Postheparin Plasma Lipase Activity in Previously Sedentary Adult
Postheparin Plasma Lipase Activity in Previously Sedentary Adult
Objective: To determine the effects of exercise, without weight loss, on insulin sensitivity (SI), postheparin plasma lipase activity (PHPL), intravenous fat clearance rate (K2), and fasting lipids in sedentary adults.
Research Design and Methods: At baseline and after 6 months of walk training (intensity 45-55 or 65-75% heart rate reserve, frequency 3-4 or 5-7 days/week, duration 30 min/session), anthropometric indexes, SI, PHPL, K2, and fasting lipids were measured in 18 sedentary adults (12 women, 6 men; 51.9 ± 5.8 years of age, BMI 28.9 ± 4.6 kg/m).
Results: Exercise increased SI (2.54 ± 2.74 vs. 4.41 ± 3.30 µU · ml · min, P < 0.005) and both lipoprotein lipase (LPL) (1,890 ± 1,380 vs. 4,926 ± 1,858 nEq free fatty acid [FFA] · ml · h) and hepatic lipase (HL) activities (3,326 ± 1,605 vs. 4,636 ± 1,636 nEq FFA · ml · h) (both P < 0.001), without altering BMI, waist circumference, K2, or fasting lipids. Correlations between changes in LPL and the total:HDL cholesterol ratio (r = -0.54) and changes in the LPL:HL ratio and waist circumference (r = -0.50) were significant (P < 0.05).
Conclusions: Exercise, without weight loss, increases SI and PHPL activity in previously sedentary adults, without changing K2 or fasting lipid levels. Furthermore, increased LPL is associated with a decreased total:HDL ratio, and an increased LPL:HL ratio is associated with a decreased waist circumference. Therefore, even modest amounts of exercise in the absence of weight loss positively affect markers of glucose and fat metabolism in previously sedentary, middle-aged adults.
Insulin resistance (IR) is defined as an inappropriately high level of insulin required to maintain metabolic homeostasis and is characterized by diminished peripheral insulin sensitivity (SI). Obesity and central body fat distribution are strong predictors of IR. Previous research demonstrates that weight loss through caloric restriction is associated with improvement in visceral adiposity, SI, and lipid risk factors for coronary artery disease.
Physical inactivity also results in markedly decreased SI. Several training studies have demonstrated that regular aerobic exercise leads to enhanced SI in previously sedentary adults. Improvements in SI with training have been accompanied by significant reductions in body weight and body composition in some, but not all, of these studies.
In addition to the profound effects of enhanced insulin action on glucose homeostasis, SI is an important independent determinant of the variation in free fatty acid (FFA) and triglyceride (TG) concentrations in adults. Exercise training is known to decrease TG concentrations and has been shown to increase the intravenous fat clearance (K2) of a TG emulsion. Enhanced K2 (92% greater clearance rate) has also been reported for endurance athletes, compared with sedentary men, in a cross-sectional study.
One potential mechanism by which exercise enhances lipid metabolism is alteration of plasma lipase activity (i.e., lipoprotein lipase [LPL] and hepatic lipase [HL]). The activity of LPL is a key determinant in the rate of catabolism of TG-rich lipoproteins, and impaired function of LPL has been found in individuals with IR. Increased LPL is a common finding in several, but not all, training studies. Furthermore, although LPL was only 2% higher, while K2 was 92% higher, in endurance-trained athletes compared with sedentary subjects, there was a direct correlation between these parameters. Together, these studies suggest that insulin may be an important regulator of LPL and that increased K2 may be at least partly explained by an increase in LPL activity. Some studies have also reported significant training-induced decrements in HL. Whereas loss of intra-abdominal fat is associated with a reduction in HL and subsequent beneficial effects on lipid levels, there is no consistent pattern in documenting positive effects of exercise per se, in the absence of weight loss, on plasma lipase activity, K2, and lipid levels.
To our knowledge, there are no investigations that have directly linked improvements in SI to enhanced postheparin plasma lipase activity (PHPL), and subsequent improvements in lipid metabolism, while body weight is maintained in sedentary adults engaged in an exercise training program. Therefore, we tested the hypothesis that aerobic exercise training, without concomitant weight loss, significantly increases SI in previously sedentary adults. We also postulated that the training-induced increase in SI would enhance PHPL, and subsequently, K2 and other markers of lipid metabolism.
Objective: To determine the effects of exercise, without weight loss, on insulin sensitivity (SI), postheparin plasma lipase activity (PHPL), intravenous fat clearance rate (K2), and fasting lipids in sedentary adults.
Research Design and Methods: At baseline and after 6 months of walk training (intensity 45-55 or 65-75% heart rate reserve, frequency 3-4 or 5-7 days/week, duration 30 min/session), anthropometric indexes, SI, PHPL, K2, and fasting lipids were measured in 18 sedentary adults (12 women, 6 men; 51.9 ± 5.8 years of age, BMI 28.9 ± 4.6 kg/m).
Results: Exercise increased SI (2.54 ± 2.74 vs. 4.41 ± 3.30 µU · ml · min, P < 0.005) and both lipoprotein lipase (LPL) (1,890 ± 1,380 vs. 4,926 ± 1,858 nEq free fatty acid [FFA] · ml · h) and hepatic lipase (HL) activities (3,326 ± 1,605 vs. 4,636 ± 1,636 nEq FFA · ml · h) (both P < 0.001), without altering BMI, waist circumference, K2, or fasting lipids. Correlations between changes in LPL and the total:HDL cholesterol ratio (r = -0.54) and changes in the LPL:HL ratio and waist circumference (r = -0.50) were significant (P < 0.05).
Conclusions: Exercise, without weight loss, increases SI and PHPL activity in previously sedentary adults, without changing K2 or fasting lipid levels. Furthermore, increased LPL is associated with a decreased total:HDL ratio, and an increased LPL:HL ratio is associated with a decreased waist circumference. Therefore, even modest amounts of exercise in the absence of weight loss positively affect markers of glucose and fat metabolism in previously sedentary, middle-aged adults.
Insulin resistance (IR) is defined as an inappropriately high level of insulin required to maintain metabolic homeostasis and is characterized by diminished peripheral insulin sensitivity (SI). Obesity and central body fat distribution are strong predictors of IR. Previous research demonstrates that weight loss through caloric restriction is associated with improvement in visceral adiposity, SI, and lipid risk factors for coronary artery disease.
Physical inactivity also results in markedly decreased SI. Several training studies have demonstrated that regular aerobic exercise leads to enhanced SI in previously sedentary adults. Improvements in SI with training have been accompanied by significant reductions in body weight and body composition in some, but not all, of these studies.
In addition to the profound effects of enhanced insulin action on glucose homeostasis, SI is an important independent determinant of the variation in free fatty acid (FFA) and triglyceride (TG) concentrations in adults. Exercise training is known to decrease TG concentrations and has been shown to increase the intravenous fat clearance (K2) of a TG emulsion. Enhanced K2 (92% greater clearance rate) has also been reported for endurance athletes, compared with sedentary men, in a cross-sectional study.
One potential mechanism by which exercise enhances lipid metabolism is alteration of plasma lipase activity (i.e., lipoprotein lipase [LPL] and hepatic lipase [HL]). The activity of LPL is a key determinant in the rate of catabolism of TG-rich lipoproteins, and impaired function of LPL has been found in individuals with IR. Increased LPL is a common finding in several, but not all, training studies. Furthermore, although LPL was only 2% higher, while K2 was 92% higher, in endurance-trained athletes compared with sedentary subjects, there was a direct correlation between these parameters. Together, these studies suggest that insulin may be an important regulator of LPL and that increased K2 may be at least partly explained by an increase in LPL activity. Some studies have also reported significant training-induced decrements in HL. Whereas loss of intra-abdominal fat is associated with a reduction in HL and subsequent beneficial effects on lipid levels, there is no consistent pattern in documenting positive effects of exercise per se, in the absence of weight loss, on plasma lipase activity, K2, and lipid levels.
To our knowledge, there are no investigations that have directly linked improvements in SI to enhanced postheparin plasma lipase activity (PHPL), and subsequent improvements in lipid metabolism, while body weight is maintained in sedentary adults engaged in an exercise training program. Therefore, we tested the hypothesis that aerobic exercise training, without concomitant weight loss, significantly increases SI in previously sedentary adults. We also postulated that the training-induced increase in SI would enhance PHPL, and subsequently, K2 and other markers of lipid metabolism.
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