Inactivity, exercise training and detraining, and plasma lipoproteins. STRRIDE: a randomized, controlled study of exercise intensity and amount.

Exercise has beneficial effects on lipoproteins. Little is known about how long the effects persist with detraining or whether the duration of benefit is effected by training intensity or amount. Sedentary, overweight subjects (n = 240) were randomized to 6-mo control or one of three exercise groups: 1) high-amount/vigorous-intensity exercise; 2) low-amount/vigorous-intensity exercise; or 3) low-amount/moderate-intensity exercise. Training consisted of a gradual increase in amount of exercise followed by 6 mo of exercise at the prescribed level. Exercise included treadmill, elliptical trainer, and stationary bicycle. The number of minutes necessary to expend the prescribed kilocalories per week (14 kcal x kg body wt(-1) x wk(-1) for both low-amount groups; 23 kcal x kg body wt(-1) x wk(-1) for high-amount group) was calculated for each subject. Average adherence was 83-92% for the three groups; minutes per week were 207, 125, and 203 and sessions per week were 3.6, 2.9, and 3.5 for high-amount/vigorous-intensity, low-amount/vigorous intensity, and low-amount/moderate-intensity groups, respectively. Plasma was obtained at baseline, 24 h, 5 days, and 15 days after exercise cessation. Continued inactivity resulted in significant increases in low-density lipoprotein (LDL) particle number, small dense LDL, and LDL-cholesterol. A modest amount of exercise training prevented this deterioration. Moderate-intensity but not vigorous-intensity exercise resulted in a sustained reduction in very-low-density lipoprotein (VLDL)-triglycerides over 15 days of detraining (P < 0.05). The high-amount group had significant improvements in high-density lipoprotein (HDL)-cholesterol, HDL particle size, and large HDL levels that were sustained for 15 days after exercise stopped. In conclusion, physical inactivity has profound negative effects on lipoprotein metabolism. Modest exercise prevented this. Moderate-intensity but not vigorous-intensity exercise resulted in sustained VLDL-triglyceride lowering. Thirty minutes per day of vigorous exercise, like jogging, has sustained beneficial effects on HDL metabolism.     

Aerobic exercise training reduces epicardial fat in obese men

The purpose of this study was to determine the effects of exercise training on ventricular epicardial fat thickness in obese men and to investigate the relationship of the change in epicardial fat thickness to changes in abdominal fat tissue following exercise training. Twenty-four obese middle-aged men [age, 49.4 +/- 9.6 yr; weight, 87.7 +/- 11.2 kg; body mass index (BMI), 30.7 +/- 3.3 kg/m(2); peak oxygen consumption, 28.4 +/- 7.2 ml.kg(-1).min(-1); means +/- SD] participated in this study. Each participant completed a 12-wk supervised exercise training program (60-70% of the maximal heart rate; 60 min/day, 3 days/wk) and underwent a transthoracic echocardiography. The epicardial fat thickness on the free wall of the right ventricle was measured from both parasternal long- and short-axis views. The visceral adipose tissue (VAT) and subcutaneous adipose tissues were measured by computed tomography. Following exercise training, the epicardial fat thickness was significantly decreased (P < 0.001). The percentage change of epicardial fat thickness was twice as high compared with those of waist, BMI, and body weight of original values (P <0.05). There was a significant relationship (r = 0.525, P = 0.008) between changes in the epicardial fat thickness and VAT with exercise training. Stepwise multiple regression analysis revealed that the change in VAT, change in systolic blood pressure, and change in quantitative insulin sensitivity check index were independently related to the change epicardial fat thickness (P < 0.05). The ventricular epicardial fat thickness is reduced significantly after aerobic exercise training and is associated with a decrease in VAT. These results suggest that aerobic exercise training may be an effective nonpharmacological strategy for decreasing the ventricular epicardial fat thickness and visceral fat area in obese middle-aged men.     

Dynamic exercise attenuates sympathetic responsiveness of canine vascular smooth muscle.

The phenomenon of reduced responsiveness of the skeletal muscle arterial vasculature to sympathetic activation during exercise (sympatholysis) remains controversial. The purpose of this study was to examine the vascular effects of sympathoactivation in dynamically exercising skeletal muscle. Mongrel dogs (19-24 kg) were instrumented chronically with transit-time ultrasonic flow probes on the external iliac arteries. After pretreatment with atropine (0.2 mg/kg), an intravenous bolus (4 microg/kg) of a nicotinic ganglion stimulant [1,1-dimethyl-4-phenylpiperazinium iodide (DMPP)] was given at rest and during treadmill exercise at graded intensities. Administration of DMPP was associated with prompt reductions in iliac blood flow and increases in arterial pressure under all conditions. There were significant reductions (P < 0.05) in iliac vascular conductance of 58 +/- 4 (SE), 48 +/- 3, 36 +/- 5, and 16 +/- 3% at rest, 3 miles/h and 0% grade, 6 miles/h and 0% grade, and 6 miles/h and 15% grade, respectively. These data demonstrate that activation of postganglionic sympathetic nerves with DMPP caused vasoconstriction in the skeletal muscle vasculature at rest and during exercise. Additionally, the magnitude of vasoconstriction was inversely related to exercise intensity. These results support the concept of exercise sympatholysis.     

Effect of exercise training on insulin sensitivity and glucose metabolism in lean, obese, and diabetic men.

To clarify the impact of vigorous physical training on in vivo insulin action and glucose metabolism independent of the intervening effects of concomitant changes in body weight and composition and residual effects of an acute exercise session, 10 lean, 10 obese, and 6 diet-controlled type II diabetic men trained for 12 wk on a cycle ergometer 4 h/wk at approximately 70% of maximal O2 uptake (VO2max) while body composition and weight were maintained by refeeding the energy expended in each training session. Before and 4-5 days after the last training session, euglycemic hyperinsulinemic (40 mU.m2.min-1) clamps were performed at a plasma glucose of 90 mg/dl, combined with indirect calorimetry. Total insulin-stimulated glucose disposal (M) was corrected for residual hepatic glucose output. Body weight, fat, and fat-free mass (FFM) did not change with training, but cardiorespiratory fitness increased by 27% in all groups. Before and after training, M was lower for the obese (5.33 +/- 0.39 mg.kg FFM-1.min-1 pretraining; 5.33 +/- 0.46 posttraining) than for the lean men (9.07 +/- 0.49 and 8.91 +/- 0.60 mg.kg FFM-1.min-1 for pretraining and posttraining, respectively) and lower for the diabetic (3.86 +/- 0.44 and 3.49 +/- 0.21) than for the obese men (P less than 0.001). Insulin sensitivity was not significantly altered by training in any group, but basal hepatic glucose production was reduced by 22% in the diabetic men. Thus, when intervening effects of the last exercise bout or body composition changes were controlled, exercise training per se leading to increased cardiorespiratory fitness had no independent impact on insulin action and did not improve the insulin resistance in obese or diabetic men.     

Substrate utilization during exercise in formerly morbidly obese women.

The purpose of this study was to compare substrate utilization during fasting and submaximal exercise in morbidly obese women after weight loss (WL) with that in weight-matched controls (C). WL were studied in the weight-stable condition approximately 24 mo after gastric bypass surgery. Energy intake (self-reported) and expenditure ((2)H(2)(18)O) were also compared. The respiratory exchange ratio during exercise at the same absolute (15 W) workload was significantly (P < or = 0.05) elevated in WL vs. C (0.90 +/- 0.02 vs. 0.83 +/- 0.03); this was reflected as lower fat utilization in WL (29.7 +/- 4.8 vs. 53.2 +/- 9.7% of energy from fat). Respiratory exchange ratio during exercise at the same relative (65% of maximal O(2) uptake) intensity was also significantly (P < 0.05) elevated in WL (0.96 +/- 0.01 vs. 0.89 +/- 0.02), and fat use was concomitantly depressed (12.4 +/- 3.0 vs. 34.3 +/- 9.9% of energy from fat). Resting substrate utilization, daily energy expenditure, and self-reported relative macronutrient intake did not differ between groups. These data suggest that lipid oxidation is depressed during physical activity in WL. This defect may, at least in part, contribute to a propensity for the development of morbid obesity.     

Fat metabolism and acute resistance exercise in trained men.

The purpose of this study was to investigate the effect of acute resistance exercise (RE) on lipolysis within adipose tissue and subsequent substrate oxidation to better understand how RE may contribute to improvements in body composition. Lipolysis and blood flow were measured in abdominal subcutaneous adipose tissue via microdialysis before, during, and for 5 h following whole body RE as well as on a nonexercise control day (C) in eight young (24 +/- 0.7 yr), active (>3 RE session/wk for at least 2 yr) male participants. Fat oxidation was measured immediately before and after RE via indirect calorimetry for 45 min. Dialysate glycerol concentration (an index of lipolysis) was higher during (RE: 200.4 +/- 38.6 vs. C: 112.4 +/- 13.1 micromol/l, 78% difference; P = 0.02) and immediately following RE (RE: 184 +/- 41 vs. C: 105 + 14.6 micromol/l, 75% difference; P = 0.03) compared with the same time period on the C day. Energy expenditure was elevated in the 45 min after RE compared with the same time period on the C day (RE: 104.4 +/- 6.0 vs. C: 94.5 +/- 4.0 kcal/h, 10.5% difference; P = 0.03). Respiratory exchange ratio was lower (RE: 0.71 +/- 0.004 vs. C: 0.85 +/- .03, 16.5% difference; P = 0.004) and fat oxidation was higher (RE: 10.2 +/- 0.8 vs. C: 5.0 +/- 1.0 g/h, 105% difference; P = 0.004) following RE compared with the same time period on the C day. Therefore, the mechanism behind RE contributing to improved body composition is in part due to enhanced abdominal subcutaneous adipose tissue lipolysis and improved whole body fat oxidation and energy expenditure in response to RE.     

Spontaneous running activity in male rats: effect of age

Alterations in the intensity and pattern of spontaneous running activity as rats increase in age from 7 wk to 1 yr was studied in male rats placed in exercise wheel cages. Daily running records were obtained on 27 rats for periods up to 12 mo, and 24-h activity recordings were made of selected runners to study the variation in activity during the day. The data indicate that for rats running over 2,940 revolutions (or 2 miles/day), the maximum intensity of running attained can be divided into a group of high achievers (approximately 8 miles/day) and moderate achievers (averaging 4.5 miles/day). For both groups, spontaneous running activity reached maximal rates after 4-5 wk. This maximal rate was sustained for 7-8 wk, then fell to levels approximately 60% of maximum for 4-5 mo, and then fell again to levels approximately 25% of maximum from 8 to 12 mo of age. The hourly pattern of running activity during the day was defined in rats of increasing age, who averaged 13,280, 6,662, 3,874, and 1,755 rev/day, corresponding to 9.0, 4.5, 2.6, and 1.2 miles/day, respectively. The overall patterns at each level indicated that the major running period occurred between 6:00 P.M. and 6:00 A.M., the greater activity of younger rats was paralleled by faster speeds and longer duration at each hour of the day, and the peak running activity for each group generally occurred between 7:00 and 9:00 P.M. In summary, there is a progressive loss in speed and duration of spontaneous running activity as male rats increase in age, with intensity of exercise falling below 2 miles/day after 7-8 mo of age.     

Weight loss increases cardiovagal baroreflex function in obese young and older men

We tested the hypothesis that reductions in total body and abdominal visceral fat with energy restriction would be associated with increases in cardiovagal baroreflex sensitivity (BRS) in overweight/obese older men. To address this, overweight/obese (25 < or = body mass index < or = 35 kg/m(2)) young (OB-Y, n = 10, age = 32.9 +/- 2.3 yr) and older (OB-O, n = 6, age = 60 +/- 2.7 yr) men underwent 3 mo of energy restriction at a level designed to reduce body weight by 5-10%. Cardiovagal BRS (modified Oxford technique), body composition (dual-energy X-ray absorptiometry), and abdominal fat distribution (computed tomography) were measured in the overweight/obese men before weight loss and after 4 wk of weight stability at their reduced weight and compared with a group of nonobese young men (NO-Y, n = 13, age = 21.1 +/- 1.0 yr). Before weight loss, cardiovagal BRS was approximately 35% and approximately 60% lower (P < 0.05) in the OB-Y and OB-O compared with NO-Y. Body weight (-7.8 +/- 1.1 vs. -7.3 +/- 0.7 kg), total fat mass (-4.1 +/- 1.0 vs. -4.4 +/- 0.8 kg), and abdominal visceral fat (-27.6 +/- 6.9 vs. -43.5 +/- 10.1 cm(2)) were reduced (all P < 0.05) after weight loss, but the magnitude of reduction did not differ (all P > 0.05) between OB-Y and OB-O, respectively. Cardiovagal BRS increased (11.5 +/- 1.9 vs. 18.5 +/- 2.6 ms/mmHg and 6.7 +/- 1.2 vs. 12.8 +/- 4.2 ms/mmHg) after weight loss (both P < 0.05) in OB-Y and OB-O, respectively. After weight loss, cardiovagal BRS in the obese/overweight young and older men was approximately 105% and approximately 73% (P > 0.05) of NO-Y (17.5 +/- 2.2 ms/mmHg). Therefore, the results of this study indicate that weight loss increases the sensitivity of the cardiovagal baroreflex in overweight/obese young and older men.     

Role of nitric oxide in exercise sympatholysis.

The production of nitric oxide is the putative mechanism for the attenuation of sympathetic vasoconstriction (sympatholysis) in working muscles during exercise. We hypothesized that nitric oxide synthase blockade would eliminate the reduction in alpha-adrenergic-receptor responsiveness in exercising skeletal muscle. Ten mongrel dogs were instrumented chronically with flow probes on the external iliac arteries of both hindlimbs and a catheter in one femoral artery. The selective alpha(1)-adrenergic agonist (phenylephrine) or the selective alpha(2)-adrenergic agonist (clonidine) was infused as a bolus into the femoral artery catheter at rest and during mild and heavy exercise. Before nitric oxide synthase inhibition with N(G)-nitro-l-arginine methyl ester (l-NAME), intra-arterial infusions of phenylephrine elicited reductions in vascular conductance of -91 +/- 3, -80 +/- 5, and -75 +/- 6% (means +/- SE) at rest, 3 miles/h, and 6 miles/h and 10% grade, respectively. Intra-arterial clonidine reduced vascular conductance by -65 +/- 6, -39 +/- 4, and -30 +/- 3%. After l-NAME, intra-arterial infusions of phenylephrine elicited reductions in vascular conductance of -85 +/- 5, -85 +/- 5, and -84 +/- 5%, whereas clonidine reduced vascular conductance by -67 +/- 5, -45 +/- 3, and -35 +/- 3%, at rest, 3 miles/h, and 6 miles/h and 10% grade. alpha(1)-Adrenergic-receptor responsiveness was attenuated during heavy exercise. In contrast, alpha(2)-adrenergic-receptor responsiveness was attenuated even at a mild exercise intensity. Whereas the inhibition of nitric oxide production eliminated the exercise-induced attenuation of alpha(1)-adrenergic-receptor responsiveness, the attenuation of alpha(2)-adrenergic-receptor responsiveness was unaffected. These results suggest that the mechanism of exercise sympatholysis is not entirely mediated by the production of nitric oxide.     

Diet-induced metabolic acidosis and the performance of high intensity exercise in man

The influence of four isolated periods of dietary manipulation upon high intensity exercise capacity was investigated in six healthy male subjects. Subjects consumed their 'normal' (N) diet (45 +/- 2% carbohydrate (CHO), 41 +/- 3% fat, 14 +/- 3% protein) for four days after which they exercised to voluntary exhaustion at a workload equivalent to 100% VO2max. Three further four-day periods of dietary manipulation took place; these were assigned in a randomised manner and each was followed by a high intensity exercise test. The dietary treatments were: a low CHO (3 +/- 1%), high fat (71 +/- 5%), high protein (26 +/- 3%) diet (HFHP); a high CHO (73 +/- 2%), low fat (12 +/- 2%), normal protein (15 +/- 1%) diet (HCLF); and a normal CHO (47 +/- 3%), low fat (27 +/- 2%), high protein (26 +/- 2%) diet (LFHP). Acid-base status and blood lactate concentration were measured on arterialised-venous blood at rest prior to dietary manipulation on each day of the different diets, immediately prior to exercise and at 2, 4, 6, 10 and 15 min post-exercise. Other metabolite concentrations were measured in the blood samples obtained prior to dietary manipulation and immediately prior to exercise. Exercise time to exhaustion after the HFHP diet (179 +/- 63 s) was shorter when compared with the N (210 +/- 65 s; p less than 0.01) and HCLF (219 +/- 69 s; p less than 0.05) diets.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of HRT and exercise training on insulin action, glucose tolerance, and body composition in older women.

The independent and combined effects of exercise training and hormone replacement therapy (HRT) on body composition, fat distribution, glucose tolerance, and insulin action were studied in postmenopausal women, aged 68 +/- 5 yr, assigned to control (n = 19), exercise (n = 18), HRT (n = 15), and exercise + HRT (n = 16) groups. The exercise consisted of 2 mo of flexibility exercises followed by 9 mo of endurance exercise. HRT was conjugated estrogens 0.625 mg/day and trimonthly medroxyprogesterone acetate 5 mg/day for 13 days. Total and regional body composition were measured by dual-energy X-ray absorptiometry. Serum glucose and insulin responses were measured during a 2-h oral glucose tolerance test. There were significant main effects of exercise on reductions in total and regional (trunk, arms, legs) fat mass, increase in leg fat-free mass, and improvements in glucose tolerance and insulin action. There were significant main effects of HRT on the reduction of total fat mass (HRT, -3.0 +/- 4.0 kg; no HRT, -1.3 +/- 2.6 kg), with a strong trend for reductions in trunk and leg fat mass (both P = 0.07). There was also a significant improvement in insulin action in response to HRT. These results suggest that there are independent and additive effects of exercise training and HRT on the reduction in fat mass and improvement in insulin action in postmenopausal women; the effect of HRT on insulin action may be mediated, in part, through changes in central adiposity.     

Concurrent exercise prevents high-fat-diet-induced macrovesicular hepatic steatosis.

The purpose of the present study was to assess the effect of an exercise training program conducted concurrently with a high-fat (HF)-diet regimen on the induction of hepatic steatosis. Two groups of rats were fed either a standard (SD) or a HF (40% kcal) diet for 8 wk and were additionally assigned either to a sedentary (Sed) or a treadmill-trained (TR) group. Training (5 days/wk) was initiated at the same time as the HF diet and was progressively increased, reaching 60 min at 26 m/min, 10% grade, for the last 4 wk. At the end of the 8-wk period, HF-Sed rats exhibited approximately 72% higher liver triacylglycerol concentration than SD-Sed rats (means +/- SE: 17.15 +/- 1.5 vs. 9.98 +/- 1.0 mg/g; P < 0.01). Histological quantification of lipid infiltration, with the use of an image analysis computing system, revealed that, although fat was mainly stored as microvesicles (<1 microm(2)), the HF-diet-induced hepatic steatosis occurred via the accumulation of macrovesicles (>1 microm(2)). Concurrent exercise training completely prevented the HF-diet-induced hepatic steatosis. The surface area of liver parenchyma infiltrated by lipid vacuoles was similar in HF-TR as in SD-Sed rats (26.4 +/- 1.8 vs. 29.3 +/- 5.9 x 10(3) microm(2)/200,000 microm(2) of liver parenchyma, respectively; P > 0.05). The different states of liver lipid infiltration after the HF diet in Sed and TR rats were associated with similar changes in plasma free fatty acids and glycerol, as well as with similar changes in fat pad weights, but not with plasma triacylglycerol levels. It is concluded that, after a HF-diet regimen of 8 wk in rats, hepatic steatosis occurs primarily via the accumulation of lipid as macrovesicles. Exercise training pursued at the same time completely prevents the HF-diet-induced macrovesicular hepatic steatosis.     

Effect of voluntary exercise on peripheral tissue glucocorticoid receptor content and the expression and activity of 11beta-HSD1 in the Syrian hamster.

Recent findings indicate that elevated levels of glucocorticoids (GC), governed by the expression of 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1) and GC receptors (GR), in visceral adipose tissue and skeletal muscle lead to increased insulin resistance and the metabolic syndrome. Paradoxically, evidence indicates that aerobic exercise attenuates the development of the metabolic syndrome even though it stimulates acute increases in circulating GC levels. To investigate the hypothesis that training alters peripheral GC action to maintain insulin sensitivity, young male hamsters were randomly divided into sedentary (S) and trained (T) groups (n = 8 in each). The T group had 24-h access to running wheels over 4 wk of study. In muscle, T hamsters had lower 11beta-HSD1 protein expression (19.2 +/- 1.40 vs. 22.2 +/- 0.96 optical density, P < 0.05), similar 11beta-HSD1 enzyme activity (0.9 +/- 0.27% vs. 1.1 +/- 0.26), and lower GR protein expression (9.7 +/- 1.86 vs. 15.1 +/- 1.78 optical density, P < 0.01) than S hamsters. In liver, 11beta-HSD1 protein expression tended to be lower in T compared with S (19.2 +/- 0.56 vs. 21.4 +/- 1.05, P = 0.07), whereas both enzyme activity and GR protein expression were similar. In contrast, visceral adipose tissue contained approximately 2.7-fold higher 11beta-HSD1 enzyme activity in T compared with S (12.9 +/- 3.3 vs. 4.8 +/- 1.5% conversion, P < 0.05) but was considerably smaller in mass (0.24 +/- 0.02 vs. 0.71 +/- 0.06 g). Thus the intracellular adaptation of GC regulators to exercise is tissue specific, resulting in decreases in GC action in skeletal muscle and increases in GC action in visceral fat. These adaptations may have important implications in explaining the protective effects of aerobic exercise on insulin resistance and other symptoms of the metabolic syndrome.     

Determinants of fat oxidation during exercise in healthy men and women: a cross-sectional study.

The aim of the present study was to establish fat oxidation rates over a range of exercise intensities in a large group of healthy men and women. It was hypothesised that exercise intensity is of primary importance to the regulation of fat oxidation and that gender, body composition, physical activity level, and training status are secondary and can explain part of the observed interindividual variation. For this purpose, 300 healthy men and women (157 men and 143 women) performed an incremental exercise test to exhaustion on a treadmill [adapted from a previous protocol (Achten J, Venables MC, and Jeukendrup AE. Metabolism 52: 747-752, 2003)]. Substrate oxidation was determined using indirect calorimetry. For each individual, maximal fat oxidation (MFO) and the intensity at which MFO occurred (Fat(max)) were determined. On average, MFO was 7.8 +/- 0.13 mg.kg fat-free mass (FFM)(-1).min(-1) and occurred at 48.3 +/- 0.9% maximal oxygen uptake (Vo(2 max)), equivalent to 61.5 +/- 0.6% maximal heart rate. MFO (7.4 +/- 0.2 vs. 8.3 +/- 0.2 mg.kg.FFM(-1).min(-1); P < 0.01) and Fat(max) (45 +/- 1 vs. 52 +/- 1% Vo(2 max); P < 0.01) were significantly lower in men compared with women. When corrected for FFM, MFO was predicted by physical activity (self-reported physical activity level), Vo(2 max), and gender (R(2) = 0.12) but not with fat mass. Men compared with women had lower rates of fat oxidation and an earlier shift to using carbohydrate as the dominant fuel. Physical activity, Vo(2 max), and gender explained only 12% of the interindividual variation in MFO during exercise, whereas body fatness was not a predictor. The interindividual variation in fat oxidation remains largely unexplained.     

Physiological responses to prolonged exercise in ultramarathon athletes

The physiological responses of 10 ultramarathon athletes to prolonged exercise at the highest intensity level they could sustain for 4 h have been examined. Energy expenditure for the 4 h of exercise was 14,146 +/- 1,789 kJ, of which 63% was provided by the oxidation of fat. Plasma free fatty acids rose, but the changes in blood lactate concentration (delta 0.2 mmol/l) and exchange ratio (delta 0.05) were small, and the postexercise glycogen content (130 +/- 42 mumol/g) of the vastus lateralis muscles was estimated to be 37-53% of normal resting values. During exercise O2 intake (VO2) increased with time from the 50th to 240th min, the rise becoming significant (P less than 0.01) after 110 min of work. The change in VO2 was equivalent to a rise in relative intensity (%VO2max) of +9.1% and a change of speed of 1.49 km/h. A rise in cardiac frequency compensated for a fall in stroke volume (SV), so that cardiac output was maintained, and the increases in rectal temperature (Tre) (delta 0.63 degree C) and sweat loss (3.49 +/- 0.50 kg, equivalent to 5.5% of body wt) and the decreased mean skin temperature (Tsk) (-1.22 degree C) were within tolerable limits during exercise. Following exercise there was a loss (-25%) of ability to generate voluntary force of the quadriceps femoris, though electrically evoked mechanical properties of the muscle remained unchanged. The results suggest that neither thermal nor cardiovascular factors are limiting to prolonged (4 h) exercise, although the ability to utilize fat as a fuel may be important in ultradistance athletes.(ABSTRACT TRUNCATED AT 250 WORDS)     

Endurance training increases fatty acid turnover, but not fat oxidation, in young men.

We examined the effects of exercise intensity and a 10-wk cycle ergometer training program [5 days/wk, 1 h, 75% peak oxygen consumption (VO2 peak)] on plasma free fatty acid (FFA) flux, total fat oxidation, and whole body lipolysis in healthy male subjects (n = 10; age = 25.6 +/- 1.0 yr). Two pretraining trials (45 and 65% of VO2 peak) and two posttraining trials (same absolute workload, 65% of old VO2 peak; and same relative workload, 65% of new VO2 peak) were performed by using an infusion of [1-13C]palmitate and [1,1,2,3, 3-2H]glycerol. An additional nine subjects (age 25.4 +/- 0.8 yr) were treated similarly but were infused with [1,1,2,3,3-2H]glycerol and not [1-13C]palmitate. Subjects were studied postabsorptive for 90 min of rest and 1 h of cycling exercise. After training, subjects increased VO2 peak by 9.4 +/- 1.4%. Pretraining, plasma FFA kinetics were inversely related to exercise intensity with rates of appearance (Ra) and disappearance (Rd) being significantly higher at 45 than at 65% VO2 peak (Ra: 8.14 +/- 1.28 vs. 6.64 +/- 0.46, Rd: 8. 03 +/- 1.28 vs. 6.42 +/- 0.41 mol. kg-1. min-1) (P 相似文献   

Adiponectin is not altered with exercise training despite enhanced insulin action

Adiponectin is an adipocytokine that is hypothesized to be involved in the regulation of insulin action. The purpose of the present investigation was to determine whether plasma adiponectin is altered in conjunction with enhanced insulin action with exercise training. An insulin sensitivity index (S(I)) and fasting levels of glucose, insulin, and adiponectin were assessed before and after 6 mo of exercise training (4 days/wk for approximately 45 min at 65-80% peak O(2) consumption) with no loss of body mass (PRE, 91.9 +/- 3.8 kg vs. POST, 91.6 +/- 3.9 kg) or fat mass (PRE, 26.5 +/- 1.8 kg vs. POST, 26.7 +/- 2.2 kg). Insulin action significantly (P < 0.05) improved with exercise training (S(I) +98%); however, plasma adiponectin concentration did not change (PRE, 6.3 +/- 1.5 microg/ml vs. POST, 6.6 +/- 1.8 microg/ml). In contrast, in a separate group of subjects examined before and after weight loss, there was a substantial increase in adiponectin (+281%), which was accompanied by enhanced insulin action (S(I), +432%). These data suggest that adiponectin is not a contributory factor to the exercise-related improvements in insulin sensitivity.     

Age-related decline in RMR in physically active men: relation to exercise volume and energy intake

We tested the hypothesis that resting metabolic rate (RMR) declines with age in physically active men (endurance exercise > or =3 times/wk) and that this decline is related to weekly exercise volume (h/wk) and/or daily energy intake. Accordingly, we studied 137 healthy adult men who had been weight stable for > or =6 mo: 32 young [26 +/- 1 (SE) yr] and 34 older (62 +/- 1 yr) sedentary males (internal controls); and 39 young (27 +/- 1 yr) and 32 older (63 +/- 2 yr) physically active males (regular endurance exercise). RMR was measured by indirect calorimetry (ventilated hood system) after an overnight fast and approximately 24 h after exercise. Because RMR is related to fat-free mass (FFM; r = 0.76, P < 0.001, current study), FFM was covaried to adjust RMR (RMR(adj)). RMR(adj) was lower with age in both the sedentary (72.0 +/- 2.0 vs. 64.0 +/- 1.3 kcal/h, P < 0.01) and the physically active (76.6 +/- 1.1 vs. 67.9 +/- 1.2 kcal/h, P < 0.01) males. In the physically active men, RMR(adj) was related to both exercise volume (no. of h/wk, regardless of intensity; r = 0.56, P < 0.001) and estimated energy intake (r = 0.58, P < 0.001). Consistent with these relations, RMR(adj) was not significantly different in subgroups of young and older physically active men matched either for exercise volume (h/wk; n = 11 each) or estimated energy intake (kcal/day; n = 6 each). These results indicate that 1) RMR, per unit FFM, declines with age in highly physically active men; and 2) this decline is related to age-associated reductions in exercise volume and energy intake and does not occur in men who maintain exercise volume and/or energy intake at a level similar to that of young physically active men.