Dataset Information

Energy replacement using glucose does not increase postprandial lipemia after moderate intensity exercise.

ABSTRACT:

Background

Aerobic exercise can decrease postprandial triglyceride (TG) concentrations but the relationship between exercise-induced energy deficits and postprandial lipemia is still unclear. The aim of the present study was to examine the effect of a single bout of aerobic exercise, with and without energy replacement, on postprandial lipemia and on peripheral blood mononuclear cell (PBMC) mRNA expression of very low density lipoprotein (VLDL) and low density lipoprotein (LDL) receptors and 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR).

Methods

Nine healthy male humans completed three two-day trials in a random order. On day 1, volunteers rested (CON), completed 60 minutes of treadmill walking at 50% of VO2peak (EX) or completed the same bout of walking but with the energy replaced afterwards with a glucose solution (EXG). On day 2, volunteers rested and consumed a high fat test meal in the morning.

Results

Total and incremental TG AUC were significantly lower on the EXG (P < 0.05) and EX (P < 0.05) trials than the CON trial with no difference between the two exercise trials. No significant difference was observed in VLDL or LDL receptor mRNA expression among the trials (P > 0.05).

Conclusions

In conclusion, energy replacement by glucose did not affect the decrease in postprandial TG concentrations observed after moderate intensity exercise and exercise does not affect changes in PBMC HMGCR, VLDL and LDL receptor mRNA expression.

SUBMITTER: Chiu CH

PROVIDER: S-EPMC4258013 | biostudies-literature | 2014 Nov

REPOSITORIES: biostudies-literature

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Publications

Energy replacement using glucose does not increase postprandial lipemia after moderate intensity exercise.

Chiu Chih-Hui CH Burns Stephen Francis SF Yang Tsung-Jen TJ Chang Yi-Hsin YH Chen Yi-Liang YL Chang Cheng-Kang CK Wu Ching-Lin CL

Lipids in health and disease 20141125

<h4>Background</h4>Aerobic exercise can decrease postprandial triglyceride (TG) concentrations but the relationship between exercise-induced energy deficits and postprandial lipemia is still unclear. The aim of the present study was to examine the effect of a single bout of aerobic exercise, with and without energy replacement, on postprandial lipemia and on peripheral blood mononuclear cell (PBMC) mRNA expression of very low density lipoprotein (VLDL) and low density lipoprotein (LDL) receptors ...[more]

PMID: 25424502

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Project description:BackgroundThere is evidence to suggest that postprandial lipemia are is linked to the impairment of endothelial function, which is characterized by an imbalance between the actions of vasodilators and vasoconstrictors. The aim of this study was to determine the effects of a 12-week high-intensity training (HIT) and moderate continuous training (MCT) protocol on postprandial lipemia, vascular function and arterial stiffness in inactive adults after high-fat meal (HFM) ingestion.MethodsA randomized clinical trial was conducted in 20 healthy, inactive adults (31.6 ± 7.1 years). Participants followed the two exercise protocols for 12 weeks. To induce a state of postprandial lipemia (PPL), all subjects received a HFM. Endothelial function was measured using flow-mediated vasodilation (FMD), normalized brachial artery FMD (nFMD), aortic pulse wave velocity (PWV) and augmentation index (AIx). Plasma total cholesterol, high-density lipoprotein cholesterol (HDL-c), triglycerides and glucose were also measured.ResultsThe effects of a HFM were evaluated in a fasted state and 60, 120, 180, and 240 min postprandially. A significant decrease in serum glucose between 0 min (fasted state) and 120 min postprandially was found in the HIT group (P = 0.035). Likewise, FMD (%) was significantly different between the fasted state and 60 min after a HFM in the HIT group (P = 0.042). The total cholesterol response expressed as area under curve (AUC)(0-240) was lower following HIT than following MCT, but no significant differences were observed (8%, P > 0.05). Similarly, triglycerides AUC(0-240) was also lower after HIT compared with MCT, which trended towards significance (24%, P = 0.076). The AUC(0-240) for the glucose response was significantly lower following HIT than MCT (10%, P = 0.008). FMD and nFMD AUC(0-240) were significantly higher following HIT than following MCT (46.9%, P = 0.021 and 67.3%, P = 0.009, respectively). PWV AUC(0-240) did not differ following between the two exercise groups (2.3%, P > 0.05).ConclusionsSupervised exercise training mitigates endothelial dysfunction and glucose response induced by PPL. Exercise intensity plays an important role in these protective effects, and medium-term HIT may be more effective than MCT in reducing postprandial glucose levels and attenuating vascular impairment.Trial registrationClinicalTrials.gov ID: NCT02738385 Date of registration: April 14, 2016.

Project description:PURPOSE:"Quantile-dependent expressivity" describes an effect of the genotype that depends upon the level of the phenotype (e.g., whether a subject's triglycerides are high or low relative to its population distribution). Prior analyses suggest that the effect of a genetic risk score (GRS) on fasting plasma triglyceride levels increases with the percentile of the triglyceride distribution. Postprandial lipemia is well suited for testing quantile-dependent expressivity because it exposes each individual's genotype to substantial increases in their plasma triglyceride concentrations. Ninety-seven published papers were identified that plotted mean triglyceride response vs. time and genotype, which were converted into quantitative data. Separately, for each published graph, standard least-squares regression analysis was used to compare the genotype differences at time t (dependent variable) to average triglyceride concentrations at time t (independent variable) to assess whether the genetic effect size increased in association with higher triglyceride concentrations and whether the phenomenon could explain purported genetic interactions with sex, diet, disease, BMI, and drugs. RESULTS:Consistent with the phenomenon, genetic effect sizes increased (P≤0.05) with increasing triglyceride concentrations for polymorphisms associated with ABCA1, ANGPTL4, APOA1, APOA2, APOA4, APOA5, APOB, APOC3, APOE, CETP, FABP2, FATP6, GALNT2, GCKR, HL, IL1b, LEPR, LOX-1, LPL, MC4R, MTTP, NPY, SORT1, SULF2, TNFA, TCF7L2, and TM6SF2. The effect size for these polymorphisms showed a progressively increasing dose-response, with intermediate effect sizes at intermediate triglyceride concentrations. Quantile-dependent expressivity provided an alternative interpretation to their interactions with sex, drugs, disease, diet, and age, which have been traditionally ascribed to gene-environment interactions and genetic predictors of drug efficacy (i.e., personalized medicine). CONCLUSION:Quantile-dependent expressivity applies to the majority of genetic variants affecting postprandial triglycerides, which may arise because the impaired functionalities of these variants increase at higher triglyceride concentrations. Purported gene-drug interactions may be the manifestations of quantile-dependent expressivity, rather than genetic predictors of drug efficacy.

Project description:Consuming a high-fat meal (HFM) may lead to postprandial lipemia (PPL) and inflammation. Postprandial exercise has been shown to effectively attenuate PPL. However, little is known about the impact of postprandial exercise on systemic inflammation and whether PPL and inflammation are associated. The purpose of this study was to determine whether moderate intensity exercise performed 60 min following a true-to-life HFM would attenuate PPL and inflammation.Thirty-nine young adults (18-40 year) with no known metabolic disease were randomized to either a control group (CON) who remained sedentary during the postprandial period or an exercise (EX) group who walked at 60 % VO2peak to expend ≈ 5 kcal/kgbw one-hour following the HFM. Participants consumed a HFM of 10 kcal/kgbw and blood draws were performed immediately before, 2 h and 4 h post-HFM.At baseline, there were no differences between EX and CON groups for any metabolic or inflammatory markers (p > 0.05). Postprandial triglycerides (TRG) increased from baseline to 4 h in the EX and CON groups (p < 0.001), with no differences between groups (p = 0.871). High density lipoprotein cholesterol (HDL-C) decreased in both groups across time (p < 0.001) with no differences between groups (p = 0.137). Interleukin-6 (IL-6) was significant as a quadratic function over time (p = 0.005), decreasing from baseline to 2 h then increasing and returning to baseline at 4 h in all participants with no difference between groups (p = 0.276). Tumor necrosis factor-alpha (TNF-α) was not different from baseline to 4 h between groups (p > 0.05). There was an increase in soluble vascular adhesion molecule (sVCAM-1) from baseline to 4 h (p = 0.027) for all participants along with a group x time interaction (p = 0.020). Changes in TRG were associated with changes in interleukin-10 (IL-10) from 0 to 2 h (p = 0.007), but were not associated with changes in any other inflammatory marker in the postprandial period (p > 0.05).Despite significant increases in PPL following a HFM, moderate intensity exercise in the postprandial period did not mitigate the PPL nor the inflammatory response to the HFM. These results indicate that in populations with low metabolic risk, PPL and inflammation following a HFM may not be directly related.

Dataset Information

Energy replacement using glucose does not increase postprandial lipemia after moderate intensity exercise.

Background

Methods

Results

Conclusions

Publications

Energy replacement using glucose does not increase postprandial lipemia after moderate intensity exercise.

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