Effect of nadolol on plasma lipids in hyperthyroidism

The effect of Nadolol treatment on lipid subfractions in a group of 23 hyperthyroid patients was assessed in a randomised double-blind placebo controlled trial lasting six weeks, carbimazole being given to both groups from weeks 2 to 6. Clinical and biochemical euthyroidism was seen in both groups at 6 weeks; no effect of nadolol on peripheral monodeiodination of T4 to T3 was observed. At time 0 there were significant negative correlations between total cholesterol and free T3 (r = 0.68), and free T4 (r = 0.54). In the Nadolol group there were significant rises between 0 and 6 weeks in total cholesterol (52.6%, P less than 0.01), LDL cholesterol (30.3%, P less than 0.01) and HDL cholesterol (18.2%, P less than 0.05). HDL cholesterol rose significantly in the placebo group (12.4%, P less than 0.05) but there were no significant increases in LDL cholesterol or total cholesterol. The rise in triglyceride during this period in the Nadolol group (64.7%, P less than 0.05) was significantly greater (P less than 0.05) than the rise in the placebo group (8.8%). Nadolol increases triglyceride more than placebo during the early management of hyperthyroidism.     

Resistance training lowers exercise-induced oxidative stress and homocysteine levels in overweight and obese older adults

Objective: To compare exercise‐induced oxidative stress and levels of homocysteine and cholesterol in normal‐weight and overweight older adults after resistance exercise (RX). Research Methods and Procedures: This interventional study was conducted at a wellness center. Forty‐nine older adults (age range, 60 to 72 years) were stratified by BMI (<25 kg/m² normal weight, ≥25 kg/m² overweight/obese) and then randomly assigned to either a control non‐exercise group or an RX group. The RX group completed a 6‐month training program. Exercise‐induced lipid hydroperoxides (PEROXs) and thiobarbituric‐reactive acid substances, homocysteine, lipoprotein a, cholesterol, and high‐density lipoprotein cholesterol were measured before and after the 6‐month RX program. Results: PEROXs and thiobarbituric‐reactive acid substances were lower in both the overweight/obese and normal‐weight RX‐trained groups compared with control groups (p < 0.05). Homocysteine levels were lower in both overweight/obese and normal‐weight RX groups compared with control groups (p < 0.05). Lipoprotein a, total cholesterol, and high‐density lipoprotein cholesterol were not different in normal‐weight and overweight/obese groups before or after RX. The change in muscle strength was correlated with homocysteine at 6 months (r = ?0.452, p < 0.05), whereas the change in PEROXs was correlated with the change in body fat (r = ?0.329). Discussion: To our knowledge, these data are the first to show that RX reduces exercise‐induced oxidative stress and homocysteine regardless of adiposity, indicating that this protection can be afforded in an older, overweight/obese population as effectively as in healthy older adults. These data suggest that RX may afford some protection against emerging cardiovascular risk factors using a mode of exercise that supports body weight.     

Effects of acute exercise intensity on plasma lipids and apolipoproteins in trained runners.

The purpose of this study was to determine the effects of exercise intensity on lipid and lipoprotein metabolism. Concentrations of triglyceride, cholesterol, high-density lipoprotein cholesterol (HDL-C) and its subfractions (HDL2-C and HDL3-C), low-density lipoprotein cholesterol, very-low-density lipoprotein cholesterol, and apolipoproteins A-I, A-II, and B were measured. Ten well-trained runners completed treadmill exercise on two different occasions: a high-intensity session at 75% maximal oxygen consumption lasting 60 min and a low-intensity session at 50% maximal oxygen consumption lasting 90 min. Energy expenditure for each session was equal. Fasted blood samples were obtained 24 h before, immediately before, immediately after, and 1, 24, 48, and 72 h after each exercise session. No significant differences were found for the blood variables across time or between treatments. However, HDL-C and HDL2-C were slightly elevated on the days after each treatment. These results suggest that acute exercise sessions lasting less than 90 min, regardless of intensity, do not elicit plasma lipid, lipoprotein, and apolipoprotein changes in men who are habitually physically active and have high initial concentrations of HDL-C.     

The effect of prolonged physical training and high fat diet on heart size and body weight in rats

White male Woodlyn Wistar rats (aged 9-10 weeks) were subjected to prolonged physical training on a treadmill for 10 weeks. After 4 weeks half of the rats received a high fat test diet (45%) (Nutritional Biochemical Corporation) while the control group was fed standard lab chow (Purina lab chow). The body weights, heart weights, and heart weight per 100 g body weight were compared in a two by two factorial analysis, the independent variables being condition (exercise or sedentary) and diet (balanced or high fat). After 10 weeks the difference in body weight between the sedentary rats (body weight (BW) equals 514.4 plus or minus 76.4 g) and the exercise rats (BW equals 389 plus or minus 44 g) was significant (p less than 0.05). The difference in body weight between the high fat diet rats (BW equals 479 plus or minus 80 g, n equals 10) and the balanced diet group (BW equals 424 plus or minus 76 g, n equals 10) was also significant (p less than 0.05). No significant differences were observed in heart weight among any of the groups whereas a significant difference was noted between the sedentary group and the exercise group with respect to heart weight : body weight ratio. Thus the exercise rats had relatively larger hearts than the sedentary group (p less than 0.05) but no evidence for cardiac hypertrophy in the exercise group compared with the sedentary group ws observed. The difference with regard to heart ratios between the balanced diet and high fat diet groups was not significant and no interaction was present (p equals 0.065). It was concluded that cardiac hypertrophy is not necessarily a consequence of prolonged physical training but is a product of the type of training, the intensity and duration, and the emotional stress involved. Prolonged physical exercise was a powerful deterrent to weight gain even in rats on a high fat diet. In the absence of the development of cardiac hypertrophy in response to prolonged training, further work is needed to quantify the factors that result in cardiac hypertrophy and to identify other changes that may be occurring in the cardiovascular system in response to prolonged physical training.     

Exercise improves plasma lipid profiles and modifies lipoprotein composition in guinea pigs

These studies were conducted to determine the effects of exercise training on plasma lipoprotein levels and metabolism in the guinea pig to evaluate potential utilization of this model for studies of exercise-mediated effects on the regulation of sterol and lipoprotein metabolism and atherosclerosis regression. Male guinea pigs (n = 5 per group) were randomly assigned to either a control or an exercise group. The exercise protocol consisted of a 7-week training program, 5 days/wk on a rodent treadmill. Final speed and duration were 33 meters/min for 30–40 min per session. Guinea pigs in the exercise group had 33% lower plasma triacylglycerol concentrations (P < 0.01), 66% higher HDL cholesterol levels (P < 0.05) and 31% lower plasma free fatty acids (P < 0.05) than guinea pigs from the non-exercised group. In addition, lipoprotein lipase activity in the heart was 50% higher (P < 0.025) in guinea pigs allocated to the exercise protocol. Exercise training resulted in modifications in composition and size of lipoproteins. The concentrations of free cholesterol in LDL and HDL were higher in the exercised guinea pigs. The LDL peak density values were lower in guinea pigs from the exercise group compared to controls suggesting that exercise training resulted in larger LDL particles. In contrast, no significant effects due to exercise were observed in hepatic cholesterol concentrations, hepatic HMG-CoA reductase activity or LDL binding to guinea pig hepatic membranes. These data indicate that exercise had a more pronounced effect on the intravascular processing of lipoproteins than on hepatic cholesterol metabolism. In addition, the pattern of changes in guinea pig lipoprotein metabolism, in response to exercise training, was similar to reported effects in humans.     

Effect of short- and long-term strength exercise on cardiac oxidative stress and performance in rat

Increase in heart metabolism during severe exercise facilitates production of ROS and result in oxidative stress. Due to shortage of information, the effect of chronic strength exercise on oxidative stress and contractile function of the heart was assessed to explore the threshold for oxidative stress in this kind of exercise training. Male Wistar rats (80) were divided into two test groups exercised 1 and 3 months and two control groups without exercise. Strength exercise was carried by wearing a Canvas Jacket with weights and forced rats to lift the weights. Rats were exercised at 70% of maximum lifted weight 6 days/week, four times/day, and 12 repetitions each time. Finally, the hearts of ten rats/group were homogenized and MDA, SOD, GPX, and catalase (CAT) were determined by ELISA method. In other ten rats/group, left ventricle systolic and end diastolic pressures (LVSP and LVEDP) and contractility indices (LVDP and +dp/dt max) and relaxation velocity (−dp/dt max) were recorded. The coronary outflow was collected. Short- and long-term strength exercise increased heart weight and heart/BW ratio (P < 0.05). In the 3-month exercise group, basal heart rate decreased (P < 0.05). LVEDP did not change but LVDP, +dp/dt max, −dp/dt max, and coronary flow significantly increased in both exercise groups (P < 0.05). None of MDA or SOD, GPX, and CAT significantly changed. The results showed that sub-maximal chronic strength exercise improves heart efficiency without increase in oxidative stress index or decrease in antioxidant defense capacity. These imply that long-time strength exercise up to this intensity is safe for cardiac health.     

Changes in LPLa and reverse cholesterol transport variables during 24-h postexercise period

We investigated the time course of exercise-induced lipoprotein lipase activity (LPLa) and reverse cholesterol transport (RCT) during the 24-h postexercise period. Subjects were 10 sedentary normolipidemic males [NTG; fasting triglyceride (TG) = 89.1 +/- 8.6 mg/dl] and 6 hyperlipidemic males (HTG; fasting TG = 296.8 +/- 64.0 mg/dl). Each subject performed a control trial (no exercise) and 4 exercise trials. In the exercise trials, a subject jogged on a treadmill at 60% of his maximal O(2) consumption for 1 h. Pre- and postheparin blood samples were taken before exercise (baseline) and at 4, 8, 12, and 24 h after exercise. There was no group difference in LPLa (P > 0.05) over the time points. When the LPLa data from the two groups were combined, LPLa at 24 h after exercise was higher than baseline or at 4, 8, 12 h after exercise (P < 0.05). Plasma TG and lecithin-cholesterol acyltransferase activity (LCATa) were higher in HTG than in NTG, and the total high-density lipoprotein-cholesterol (HDL(tot)-Chol) was lower in HTG than in NTG (P < 0.05). HDL(2)-Chol, LCATa, and cholesterol ester transfer protein activity did not differ during the 24-h postexercise period (P > 0.05). These results suggest that LPLa is still increasing 24 h after an acute aerobic exercise and that the magnitude of the increase in exercise-induced LPLa in HTG was similar to that in NTG. Furthermore, in the sedentary population with or without HTG, the variables related to RCT do not change during the 24-h period after exercise.     

Time course of endothelial adaptation after acute and chronic exercise in patients with metabolic syndrome

Clustering of cardiovascular risk factors may lead to endothelial dysfunction. Physical exercise is an important factor in prevention and treatment of endothelial dysfunction. We wanted to determine the time course of adaptation to a single bout of exercise at either high or moderate intensity upon endothelial function both before and after a 16-week fitness program in patients with metabolic syndrome. Twenty-eight patients with metabolic syndrome participated in the study and were randomized and stratified (according to age and sex) into an aerobic interval exercise training group (AIT, n = 11), a continuously moderate-intensity exercise training group (CME, n = 8) or to a control group (n = 9). Flow-mediated dilatation (FMD) was determined at baseline, immediately, 24, 48, and 72 hours after 1 bout of exercise and repeated after 16 weeks of exercise. In the untrained state, FMD improved from 5 to 11% (p = 0.003) immediately after a single bout of aerobic interval training (AIT), an effect lasting 72 hours postexercise. In comparison, continuous moderate exercise (CME) improved FMD immediately after a single bout of exercise from 5 to 8% (p = 0.02), an effect lasting 24 hours postexercise (group difference, p < 0.001). In the trained state, a single bout of AIT resulted in a 2% (p = 0.007) acute increase of FMD lasting 48 hours postexercise. The CME increased FMD by 3% (p < 0.01), an effect lasting 24 hours postexercise (group difference p = 0.0012). Blood glucose level decreased after 1 single bout of AIT in the untrained state (p < 0.05), and the effect lasted at least 72 hours postexercise (p < 0.01). Acute CME decreased blood glucose with normalization of the values 24 hours postexercise (p < 0.01). A single bout of exercise in the trained state reduced fasting blood glucose by 10% (p < 0.05) after both AIT and CME. Exercise training, especially high intensity, thus appears to be highly beneficial in reducing blood glucose and improving endothelial function.     

Does beta(3)-adrenoreceptor blockade attenuate acute exercise-induced reductions in leptin mRNA?

We investigated the effect of a single bout of exercise on leptin mRNA levels in rat white adipose tissue. Male Sprague-Dawley rats were randomly assigned to an exercise or control group. Acute exercise was performed on a rodent treadmill and was carried out to exhaustion, lasting an average of 85.5 +/- 1.5 min. At the end of exercise, soleus muscle and liver glycogen were reduced by 88% (P < 0.001). Acutely exercised animals had lower (P < 0.05) leptin mRNA levels in retroperitoneal but not epididymal fat, and this was independent of fat pad weight. To test the hypothesis that beta(3)-adrenergic-receptor stimulation was involved in the downregulation of leptin mRNA in retroperitoneal fat, a second experiment was performed in which rats were randomized into one of four groups: control, control + beta(3)-antagonist, exercise, and exercise + beta(3)-antagonist. A highly selective beta(3)-antagonist (SR-59230A) or vehicle was given by gavage 30 min before exercise or control experiment. Exercise consisted of 55 min of treadmill running, sufficient to reduce liver and muscle glycogen by 70 and 80%, respectively (both P < 0.0001). Again, acute exercise reduced leptin mRNA in retroperitoneal fat (exercise vs. control; P < 0.05), but beta(3)-antagonism blocked this effect (exercise + beta(3)-antagonist vs. control + beta(3)-antagonist; P = 0.42). Unexpectedly, exercise increased serum leptin. This would be consistent with the idea that there are releasable, preformed pools of leptin within adipocytes. We conclude that beta(3)-receptor stimulation is a mechanism by which acute exercise downregulates retroperitoneal adipose tissue leptin mRNA in vivo.     

The therapeutic effect of aerobic exercise with resistance training in elderly men with type 2 diabetes mellitus

Objective: This study was conducted to examine the effects of aerobic exercise alone and aerobic exercise with resistance training on the quality of life in men over the age of 55 years with type 2 diabetes mellitus. Methods: A total of 54 participants were divided into the following three groups so that there were no significant differences in blood chemistry or physical ability indexes among the three groups: control, aerobic exercise, and aerobic exercise with resistance training. The latter two groups exercised for 24 weeks, while the control group performed no exercise. Blood chemistry levels and measures of physical ability in each group members were examined one day before and one day after the exercise regimens. Results: Compared with those before the study, blood glucose, glycated hemoglobin, triglycerides, cholesterol, and low-density lipoprotein levels as well as vital capacity, reaction time, sit-and-reach ability, and balancing while standing on one leg with closed eyes were significantly improved in the aerobic exercise only group(P 0.05). All these measures as well as high-density lipoprotein levels and grip, back, and leg strength were significantly improved in the combined aerobic and resistance training group(P 0.05). By contrast, no significant differences before and after the experiment were found in any measure for the control group(P 0.05). Conclusion: Although both aerobic exercise and aerobic exercise combined with resistance training for 24 weeks effectively improved the quality of life in patients with type 2 diabetes, the effect of the combined training was better than that of aerobic exercise alone. These results suggest that resistance training may be safely added to the rehabilitation training regimen of patients with type 2 diabetes mellitus.     

Increase in hepatic mitochondria on administration of ethyl α-p-chlorophenoxyisobutyrate to the rat

1. The antihypercholesterolaemic drug ethyl alpha-p-chlorophenoxyisobutyrate when fed to the rat orally or mixed with the diet increased the content of mitochondria in the liver by 50-100%. Other subcellular fractions did not show any significant change. 2. In oxidative activity, respiratory control and phosphorylating ability no significant difference was observed between the mitochondria isolated from the livers of the drug-treated rats and those from normal animals. 3. In agreement with earlier reports, administration of the drug depressed the concentration of serum cholesterol and increased liver weight and the liver content of ubiquinone. However, the increase of ubiquinone was greater in the nuclear than in the mitochondrial protein.     

nHAP对大鼠肝线粒体的生物活性作用

为了探讨羟基磷灰石纳米粒子(nHAP)对大鼠肝线粒体生物活性的影响,将nHAP直接作用于线粒体,在不同浓度和时间下测定线粒体标志酶琥珀酸脱氢酶(SDH)比活性,并与对照组进行比较。结果显示,当nHAP中水含量在10%以下时,线粒体生物活性未发现改变;当nHAP浓度递增时,在等时间段内,对线粒体SDH比活性呈逐步抑制作用;在不等时间段内,nHAP对线粒体SDH比活性的抑制作用与对照组相比较差异有显著性(p<0.05)。因此,nHAP对线粒体SDH比活性的抑制有浓度和时间的依赖性。     

Effect of aging on the activity of the phosphate carrier and on the lipid composition in rat liver mitochondria

The effect of aging on the activity of the phosphate carrier and on the lipid composition in rat liver mitochondria has been investigated. It was found that the rate of phosphate transport in mitochondria from aged rats (28 months old) is significantly reduced (around 40%) compared to that obtained in mitochondria from young control rats (5 months old). Kinetic analysis of the phosphate transport indicates that only the Vmax of this process is affected, while there is no change in the Km values. The lower activity of the phosphate carrier in mitochondria from aged rats is also documented by swelling experiments. The age-related decrement in the activity of the phosphate carrier was found not to be due neither to a change in the endogenous content of phosphate nor to a change in the transmembrane delta pH value. Inhibitor titrations with mersalyl provide no evidence for a lower content of functional phosphate translocase in mitochondria from aged rats. There is no difference either in the respiratory control ratios or in the ADP/O ratios between mitochondria from young and aged animals. The hepatic mitochondrial lipid composition is altered significantly in aged rats: the total cholesterol increases (31%), the phospholipids decrease (12%), and the cholesterol/phospholipid molar ratio increases (44%). Among the phospholipids cardiolipin shows the greatest alteration (30% decrease with age). Alterations were also found in the pattern of fatty acids. The age-related decrement in the activity of the phosphate carrier appears to be dependent on changes in the lipid domain surrounding the carrier protein molecule in the mitochondrial membrane.     

Health checks and coronary risk: further evidence from a randomised controlled trial.

OBJECTIVE: To determine the effectiveness of a health check and assess any particular benefits resulting from feedback of plasma cholesterol concentration or coronary risk score, or both. DESIGN: Randomised controlled trial in two Glasgow work sites. SUBJECTS: 1,632 employees (89% male) aged 20 to 65 years. INTERVENTIONS: At the larger work site, (a) health education; (b) health education and feedback on cholesterol concentration; (c) health education and feedback on risk score; (d) health education with feedback on cholesterol concentration and risk score (full health check); (e) no health intervention (internal control). At the other work site there was no health intervention (external control). MAIN OUTCOME MEASURES: Changes in Dundee risk score, plasma cholesterol concentration, diastolic blood pressure, body mass index and self-reported behaviours (smoking, exercise, alcohol intake, and diet) in comparison with internal and external control groups. RESULTS: Comparisons between the full health check and the internal control groups showed a small difference (0.13 mmol/l) in the change in mean cholesterol concentration (95% confidence interval 0.02 to 0.22, P = 0.02) but no significant differences for changes in Dundee risk score (P = 0.21), diastolic blood pressure (P = 0.71), body mass index (P = 0.16), smoking (P = 1.00) or exercise (P = 0.41). Significant differences between the two groups were detected for changes in self-reported consumption of alcohol (41% in group with full health check v 17% in internal control group, P = 0.001) fruit and vegetables (24% v 12%, P < 0.001), and fat (30% v 9%, P < 0.001). Comparison of all groups showed no advantage from feedback of cholesterol concentration or risk score, or both. CONCLUSIONS: The health check only had a small effect on reversible coronary risk. It was effective in influencing self reported alcohol consumption and diet. Feedback on cholesterol concentration and on risk score did not provide additional motivation for a change in behaviour.     

Left ventricular function during graded exercise in patients with coronary artery disease and in control subjects.

The left ventricular function of 30 patients with coronary artery disease and 11 control subjects was studied by electrocardiography gated cardiac blood pool scintigraphy as the participants lay on their backs and either rested or exercised on a cycle ergometer at graded levels on intensity. The control subject showed a progressive increase in ejection fraction from rest (51% +/- 7%) to intermediate (56% +/- 10%, P less than 0.05) and maximum levels of exercise (64% +/- 10%, P less than 0.001). All the patients showed a decrease in ejection fraction from rest (42% +/- 16%) to their maximal level of exercise (36% +/- 11%, P less than 0.001). However, the response of some of the patients to intermediate exercise ranged from a decrease or no change to an increase in ejection fraction. Thus, exercise at maximal intensity is necessary to induce the left ventricular dysfunction that is diagnostic of coronary artery disease.     

Decreased activity of the phosphate carrier and modification of lipids in cardiac mitochondria from senescent rats.

1. A comparative study of the effects of aging on the transport of phosphate and on the lipid composition in cardiac mitochondria isolated from young and aged rats was carried out. 2. Mitochondria from aged rats (26 month old) translocate phosphate much more slowly than do mitochondria from young control rats (4 month old). 3. Kinetic analysis of the phosphate transport show that only the Vmax of this process is decreased while there is no change in the Km value. 4. There is no appreciable difference in either the respiratory control ratios or in the ADP/O ratios between mitochondria from young and aged rats. 5. The heart mitochondrial lipid composition is altered in aged rats; in particular, the cholesterol/phospholipid molar ratio increases and the content of cardiolipin decreases with aging.     

Physical Activity as a Predictor of Weight Maintenance in Previously Obese Subjects

We examined the association between exercise and weight loss maintenance in a group of 45 previously obese subjects 2 years post very-low-calorie diet (VLCD) to suggest exercise goals for this population. At baseline, subjects weighed a mean 100 kg and had a mean total cholesterol (TC) of 5.8 mmol/L. With VLCD they lost an average 28 kg and decreased their TC by 1.6 mmol/L. Two years post-VLCD their weight and lipids were measured and they completed a physical activity survey (Paffenbarger). Subjects were grouped into tertiles by reported exercise levels: low active (< 850 kcals per week), moderate active (850–1575 kcals per week) and high active (> 1575 kcals per week). Walking accounted for the greatest calorie expenditure (65%). Analysis of variance showed that baseline characteristics and weight and blood lipid changes during the VLCD did not differ (P>0.05) among groups. At follow-up, high active patients maintained significantly greater weight loss, had a lower percent regain and a significantly greater decrease in total cholesterol (P < 0.05) than less active patients. Multiple regression analysis indicated that total exercise calories independently predicted overall weight loss and percent regain (r = 0.66 and r = 0.62, respectively). Exercise calories also predicted total cholesterol change (r=-0.37). The high active group walked more miles (16.2 per week) than the low and moderate active groups (4.8 and 9.1 per week, respectively) and exercised more days per week (5.3 vs. 1.9 and 3.7). The low and moderate active groups regained virtually equal amounts of weight, even though the moderate group expended twice as many kcals per week as the low active group. These data demonstrate that increased exercise levels enhance weight loss maintenance.     

Exercise training alters length dependence of contractile properties in rat myocardium.

Myocardial function is enhanced by endurance exercise training, but the cellular mechanisms underlying this improved function remain unclear. Exercise training increases the sensitivity of rat cardiac myocytes to activation by Ca(2+), and this Ca(2+) sensitivity has been shown to be highly dependent on sarcomere length. We tested the hypothesis that exercise training increases this length dependence in cardiac myocytes. Female Sprague-Dawley rats were divided into sedentary control (C) and exercise-trained (T) groups. The T rats underwent 11 wk of progressive treadmill exercise. Heart weight increased by 14% in T compared with C rats, and plantaris muscle citrate synthase activity showed a 39% increase with training. Steady-state tension was determined in permeabilized myocytes by using solutions of various Ca(2+) concentration (pCa), and tension-pCa curves were generated at two different sarcomere lengths for each myocyte (1.9 and 2.3 microm). We found an increased sarcomere length dependence of both maximal tension and pCa(50) (the Ca(2+) concentration giving 50% of maximal tension) in T compared with C myocytes. The DeltapCa(50) between the long and short sarcomere length was 0.084 +/- 0.023 (mean +/- SD) in myocytes from C hearts compared with 0.132 +/- 0.014 in myocytes from T hearts (n = 50 myocytes per group). The Deltamaximal tension was 5.11 +/- 1.42 kN/m(2) in C myocytes and 9.01 +/- 1.28 in T myocytes. We conclude that exercise training increases the length dependence of maximal and submaximal tension in cardiac myocytes, and this change may underlie, at least in part, training-induced enhancement of myocardial function.     

Adaptation of the left ventricle to exercise-induced hypertrophy

Cardiac functional and structural adaptations to exercise-induced hypertrophy were studied in 68 pigs. Pigs were exercise trained on a treadmill for 10 wk. Sequential measurements were made of cardiac dimensions, [left ventricular end-diastolic diameter (EDD), changes in diameter (delta D%), wall thickness (WTh), wall thickening (WTh%), left ventricular pressure (LVP), time derivative of pressure (dP/dt), stroke volume, total body O2 consumption (VO2), blood gases, and systemic hemodynamics] at rest and during moderate and severe exercise. Postmortem studies included morphometric measurements of capillary density, arteriolar density, mitochondria, and myofibrils. All of the exercise-trained pigs showed significant increases in aerobic capacity. Maximum O2 consumption (VO2 max) increased by 37.5% in group 1 (moderate exercise training) and 34% in group 3 (heavy exercise training). Cardiac hypertrophy ranged from less than 15% in a group (n = 8) subjected to moderate exercise training to greater than 30% in a group (n = 11) subjected to heavy exercise training. Before training, exercise was characterized by a decreasing EDD during progressive exercise; this was reversed after exercise training. Stroke volume and end-diastolic volumes during exercise showed a highly significant increase after exercise training and hypertrophy. Morphometric measurements showed that mitochondria and cell membranes increased with increasing myocyte growth in all exercise groups, but there was only a partially compensated adaptation of capillary proliferation. Arteriolar number and length increased in all exercise groups. Intrinsic contractility as measured by delta D%, WTh%, or left ventricular dP/dt did not increase with exercise training and in some instances decreased. Therefore, left ventricular adaptation to strenuous exercise in the pig heart is primarily one of changes in left ventricular dimensions and a compensated hypertrophy. Exercise-induced increases in EDD and stroke volume can be accounted for by decreases in peripheral resistance and increased cardiac dimensions.     

Effect of endurance training upon lipid metabolism in the liver of cachectic tumour-bearing rats

The syndrome of cancer cachexia is accompanied by several alterations in lipid metabolism, and the liver is markedly affected. Previous studies showed that moderate exercise training may prevent liver fat accumulation through diminished delivery of lipids to the liver, increased hepatic oxidation and increased incorporation of triacylglycerol (TAG) into very low density lipoprotein (VLDL). Our aim was to examine the influence of moderate intensity training (8 weeks) upon TAG content, VLDL assembly and secretion, apolipoprotein B (apoB) and microsomal transfer protein (MTP) gene expression in the liver of cachectic tumour-bearing rats. Animals were randomly assigned to a sedentary control (SC), sedentary tumour-bearing (ST) or exercise-trained control (EC) or to an exercise trained tumour-bearing (ET) group. Trained rats ran on a treadmill (60% VO(2max)) for 60 min day(-1), 5 day week(-1), for 8 weeks. TAG content and the rate of VLDL secretion (followed for 3 h), as well as mRNA expression of apoB and MTP, and total cholesterol, VLDL-TAG, VLDL-cholesterol, high density lipoprotein cholesterol (HDL-cholesterol) and tumour weight were evaluated. VLDL-cholesterol showed a decrease in ST (p < 0.05) in relation to SC. Serum TAG, VLDL-TAG and tissue TAG content were all increased in ST (p < 0.01), when compared with SC. ST showed a lower rate of VLDL secretion (p < 0.05) and reduced expression of apoB (p < 0.001) and MTP (p < 0.001), when compared with SC. These parameters were restored to control values (p < 0.05) when the animals were submitted to the exercise training protocol. Tumour weight decreased 10-fold after training (p < 0.001). It is possible to affirm, therefore, that endurance training promoted the re-establishment of lipid metabolism in cachectic tumour-bearing animals, especially in relation to VLDL secretion and assembly.