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Effects of percutaneous balloon mitral valvuloplasty and exercise training on the kinetics of recovery oxygen consumption after exercise in patients with mitral stenosis.

AIMS: Kinetics of recovery oxygen consumption after exercise plays an important role in determining exercise capacity. This study was performed to assess the kinetics of recovery oxygen consumption in mitral stenosis and evaluate the effects of percutaneous balloon mitral valvuloplasty and exercise training on the kinetics. METHODS AND RESULTS: Thirty patients with mitral stenosis (valve area < or =1.0 cm2) and same sized age- and size-matched healthy volunteers were included for this study. All subjects performed maximal upright graded bicycle exercise. Thirty consecutive patients who underwent successful percutaneous balloon mitral valvuloplasty (valve area > or =1.5 cm2 and mitral regurgitation grade < or =2), were randomized to an exercise training group or non-training group. The exercise group performed daily exercise training for 3 months. Half-recovery time of peak oxygen consumption was significantly delayed in mitral stenosis as compared to normal subjects (120+/-42 s vs 59+/-5, P<0.01). Peak oxygen consumption (ml x min(-1) x kg(-1)) was significantly increased in both the training (16.8+/-4.9 to 25.3+/-6.9) and non-training groups (16.3+/-5.1 to 19.6+/-6.0) 3 months after percutaneous balloon mitral valvuloplasty. Half-recovery time of peak oxygen consumption was significantly shortened in the training group (124+/-39 to 76+/-13, P<0.01), but not in the non-training group (114+/-46 to 109+/-44 s, P=0.12) at 3 months follow-up. The degrees of symptomatic improvement after percutaneous balloon mitral valvuloplasty were more closely correlated with the changes of the half-recovery time of peak oxygen consumption than those of peak oxygen consumption. CONCLUSION: Kinetics of recovery oxygen consumption was markedly delayed in mitral stenosis, which was improved after exercise training but not after percutaneous balloon mitral valvuloplasty alone. These results suggest that adjunctive exercise training may be useful for improvement of recovery kinetics and subjective symptoms after percutaneous balloon mitral valvuloplasty.

Adult↗

Exercise training induces glycogen sparing during exercise by old rats.

Glycogen utilization during exercise appears to be related to muscle respiratory capacity. Since the decline in hindlimb muscle respiratory capacity that occurs in rats during old age is eliminated when young and old rats undergo an identical exercise training protocol, liver and gastrocnemius glycogen concentrations were determined in identically trained young and old Fischer 344 rats at rest and immediately after a 30-min run requiring approximately 75% of maximal O2 consumption. These values were also compared with untrained age-matched control animals. The animals, which were 10 or 24 mo old after 6 mo of training, were fasted for 24 h before they were killed. Resting gastrocnemius glycogen did not differ among the groups. After 30 min of running, gastrocnemius glycogen was lower in the untrained than the trained groups and was not different between the trained groups. Resting liver glycogen was lower in the old trained group than the untrained groups but not statistically different from the young trained group. The postrun liver glycogen did not differ among the groups. Estimated gastrocnemius and liver glycogen utilization during exercise was decreased in both trained groups compared with untrained age-matched controls. These results indicate that the training-induced glycogen sparing during exercise of the same relative intensity was not diminished with age in identically trained young and old rats.

Aging↗

Effect of physical exercise training on health-related quality of life and exercise tolerance in patients with left ventricular dysfunction.

OBJECTIVES: The improvement of exercise tolerance and quality of life (QOL) are essential in the treatment of patients with heart failure. The influence of physical exercise training on QOL was investigated in patients with left ventricular dysfunction. METHODS: Health-related QOL was evaluated using the Medical Outcomes Study Short-Form 36 Health Status Survey (SF-36) before and 3 months after individualized exercise training determined by cardiopulmonary exercise testing in 65 patients. The 44 patients who could carry out more than two-thirds of the prescribed exercise were classified into two groups: Group A (11 patients)with left ventricular ejection fraction < 40% and Group B (33 patients) with left ventricular ejection fraction > or = 40%. The remaining 21 patients served as the control group. RESULTS: The mean value of SF-36 improved significantly with exercise training only in Group A (50.8 +/- 25.3 to 62.1 +/- 22.2, p < 0.05). Group A also had an increase in peak Vo2 (18.9 +/- 3.5 to 21.4 +/- 3.6 ml/min/kg, p < 0.005) and a decrease in brain natriuretic peptide. The 24 patients (9 in Group A, 15 in Group B) with improved SF-36 values after the exercise training showed a negative correlation between the change of the mental component summary and the peak Vo2 (r = - 0.606, p < 0.05). CONCLUSIONS: Exercise training improves both the QOL, especially the mental component, and the exercise tolerance in patients with left ventricular dysfunction.

Adult↗

Human gender differences in fibrinolytic responses to exercise training and their determinants.

Endurance exercise training improves fibrinolysis, but this training-induced adaptation may differ somewhat between men and women. We sought to determine whether the potential gender differences in training-induced changes in selected fibrinolysis measures were related to changes in adiposity and/or plasma lipoprotein lipid levels. Seventeen men and 28 women, 50-75 years old, who were generally overweight to obese, were assessed for plasminogen activator inhibitor-1 (PAI-1) and tissue plasminogen activator (t-PA) activity, t-PA antigen and plasma lipoprotein-lipid levels, and body composition before and after 6 months of endurance exercise training while on a low-fat diet. At baseline, there were no differences in fibrinolytic measures between the men and women. Baseline levels of these fibrinolytic markers in both men and women were primarily related to other fibrinolytic measures and body composition, with a smaller contribution from plasma high-density lipoprotein cholesterol (HDL-C) levels. Exercise training reduced t-PA antigen levels in both men and women, but the reduction was significantly greater in men (-1.6 +/- 0.3 versus -0.5 +/- 0.2 ng ml(-1), P = 0.007). Exercise training decreased PAI-1 activity more in men than in women (-2.6 +/- 1.4 versus +0.9 +/- 0.9 IU ml(-1), P = 0.03). Men and women both showed increased t-PA activity with exercise training to the same extent (+0.38 +/- 0.12 versus +0.36 +/- 0.24 U ml(-1)). The changes in fibrinolytic measures with exercise training in men and women were correlated with changes in other fibrinolytic measures, although in men abdominal fat changes were a strong predictor of fibrinolytic changes with training. These findings suggest that training-induced improvements in endogenous fibrinolysis markers are somewhat greater in men compared to women and may be more strongly associated with abdominal obesity in men.

Aged↗

Effect of a three-day interruption of exercise-training on resting metabolic rate and glucose-induced thermogenesis in training individuals.

Exercise-training has been shown to influence resting components of energy expenditure in lean and obese individuals. Moreover, experimental data suggest that the effect of training on these components could represent an acute effect of exercise. In this regard, the present study was undertaken to determine whether resting metabolic rate (RMR) and glucose-induced thermogenesis (GIT) could be modified depending on the delay elapsing between the last exercise session of a training program and calorimetric measurements. Eight trained individuals were tested 16 h after a 90-min exercise bout and following a 3-day interruption of training. A significant decrease in RMR (-6.6 percent, P less than 0.05) was observed in response to exercise cessation. On the other hand, an increased GIT was noted following the 3-day rest period and this effect was also statistically significant. These results show that short-term interruption of training can affect substantially RMR and GIT in trained individuals, indicating that the time elapsing since the last exercise session must be taken into account in the interpretation of the effects of physical training on both these parameters.

Basal Metabolism↗

Site of enhanced insulin sensitivity in exercise-trained rats at rest.

Spontaneously exercised rats show at rest enhanced responsiveness to exogenous insulin and lower plasma insulin levels after oral glucose than sedentary control rats. To assess insulin sensitivity of specific organs, glucose uptake by perfused hindlimb muscle and liver from resting exercise-trained rats was compared with perfused organs from control rats. Glucose uptake, assessed by metabolic clearance formulas, was 17% faster in hindlimbs from exercise-trained rats when perfused without added insulin and 43% faster at perfusate insulin levels of 40 microU/ml. After an overnight fast, glucose clearance in exercise-trained hindlimbs increased over controls by 57% in the basal state and by 97% at low perfusate levels. In contrast, glucose clearance by livers from both fed and fasted exercise-trained rats was less than one-half that of livers from control rats. These results suggest that skeletal muscle, and not liver, is the organ primarily responsible for the increased sensitivity to insulin-induced glucose uptake with exercise training and that this response is enhanced after overnight fasting.

Animals↗

Cardiopulmonary stress during exercise training in patients with COPD.

Exercise training is an essential component of pulmonary rehabilitation. However, the cardiopulmonary stress imposed during different modalities of exercise training is not yet known. In the present study, the cardiopulmonary stress of a 12-week exercise training programme in 11 chronic obstructive pulmonary disease (COPD) patients (forced expiratory volume in one second 42+/-12%pred, age 69+/-6 yrs) was measured. Pulmonary gas exchange and cardiac frequency (f(C)) of three training sessions were measured with a portable metabolic system at the beginning, mid-term and end of the programme. Symptoms were assessed with Borg scores. The exercise intensity was compared with the recommendations for exercise training by the American College of Sports Medicine (ACSM). Training effects were significant (maximum change in work: 14+/-11 Watts, 6-min walk test: 44+/-36 m). Whole body exercises (cycling, walking and stair climbing) consistently resulted in higher cardiopulmonary stress (oxygen uptake (V'(O(2))), minute ventilation and f(C)) than arm cranking and resistance training. Dyspnoea was higher during cycling than resistance training. Patients exercised for >70% (>20 min) of the total exercise time at >40% of the V'(O(2)) reserve and f(C) reserve ("moderate" intensity according to the ACSM) throughout the programme. The cardiopulmonary stress resistance training is lower than during whole-body exercise and results in fewer symptoms. In addition, exercise testing based on guidelines using a fixed percentage of baseline peak performance and symptom scores achieves and sustains training intensities recommended according to the American College of Sports Medicine.

Aged↗

Effects of exercise training and activity restriction on 6-minute walking test performance in patients with chronic heart failure.

Eighteen hospitalized patients with severe chronic heart failure (ejection fraction [mean +/- SEM] 21% +/- 1%) underwent 3 weeks of exercise training (interval bicycle ergometer and treadmill walking training exercises) and 3 weeks of activity restriction in a random-order crossover trial. Before and after exercise training and after activity restriction, a 6-minute walking test was performed to determine the maximum distance walked, hemodynamic and cardiopulmonary responses, norepinephrine levels, and ratings of leg fatigue and dyspnea while walking. A ramp test on bicycle ergometer (increments of 12.5 W/min) was performed before and after exercise training and activity restriction to determine peak oxygen uptake. After training, the maximum distance walked was increased by 65% (from 232 +/- 21 m at baseline to 382 +/- 20 m; p < 0.001), whereas after activity restriction (253 +/- 19 m) there was no significant difference compared with baseline. No significant differences in hemodynamic and cardiopulmonary parameters (with the exception of the ventilatory equivalent for carbon dioxide and perceived exertion) or norepinephrine levels were observed during walking tests. Improvement in maximum distance walked correlated significantly with training-induced increase in peak oxygen uptake measured during bicycle ergometry (r = 0.47, p < 0.05). The lower the maximum distance walked at baseline, the more pronounced the training-induced prolongation of maximum distance (r= -0.73; p < 0.001). These data support the value of exercise training in patients with severe chronic heart failure for improving maximum distance walked, as documented by the 6-minute walking test. The impairment of walking test performance during activity restriction suggests a need for long-term exercise training programs.

Activities of Daily Living↗

Desensitization of the inhibitory effect of norepinephrine on insulin secretion from pancreatic islets of exercise-trained rats.

The effect of exercise training (9 weeks of running) on norepinephrine-induced inhibition of insulin secretion was examined in rat islets. Insulin secretions from islets in the presence of glucose (> or =5.5 mmol/L) were significantly lower in trained (TR) than in control rats (CR). Norepinephrine inhibited 5.5 mmol/L glucose-stimulated insulin secretions and cyclic adenosine monophosphate (cAMP) contents in a dose-dependent manner in CR. Norepinephrine (10 micromol/L)-induced inhibition of insulin secretion was reversed by the blockade of the alpha(2)-adrenergic receptor in CR, but not in TR. Exercise training substantially shifted the dose-dependent curve for clonidine-induced inhibition of insulin secretions and that of cAMP contents to the right. Exercise training did not alter the density of the alpha(2)-adrenergic receptor either per islet or per protein of islet crude membrane. However, exercise training significantly reduced the protein expression of G alpha i-2 without change in G alpha i-2 mRNA. In CR but not in TR, norepinephrine significantly inhibited insulin secretions elicited by a combination of high glucose, a protein kinase C activator, and an adenylate cyclase activator under Ca(2+)-free conditions. Thus, exercise training appears to provoke a decreased expression of G alpha i-2 protein. This, at least in part, results in loss of the inhibitory effect of norepinephrine either on cAMP content or on insulin secretion at the post-calcium events in stimulus-secretion coupling, which, in turn, leads to the blunted inhibitory effects of norepinephrine on insulin secretion.

Adrenergic alpha-Agonists↗

SOD-1 expression in pig coronary arterioles is increased by exercise training.

Coronary arterioles of exercise-trained (EX) pigs have enhanced nitric oxide (NO.)-dependent dilation. Evidence suggests that the biological half-life of NO. depends in part on the management of the superoxide anion. The purpose of this study was to test the hypothesis that expression of cytosolic copper/zinc-dependent superoxide dismutase (SOD)-1 is increased in coronary arterioles as a result of exercise training. Male Yucatan pigs either remained sedentary (SED, n = 4) or were EX (n = 4) on a motorized treadmill for 16-20 wk. Individual coronary arterioles ( approximately 100-microm unpressurized internal diameter) were dissected and frozen. Coronary arteriole SOD-1 protein (via immunoblots) increased as a result of exercise training (2.16 +/- 0.35 times SED levels) as did SOD-1 enzyme activity (measured via inhibition of pyrogallol autooxidation; approximately 75% increase vs. SED). In addition, SOD-1 mRNA levels (measured via RT-PCR) were higher in EX arterioles (1.68 +/- 0.16 times the SED levels). There were no effects of exercise training on the levels of SOD-2 (mitochondrial), catalase, or p67(phox) proteins. Thus chronic aerobic exercise training selectively increases the levels of SOD-1 mRNA, protein, and enzymatic activity in porcine coronary arterioles. Increased SOD-1 could contribute to the enhanced NO.-dependent dilation previously observed in EX porcine coronary arterioles by improving management of superoxide in the vascular cell environment, thus prolonging the biological half-life of NO.

Animals↗

The metabolic and psychological effects of exercise training in hemodialysis patients.

The effect of exercise training on metabolic abnormalities and psychological function was assessed in seven hemodialysis patients. Their initial work capacity was low and improved after 8 months of training. Exercise was associated with a reduction in the dose of antihypertensive medications in four patients and a decrease in phosphate binder therapy in three patients. There was also a rise in hematocrit levels (% delta = 34 +/- 20%, P less than 0.03) and the hemoglobin concentration (% delta = 37 +/- 23%, P less than 0.05) of five males. Plasma glucose levels fell (-5 +/- 2%, P less than 0.05, n = 5) and the glucose disappearance rate improved (20 +/- 7%, P less than 0.02), while hyperinsulinism decreased (-36 +/- 20%, P less than 0.02, n = 5) during training. There was no change in body weight or diet. Exercise lowered plasma triglyceride levels (-41 +/- 28%, P less than 0.02, n = 6) and raised the high-density lipoprotein cholesterol concentration (20 +/- 21%, P less than 0.05, n = 6). Psychological testing (n = 4) demonstrated that exercise training was associated with an improvement in depression, hostility, anxiety, social interaction, and outlook for the future. These results suggest that exercise can improve some of metabolic abnormalities and psychological dysfunction which exists in some dialysis patients.

Adult↗

Voluntary exercise training enhances glucose transport but not insulin signaling capacity in muscle of hypertensive TG(mREN2)27 rats.

Male heterozygous TG(mREN2)27 rats (TGR) overexpress a murine renin transgene, display marked hypertension, and have insulin resistance of skeletal muscle glucose transport and insulin signaling. We have shown previously that voluntary exercise training by TGR improves insulin-mediated skeletal muscle glucose transport (Kinnick TR, Youngblood EB, O'Keefe MP, Saengsirisuwan V, Teachey MK, and Henriksen EJ. J Appl Physiol 93: 805-812, 2002). The present study evaluated whether this training-induced enhancement of muscle glucose transport is associated with upregulation of critical insulin signaling elements, including insulin receptor substrate-1 (IRS-1), phosphatidylinositol 3-kinase, Akt, and glycogen synthase kinase-3. TGR remained sedentary or ran spontaneously in activity wheels for 6 wk, averaging 7.1 +/- 0.8 km/day by the end of week 3 and 4.3 +/- 0.5 km/day over the final week of training. Exercise training reduced total abdominal fat by 20% (P < 0.05) in TGR runners (2.64 +/- 0.01% of body weight) compared with sedentary TGR controls (3.28 +/- 0.01%). Insulin-stimulated (2 mU/ml) glucose transport activity in soleus muscle was 36% greater in TGR runners compared with sedentary TGR controls. However, the protein expression and functionality of tyrosine phosphorylation of insulin receptor and IRS-1, IRS-1 associated with the p85 regulatory subunit of phosphatidylinositol 3-kinase, and Ser473 phosphorylation of Akt were not altered by exercise training. Only insulin-stimulated glycogen synthase kinase-3beta Ser9 phosphorylation was increased (22%) by exercise training. These results indicate that voluntary exercise training in TGR can enhance insulin-mediated glucose transport in skeletal muscle, as well as reduce total abdominal fat mass. However, this adaptive response in muscle occurs independently of modifications in the proximal elements of the insulin signaling cascade.

Animals↗

Exercise training in COPD patients: the basic questions.

Pulmonary rehabilitation programmes aim at improving exercise capacity, activities of daily living, quality of life and perhaps survival in patients with chronic obstructive pulmonary disease (COPD). Recently, well-designed studies investigated and confirmed the efficacy of comprehensive pulmonary rehabilitation programmes, including exercise training, breathing exercises, optimal medical treatment, psychosocial support and health education. In the present overview, the contribution of exercise training in clinical practice to the demonstrated effects of pulmonary rehabilitation is discussed by means of six basic questions. These include: 1) the significance of exercise training; 2) the optimal intensity for exercise training; 3) prescribing training modalities; 4) the effects of exercise training combined with medication, nutrition or oxygen; 5) how training effects should be maintained; and 6) where the rehabilitation programme should be performed: in-patient, out-patient or homecare? First, exercise training has been proven to be an essential component of pulmonary rehabilitation. Training intensity is of key importance. High-intensity training (>70% maximal workload) is feasible even in patients with more advanced COPD. In addition, the effects on peripheral muscle function and ventilatory adaptations are superior to low-intensity training. There is, however, no consensus on the optimal training modalities. Both walking and cycling improved exercise performance. Since peripheral muscle function has been recognized as an important contributor to exercise performance, specific peripheral muscle training recently gained interest. Improved submaximal exercise performance and increased quality of life were found after muscle training. The optimal training regimen (strength or endurance) and the muscle groups to be trained, remain to be determined. Training of respiratory muscles is recommended in patients with ventilatory limitation during exercise. The additional effects of anabolic-androgenic drugs, oxygen and nutrition are not well-established in COPD patients and need further research. In order to maintain training effects, close attention of the rehabilitation team is required. The continuous training frequency necessary to maintain training effects remains to be defined. At this point in time, out-patient-based programmes show the best results and guarantee the best supervision and a multidisciplinary approach. Future research should focus on the role of homecare programmes to maintain improvements.

Exercise↗

Insulin activation of pyruvate dehydrogenase complex is enhanced by exercise training.

We studied the effects of exercise training on the activity of the pyruvate dehydrogenase (PDH) complex in rat gastrocnemius muscle (experiment 1) and the response of the complex to glucose and insulin infusion (euglycemic clamp) in trained and sedentary rats (experiment 2). In experiment 1, half of the rats were randomly allocated as sedentary animals and the other half were trained by voluntary running exercise for 8 weeks. The total activity of the PDH complex was not affected by exercise training, and the activity state (proportion of the active form) of the PDH complex was decreased from 15.0%+/-2.4% to 7.5%+/-1.1% by exercise training. The activity of 3-hydroxyacyl-coenzyme A (CoA) dehydrogenase ([3-HADH] an enzyme in beta-oxidation) was significantly higher in trained versus sedentary rats. In experiment 2, sedentary and trained rats were starved for 24 hours before performing the euglycemic clamp. Glucose and insulin infusion was performed by a euglycemic clamp (insulin infusion rate, 6 mU/kg/min) for 90 minutes. The PDH complex was inactivated to less than 1% in both sedentary and trained rats after 24 hours of starvation. The glucose infusion rate (GIR) during the euglycemic clamp was higher in trained versus sedentary rats. The euglycemic clamp resulted in activation of the PDH complex in both sedentary and trained rats, but the response of the PDH complex to the euglycemic clamp was significantly higher in trained rats (5.8%+/-0.5%) than in sedentary rats (2.9%+/-0.5%). These results suggest that exercise training promotes fatty acid oxidation in association with suppression of glucose oxidation in skeletal muscle under resting conditions, but increases the rate of carbohydrate oxidation when glucose flux into muscle cells is stimulated by insulin.

Animals↗

Changes in the rat heart proteome induced by exercise training: Increased abundance of heat shock protein hsp20.

Chronic exercise training elicits adaptations in the heart that improve pump function and confer cardioprotection. To identify molecular mechanisms by which exercise training stimulates this favorable phenotype, a proteomic approach was employed to detect rat cardiac proteins that were differentially expressed or modified after exercise training. Exercise-trained rats underwent six weeks of progressive treadmill training five days/week, 0% grade, using an interval training protocol. Sedentary control rats were age- and weight-matched to the exercise-trained rats. Hearts were harvested at various times (0-72 h) after the last bout of exercise and were used to generate 2-D electrophoretic proteome maps and immunoblots. Compared with hearts of sedentary rats, 26 protein spot intensities were significantly altered in hypertrophied hearts of exercise-trained rats (p <0.05), and 12 spots appeared exclusively on gels from hearts of exercise-trained rats. Immunoblotting confirmed that chronic exercise training, but not a single bout of exercise, elicited a 2.5-fold increase in the abundance of one of the candidate proteins in the heart, a 20 kDa heat shock protein (hsp20) that persisted for at least 72 h of detraining. Thus, exercise training alters the cardiac proteome of the rat heart; the changes include a marked increase in the expression of hsp20.

Animals↗

Synergistic improvement of glucose tolerance by sucrose feeding and exercise training.

The interactive effects of exercise training (5-7 wk) and sucrose consumption (ad libitum feeding of a 32% sucrose solution and Purina chow) on intravenous glucose tolerance and plasma insulin levels were investigated using a 2 X 2 experimental design. Rats were divided in Purina-sedentary, Purina-trained, sucrose-sedentary, and sucrose-trained groups. Sucrose feeding of sedentary animals significantly increased basal and glucose-stimulated insulin levels and improved basal glycemia and glucose tolerance. On the other hand, exercise training of Purina-fed animals significantly reduced basal as well as glucose-stimulated insulinemia without altering basal glycemia or glucose tolerance. Such a sparing effect of exercise training on insulin requirements was not as evident in rats consuming sucrose. These animals displayed a reduced basal glycemia (P less than 0.01) with normal basal insulin levels. Their glucose tolerance was markedly improved (P less than 0.01) but their insulin response during intravenous glucose tolerance test remained as high as in sucrose-sedentary animals. Results from these studies indicate that sucrose feeding of sedentary animals leads to hyperinsulinemia without compensatory insulin resistance, resulting in an improvement of glucose tolerance, exercise training increases the sensitivity of peripheral tissues to insulin, and the marked improvement of glucose tolerance observed in sucrose-trained animals results from a synergistic combination of the above two factors, i.e., increased insulinemia (induced by diet) and enhanced insulin sensitivity (induced by training).

Adipose Tissue↗

Exercise training increases baroreceptor gain sensitivity in normal and hypertensive rats.

Exercise training attenuates arterial hypertension and increases baroreflex sensitivity in spontaneous hypertension. However, no information exists regarding the portion of the baroreflex arch in which this attenuation takes place. We tested the hypothesis that exercise training increases the afferent pathway sensitivity of baroreflex control in both normotensive and spontaneously hypertensive rats (SHR). Arterial pressure and whole-nerve activity of the aortic baroreceptor (multifiber preparation) were evaluated in 30 male rats assigned to 4 groups: sedentary and exercise-trained normotensive rats and sedentary and exercise-trained SHR. Exercise training was performed on a motor treadmill, 5 d/wk for 60 minutes, gradually progressing toward a speed of 26.8 m/min. Exercise training reduced mean arterial pressure in conscious exercise-trained SHR (183+/-4 versus 165+/-7 mm Hg). The relation between changes in aortic baroreceptor discharge and changes in systolic arterial pressure increased significantly in exercise-trained normotensive rats (2.09+/-0.1 versus 1.44+/-0.1%/mm Hg) and exercise-trained SHR (0.92+/-0.1 versus 0.71+/-0.1%/mm Hg) compared with their respective sedentary rats. Likewise, the average aortic baroreceptor gain sensitivity (calculated by logistic equation) was significantly higher in exercise-trained normotensive rats (2.25+/-0.19 versus 1.77+/-0.03%/mm Hg) and exercise-trained SHR (1.07+/-0.04 versus 0.82+/-0.05%/mm Hg) compared with their respective sedentary control rats. In conclusion, exercise training increases aortic baroreceptor gain sensitivity in normotensive and SHR, thus improving baroreceptor sensitivity, which may result in a more efficient arterial pressure regulation by the baroreflexes.

Afferent Pathways↗

Effects of exercise training in patients with heart failure: the Exercise Rehabilitation Trial (EXERT).

BACKGROUND: The purpose of this study was to examine the effects of exercise training on functional capacity in patients with heart failure. METHODS: One hundred eighty-one patients in New York Heart Association class I to III, with ejection fraction <40% and 6-minute walk distance <500 meters, were recruited into a randomized, controlled, single-blind trial comparing 3 months of supervised training, then 9 months of home-based training with usual care. RESULTS: There was a significant increase in 6-minute walk distance at 3 and 12 months but no between-group differences. Incremental peak oxygen uptake increased in the exercise group compared with the control group at 3 months (0.104 +/- 0.026 L/min vs 0.025 +/- 0.023 L/min; P =.026) and 12 months (0.154 +/- 0.074 L/min vs 0.024 +/- 0.027 L/min; P =.081). Compared with the control group, significant increases were observed in the exercise group for arm and leg strength. No significant changes were observed in cardiac function or quality of life. Adherence to exercise was good during supervised training but reduced during home-based training. CONCLUSIONS: Exercise training improves peak oxygen uptake and strength during supervised training. Over the final 9 months of the study, there was little further improvement, suggesting that some supervision is required for these patients. There were no adverse effects on cardiac function or clinical events.

Aged↗