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PubMed1977

Adrenocortical function in aging exercise-trained rats.

Plasma corticosterone concentrations and in vitro adrenal secretion of corticosterone were determined in exercise-trained rats. Rats, 100, 200, and 300 days of age, were trained for a 10-wk period by treadmill running. Following the training program, rats were subjected to an acute bout of swimming. Acute swimming elevated plasma corticosterone concentrations in all age groups. At 170 days of age, the plasma corticosterone concentration following swimming was higher in exercise-trained rats than in controls. The opposite was true of acutely swum rats at 270 and 370 days of age. Acute swimming elevated the in vitro adrenal gland response to adrenocorticotropic hormone stimulation in control rats at all ages and in trained rats at 170 days of age. The in vivo relationship of epinephrine and the pituitary adrenal system is suggested as a mechanism which could have caused this response. The relationship of secretion rates to plasma corticosterone concentrations indicated that extra-adrenal mechanisms, such as decreased turnover, were also responsible for the elevated plasma corticosterone levels observed in response to acute swimming.

Adrenal Cortex↗

PubMed2006

Beneficial effects of a long-term oral L-arginine treatment added to a hypocaloric diet and exercise training program in obese, insulin-resistant type 2 diabetic patients.

Because chronic L-arginine supplementation improves insulin sensitivity and endothelial function in nonobese type 2 diabetic patients, the aim of this study was to evaluate the effects of a long-term oral L-arginine therapy on adipose fat mass (FM) and muscle free-fat mass (FFM) distribution, daily glucose levels, insulin sensitivity, endothelial function, oxidative stress, and adipokine release in obese type 2 diabetic patients with insulin resistance who were treated with a combined period of hypocaloric diet and exercise training. Thirty-three type 2 diabetic patients participated in a hypocaloric diet plus an exercise training program for 21 days. Furthermore, they were divided into two groups in randomized order: the first group was also treated with L-arginine (8.3 g/day), and the second group was treated with placebo. Although in the placebo group body weight, waist circumference, daily glucose profiles, fructosamine, insulin, and homeostasis model assessment index significantly decreased, L-arginine supplementation further decreased FM (P < 0.05) and waist circumference (P < 0.0001), preserving FFM (P < 0.03), and improved mean daily glucose profiles (P < 0.0001) and fructosamine (P < 0.03). Moreover, change in area under the curve of cGMP (second messenger of nitric oxide; P < 0.001), superoxide dismutase (index of antioxidant capacity; P < 0.01), and adiponectin levels (P < 0.02) increased, whereas basal endothelin-1 levels (P < 0.01) and leptin-to-adiponectin ratio (P < 0.05) decreased in the L-arginine group. Long-term oral L-arginine treatment resulted in an additive effect compared with a diet and exercise training program alone on glucose metabolism and insulin sensitivity. Furthermore, it improved endothelial function, oxidative stress, and adipokine release in obese type 2 diabetic patients with insulin resistance.

Administration, Oral↗

PubMed1999

Effect of dietary fish and exercise training on urinary F2-isoprostane excretion in non-insulin-dependent diabetic patients.

Despite the potential benefits of dietary treatment with marine omega3 fatty acids in cardiovascular disease, there remains concern with respect to their potential for increased lipid peroxidation. Thus far, data from in vivo studies are inconclusive. Increased lipid peroxidation has also been associated with acute exercise in some studies, but the methods have been nonspecific. The quantitation of F2-isoprostanes provides a more reliable and useful assessment of in vivo lipid peroxidation. We therefore aimed to assess the independent and combined effects of dietary omega3 fatty acids and aerobic exercise training on urinary F2-isoprostane levels in dyslipidemic non-insulin-dependent diabetic (NIDDM) patients. In a randomized controlled trial, 55 untrained, sedentary, dyslipidemic NIDDM patients were randomly assigned to a low-fat diet (30% of daily energy) with or without one daily fish meal (3.6 g omega3 fatty acids per day) and further randomized to either a moderate (55% to 65% maximal oxygen consumption [VO2max]) or light (heart rate <100 bpm) exercise training program for 8 weeks. Twenty-four-hour urine samples from 49 subjects were collected for measurement of urinary F2-isoprostanes by gas chromatography-mass spectrometry before and after intervention. The fish diets reduced urinary F2-isoprostanes by 830+/-321 pmol/24 h (20%, P = .013) relative to the low-fat diet alone. This effect was independent of age, gender, and body weight change. Moderate exercise training did not alter F2-isoprostanes. These findings show that, at least in the short-term, exercise had no effect, whereas the inclusion of regular fish meals as part of a low-fat diet reduced in vivo lipid peroxidation in dyslipidemic NIDDM patients. This response could further complement the known benefits of omega3 fatty acids and exercise favoring a reduced cardiovascular risk in diabetic patients.

Adult↗

PubMed1988

Effects of exercise training on high density lipoproteins and apolipoprotein A-I in old and young men.

Although exercise training has been demonstrated to improve lipid profiles in young and middle-aged subjects, the response in training in the elderly has received little attention. In this study, we assessed and compared the changes in aerobic capacity, lipid profiles, and body composition in young (Y, 31.9 +/- 5.5 years; n = 18) and older (O, 65.1 +/- 6.1 years; n = 10) subjects in response to similar 3-month exercise training programs (80% to 85% of heart rate reserve, three times per week). We hypothesized that the responses would be qualitatively similar for the two groups, although the absolute quantitative response might be somewhat less in the elderly. The two groups were quite similar at baseline for percent body fat (Y, 30.1% +/- 7.2% v O, 30.3% +/- 4.7%; P = NS) and maximal aerobic capacity (Y, 36.8 +/- 8.1 v O, 36.3 +/- 8.3 mL/kg/min; P = NS). In addition, there were no significant differences in the baseline lipid profiles between the groups. After training, the improvements in body composition were similar, with both groups losing similar amounts of fat (Y, 2.86% +/- 3.14% v O, -2.85% +/- 1.78%) and neither group significantly changing their fat-free mass. Maximal aerobic capacity improved in both groups, but the increment was greater in the young (18% v 10%, P less than .05). HDL-cholesterol (+6%, P less than .01) and apolipoprotein A-I (+6%, P less than .01) concentrations increased significantly only in the young. These increments, however, were not different from those observed in the older subjects (+7% and +4%, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1980

Histochemical fiber type alterations secondary to exercise training of reinnervating adult rat muscle.

The purpose of this study was to evaluate the effect of exercise training on reinnervating rat muscle histochemistry. Adult female Wistar rats in 5 groups (1 control and 4 experimental) underwent bilateral sciatic nerve crush. The 4 experimental groups were exercised on a motorized treadmill at 35% grade and a speed of 27m/min once (groups J and L) or twice (groups K and M) daily, 5 days/week from the 2nd (groups J and K), and 3rd (groups L and M), to the 6th week after the crush. The exercise sessions lasted 1 hour. The fiber diameter and percent of type I and II fibers (weak and strong myosin ATPase reaction, pH .94) were evaluated in the soleus and superficial and deep regions of the plantaris muscles. Exercise training did not affect the fiber diameters. There was no change in the fiber type distribution in the soleus and superficial region of the plantaris. However, the percent of type II fibers increased significantly (p less than 0.05) in the deep region of the plantaris groups J, K, L and M bu 12%, 7%, 15% and 10%, respectively. This study indicated that exercise did not interfere with reinnervation and that there was an increase in the proportion of fibers with a strong myosin ATPase reaction in the deep region of the plantaris.

Adenosine Triphosphatases↗

PubMed2003

Benefits of supplemental oxygen in exercise training in nonhypoxemic chronic obstructive pulmonary disease patients.

Supplemental oxygen improves exercise tolerance of normoxemic and hypoxemic chronic obstructive pulmonary disease (COPD) patients. We determined whether nonhypoxemic COPD patients undergoing exercise training while breathing supplemental oxygen achieve higher intensity and therefore improve exercise capacity more than patients breathing air. A double-blinded trial was performed involving 29 nonhypoxemic patients (67 years, exercise SaO2 > 88%) with COPD (FEV1 = 36% predicted). All exercised on cycle ergometers for 45 minutes, 3 times per week for 7 weeks at high-intensity targets. During exercise, they received oxygen (3 L/minute) (n = 14) or compressed air (3 L/minute) (n = 15). Both groups had a higher exercise tolerance after training and when breathing oxygen. However, the oxygen-trained group increased the training work rate more rapidly than the air-trained group. The mean +/- SD work rate during the last week was 62 +/- 19 W (oxygen-trained group) and 52 +/- 22 W (air-trained group) (p < 0.01). After training, endurance in constant work rate tests increased more in the oxygen-trained group (14.5 minutes) than in the air-trained group (10.5 minutes) (p < 0.05). At isotime, the breathing rate decreased four breaths per minute in the oxygen-trained group and one breath per minute in the air-trained group (p = 0.001). We conclude that supplemental oxygen provided during high-intensity training yields higher training intensity and evidence of gains in exercise tolerance in laboratory testing.

Aged↗

PubMed1990

Beneficial effect of exercise training on cardiac long-chain acylcarnitine levels in diabetic rats.

Long-chain acylcarnitines are markedly elevated in the diabetic rat heart. This could be associated with the increased rate of fatty acid metabolism in this tissue seen in the diabetic animal. The effect of exercise training on this carnitine derivative in the diabetic rat, however, has received little attention. We therefore examined the effect of exercise training on this derivative as well as other carnitine esters in hearts of diabetic rats. Four groups of male Wistar rats were used: sedentary-control (SC), trained-control (TC), sedentary-diabetic (SD), and trained-diabetic (TD). Diabetes was induced by the I.V. injection of streptozotocin at the dose of 50 mg/kg. Training was performed on a motor-driven treadmill according to a 10-week program. Sixty hours after the last bout of exercise, the rats were killed by decapitation and the hearts were quickly excised and placed in liquid nitrogen for measurement of total carnitine and its acyl derivatives. SD and TD had significantly lower levels of total (p less than 0.001) and free carnitine (p less than 0.01) compared to the respective control groups. Exercise had no effect on total and free carnitine levels in both control and diabetic groups. Short-chain acylcarnitine levels were neither altered by training nor diabetes. Heart tissue levels of long-chain acylcarnitine were increased (p less than 0.01) in SD compared to SC. However, exercise training resulted in a significant (p less than 0.05) reduction in long-chain acylcarnitines in diabetic rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Acylation↗

PubMed1991

Plasma catecholamine response to acute psychological stress in humans: relation to aerobic fitness and exercise training.

Existing cross-sectional studies on plasma catecholamine activity provide no support for the concept that a markedly high level of aerobic fitness modifies sympathoadrenal response to an acute psychological challenge in humans. In contrast, compromised sympathetic nervous system activity has been observed in individuals with low aerobic fitness and the relationship probably reflects a global deconditioning syndrome involving both psychological and physiological processes. The relationship between low levels of fitness and plasma norepinephrine may appear as a blunted or augmented response depending upon the nature of the task. Short-term (3-4 months) exercise training studies conducted with humans have not indicated a substantial adaptation in the relative plasma catecholamine change from a preexisting baseline during exposure to acute psychological stress. Exercise training can lower basal circulating plasma norepinephrine, resulting in lower absolute concentrations during an acute challenge, but the studies in this area lack consistency and the absolute change tends to be modest. There is no evidence that fitness or exercise training is significantly associated with plasma epinephrine activity during short-term psychological stress.

Analysis of Variance↗

PubMed2001

Endothelium-mediated relaxation of porcine collateral-dependent arterioles is improved by exercise training.

BACKGROUND: Endothelium-dependent modulation of coronary tone is impaired in the collateral-dependent coronary microcirculation. We used a porcine model of chronic coronary occlusion and collateral development to evaluate the hypothesis that exercise training enhances endothelium-mediated relaxation and increases endothelial nitric oxide synthase (ecNOS) mRNA levels of collateral-dependent microvasculature. METHODS AND RESULTS: Adult female miniature swine were subjected to chronic, progressive ameroid occlusion of the proximal left circumflex coronary artery (LCx); after 2 months, animals were randomly exposed to 16-week exercise-training (EX group; treadmill running) or sedentary (SED group; cage confinement) protocols. After completion of EX or SED programs, coronary arterioles ( approximately 100 microm in diameter) were isolated from collateral-dependent LCx (distal to occlusion) and nonoccluded left anterior descending coronary artery (LAD) regions of each heart. Arterioles were studied by in vitro videomicroscopy or frozen for ecNOS mRNA analysis (RT-PCR techniques). Relaxation to the endothelium-dependent vasodilator bradykinin was decreased (P<0.05) in arterioles isolated from collateral-dependent LCx versus nonoccluded LAD regions of SED animals. Bradykinin-mediated relaxation, however, was not different in LCx versus LAD arterioles isolated from EX animals. Nitroprusside-induced relaxation was unaffected by either chronic occlusion or exercise. Importantly, ecNOS mRNA expression was significantly decreased in arterioles isolated from LCx versus LAD regions of SED animals. After training, ecNOS mRNA expression was not different between LAD and LCx arterioles. CONCLUSIONS: These data indicate that exercise training enhances bradykinin-mediated relaxation of collateral-dependent LCx arterioles isolated after chronic coronary occlusion, most likely because of effects on ecNOS mRNA expression and increased production of NO.

Animals↗

PubMed2007

Mild exercise training, cardioprotection and stress genes profile.

To improve current knowledge of the molecular mechanisms underlying exercise-induced cardioprotection in a rat model of mild exercise training, Sprague-Dawley rats were trained to run on a treadmill up to 55% of their maximal oxygen uptake for 1 h/day, 3 days/week, 14 weeks, with age-matched sedentary controls (n = 20/group). Rats were sacrificed 48 h after the last training session. Despite lack of cardiac hypertrophy, training decreased blood hemoglobin (7.94 +/- 0.21 mM vs. 8.78 +/- 0.23 mM, mean +/- SE, P = 0.01) and increased both plasma malondialdehyde (0.139 +/- 0.005 mM vs. 0.085 +/- 0.009 mM, P = 0.05) and the activity of Mn-superoxide dismutase (11.6 +/- 0.6 vs. 16.5 +/- 1.6 mU/microg, P = 0.01), whereas total superoxide dismutase activity was unaffected. When subjected to 30-min ischemia followed by 90-min reperfusion, hearts from trained rats (n = 5) displayed reduced infarct size as compared to controls (37.26 +/- 0.92% vs. 49.09 +/- 2.11% of risk area, P = 0.04). The biochemical analyses in the myocardium, which included gene expression profiles, real-time PCR, Western blot and determination of enzymatic activity, showed training-induced upregulation of the following mRNAs and/or proteins: growth-arrest and DNA-damage induced 153 (GADD153/CHOP), heme-oxygenase-1 (HO-1), cyclooxygenase-2 (Cox-2), heat-shock protein 70/72 (HSP70/72), whereas heat-shock protein 60 (HSP60) and glucose-regulated protein 75 (GRP75) were decreased. As a whole, these data indicate that mild exercise training activates a second window of myocardial protection against ischemia/reperfusion by upregulating a number of protective genes, thereby warranting further investigation in man.

Animals↗

PubMed1999

Effects of exercise training on older patients with major depression.

BACKGROUND: Previous observational and interventional studies have suggested that regular physical exercise may be associated with reduced symptoms of depression. However, the extent to which exercise training may reduce depressive symptoms in older patients with major depressive disorder (MDD) has not been systematically evaluated. OBJECTIVE: To assess the effectiveness of an aerobic exercise program compared with standard medication (ie, antidepressants) for treatment of MDD in older patients, we conducted a 16-week randomized controlled trial. METHODS: One hundred fifty-six men and women with MDD (age, > or = 50 years) were assigned randomly to a program of aerobic exercise, antidepressants (sertraline hydrochloride), or combined exercise and medication. Subjects underwent comprehensive evaluations of depression, including the presence and severity of MDD using Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition criteria and Hamilton Rating Scale for Depression (HAM-D) and Beck Depression Inventory (BDI) scores before and after treatment. Secondary outcome measures included aerobic capacity, life satisfaction, self-esteem, anxiety, and dysfunctional cognitions. RESULTS: After 16 weeks of treatment, the groups did not differ statistically on HAM-D or BDI scores (P = .67); adjustment for baseline levels of depression yielded an essentially identical result. Growth curve models revealed that all groups exhibited statistically and clinically significant reductions on HAM-D and BDI scores. However, patients receiving medication alone exhibited the fastest initial response; among patients receiving combination therapy, those with less severe depressive symptoms initially showed a more rapid response than those with initially more severe depressive symptoms. CONCLUSIONS: An exercise training program may be considered an alternative to antidepressants for treatment of depression in older persons. Although antidepressants may facilitate a more rapid initial therapeutic response than exercise, after 16 weeks of treatment exercise was equally effective in reducing depression among patients with MDD.

Aged↗

PubMed1990

Beneficial effect of exercise training on cardiac long-chain acylcarnitine levels in diabetic rats.

Long-chain acylcarnitines are markedly elevated in the diabetic rat heart. This could be associated with the increased rate of fatty acid metabolism in this tissue seen in the diabetic animal. The effect of exercise training on this carnitine derivative in the diabetic rat, however, has received very little attention. We therefore examined the effect of exercise training on this derivative as well as other carnitine esters in hearts of diabetic rats. Four groups of male Wistar rats were used: sedentary-control (SC), trained-control (TC), sedentary-diabetic (SD), and trained-diabetic (TD). Diabetes was induced by the I.V. injection of streptozotocin at the dose of 50 mg/kg. Training was performed on a motor-driven treadmill according to a ten-week program. 60 hr after the last bout of exercise, the rats were killed by decapitation and the hearts were quickly excised and placed in liquid nitrogen for measurement of total carnitine and its acyl derivatives. SD and TD had significantly lower levels of total (p less than 0.001) and free carnitine (p less than 0.01) compared to the respective control groups. Exercise had no effect on total and free carnitine levels in both control and diabetic groups. Short-chain acylcarnitine levels were neither altered by training nor diabetes. Heart tissue levels of long-chain acylcarnitine were increased (p less than 0.01) in SD compared to SC. However, exercise training resulted in a significant (p less than 0.05) reduction in long-chain acylcarnitines in diabetic rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Acylation↗

PubMed1985

Exercise training and "ventilation threshold" in elderly.

Dynamic exercise training of the elderly increases maximal O2 uptake (VO2max); however, the effects of training on the ventilation threshold (VET) have not been studied. VET was identified as the final point before the ventilatory equivalent for O2 (VE/VO2) increased, without an increase in the ventilatory equivalent for CO2 (VE/VCO2). Inactive elderly males (mean age, 62 yr) were randomly assigned to a control (C, n = 44) or activity (A, n = 45) group. VO2max and VET were determined from an incremental treadmill test. Initial VO2max was not different between the C (2.34 +/- 0.42 l X min-1) and A (2.28 +/- 0.44 l X min-1) groups, nor was there a significant difference in the VO2 at the VET (C = 1.39 +/- 0.26 l X min-1; A = 1.31 +/- 0.23 l X min-1). The activity group trained for 30 min/day, 3 days/wk at an intensity of approximately 65-80% of VO2max. After 1 yr of training the activity group exhibited an 18% increase in VO2max (A = 2.70 +/- 0.54 l X min-1), but the change in VET was not significant (A = 1.39 +/- 0.28 l X min-1). There was no significant change in VO2max (C = 2.45 +/- 0.68 l X min-1) or VET (C = 1.38 +/- 0.31 l X min-1) in the control group. VET/VO2max declined significantly in the activity group (from 58 to 52% of VO2max). Change in VET/VO2max with training was not correlated with the initial VO2max value. We conclude that increases in aerobic capacity are more readily effected than alterations of the VET in elderly subjects.

Humans↗

PubMed1984

Effects of intense exercise training on plasma catecholamines in coronary patients.

This paper reports the effect of 12 mo of intense endurance exercise training on the plasma catecholamine response to exercise in 11 male patients [aged 50 +/- 8 yr (mean +/- SD)] with coronary artery disease. A substantial adaptation to training was attained as evidenced by a 42% increase in maximum O2 uptake capacity. At rest, heart rate was lower after training, but resting blood pressure and plasma catecholamines were unchanged. At the same absolute work rate, plasma norepinephrine and epinephrine levels, rate pressure product, and ischemic S-T segment depression were all significantly lower after training. A higher plasma norepinephrine level was attained at maximal exercise after training (2,049 +/- 654 before vs. 3,408 +/- 1,454 pg/ml after, P less than 0.025); this was associated with a higher systolic blood pressure (175 +/- 25 before vs. 188 +/- 22 mmHg after, P less than 0.025) and a higher rate-pressure product (25.3 X 10(3) +/- 4.5 X 10(3) before vs. 27.6 X 10(3) +/- 5.2 X 10(3) after, P less than 0.025). Despite the higher plasma norepinephrine level and rate pressure product, S-T segment depression at maximal exercise was unchanged. These findings suggest that some patients with coronary arterial disease can attain a higher myocardial O2 requirement, without electrocardiographic evidence of increased ischemia, after prolonged strenuous exercise training.

Adaptation, Physiological↗

PubMedDate not supplied

Exercise training attenuates age-induced changes in apoptotic signaling in rat skeletal muscle.

The aging process in skeletal muscle is characterized by a loss of myocytes and reduction in cross-sectional area of the remaining myocytes, particularly in Type II (fast-twitch) muscle fibers. In multinucleated skeletal muscle, apoptosis may contribute to both fiber atrophy and loss of muscle fibers. Recent evidence suggests that the mitochondrial Bcl-2 family pathway may be a target of aging. Here the authors demonstrated that aging increased DNA fragmentation, cleaved caspase-3, and pro-apoptotic Bax in rat skeletal muscle. Twelve weeks of treadmill exercise training increased anti-apoptotic Bcl-2, while markedly reducing DNA fragmentation, and cleaved caspase-3, Bax, and Bax/Bcl-2 ratio in the white gastrocnemius and soleus muscles of old rats. Upstream anti-apoptotic NF-kappaB activity decreased in aging skeletal muscle, and increased with exercise training. Regulation of NF-kappaB activity with aging and exercise was not related to changes in NF-kappaB subunit protein levels. Instead, changes in post-translational activation of NF-kappaB occurred as a function of altered phosphorylation of IkappaB. These results indicate that treadmill exercise training attenuates fiber atrophy and pro-apoptotic signaling in aging skeletal muscle.

Animals↗

PubMed1993

Changes in skeletal muscle with aging: effects of exercise training.

There is an approximate 30% decline in muscle strength and a 40% reduction in muscle area between the second and seventh decades of life. Thus, the loss of muscle mass with aging appears to be the major factor in the age-related loss of muscle strength. The loss of muscle mass is partially due to a significant decline in the numbers of both Type I and Type II muscle fibers plus a decrease in the size of the muscle cells, with the Type II fibers showing a preferential atrophy. There appears to be no loss of glycolytic capacity in senescent skeletal muscle whereas muscle oxidative enzyme activity and muscle capillarization decrease by about 25%. Vigorous endurance exercise training in older people, where the stimulus is progressively increased, elicits a proliferation of muscle capillaries, an increase in oxidative enzyme activity, and a significant improvement in VO2max. Likewise, progressive resistive training in older individuals results in muscle hypertrophy and increased strength, if the training stimulus is of a sufficient intensity and duration. Since older individuals adapt to resistive and endurance exercise training in a similar fashion to young people, the decline in the muscle's metabolic and force-producing capacity can no longer be considered as an inevitable consequence of the aging process. Rather, the adaptations in aging skeletal muscle to exercise training may prevent sarcopenia, enhance the ease of carrying out the activities of daily living, and exert a beneficial effect on such age-associated diseases as Type II diabetes, coronary artery disease, hypertension, osteoporosis, and obesity.

Adult↗

PubMed2006

Endothelial function and biochemical vascular markers in first-degree relatives of type 2 diabetic patients: the effect of exercise training.

Endothelial dysfunction (ED) is associated with the presence of atherosclerosis. However, ED is also considered a sign of the early vascular changes preceding atherosclerosis. By measuring flow-mediated vasodilation (FMD) and circulating markers of endothelial function we sought to explore whether impaired endothelial function is already present in healthy subjects at increased risk of developing type 2 diabetes mellitus. Furthermore, we aimed to assess the impact of short-term lifestyle intervention (10 weeks endurance exercise) on the potentially primary defects of endothelial function. Twenty-nine healthy but insulin-resistant first-degree relatives of patients diagnosed with type 2 diabetes mellitus (33 +/- 5 years; body mass index, 26.3 +/- 1.6 kg/m2) were compared with 19 control subjects without a family history of diabetes mellitus (31 +/- 5 years; body mass index, 25.8 +/- 3.0 kg/m2). At baseline the von Willebrand factor was significantly increased in the relatives (P < .05). Furthermore, mannose-binding lectin (P = .06), soluble intercellular adhesion molecule 1 (P = .08), and osteoprotegerin (P = .08) tended to be increased in relatives. The following markers of endothelial function were comparable at baseline: FMD, C-reactive protein, plasminogen activator inhibitor 1, and soluble vascular cell adhesion molecule 1. Exercise training resulted in a decrease in mannose-binding lectin (P = .02) and osteoprotegerin (P < .01) in relatives only, whereas other biochemical markers were unaffected in both groups. Moreover, the relatively high-intensity exercise training tended weakly to reduce FMD in the relatives (P = .15). In conclusion, healthy subjects predisposed for type 2 diabetes mellitus show only minor signs of endothelial dysfunction. Under these almost normal vascular conditions, exercise training has little effect on endothelial function.

Adult↗

PubMed1977

Contractile function and myofibrillar ATPase activity in the exercise-trained dog heart.

Myocardial contractility and the enzymatic (ATPase) activity of cardiac contractile proteins were examined after exercise training using the chronically instrumented, unanesthetized dog as an experimental model. Before training, heart rate and the maximum rate of left ventricular pressure development (max dP/dt) were measured at rest and during submaximal exercise. Animals were then subjected to an 8- to 10-wk treadmill running program. Training was verified by the establishment of a 10- to 20-beat/min reduction in heart rate during submaximal exercise. After training max dP/dt was within normal limits at rest, but significantly elevated during submaximal exercise. When max dP/dt was plotted as a function of heart rate, either with the animal standing quietly on the treadmill or during submaximal exercise, a marked elevation in max dP/dt at any given heart rate was observed following training. Myofibrillar protein yield and ATPase activity values were nearly identical in left ventricles from exercise-trained and sedentary control dogs. Although exercise training by treadmill running improved contractile function in the unanesthetized dog myocardium, this response does not appear to involve alterations in myofibrillar ATPase activity.

Adenosine Triphosphatases↗