the postprandial period. In conclusion, aerobic exercise performed 14h before a moderate-fat meal reduced postprandial lipaemia in women in the luteal phase. This effect shows the potential of exercise to mitigate even moderate lipaemic responses in eumenorrhoeic women.

The role of bicarbonated mineral waters on lipid metabolism and lipoprotein concentrations in man has scarcely been investigated. The present study aimed to investigate whether drinking sodium bicarbonated mineral water affects postprandial cholesterol and triacylglycerol metabolism in postmenopausal women. In a three-way, randomised, crossover study, eighteen healthy postmenopausal women consumed two sodium bicarbonated mineral waters (bicarbonated mineral water 1 and bicarbonated mineral water 2) and a low mineral water (500 ml of each) with a standard fat-rich meal (4552 kJ; 75·3 g fat). The bicarbonated waters were rich in sodium and bicarbonate and bicarbonated mineral water 1 contained 5·7 times more fluoride than bicarbonated mineral water 2. Fasting blood samples and postprandial blood samples were taken at 30, 60, 120, 240, 360 and 420 min after the end of the meal consumption. Cholesterol and triacylglycerols were determined in serum and chylomicrons. A significant water consumption effect was observed in the total area under the curve (TAUC) of serum and chylomicron triacylglycerols (ANOVA, P=0·008 and P=0·027, respectively). TAUC of serum triacylglycerols for bicarbonated mineral water 2 was significantly lower compared to low mineral water (Bonferroni, P=0·039). Peak concentration of serum triacylglycerols showed a significant water effect (P=0·025). Changes in chylomicron cholesterol were not significantly affected by the type of water. Bicarbonated mineral waters 1 and 2 did not show any significant differences. Drinking sodium bicarbonate-rich mineral waters reduces postprandial lipaemia in healthy postmenopausal women compared to drinking a low mineral water.