Effects of Exercise on Fructose-induced Postprandial Lipemia
Condition: Sedentary Lifestyle; Dyslipidemias; Lipid Metabolism Disorders; Carbohydrate Inducible Hyperlipemia
MeSH terms: Hyperlipoproteinemia Type IV; Dyslipidemias; Metabolic Diseases; Hyperlipidemias; Lipid Metabolism Disorders
Study type: Interventional

Summary: 
      Cardiovascular Diseases (CVDs) are the leading causes of death in the world and in Brazil. In
      2001, 12.45 million deaths on the globe (21% of the total) were caused by some CVD.

      The composition of modern man's diet has changed drastically with the industrialization of
      food, resulting in the transition from a diet rich in fibers and complex carbohydrates to one
      with a high content of sugars and fats. Since the current dietary pattern is characterized by
      the consumption of three or more meals a day, containing a quantity of fat in the range of 20
      to 70 g, individuals spend a large part of the day in the postprandial state, with continuous
      fluctuation of lipemia Over 18 hours. Food intake (postprandial state) is the dynamic,
      unstable response of the body that refers to rapid hormonal and lipoprotein remodeling. It is
      well established in the literature that high-fat meals (lipid overload) cause an increase in
      plasma triglycerides. Hypertriglyceridemia and / or elevated triglyceride-rich lipoproteins
      (LRT) (chylomicrons, VLDL and their remnants) in the postprandial state induces endothelial
      dysfunction via increased oxidative stress and is an independent risk factor for CVDs.
      Therefore, Postprandial Lipemia (PPL) is counted as an early marker of atherosclerotic
      process, metabolic abnormalities and endothelial dysfunction.

      High-carbohydrate (CHO) diets may promote increased LDL-c, TG, VLDL and HDL-c reduction, as
      well as PPL, generating a lipid profile associated with an increased risk of CVDs. This
      effect appears to be more pronounced with the inclusion of simple carbohydrates (mono and
      disaccharides), although it also occurs with diets rich in complex carbohydrates
      (polysaccharides).

      High fructose diets (HFDs) are a known model of induction of insulin resistance, dyslipidemia
      and DM2 in primates and humans. The chronic effect of fructose consumption has been well
      studied in the last decades due to its connection with obesity, resistance to Insulin,
      accumulation of visceral fat and dyslipidemia.

      As the consumption of fructose is progressively increasing in society and its chronic
      exposure can generate a phenotypic effect of dyslipidemia and, consequently, the increased
      risk of CVDs, prevention and treatment strategies should be seen as an important public
      health issue . Thus, the objective of this study is to understand the effects of exercise on
      fat metabolism, since there is a lack of robust evidence about the possible cardioprotective
      and hypolipemic role of the same on HFD.
    

Detailed description: 
      Background: Cardiovascular Diseases (CVDs) are the leading causes of death in the world and
      in Brazil. In 2001, 12.45 million deaths on the globe (21% of the total) were caused by some
      CVD.

      Different studies agree that CVDs can be prevented by reducing risk factors, such as:
      smoking, inadequate diet (high in fat, simple carbohydrates and salt), physical inactivity,
      obesity, diabetes mellitus (DM), high levels of Lipids in the blood (dyslipidemia) and
      hyperglycemia even in the absence of a diagnosis of DM.

      The composition of modern man's diet has changed drastically with the industrialization of
      food, resulting in the transition from a diet rich in fibers and complex carbohydrates to one
      with a high content of sugars and fats. Since the current dietary pattern is characterized by
      the consumption of three or more meals a day, containing a quantity of fat in the range of 20
      to 70 g, individuals spend a large part of the day in the postprandial state, with continuous
      fluctuation of lipemia Over 18 hours.

      Food intake (postprandial state) is the dynamic, unstable response of the body that refers to
      rapid hormonal and lipoprotein remodeling. It is well established in the literature that
      high-fat meals (lipid overload) cause an increase in plasma triglycerides.
      Hypertriglyceridemia and / or elevated triglyceride-rich lipoproteins (LRT) (chylomicrons,
      VLDL and their remnants) in the postprandial state induces endothelial dysfunction via
      increased oxidative stress and is an independent risk factor for CVDs. Therefore,
      Postprandial Lipemia (PPL) is counted as an early marker of atherosclerotic process,
      metabolic abnormalities and endothelial dysfunction.

      High-carbohydrate (CHO) diets may promote increased LDL-c, TG, VLDL and HDL-c reduction, as
      well as PPL, generating a lipid profile associated with an increased risk of CVDs. This
      effect appears to be more pronounced with the inclusion of simple carbohydrates (mono and
      disaccharides), although it also occurs with diets rich in complex carbohydrates
      (polysaccharides).

      High fructose diets (HFDs) are a known model of induction of insulin resistance, dyslipidemia
      and DM2 in primates and humans. The chronic effect of fructose consumption has been well
      studied in the last decades due to its connection with obesity, resistance to Insulin,
      accumulation of visceral fat and dyslipidemia.

      Due to the increase in fructose consumption from beverages and processed foods, changes in
      lifestyle, mainly related to diet and exercise, should be seen as a means of prevention and
      first form of treatment of CVDs and changes in lipid metabolism.

      Acute and chronic aerobic exercise seems to reduce the risk of atherosclerosis and CVD by
      reducing lipemia (improvement of TG, CT, LDL-c and HDL-c) and endothelial function. In
      addition, the exercise when performed the previous day has the ability to prevent the
      increase of PPL after a hyperlipidic meal, regardless of body mass. This effect may be
      considered a cardiometabolic protection and seems to occur as a result of the increase in
      lipoprotein lipase (LPL) activity and / or reduction of VLDL secretion in the liver.

      As the consumption of fructose is progressively increasing in society and its chronic
      exposure can generate a phenotypic effect of dyslipidemia and, consequently, the increased
      risk of CVDs, prevention and treatment strategies should be seen as an important public
      health issue . Thus, the objective of this study is to understand the effects of exercise on
      fat metabolism, since there is a lack of robust evidence about the possible cardioprotective
      and hypolipemic role of the same on HFD.

      Methods: The study was characterized as a crossover randomized clinical trial, with a 7 day
      washout period. The sample was composed of 12 sedentary men, aged between 20 and 40 years.
      All volunteers who agreed to participate in the study signed a two-way informed consent form
      (TCLE). The study protocol followed the recommendations of the Helsinki Declaration. Subjects
      were invited to perform three (3) protocols, in a randomized fashion, with a minimum period
      of one week interval (washout period). On day 0, they arrived to the laboratory at the end of
      the day, between 6 and 7pm, to perform 45min of treadmill exercise at 60% of the VO2peak or
      rest, depending on randomization. Soon after, he received a Standard Meal (SM; 60%
      carbohydrate, 20% fat, 20% protein) in the laboratory and was instructed to perform a 12-hour
      fast. On day 1, they arrived at the laboratory between 7 and 8 a.m and were submitted to
      basal blood collection. Soon after, they received a High Fat Meal (HFM) which consisted of
      sandwich with cream and cheese, added to the drink rich in FRUCTose (0.5 g / kg) or DEXtrose
      (isoenergetic). The meals had the same energy and macronutrients (50% fat, 40% carbohydrate
      and 10% protein) and should be consumed in 10 minutes. Blood samples were collected from 1 to
      4 h after the meal consumption to analyze the postprandial parameters. Subsequently the
      subject was released to perform his daily activities outside the laboratory. On the same day,
      between 6 pm and 7 pm, the subject returned to the laboratory to remain at rest and receive a
      SM again and be instructed to perform 12 hours of fasting. On day 2, subjects reached the
      laboratory between 7 and 8 a.m. and again submitted to baseline blood collection. Soon after,
      they received HFM with a drink rich in DEXtrose (0.5g / kg). Blood samples were collected
      from 1 to 4 hours after eating the meal. A 24h food record was done to control subject's
      diet. Body composition was evaluated before intervention. The data were analyzed using the
      statistical package IBM SPSS statistics (Statistical Package for Social Sciences) version
      20.0 (IBM, USA) for Windows. The distribution of all variables was analyzed using the
      Shapiro-Wilk test, and the analysis sphericity by the Mauchly test. In cases where the data
      did not pass the normality tests, the respective nonparametric tests were performed. Data
      from the experimental groups were treated by two-way ANOVA for repeated measurements (2 x 5).
      If necessary, the Bonferroni post-hoc was used to identify differences. Incremental and total
      area under the curve were analyzed by trapezoidal method. The difference between AUC was
      verified by one-way ANOVA with post-hoc Bonferroni. All results were expressed as mean and
      standard deviation, or median, where appropriate, and the accepted level of significance was
      5%.
    

Intervention name(s): FRUCTOSE; DEXTROSE; EXERCISE
Intervention type(s): Dietary Supplement; Dietary Supplement; Dietary Supplement
Intervention description(s): Fructose-rich beverage with a high fat meal, without exercise.; Dextrose-rich beverage with a high fat meal (control), without exercise.; 45 minutes of 60% VO2peak aerobic exercise
Other intervention name(s): High fat meal; High fat meal
Allocation: Randomized
Intervention model: Crossover Assignment
Masking: Double (Participant, Outcomes Assessor)
Primary purpose: Prevention
Keywords: fat metabolism; fructose; exercise