Exercise Training, Without Weight Loss, Increases Insulin Sensitivity and Postheparin Plasma Lipase Activity in Previously Sedentary Adults

Abstract

OBJECTIVE -To determine the effects of exercise, without weight loss, on insulin sensitivity (S I ), postheparin plasma lipase activity (PHPL), intravenous fat clearance rate (K 2 ), 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, S I , PHPL, K 2 , and fasting lipids were measured in 18 sedentary adults (12 women, 6 men; 51.9 Ϯ 5.8 years of age, BMI 28.9 Ϯ 4.6 kg/m 2 ). ⅐ h Ϫ1 ) (both P Ͻ 0.001), without altering BMI, waist circumference, K 2 , or fasting lipids. Correlations between changes in LPL and the total:HDL cholesterol ratio (r ϭ Ϫ0.54) and changes in the LPL:HL ratio and waist circumference (r ϭ Ϫ0.50) were significant (P Ͻ 0.05). RESULTSCONCLUSIONS -Exercise, without weight loss, increases S I and PHPL activity in previously sedentary adults, without changing K 2 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. Diabetes Care 26:557-562, 2003I nsulin resistance (IR) is defined as an inappropriately high level of insulin required to maintain metabolic homeostasis (1) and is characterized by diminished peripheral insulin sensitivity (S I ). Obesity and central body fat distribution are strong predictors of IR (2). Previous research demonstrates that weight loss through caloric restriction is associated with improvement in visceral adiposity, S I , and lipid risk factors for coronary artery disease (3).Physical inactivity also results in markedly decreased S I (4). Several training studies (5-7) have demonstrated that regular aerobic exercise leads to enhanced S I in previously sedentary adults. Improvements in S I with training have been accompanied by significant reductions in body weight and body composition in some (5), but not all (6,7), of these studies.In addition to the profound effects of enhanced insulin action on glucose homeostasis, S I is an important independent determinant of the variation in free fatty acid (FFA) and triglyceride (TG) concentrations in adults (8). Exercise training is known to decrease TG concentrations (9,10) and has been shown to increase the intravenous fat clearance (K 2 ) of a TG emulsion (11,12). Enhanced K 2 (92% greater clearance rate) has also been reported for endurance athletes, compared with sedentary men, in a cross-sectional study (13).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 (14), and impaired function of LPL has been found in individuals with IR (15,1...

Effects of resistance versus endurance training on serum adiponectin and insulin resistance index

“…An interesting finding from the present study is that insulin sensitivity was improved without changes in body weight, WHR and BMI. This finding supports those of previous studies (35,36) and suggests that both endurance and circuit weight training improve insulin sensitivity independent of changes in body composition. Restoring insulin sensitivity by aerobic exercise and circuit weight training might be mediated mainly by mechanisms other than adiponectin, for instance, by the AMP-activated protein kinase pathway (10).…”

Low-intensity physical activity is associated with reduced risk of incident type 2 diabetes in older adults: evidence from the English Longitudinal Study of Ageing

“…As weight loss is not the only mechanism through which physical activity is associated with type 2 diabetes, it is important to establish what other non-obesity-related biological mechanisms may play a role. Structural and biochemical changes in skeletal muscle and systemic changes such as improved hormonal homeostasis and improvements in dyslipidaemia and inflammation [4,5,[24][25][26]] may be such mechanisms. Other studies have also examined the association between acute exercise and rapid and pronounced induction of hepatic metabolic enzymes and regulators of metabolism or transcription, such as insulin receptor substrate in animals [27] and the role of proteins that regulate translocation of the glucose transporter isoform GLUT-4 such as Akt substrate [28].…”

Influence of Pro12Ala peroxisome proliferator-activated receptor γ2 polymorphism on glucose response to exercise training in type 2 diabetes

“…Exercise training and the Ala allele must act either independently or in unison to modify glucose homeostasis through increasing glucose uptake or by decreasing hepatic glucose output. At the whole-body level, exercise training has been shown to increase insulin sensitivity [53][54][55] and has also been shown to decrease basal hepatic glucose production in patients with type 2 diabetes [56]. At baseline, the association of the Ala allele with lower fasting glucose or insulin is inconsistent [31,42,49,57,58].…”