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PubMed1995

Effects of exercise training in patients with congestive heart failure: a critical review.

Congestive heart failure is a potentially debilitating disorder that affects a significant number of patients. The age-adjusted death rate has doubled over the past decade. Patients live an average of 4 to 5 years, and nearly all suffer from fatigue and breathlessness, which limits exercise capacity and produces a poor quality of life. Patients have usually been advised to avoid exercise because of concerns that they would experience a further decline in cardiac function. However, it has been demonstrated that exercise capacity is not related to the degree of left ventricular systolic dysfunction. This has led to the suggestion that peripheral changes in skeletal muscle and blood supply may play a major role in determining the exercise capacity of patients with congestive heart failure. Studies have demonstrated abnormalities of skeletal muscle blood flow, metabolism and structure, all of which are consistent with the impaired performance observed in these patients. Although the effects of exercise training have been examined in only a relatively few number of patients, the results have been promising. Exercise training has been found to improve exercise capacity and reduce symptoms. However, to our knowledge no data exist as to the impact of exercise training on left ventricular function, hospital stay or mortality in this population. Even though the early results are promising, they require confirmation of feasibility, clinical benefit and safety in larger, long-term randomized trials. It should be determined whether training has a long-term beneficial impact on measures more closely related to daily activities and quality of life. Ultimately, it would be important to determine whether training has an impact on mortality and morbidity.

Clinical Trials as Topic↗

PubMed2003

Exercise training in patients with chronic heart failure improves endothelial function predominantly in the trained extremities.

The present study investigates whether lower-limb dominant exercise training in patients with chronic heart failure (CHF) improves endothelial function primarily in the trained lower extremities or equally in the upper and lower extremities. Twenty-eight patients with CHF were randomized to the exercise or control group. The exercise group underwent cycle ergometer training for 3 months while controls continued an inactive sedentary lifestyle. Exercise capacity (6-min walk test) and flow-mediated vasodilation in the brachial and posterior tibial arteries were evaluated. After 3 months, walking performance increased only in the exercise group (488+/-16 to 501+/-14 m [control]; 497+/-23 to 567+/-39 m [exercise, p<0.05]). The flow-mediated vasodilation in the brachial arteries did not change in either group (4.2+/-0.5 to 4.5+/-0.4% [control]; 4.3+/-0.5 to 4.6+/-0.4% [exercise]), but that in the posterior tibial arteries increased only in the exercise group (4.1+/-0.5 to 4.1+/-0.3% [control]; 3.6+/-0.3 to 6.4+/-0.6% [exercise, p<0.01]). Cycle ergometer training improved flow-mediated vasodilation in the trained lower limbs, but not in the untrained upper limbs. Exercise training appears to correct endothelial dysfunction predominantly by a local effect in the trained extremities.

Arm↗

PubMed1991

Exercise training improves left ventricular systolic function in older men.

To determine whether endurance exercise training can improve left ventricular systolic function in older men, 10 healthy sedentary men (64 +/- 3 years old; mean +/- SD) were studied. Training consisted of endurance exercise 4 +/- 0.3 days per week for 11.8 +/- 2.5 months at a progressively increasing intensity of 60-80% of maximal O2 uptake (Vo2max) with additional brief bouts of exercise equal to 93 +/- 13% of Vo2max. Vo2max increased from 29.6 +/- 4.1 to 37.2 +/- 5.7 ml/kg/min (p less than 0.001). Percent body fat was decreased (17.8 +/- 3.6% versus 15.6 +/- 3.6%; p less than 0.001). Before training, left ventricular ejection fraction, determined by electrocardiographic-gated equilibrium blood pool imaging, increased only modestly during exercise (from 66.3 +/- 6.7% at rest to 70.6 +/- 6.9% at peak exercise). After training, the increase in ejection fraction during exercise was significantly greater (from 67 +/- 4.8% at rest to 77.6 +/- 7.5% at peak exercise) than that observed before training and was similar to that in young sedentary men (64 +/- 7% at rest versus 74 +/- 9% at peak exercise). Although the changes in systolic pressure from rest to exercise were similar, end-systolic volume decreased significantly at peak exercise after (51 +/- 12 versus 38 +/- 13 ml; p less than 0.005) but not before (46 +/- 8 versus 43 +/- 13 ml; p = NS) training with a shift in the end-systolic volume-systolic blood pressure relation to the left compatible with enhanced inotropic state.(ABSTRACT TRUNCATED AT 250 WORDS)

Adaptation, Physiological↗

PubMedDate not supplied

Modest effects of exercise training alone on coronary risk factors and body composition in coronary patients.

BACKGROUND: Cardiac rehabilitation programs have evolved to become secondary prevention centers. However, the independent effect of exercise alone on coronary risk factors and body composition in patients with coronary artery disease has not been well studied. OBJECTIVE: The aim of this study was to determine the effect of exercise training alone, without modification of dietary intake, on coronary risk factors and body composition in a coronary population. METHODS: The authors studied 82 coronary patients (23 females and 59 males) aged 61.2 +/- 12.2 years (mean +/- SD) before and after a 3-month exercise training program. Outcome variables included serum lipid values, glucose, insulin, body composition, body fat distribution, macronutrient intake, and peak aerobic capacity. RESULTS: Neither male nor female patients experienced a significant overall improvement in plasma cholesterol, low-density lipoprotein (LDL)-cholesterol, triglycerides, glucose, or insulin levels after the 3-month exercise training program. Dietary macronutrient intake was unaltered during the study period. Peak aerobic capacity increased by 3.4 +/- 4.7 ml/kg/min (17%, P < 0.0001) and high-density lipoprotein (HDL)-cholesterol increased from 38 +/- 10 to 41 +/- 11 mg/dL (8%, P < 0.001) after the rehabilitation program. Patients with baseline triglyceride levels over 200 mg/dL experienced a 22% decrease (from 374 +/- 205 to 293 +/- 190 mg/dL; P < 0.05) after conditioning. Patients with baseline HDL-cholesterol levels under 35 mg/dL also improved overall by 17% (from 29 +/- 3 to 34 +/- 5 mg/dL; P < 0.0001). Exercise-induced changes in plasma HDL-cholesterol were more related to changes in body composition and/or body fat distribution, rather than changes in peak aerobic capacity. CONCLUSION: Exercise conditioning alone resulted in relatively modest risk factor improvements in coronary patients after 3 months. High-density lipoprotein cholesterol measures increased by 3 +/- 8 mg/dL (8%). Patients with baseline triglyceride elevations experienced a 22% decrease. On the other hand, there were no overall effects on body weight, total cholesterol, LDL-cholesterol, triglycerides, glucose, or insulin levels. For most patients, exercise effects were minimal and nutritional and medical therapy will need to be used more aggressively to attain nationally recognized risk factor goals.

Adult↗

PubMed2004

Effect of exercise training on central aortic pressure wave reflection in coronary artery disease.

BACKGROUND: Arterial stiffness is an important factor for cardiovascular performance and a predictor of cardiovascular risk. We investigated the effect of exercise training on arterial stiffness in coronary artery disease (CAD). METHODS: Arterial stiffness was assessed before and after 12 weeks of either exercise training or standard care in CAD patients. Arterial stiffness was evaluated by aortic augmentation index and time delay of the reflected wave (Deltat) using the SphygmoCor system. RESULTS: The augmentation index decreased (30% v 26%, P <.05) and Deltat increased (136 msec v 144 msec, P <.05) in patients with CAD after 12 weeks of exercise. CONCLUSION: These results suggest that endurance exercise training improves systemic arterial stiffness in individuals with CAD.

Aged↗

PubMed2005

Resistance exercise training decreases oxidative damage to DNA and increases cytochrome oxidase activity in older adults.

Regular resistance exercise increases muscle strength and induces muscle fibre hypertrophy in older adults. Although the underlying causes of aging remain unclear, like acute exercise, aging is associated with oxidative stress. In ageing, however, oxidative stress is closely associated with mitochondrial dysfunction as proposed by the mitochondrial theory of aging. The effect of regular resistance exercise upon mitochondrial function and oxidative stress in older adults is unknown. Twenty-eight older men and women (approximately 68.5+/-5.1 yr) performed whole-body resistance exercise training for 14 weeks. Muscle biopsies were taken before and 72 h following the last exercise bout from the vastus lateralis. Urine samples were also taken at the time of tissue collection. Resistance exercise training was associated with a decrease in 8-OHdG (Pre: 10783+/-5856, Post: 8897+/-4030 ng g(-1) creatinine; p<0.05). Protein content for CuZnSOD, MnSOD, and catalase, and enzyme activities for citrate synthase, mitochondrial ETC complex I+III, and complex II+III were not significantly different from baseline. However, complex IV activity was significantly higher after training as compared to before training (Pre: 2.2+/-0.5, Post: 2.9+/-0.9 micromol min(-1) g(-1)ww; p<0.05), as was the ratio of complex IV to complex I (Pre: 11.1+/-9.3, Post: 14.5+/-10.3; p<0.05). There were no apparent changes in normal mtDNA content or visible mtDNA deletion products as a function of training. These data suggest that regular resistance exercise decreases oxidative stress, but does not affect mtDNA. Moreover, increases in complex IV of the electron transport chain may have an indirect antioxidant effect in older adults and may improve function in daily activities.

8-Hydroxy-2'-Deoxyguanosine↗

PubMed2001

Resistance exercise training attenuates wasting of the extensor digitorum longus muscle in mice bearing the colon-26 adenocarcinoma.

Progressive wasting of skeletal muscle is a significant side effect of malignancy. Perturbations in protein metabolism contribute to this state of wasting. Resistance exercise increases protein synthesis and mass of healthy muscles and counteracts muscle wasting associated with several catabolic conditions. It is not known whether resistance exercise training can counteract cancer-induced muscle wasting. This study examined the effect of resistance exercise training on muscle mass and protein content in 9 mice bearing the colon-26 adenocarcinoma. The dorsiflexor (extensor digitorum longus [EDL] and tibialis anterior) and plantar flexor (soleus, plantaris, and gastrocnemius) muscles of 1 leg of the tumor-bearing and the control mice were stimulated to contract eccentrically and concentrically, respectively, using an electrical stimulation protocol consisting of 10 sets of 6 repetitions per session. The muscles were stimulated on alternate days for a total of 8 sessions. The weight and protein content of the stimulated EDL muscle in the tumor-bearing mice were significantly higher (62% and 25%, respectively) than those of the nonstimulated EDL. Training did not have significant effects on the weight or protein content of the other muscles of the tumor-bearing mice, nor did it have significant effects on the muscles of the controls. These findings demonstrated that resistance training attenuated cancer-induced muscle wasting and protein depletion in the EDL muscle. The lack of an effect of the same training protocol on the EDL muscle in the control mice suggests that the amount and intensity of exercise training that is adequate to attenuate muscle wasting may not be adequate to induce hypertrophy of healthy muscles.

Adenocarcinoma↗

PubMed1995

Exercise-training reduces BAT thermogenesis in rats.

In the energy balance equation, physical activity represents one component of energy expenditure. From various studies it appears that exercise-training does not affect clearly thermogenesis which depends on brown adipose tissue (BAT) activity. In the present work we examine how exercise-training can influence food intake and body weight regulation in relation to BAT thermogenesis. The proton conductance of the uncoupling protein of BAT was examined in male adult Wistar trained 2 h/day for 20 days and compared to that of sedentary (2 h of fasting instead of exercise) or control animals. All animals were provided with separate sources of the 3 macronutrients (protein, fat and carbohydrate) containing an identical percentage of vitamins, salt mixture and cellulose powder. At the end of training, rats were placed at 5 degrees C during 10 days, then during 4 days at 28 degrees C. This condition has been demonstrated to favour and amplify BAT responsiveness to moderate modifications of stimulation. The body weight of trained rats became significantly lower than that of the control and sedentary rats and this difference persisted all throughout the experiment. When placed at 5 degrees C, all rats increased their total ingestion: control rats enhanced fat intake, while sedentary and trained rats enhanced carbohydrate ingestion. When placed at 28 degrees C, all rats had identical total energy and that of the 3 items intakes. BAT proton conductance was about 40% lower in the trained compared with the sedentary plus the control rats. This indicated a lower BAT thermogenic activity in the trained animals. It could be concluded that exercise-training in rats induces negative energy balance; the reduced BAT activity could restrain weight loss and overeating.

Adipose Tissue, Brown↗

PubMed2004

Effect of exercise training in patients with an implantable cardioverter defibrillator.

AIMS: Little research exists on exercise performance and training in patients with an implemented cardioverter defibrillator (ICD) and only in a limited number of patients. This study aims to investigate the effect of exercise training in ICD patients in comparison to the effects in other cardiac patients without an ICD. METHODS AND RESULTS: 92 ICD patients were compared with a control group of 473 patients. A maximal cycle-spiroergometric test was performed until exhaustion before and after an ambulatory exercise training programme. Exercise training was offered 3 times a week for 3 months. The cut-off heart rate was set at (ICD detection rate -20 beats/min). At baseline, the ICD patients had a lower peak oxygen uptake (VO(2)) compared to the control group. Training effects were smaller for peak VO(2) (mL/min/kg) and oxygen pulse in the ICD group (18 vs. 27%, p = 0.006 and 11 vs. 17%, p = 0.016, respectively). Several appropriate shocks were delivered during (n = 5), and in between (n = 7), testing or training and one inappropriate shock during training. CONCLUSIONS: ICD patients can safely participate in an exercise training programme with favorable results. A randomised control study with evaluation of the physical and the psychosocial effects is warranted.

Defibrillators, Implantable↗

PubMed2000

Randomized controlled trial of exercise training for older people (Sendai Silver Center Trial; SSCT): study design and primary outcome.

Physical exercise is expected to improve and maintain physical function in older people, thus promoting health and preventing or postponing the onset of disability in later life. The Sendai Silver Center Trial (SSCT) was a randomized controlled trial designed to evaluate the efficacy of exercise training among healthy free-living older people. Sixty-five eligible participants, aged from 60 to 81 years, were randomly allocated to an exercise group or a control group. The subjects in the exercise group were asked to attend training classes at the Sendai Silver Center, a municipal health and welfare facility in the center of Sendai City, at least twice a week for 25 weeks. Each training class, lasting two hours, started with a warm-up session, followed by an endurance session with a bicycle ergometer, and a resistance exercise training session using rubber films, and ended with a cool-down session. The subjects in the control group were asked to attend recreational classes at the Center twice a month. There were no drop-outs or accidents during the intervention. Comparison of maximum oxygen consumption (VO2max) before and after the 25-week intervention revealed a significant increase in the exercise group (2.1 ml/kg/min) but no significant change in the control group. Our result is equivalent to the participants becoming younger in aerobic capacity by five years after six months of exercise training.

Aged↗

PubMed2004

Effects of high-intensity endurance exercise training in the G93A mouse model of amyotrophic lateral sclerosis.

The G93A transgenic mouse has a mutation in copper/zinc superoxide dismutase (CuZnSOD) that results in oxidative stress and motor neuron loss. Endurance exercise training is known to increase antioxidant capacity in skeletal muscle. Therefore, we hypothesized that endurance training may extend onset of disease or survival in the G93A mouse. We examined the effects of high-intensity endurance exercise training (45 min/day, 5 times/week, progressive increase from 9 to 22 m/min) on disease onset and survival in G93A mice. Endurance training did not affect clinical onset, although it hastened death in male mice (P < 0.05). Endurance-trained males had a statistically significant decrease in rotarod performance at 112 days (P < 0.05), whereas sedentary males decreased at 119 days (P < 0.05). Endurance-trained and sedentary females decreased at 126 days and 129 days, respectively (P < 0.05). Female mice lived longer than males (P < 0.05), and there was a trend for hastened clinical onset in males (P = 0.062). We conclude that high-intensity endurance exercise training does not affect onset of clinical symptoms in G93A mice but hastens a decrease in motor performance and death following onset of clinical symptoms in male mice only. In light of a recent report describing increased survival following low-intensity endurance training, it appears that training intensity is an important determinant of survival in the G93A mouse.

Alanine↗

PubMed2006

Kinematics of stair descent in young and older adults and the impact of exercise training.

Stair descent is a challenging task in old age. This study firstly investigated lower extremity kinematics during stair descent in young (YOU) and healthy, community dwelling older adults (OLD). Secondly, the impact of an exercise training intervention on age-related differences in stair descent was assessed. At baseline, a motion analysis system was used to determine spatio-temporal gait variables and lower extremity kinematics as YOU (n=23, age=27+/-3 years) and OLD (n=34, age=73+/-4 years) descended a three step staircase. The older adults were then divided into training (TRA) and control (CON) groups. For 12 months, TRA performed resistance, aerobic, balance, and flexibility exercises under supervision in a class environment (twice per week) and unsupervised at home (once per week). CON carried on with normal daily activities. Following the intervention, baseline measurements were repeated in TRA and CON. At baseline, total descent, stride cycle, and single support times were longer in OLD than in YOU. In addition, sagittal plane knee motion was lower in OLD whilst frontal and transverse plane pelvis and hip motion were higher in OLD. Exercise training did not reduce the age-related differences observed. In conclusion healthy older adults perform stair descent at a slower speed and with greater motion outside the plane of progression than young adults. We found no evidence that these differences are reduced by generic exercise training, at least in non-frail older adults.

Adult↗

PubMed2002

Regulation of nitric oxide production in limb and ventilatory muscles during chronic exercise training.

In this study, we evaluated the differential influence of chronic treadmill training (30 m/min, 15% incline, 1 h/day, 5 days/wk) on nitric oxide (NO) production and NO synthase (NOS) isoform expression as well as 3-nitrotyrosine formation (footprint of peroxynitrite) both in limb (gastrocnemius) and ventilatory (diaphragm) muscles. A group of exercise-trained rats and a control group (no training) were examined after a 4-wk experimental period. Exercise training elicited an approximate fourfold rise in gastrocnemius NOS activity and augmented protein expression of the endothelial (eNOS) and neuronal (nNOS) isoforms of NOS to approximately 480% and 240%, respectively. Qualitatively similar but quantitatively smaller elevations in NOS activity and eNOS and nNOS expression were observed in the diaphragm. No detectable inducible NOS (iNOS) protein expression was found in any of the muscle samples. Training increased the intensity of 3-nitrotyrosine only in the gastrocnemius muscle. We conclude that whole body exercise training enhances both limb and ventilatory muscle NO production and that constitutive and not iNOS isoforms are responsible for increased protein tyrosine nitration in trained limb muscles.

Animals↗

PubMed2000

Angiotensin II receptor blockade attenuates the deleterious effects of exercise training on post-MI ventricular remodelling in rats.

OBJECTIVES: The effects of exercise training on LV remodelling following large anterior myocardial infarction (MI) remains controversial. Blockade of the renin-angiotensin system has been shown to prevent ventricular dilation and deleterious remodeling. We therefore tested, in a rat model of chronic MI, whether any potentially deleterious effects of exercise on post-MI remodelling could be ameliorated by angiotensin II receptor blockade. METHODS: Male Wistar rats underwent coronary ligation or sham operation. Treatment with losartan (10 mg/kg/day) began 1 week post-MI and moderate treadmill exercise (25 m/min, 60 min/day, 5 days/week) was initiated 2 weeks post-MI. Systolic and diastolic pressure-volume relationships were measured in isolated, red-cell perfused, isovolumically beating hearts 8 weeks post-MI. Morphometric measurements were performed in trichrome stained cross sections of the heart. Five groups of animals were compared: sham (n=13), control MI (MI; n=11), MI plus losartan (MI-Los; n=13), MI plus exercise (MI-Ex; n=10) and MI plus exercise and losartan (MI-Ex-Los; n=12). RESULTS: Infarct size (% of left ventricle, LV) was similar among the infarcted groups [MI=43+/-4%, MI-Los=49+/-2%, MI-Ex=45+/-1%, MI-Ex-Los=48+/-2% (NS)]. Exercise, losartan and exercise+losartan treatments all attenuated LV dilation post-MI to a similar degree. Exercise training increased LV developed pressure in both untreated and losartan treated hearts (P<0.05 vs. other MI groups). In addition, exercise resulted in additional scar thinning in untreated hearts, while no additional scar thinning was seen in post-infarct hearts receiving both losartan and exercise. CONCLUSIONS: Following large anterior MI, losartan attenuated LV dilation and scar thinning. In untreated animals, exercise decreased dilation, but also contributed to scar thinning. Therefore, exercise concurrent with blockade of the renin-angiotensin system may provide optimal therapeutic benefit following large anterior MI.

Analysis of Variance↗

PubMed2002

Increased expression of vascular endothelial growth factor in human skeletal muscle in response to short-term one-legged exercise training.

The effects of short-term exercise training on vascular endothelial growth factor (VEGF) and one of its regulatory transcription factors, the hypoxia inducible factor 1 (HIF-1) subunit, were studied in eight healthy males. Muscle and blood samples were obtained before the 1st, and 24 h after the 7th training session. VEGF and HIF-1 mRNA were analysed using RT-PCR, VEGF mRNA localization with in situ hybridization and VEGF protein with ELISA. Concurrent increases in VEGF mRNA and protein levels were observed in skeletal muscle, and the mRNA was expressed within the skeletal muscle fibres and in cells in the interstitium. These data support the idea of a pretranslational regulation of exercise-induced changes in VEGF mRNA, and indicate that increased VEGF protein expression is an early event in skeletal muscle adaptation to training. Furthermore, different cell types may act as sources for the production of angiogenic factors in response to exercise. The levels of HIF-1 mRNA subunits did not change, suggesting no change in HIF-1 mRNA transcript levels in the regulation of training-induced VEGF expression. In contrast to increased tissue VEGF expression, the arterial and femoral venous plasma levels of VEGF were decreased by training, which may indicate an exercise-induced enhancement of the peripheral uptake of VEGF.

Adult↗

PubMed1996

Exercise training and the glucose transport system in obese SHHF/Mcc-fa(cp) rats.

The effects of a similar exercise training stimulus on maximal insulin-stimulated (MIS) plasma membrane glucose transporter number and glucose transport were determined in lean and obese SHHF/Mcc-facp rats. Six-week-old lean and obese male rats were randomly divided into four groups: lean sedentary (LSed), obese sedentary (OSed), lean exercise (LEx), and obese exercise (OEx). An 8- to 12-wk treadmill running program equalized daily muscular work for LEx and OEx. Plasma membranes were isolated from control and MIS muscles of mixed fiber types. MIS significantly increased glucose transport (3.4- and 2.8-fold) in LSed and OSed, respectively. MIS significantly increased glucose transporter number (2.5-fold) in LSed, but there was no increase in glucose transporter number in OSed. Peak oxygen uptake and citrate synthase activity were increased a similar amount for LEx and OEx groups, demonstrating a similar training stimulus. MIS significantly and similarly increased glucose transport in LEx and OEx (4.4- and 5.1-fold, respectively). The effects of MIS on plasma membrane glucose transporter number in the exercise-trained rats were similar to the responses observed in the sedentary lean and obese groups. MIS significantly increased glucose transporter number (2.6-fold) in LEx, whereas there was no increase in glucose transporter number in OEx. The reduction in MIS glucose transport in OSed appears to be related to a defect in the processes associated with the translocation of glucose transporters to the plasma membrane. Exercise training of the obese rats apparently did not alter this defect. Similar increases in peak oxygen uptake, citrate synthase, and MIS glucose transport in LEx and OEx groups suggest that insulin resistance does not limit the ability of the glucose transport system to adapt to exercise training in the obese male SHHF/Mcc-facp rats.

4-Nitrophenylphosphatase↗

PubMedDate not supplied

Exercise training improves outcomes of a dyspnea self-management program.

PURPOSE: The purpose of this study was twofold: (1) to determine whether exercise training adds to the benefit of a dyspnea self-management (DM) program; and (2) to determine if there is a "dose response" to supervised exercise training (0, 4, or 24 sessions) in dyspnea, exercise performance, and health-related quality of life. METHODS: Subjects with chronic obstructive pulmonary disease (n = 103, 46 men, 57 women; age 66 +/- 8 years; forced expiratory volume in 1 second 44.8 +/- 14% predicted) were randomized to DM, DM-exposure, or DM-training. Dyspnea self-management included individualized education about dyspnea management strategies, a home-walking prescription, and daily logs. Outcomes were measured at baseline and 2 months as part of a 1-year longitudinal randomized clinical trial. Outcomes included dyspnea during laboratory exercise and with activities of daily living (Chronic Respiratory Questionnaire [CRQ]), Shortness of Breath Questionnaire, Baseline/Transitional Dyspnea Index), exercise performance (incremental treadmill tests (ITTs) and endurance treadmill tests (ETTs), 6-minute walk (6MW), and health-related quality of life (SF-36). RESULTS: The DM-training group had significantly greater improvements than the DM-exposure and the DM groups in dyspnea at isotime during ITT (P =.006); exercise performance during ITT (P =.005), ETT (P =.003), and 6MW (P =.01); SF-36 Vitality (P =.031); and CRQ mastery (P =.007). There was a dose-dependent improvement in CRQ dyspnea scores (P <.05) with significant improvements only in the DM-training and DM-exposure groups. CONCLUSION: Exercise training substantially improved the impact of a dyspnea self-management program with a home walking prescription (DM). This impact tended to be dependent on the "dose" of exercise.

Activities of Daily Living↗

PubMed1989

[The effects of exercise training on metabolic phases. With special reference to intraorganic fat and amino acids in Sprague-Dawley rats with streptozotocin diabetes].

We attempted to clarify the effects of aging and the difference between heavy and mild exercise training on the fat and amino acid (AA) systems of streptozotocin diabetic Sprague-Dawley rats in vivo. We exercised two groups of rats, both composed of juvenile and aged rats. The first group, however, consisted of diabetic rats only, the second of normal rats only. Both groups underwent mild training, 20 cm/s, or heavy training, 33 cm/s, for an hour a day, five times a week for four weeks. We looked for fat and amino acids in the serum, liver, red skeletal muscles and heart muscles at the pre- and post-training stages. The results were as follows: Although we observed decreased triglyceride (TG) levels in the serum, liver and intraskeletal muscles in the normal control group, similar decreases were also observed in the diabetic group undergoing insulin treatment with mild exercise training. On the other hand, we observed a clear increase in the rats subjected to heavy exercise training. This increase was particularly significant in the aged rats. There was, however, no significant change in the TG levels in the intraheart muscles of either the juvenile or aged rats, including the diabetic ones. Exercise training in the normal control group produced decreases in total AA, glycogenic AA, branched chain AA and ketogenic AA. Although there was no significant decrease in the TG levels in the serum, we could see clear signs of a decrease in the liver and the intraskeletal muscles. By contrast, the more the rats undergoing insulin treatment for diabetes were exercised, the greater the increase in the amount of AA in the livers and intraskeletal muscles. These changes were especially significant in the aged group. Consistent with previous reports, the diabetic groups produced different results for fat and AA in proportion to the intensity of exercise training and age of the rats. We also demonstrated that the differences were very small in the serum, but significant in the organs, livers and skeletal muscles. From the above findings, we have concluded that exercise training should play a major role in the treatment of diabetes in consideration not only of serum, but also transitions of the whole body's metabolic phases, including the intraorganic systems.

Aging↗