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PubMedDate not supplied

Effects of aerobic exercise training on hemodynamic responses during psychosocial stress in normotensive and borderline hypertensive type A men: a preliminary report.

This study assessed the effects of aerobic exercise training on cardiovascular responses to a 5-min reaction time competition task. Twenty-seven Type A men (aged 30-56) participated in this randomized study in which 14 underwent supervised aerobic training and 13 strength training, with sessions scheduled three times per week for 12 consecutive weeks. Aerobic exercise training was associated with a 13.6% increase in VO2max compared to 2.9% for the strength group. The effects of aerobic exercise training were most evident in subjects whose initial casual blood pressure readings fell in the borderline hypertensive range (N = 5). These individuals exhibited a general reduction in diastolic blood pressure (i.e., during rest, competition, and recovery) which was associated with a fall in both heart rate and total peripheral vascular resistance. Furthermore, diastolic pressure reactivity to the competition task was attenuated in borderline hypertensive subjects who underwent aerobic conditioning. These data are interpreted as preliminary findings suggesting that borderline hypertensives may be particularly responsive to the cardiovascular benefits of aerobic conditioning. For patients who have progressed to this stage of hypertensive disease, aerobic exercise may be of ameliorative value.

Adult↗

PubMedDate not supplied

Central and peripheral adaptations after 12 weeks of exercise training in post-coronary artery bypass surgery patients.

PURPOSE: Training adaptations in patients with coronary artery disease (CAD) have been reported previously, but little is known about central and peripheral adaptations in those recovering from coronary artery bypass graft surgery (CABG). The purpose of this study was to examine the effects of 12 weeks of endurance exercise training on exercise performance and left ventricular and peripheral vascular reserve in a group of uncomplicated CABG patients. METHODS: Thirty-one patients were recruited and began training 8 to 10 weeks after uncomplicated CABG. Patients underwent progressive exercise training consisting of walking and jogging, at 75% to 80% maximal oxygen intake (VO2max). Measures of left ventricular function included ejection fraction (EF), ventricular volumes, and the pressure volume ratio, an index of contractility. Peak ischemic exercise calf blood flow and vascular conductance was determined using strain-gauge plethysmography. Maximal oxygen intake and submaximal blood lactate concentration also was determined. RESULTS: A significant improvement in VO2max (1497 +/- 60 mL/min versus 1691 +/- 71 mL/min) was observed after training. This change was accompanied by an increase in the EF during submaximal exercise (60 +/- 3% versus 63 +/- 2% at 40% VO2max; 61 +/- 3% versus 64 +/- 3% at 70% VO2max) (P < 0.05), and the change in EF from rest to exercise (delta EF). No changes were observed for ventricular volumes during exercise, although there was a trend for a higher stroke volume at 70% VO2max. A significant increase (18%) was observed for peak ischemic exercise calf blood flow and vascular conductance. In addition, submaximal blood lactate concentration was lower after training. CONCLUSIONS: These data indicate that exercise training for 12 weeks in patients recovering from CABG can elicit significant improvements in functional capacity that, for the most part, are secondary to peripheral adaptations, with limited support for improvement in left ventricular function.

Adaptation, Physiological↗

PubMed1988

Decreased insulin response to sustained hyperglycemia in exercise-trained rats.

Male Wistar rats were studied to determine if exercise training reduces the insulin response to sustained hyperglycemia. Training (TN) for 8 wk on a treadmill resulted in significantly (P less than 0.05) increased time to exhaustion in TN compared to control animals (CN). Hyperglycemic glucose clamps at 11 mM for 90 min resulted in elevations of arterial plasma insulin to 23.6 +/- 4.3 ng.ml-1 (mean +/- SE, N = 7) in CN and 11.8 +/- 1.1 ng.ml-1 (N = 7) in TN (P less than 0.05). No significant difference between groups existed for the level of imposed hyperglycemia. Glucose infusion rates required to maintain the sustained hyperglycemia were 62.7 +/- 3.2 mg.kg-1 min-1 in CN and 68.5 +/- 3.0 mg.kg-1.min-1 in TN (P greater than 0.05) at the end of the glucose clamp. These data show that exercise training reduces the insulin response to sustained steady state hyperglycemia.

Animals↗

PubMed2001

Modification by exercise training of activity and enzyme expression of hepatic branched-chain alpha-ketoacid dehydrogenase complex in streptozotocin-induced diabetic rats.

The branched-chain alpha-ketoacid dehydrogenase (BCKDH) complex is the rate-limiting enzyme in the catabolism of branched-chain amino acids. In the present study, we examined the effects of exercise training on the activity and enzyme expression of the hepatic BCKDH complex in diabetic rats. The rats were prepared by intravenous injections of streptozotocin (50 mg/kg BW), and exercise training was accomplished by treadmill running for 45 min/d for 4 wk. The total and actual activities of hepatic BCKDH complex were significantly increased to approximately 160% by 4 wk of diabetes. On the other hand, diabetic rats in the trained group had the same level of activities as those in the normal rats, indicating that exercise training inhibited the diabetes-induced increase in the enzyme activities. The activity state (% active form) of the enzyme complex was about 100% in all groups and was not affected by diabetes or training. The protein amounts of the enzyme subunits (E1alpha and E2) and the abundance of mRNA for the E2 subunit, but not for the other subunits, in the liver had the same trend as the activities. These results suggest that the capacity for branched-chain amino acid catabolism in streptozotocin-induced diabetic rats is reduced by exercise training and that this modification is associated with the suppression of diabetes-induced BCKDH complex expression in the liver.

3-Methyl-2-Oxobutanoate Dehydrogenase (Lipoamide)↗

PubMed2003

Gender, exercise training, and eNOS expression in porcine skeletal muscle arteries.

Our purpose was to determine the effects of gender and exercise training on endothelial nitric oxide synthase (eNOS) and superoxide dismutase (SOD) protein content of porcine skeletal muscle arteries and to evaluate the role of 17beta-estradiol (E2) in these effects. We measured eNOS and SOD content with immunoblots and immunohistochemistry in femoral and brachial arteries of trained and sedentary male and female pigs and measured estrogen receptor (ER) mRNA and alpha-ER and beta-ER protein in aortas of male and female pigs. Results indicate that female arteries contain more eNOS than male arteries and that exercise training increases eNOS content independent of gender. Male and female pigs expressed similar levels of alpha-ER mRNA and protein and similar amounts beta-ER protein in their arteries. E2 concentrations as measured by RIA were 180 +/- 34 pg/ml in male sera and approximately 5 pg/ml in female sera, and neither was changed by training. However, bioassay indicated that biologically active estrogen equivalent to only 35 +/- 5 pg/ml was present in male sera. E2 in female pigs, whether measured by RIA or bioassay, was approximately 24 pg/ml at peak estrous and 2 pg/ml on day 5 diestrus. The free fraction of E2 in sera did not explain the low measurements, relative to RIA, of E2. We conclude that 1). gender has significant influence on eNOS and SOD content of porcine skeletal muscle arteries; 2). the effects of gender and exercise training vary among arteries of different anatomic origin; 3). male sera contains compounds that cause RIA to overestimate circulating estrogenic activity; and 4). relative to human men, the male pig is not biologically estrogenized by high levels of E2 reported by RIA, whereas in female pigs E2 levels are lower than in the blood of human women.

Animals↗

PubMed2002

Exercise training and heart failure: a systematic review of current evidence.

Chronic heart failure (CHEF) is a growing public health problem. Current guidelines provide detailed information regarding pharmacotherapy but little guidance about the value of exercise/cardiac rehabilitation programmes for individuals with this condition. To investigate the effects of exercise training upon CHF patients, a systematic literature review was carried out of trials (from 1966 to December 2000) which used as their main outcome measures the effects of exercise training upon: (a) physical performance; or (b) quality of life; or (c) morbidity/mortality. Databases searched include: MedLine; Science Citation Index; Social Sciences Citation Index; BIDS, Bandolier; Cochrane Database of Systematic Reviews (CDSR); NHS National Research Register (NRR); and Current Research in Britain (CRIB). Relevant bibliographic references from identified articles were also reviewed. Thirty-one trials were identified, comprising randomised controlled trials (RCTs) (14/31), randomised crossover trials (8/31), non-RCTs (2/31), and pre-test/post-test (7/31). Sample sizes were: 25 participants or fewer (20/31); 26 to 50 participants (7/31); 51 to 150 participants (4/31). Participants were predominantly younger with a mean age in 23/31 studies of 65 years or less, and male. Patients with comorbidities were often excluded. Positive effects were reported on physical performance (27/31), quality of life (11/16), mortality (1/31), and readmission rates (1/31). No cost-effectiveness analyses were identfied. We conclude that short-term physical exercise training in selected subgroups of patients with CHF has physiological benefits and positive effects on quality of life. This review highlights the continuing problem of clinical trials that include participants who are not representative of the general population of CHF patients seen in primary care. Further investigation of the utility and applicability of exercise training is essential.

Adult↗

PubMed2006

Exercise training and the antioxidant alpha-lipoic acid in the treatment of insulin resistance and type 2 diabetes.

One hallmark of the insulin-resistant state of prediabetes and overt type 2 diabetes is an impaired ability of insulin to activate glucose transport in skeletal muscle, due to defects in IRS-1-dependent signaling. An emerging body of evidence indicates that one potential factor in the multifactorial etiology of skeletal muscle insulin resistance is oxidative stress, an imbalance between the cellular exposure to an oxidant stress and the cellular antioxidant defenses. Exposure of skeletal muscle to an oxidant stress leads to impaired insulin signaling and subsequently to reduced glucose transport activity. Numerous studies have demonstrated that treatment of insulin-resistant animals and type 2 diabetic humans with antioxidants, including alpha-lipoic acid (ALA), is associated with improvements in skeletal muscle glucose transport activity and whole-body glucose tolerance. An additional intervention that is effective in ameliorating the skeletal muscle insulin resistance of prediabetes and type 2 diabetes is endurance exercise training. Recent investigations have demonstrated that the combination of exercise training and antioxidant treatment using ALA in an animal model of obesity-associated insulin resistance provides a unique interactive effect resulting in a greater improvement in insulin action on skeletal muscle glucose transport than either intervention individually. Moreover, this interactive effect of exercise training and ALA is due in part to improvements in IRS-1-dependent insulin signaling. These studies highlight the effectiveness of combining endurance exercise training and antioxidants in beneficially modulating the molecular defects in insulin action observed in insulin-resistant skeletal muscle.

Animals↗

PubMed1987

Mechanisms responsible for enhanced stroke volume after exercise training in coronary heart disease.

High intensity endurance exercise training increases maximal attainable O2 uptake (VO2max) and stroke volume (SV) in patients with ischaemic heart disease. To determine the mechanisms responsible for enhanced SV after training, 18 patients, 51 +/- 3 years (mean +/- SE) were studied. Patients completed 12 months of endurance exercise with a peak intensity of 89.7 +/- 2% of attainable VO2max. Attainable VO2max increased from 23 +/- 1 to 32 +/- 2 ml/kg/min (P less than 0.0001). Left ventricular function was assessed using radionuclide ventriculography. To control for afterload, haemodynamic variables were evaluated at comparable mean blood pressure (mBP). SV was increased after training both at rest (77 +/- 3 vs 81.5 +/- 5 ml; P less than 0.025) and during exercise (78 +/- 6 vs 93 +/- 6 ml; P less than 0.025) at comparable mBP. Before training, ejection fraction decreased during exercise (59 +/- 3 vs 55 +/- 3%, P less than 0.005) but increased after training from the resting level (59 +/- 3 vs 63 +/- 3%, P less than 0.025). Left ventricular end diastolic volume during exercise did not change. Thus, the results suggest that enhanced SV during exercise is, in part, due to improved left ventricular function after exercise training.

Coronary Disease↗

PubMed2026

Effects of Intravenously Administered Plasma from Exercise-Trained Donors on Mitochondrial Respiration in a Rat Model of Alzheimer's Disease.

PURPOSE: Dysfunction of mitochondria is observed early in Alzheimer's disease (AD), possibly driving the pathogenesis of the disease. This study aims to assess whether plasma from exercise-trained donors can enhance mitochondrial function in a transgenic AD model and to gain insight into the proteomic profile of the donor plasma. METHODS: Male McGill-R-Thy1-APP rats (n = 3 per treatment group) were treated at either an early preplaque stage (2.2 months) or a later stage (5.2 months) with plasma from exercise-trained donors (ExPlas), sedentary donors (SedPlas), or saline. The rats received 14 transfusions over 6 wk. Mitochondrial respiration was assessed in cornu ammonis (CA), dentate gyrus (DG), gastrocnemius, and left ventricle using high-resolution respirometry. Proteomic analyses were performed in donor blood using mass spectrometry. RESULTS: In early-stage AD rats, ExPlas improved hippocampal mitochondrial respiration. Compared with saline, CA oxidative phosphorylation (OXPHOS) capacity for complex I increased by +30.8 pmol O2·s-1·mg-1 (P < 0.001) and CI+II by +37.8 pmol O2·s-1·mg-1 (P < 0.001). Compared with SedPlas, CA OXPHOS for CI increased by +16.9 pmol O2·s-1·mg-1 (P = 0.01) and CI+II by +23.8 pmol O2·s-1·mg-1 (P = 0.007). In DG, similar improvements were only seen compared with saline. In CA, but not DG, of later-stage rats, ExPlas produced smaller but significant increases in CI and CI+II OXPHOS compared with saline, but no significant differences compared with SedPlas. No changes were observed in muscle or heart. Proteomics revealed enrichment of complement and platelet-related pathways in ExPlas. CONCLUSIONS: This proof-of-concept study shows that exercise-trained donor plasma enhances hippocampal mitochondrial respiration in early-stage AD rats and, to a lesser extent, in later-stage AD rats. The proteomic profile of the exercise-trained donor plasma indicates a role of altered complement and platelet functions.

Animals↗

PubMed2004

Effects of ageing and exercise training on endothelium-dependent vasodilatation and structure of rat skeletal muscle arterioles.

Ageing reduces endothelium-dependent vasodilatation in humans and animals, and in humans, exercise training reverses the ageing-associated reduction in endothelium-dependent vasodilatation. The purpose of this study was to determine the mechanism(s) by which 10-12 weeks of treadmill exercise enhances endothelium-dependent vasodilatation in muscles of differing fibre composition from young and old rats. Three- and 22-month-old male Fischer 344 rats were assigned to young sedentary, young exercise-trained, old sedentary, or old exercise-trained groups. Arterioles were isolated from the soleus and gastrocnemius muscles; luminal diameter changes were determined in response to the endothelium-dependent vasodilator acetylcholine (ACh, 10(-9)-10(-4) mol l(-1)) alone and in the presence of the nitric oxide synthase (NOS) inhibitor l-NAME (10(-5) mol l(-1)) or the combination of l-NAME and the cyclooxygenase inhibitor indomethacin (10(-5) mol l(-1)). Training ameliorated the ageing-induced reduction in endothelium-dependent vasodilatation in soleus muscle arterioles. Treatment with l-NAME alone and in combination with indomethacin abolished differences in ACh vasodilatation occurring with ageing and training. Expression of endothelial NOS (eNOS) mRNA in soleus arterioles was unaltered by ageing, whereas eNOS protein was increased with age; training elevated both eNOS mRNA and protein. In gastrocnemius muscle arterioles, ageing did not alter maximal vasodilatation, but ageing and training increased maximal arteriolar diameter. These results demonstrate that ageing-induced reductions and training-induced enhancement of endothelial vasodilatation both occur through the nitric oxide signalling mechanism in highly oxidative skeletal muscle, but ageing and training do not appear to act on the same portion of the signalling cascade.

Acetylcholine↗

PubMedDate not supplied

Exercise training, indomethacin, and isoproterenol-induced myocardial necrosis in the rat.

It was hypothesized that endurance exercise training would attenuate isoproterenol-induced myocardial necrosis in the rat by increasing the concentration of prostacyclin in the myocardial vasculature. Rats were randomly assigned to exercise and control groups. Exercisers ran on a motorized treadmill 1 h.d-1, 5 d.week-1 for 14 weeks. Immediately following the training program subgroups of rats were injected with 4 mg.kg-1 indomethacin or saline. One day later, all rats were given a subcutaneous injection of isoproterenol (20 mg.kg-1); after another 24 h they were sacrificed. A decrease of myocardial creatine kinase (CK) activity was used as a marker for myocardial necrosis. Endurance exercise training attenuated the isoproterenol-induced decrease in myocardial CK relative to control by approximately 37% (exercise: 16.4 +/- 0.6 U.mg-1 protein; control: 10.5 +/- 0.6 U.mg-1 protein; p less than 0.05). Pretreatment with indomethacin decreased myocardial CK in the exercise-trained rats (indomethacin: 15.4 +/- 0.8 U.mg-1 protein; saline: 17.7 +/- 0.7 U.mg-1 protein; p less than 0.05), but not in the controls (indomethacin: 10.3 +/- 1.0 U.mg-1 protein; saline: 10.8 +/- 0.6 U.mg-1 protein; p greater than 0.05). The concentration of myocardial 6-keto-PGF1 alpha, a marker for prostacyclin, was not altered by exercise but, as expected, was reduced by indomethacin pretreatment (p less than 0.05). Thus, exercise training reduces myocardial damage caused by isoproterenol, but the evidence does not support the hypothesis that prostacyclin mediated this effect of training. Further research is needed to determine the extent to which exercise training-induced alterations in sensitivity to PGI2 or TXA2 affect myocardial damage from isoproterenol.(ABSTRACT TRUNCATED AT 250 WORDS)

6-Ketoprostaglandin F1 alpha↗

PubMed2004

Exercise training improves cardiac function-related gene levels through thyroid hormone receptor signaling in aged rats.

Exercise training improves the aging-induced downregulation of myosin heavy chain (MHC) and sarcoplasmic reticulum (SR) Ca(2+)-ATPase, which participate in the regulation of cardiac contraction and relaxation. Thyroid hormone receptor (TR), a transcriptional activator, affected the regulation of gene expression of MHC and SR Ca(2+)-ATPase. We hypothesized that myocardial TR signaling contributes to a molecular mechanism of exercise training-induced improvement of MHC and SR Ca(2+)-ATPase genes with cardiac function in old age. We investigated whether TR signaling and gene expression of MHC and SR Ca(2+)-ATPase in the aged heart are affected by exercise training, using the hearts of sedentary young rats (4 mo old), sedentary aged rats (23 mo old), and trained aged rats (23 mo old, swimming training for 8 wk). Trained aged rats showed improvement in cardiac function. Expression of TR-alpha1 and TR-beta1 proteins in the heart were significantly lower in sedentary aged rats than in sedentary young rats and were significantly higher in trained aged rats than in sedentary aged rats. The activity of TR DNA binding to the transcriptional regulatory region in the alpha-MHC and SR Ca(2+)-ATPase genes and the mRNA and protein expression of alpha-MHC and SR Ca(2+)-ATPase in the heart and plasma 3,3'-triiodothyronine and thyroxine levels were altered in association with changes in the myocardial TR protein levels. These findings suggest that exercise training improves the aging-induced downregulation of myocardial TR signaling-mediated transcription of MHC and SR Ca(2+)-ATPase genes, thereby contributing to the improvement of cardiac function in trained aged hearts.

Aging↗

PubMed1998

An exercise training combined with dietary program for patients with hypertension.

A controlled clinical trial was conducted to determine whether combined exercise training and diet alone reduce blood pressure (BP), body weight and body mass index (BMI) in three weeks. Twenty eight patients with diastolic BP < or = 110 mmHg were assigned to a hypertensive group and another 28 subjects with diastolic BP < or = 90 mmHg were subjected to the same intervention as control group (normotensive group). Exercise training and diet reduced diastolic BP by 24.7 mmHg and systolic BP by 32.8 mmHg in hypertensive group. There was a mean decreased of 5.3 mmHg in the diastolic BP in the normotensive group (P < 0.001). The systolic BP decreased only minimally. The weight loss ranged from 1 kg to 3 kg in hypertensive and 1 kg to 2 kg in the normotensive group. The mean weight loss was 1.6 kg (0.7) in hypertensive and 1.5 kg (0.5) in the normotensive group. In both the groups the weight reduction was highly significant (P < 0.001) and moderately positive correlation was also noted with the fall of BPs. The mean fall of BMI was 0.61 kg/m2 (0.21) and 0.51 (0.2) kg/m2 in the hypertensive and normotensive groups respectively. The findings indicated that a combined exercise training and dietary program could lower BP in patients with mild to moderate hypertension, but its long-term consequences on morbidity and mortality remain to be determined.

Adult↗

PubMed2002

The effect of endurance exercise training on plasma lipoprotein AI and lipoprotein AI:AII concentrations in sedentary adults.

The effect of 6 months of endurance exercise training on plasma concentrations of lipoprotein (Lp)AI and LpAI:AII was determined in 39 sedentary subjects (17 men, 22 women, average age, 57 years) with abnormal cholesterol concentrations (total cholesterol [TC] > 200 mg/dL, or high-density lipoprotein-cholesterol [HDL-C] < 35 mg/dL). Following exercise training, plasma LpAI concentrations increased (+5.9 +/- 1.2 mg/dL; P <.001), but there was no change in total apolipoprotein (apo) A-I or LpAI:AII concentrations. The change in plasma LpAI concentration was positively correlated to changes in total HDL-C (r =.495, P =.001), the sum of HDL4-C(nmr) + HDL5-C(nmr) (r =.417, P =.008), and average HDL particle size (r =.415, P =.009), but not to changes in body composition or Vo2max. In the 8 subjects with the greatest change in LpAI concentration following training, the size distribution of LpAI and LpAI:AII particles in plasma also was measured before and after training. In these subjects, the size distribution of LpAI:AII particles did not change with training, but there was a significant increase (0.1 nm; P =.048) in the peak size of the "medium" (7.8 to 9.8 nm) LpAI particles after training. In 7 subjects who served as age- and weight-matched sedentary controls, plasma concentrations of total apo A-I, the LpAI and LpAI:AII subfractions, and plasma lipoprotein-lipids did not differ significantly between baseline and final testing. These data indicate that endurance exercise training increases the average size and plasma concentrations of LpAI, but not LpAI:AII, particles, which may represent possible enhancements of reverse cholesterol transport and may provide insight into the role that exercise plays in reducing cardiovascular disease risk.

Aged↗

PubMed2005

Exercise training modulates cytokines activity in coronary heart disease patients.

BACKGROUND: Physical activity may lower the risk for coronary artery disease (CAD) by mitigating inflammation, which plays a key role in the pathophysiology of atherosclerosis. The purpose of this study was to determine the effect of aerobic exercise training on levels of pro- and anti-inflammatory cytokines, IL-1, IL-6, IL-10, INF-gamma, and C-reactive protein (CRP), in CAD patients participating in a cardiac rehabilitation program. METHODS AND RESULTS: Twenty-eight patients, age 64+/-7.1 years, participated in a 12-week aerobic exercise training program at 70-80% of individual maximal heart rate. Training resulted in a significant reduction of all pro-inflammatory cytokines, CRP from 7.5+/-4.2 to 3.9+/-3.5 mg/l, p<0.001, IL-1, 0.33+/-0.23 to 0.51+/-0.12 pg/ml, p=0.014, IL-6, 2.50+/-1.50 to 1.44+/-0.57 pg/ml, p=0.002, INF-gamma, 18.63+/-3.31 to 16.77+/-2.49 pg/ml, p<0.001, as well as a significant increase in the anti-inflammatory, cytokine IL-10, from 1.61+/-1.40 to 2.29+/-2.01 pg/ml, p=0.008. Baseline CRP levels were 36% (p=0.006) higher among diabetes mellitus patients and training was associated with a 40.5% CRP reduction in these patients compared to 19% reduction in non-diabetics, p<0.01. At baseline 72% of patients were in a high risk category (CRP>3 mg/l), 28% in an intermediate (CRP=1-3 mg/l), with none in a low risk category (<1 mg/l). Following exercise training, 11% were in the low risk, 50% in the intermediate and 39% in the high risk category, indicating 46% reduction in the number of subjects in the high risk category. CONCLUSIONS: Aerobic exercise training in CAD patients is an effective mean in inducing reduction in CRP, IL-1, IL-6, INF-gamma levels, and increase in IL-10, thus, possibly improving coronary risk profile.

Aged↗

PubMedDate not supplied

Tai Chi as an adjunct to cardiac rehabilitation exercise training.

Heart disease is a chronic condition needing lifetime secondary prevention measures to decrease morbidity and mortality, and to improve quality of life. Cardiac rehabilitation exercise training, one aspect of cardiac recovery, traditionally includes some form of aerobic fitness and, more recently, muscle strength training to improve exercise tolerance. Tai chi, widely practiced in China for centuries, is a popular form of exercise among older Chinese persons associated with enhanced well-being and health among traditional Chinese practitioners. Recent research has reported improvement in cardiorespiratory function, balance and postural stability, fall prevention, and stress reduction. A review of the literature suggests potential benefits from tai chi exercise performed as an adjunct to cardiac rehabilitation exercise training. Tai chi is cost-effective and facilitates a lifestyle of health-related behavior practices.

Accidental Falls↗

PubMedDate not supplied

Interaction of exercise training and chronic ethanol ingestion on antioxidant system of rat brain regions.

This study investigates the interactive effects of chronic ethanol ingestion and exercise training on the antioxidant system and lipid peroxidation in cortex, cerebellum, medulla, striatum and hypothalamus of the rat brain. Exercise training (6.5 weeks) significantly increased superoxide dismutase (SOD) activity in striatum, the region associated with motor activity, but decreased SOD activity in other brain regions. Catalase (CAT) activity decreased significantly in hypothalamus, the region associated with behavior, due to exercise. The training significantly increased glutathione peroxidase (GSH-Px) activity in brain regions studied with the exception of cerebellum. In addition, glutathione reductase (GR) activity increased in brain regions, with the exception of medulla. The training significantly decreased malondialdehyde (MDA) levels in all brain regions studied, which is due to training adaptation. Ethanol (20%) (2.0 g kg[-1], p.o. for 6.5 weeks) significantly decreased SOD activity in all regions except cortex, CAT activity in cortex, striatum and hypothalamus, GSH-Px activity in cerebellum and GR activity in medulla. Similarly, ethanol significantly decreased the GSH level in cortex, medulla and striatum and the GSH/GSSG ratio in medulla and cerebellum. Conversely, ethanol significantly augmented GR activity in cortex, cerebellum and striatum. When ethanol and exercise were combined, there was significantly increased SOD and CAT activity in striatum, GSH-Px activity in cortex, striatum and hypothalamus and GR activity in cortex and striatum. The GSH level was significantly depleted in cortex, striatum and medulla. Combining training and ethanol also decreased MDA levels in medulla and cerebellum. In conclusion, the sensitivity of specific brain regions in reaction to chronic ethanol ingestion or training is a function of variability in antioxidant system activity. Thus, exercise training protects specific brain regions against ethanol-induced oxidative injury.

Animals↗

PubMed2005

Exercise training and 3-day head down bed rest deconditioning: exercise thermoregulation.

UNLABELLED: Bed rest (BR) deconditioning causes excessive increase of exercise core body tempera-ture, while aerobic training improves exercise thermoregulation. The study was designed to determine whether 3 days of 6 degrees head-down bed rest (HDBR) affects body temperature and sweating dynamics during exercise and, if so, whether endurance training before HDBR modifies these responses. Twelve healthy men (20.7+/-0.9 yrs, VO2max: 46+/-4 ml x kg(-1) x min(-1) ) underwent HDBR twice: before and after 6 weeks of endurance training. Before and after HDBR, the subjects performed 45 min sitting cycle exercise at the same workload equal to 60% of VO2max determined before training. During exercise the VO2, HR, tympanic (Ttymp) and skin (Tsk) temperatures were recorded; sweating dynamics was assayed from a ventilated capsule on chest. Training increased VO2max by 12.1% (p<0.001). Resting Ttymp increased only after first HDBR (by 0.22 +/- 0.08 degrees C, p<0.05), while exercise equilibrium levels of Ttymp were increased (p<0.05) by 0.21 +/- 0.07 and 0.26 +/- 0.08 degrees C after first and second HDBR, respectively. Exercise mean Tsk tended to be lower after both HDBR periods. Total sweat loss and time-course of sweating responses were similar in all exercise tests. The sweating threshold related to Ttymp was elevated (p<0.05) only after first HDBR. IN CONCLUSION: six-week training regimen prevents HDBR-induced elevation of core temperature (Ttymp) at rest but not during ex-ercise. The post-HDBR increases of Ttymp without changes in sweating rate and the tendency for lower Tsk suggest an early (<3d) influence of BR on skin blood flow.

Adult↗