Effects of prior moderate exercise on exogenous and endogenous lipid metabolism and plasma factor VII activity

Abstract

Moderate exercise reduces postprandial triacylglycerol concentrations, which are a risk marker for coronary heart disease. The present study sought to determine the qualitative nature of exercise-induced changes in lipid metabolism and their association (if any) with changes in factor VII activation. Eleven normotriglyceridaemic men, aged 51.7+/-6.1 years (mean+/-S.D.), participated in two oral fat tolerance tests after different pre-conditions: control (no exercise), and exercise (90 min of brisk walking the day before). Venous blood samples were obtained in the fasted state and for 8 h after ingestion of a high-fat meal (1.32 g of fat, 1.36 g of carbohydrate, 0.30 g of protein and 10 mg of [1,1,1-(13)C] tripalmitin x kg(-1) body mass). Prior exercise reduced postprandial plasma triacylglycerol concentrations by 25+/-3% (mean+/-S.E.M.), with lower concentrations in the Svedberg flotation rate (Sf) 20--400 (very-low-density lipoprotein) fraction accounting for 79+/-10% of this reduction. There was no effect on plasma factor VII coagulant activity or on the concentration of the active form of factor VIIa. Prior exercise increased postprandial serum 3-hydroxybutyrate and plasma fatty acid concentrations, decreased serum postprandial insulin concentrations and increased exogenous (8 h (13)C breath excretion of 15.1+/-0.9% of ingested dose compared with 11.9+/-0.8%; P=0.00001) and endogenous postprandial fat oxidation. These data raise the possibility that reduced hepatic secretion of very-low-density lipoprotein plays a role in the attenuation of plasma triacylglycerol concentrations seen after exercise, although it is possible that increased triacylglycerol clearance also contributes to this effect.

Effects of continuous versus accumulated activity patterns on postprandial triacylglycerol concentrations in obese men

“…19 The other mechanism is a reduced rate of hepatic very low-density lipoprotein (VLDL)-TAG secretion. 26 It is difficult to tell which of these mechanisms predominates in the present study. NEFAs concentrations did not differ among trials in the present study suggesting that substrate delivery to the liver for TAG synthesis and secretion in VLDLs was not different among trials.…”

Effect of prior exercise on lipemia after a meal of moderate fat content

“…This is the first attempt to determine whether exercise can suppress the lipemic response to a meal approximating the macronutrient composition of the typical Western diet, that is (in terms of energy) 35-40% fat, about 47% carbohydrate, and about 16% protein (Williams, 2002). In fact, with the exception of Murphy et al (2000), who employed a diet providing 47% of energy from fat over the course of 1 day, all studies on the effect of exercise on postprandial lipemia have used test meals containing 60-93% of energy as fat, or 1.0-1.5 g/kg body mass (Maruhama et al, 1977;Schlierf et al, 1987;Klein et al, 1992;Aldred et al, 1994;Hardman & Aldred, 1995;Tsetsonis & Hardman, 1996a, b;Tsetsonis et al, 1997;Gill et al, 1998Gill et al, , 2001aGill et al, , b, 2002Hardman et al, 1998;Herd et al, 1998Herd et al, , 2000Herd et al, , 2001Zhang et al, 1998;Malkova et al, 1999;Gill & Hardman, 2000;Thomas et al, 2001;Petitt et al, 2003). Since the lipemic response to a fat meal is expected and has been shown to be positively related to the amount of fat ingested (Dubois et al, 1998), one could claim that exercise might not have a significant effect on lipemia after a meal of moderate fat content.…”

“…Physical exercise has been repeatedly shown to be effective to this end, especially when performed on the day before a fat-rich meal (Aldred et al, 1994;Tsetsonis & Hardman, 1996a, b;Tsetsonis et al, 1997;Gill et al, 1998Gill et al, , 2001aGill et al, , b, 2002Zhang et al, 1998;Malkova et al, 1999Malkova et al, , 2000Gill & Hardman, 2000;Herd et al, 2001;Thomas et al, 2001;Petitt et al, 2003). However, there does not seem to be a chronic effect extending beyond 2 days after the interruption of training Herd et al, 1998Herd et al, , 2000.…”

“…This hypothesis has been based on the fact that the attenuation of postprandial lipemia is observed within the time frame of enhanced LPL expression and activity after acute exercise (Seip & Semenkovich, 1998), but experimental evidence is either weak (Herd et al, 2001; or not supportive Gill et al, 2001b;Thomas et al, 2001). An alternative (or complementary) mechanism, decreased secretion of TG by the liver, has gained indirect experimental support Gill et al, 2001a). A third possibility, reduced output of dietary TG from the intestine, has been usually dismissed by the argument that too many hours have elapsed since the exercise stimulus (Tsetsonis & Hardman, 1996b;Gill & Hardman, 2000;Gill et al, 2001a).…”

“…An alternative (or complementary) mechanism, decreased secretion of TG by the liver, has gained indirect experimental support Gill et al, 2001a). A third possibility, reduced output of dietary TG from the intestine, has been usually dismissed by the argument that too many hours have elapsed since the exercise stimulus (Tsetsonis & Hardman, 1996b;Gill & Hardman, 2000;Gill et al, 2001a). However, this hypothesis has not been tested.…”