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PubMed1997

Effect of high intensity exercise training on central hemodynamic responses to exercise in men with reduced left ventricular function.

OBJECTIVES: The aim of this study was to evaluate the effects of high intensity exercise training on left ventricular function and hemodynamic responses to exercise in patients with reduced ventricular function. BACKGROUND: Results of studies on central hemodynamic adaptations to exercise training in patients with chronic heart failure have been contradictory, and some research has suggested that training causes further myocardial damage in these patients after a myocardial infarction. METHODS: Twenty-five men with left ventricular dysfunction after a myocardial infarction or coronary artery bypass graft surgery were randomized to an exercise training group (mean age +/- SD 56 +/- 5 years, mean ejection fraction [EF] 32 +/- 7%, n = 12) or a control group (mean age 55 +/- 7 years, mean EF 33 +/- 6%, n = 13). Patients in the exercise group performed 2 h of walking daily and four weekly sessions of high intensity monitored stationary cycling (40 min at 70% to 80% peak capacity) at a residential rehabilitation center for a period of 2 months. Ventilatory gas exchange and upright hemodynamic measurements (rest and peak exercise cardiac output; pulmonary artery, wedge and mean arterial pressures; and systemic vascular resistance) were performed before and after the study period. RESULTS: Maximal oxygen uptake (VO2max) increased by 23% after 1 month of training, and by an additional 6% after month 2. The increase in VO2max in the trained group paralleled an increase in maximal cardiac output (12.0 +/- 1.8 liters/min before training vs. 13.7 +/- 2.5 liters/min after training, p < 0.05), but maximal cardiac output did not change in the control group. Neither stroke volume nor hemodynamic pressures at rest or during exercise differed within or between groups. Rest left ventricular mass, volumes and EF determined by magnetic resonance imaging were unchanged in both groups. CONCLUSIONS: High intensity exercise training in patients with reduced left ventricular function results in substantial increases in VO2max by way of an increase in maximal cardiac output combined with a widening of maximal arteriovenous oxygen difference, but not changes in contractility. Training did not worsen hemodynamic status or cause further myocardial damage.

Cardiac Output↗

PubMed2000

Effect of long-term exercise training on blood viscosity during endurance exercise at an anaerobic threshold intensity.

Blood viscosity (etaB) is low in athletes, but the effect of exercise training on etaB during endurance exercise at an anaerobic threshold (AT) intensity in non-athletes is not well known, although it is known that exercise training sometimes induces the hyperviscosity syndrome. Fourteen subjects were recruited and divided into 2 groups: those who trained at an AT intensity for 30 min/day, 3 times weekly for 1 year (Group T, n=8), and sedentary subjects (Group C, n=6). The test protocol consisted of a single 30-min treadmill exercise at each individual's AT intensity, which was determined in advance. The etaB, plasma viscosity (etaP), and hematocrit were measured just before and at the end of the treadmill exercise. The subjects were not allowed to drink any water before exercise. In the Group C subjects, the hematocrit and etaP increased significantly and the etaB tended to increase. However, in the Group T subjects, the hematocrit and etaP did not increase and the etaB decreased significantly. These data indicate that long-term exercise training attenuates the increase in blood viscosity during exercise.

Adult↗

PubMed2002

Resistance exercise training attenuates exercise-induced lipid peroxidation in the elderly.

This study examined the effects of 6 months of resistance exercise (RX) on basal and post-aerobic exercise lipid peroxidation (LIPOX). Men and women [n = 62, mean (SD) age 68.4 (6) years] were divided randomly into either a control (n = 16, CON), low-intensity training [LEX n = 24; 50% one-repetition maximum (1RM), 13 repetitions/exercise], or high-intensity training (HEX n = 22, 80% 1RM, 8 repetitions/exercise) group. Pre- and post-training, subjects performed a graded aerobic exercise test (GXT). Blood samples were collected prior to and 10 min following each GXT. Subjects trained 3 times per week for 6 months using 12 RX machines. LIPOX was determined by measuring levels of thiobarbituric reactive acid substances (TBARS) and lipid hydroperoxides (PEROX). RX had no effect on resting LIPOX. Post-training, post-GXT TBARS were lower in the LEX and HEX groups by 14% and 18%, respectively, compared to CON (P < 0.05). Post-GXT PEROX levels were lower (P < 0.05) in LEX and HEX compared to CON [CON 3.51 (0.56) nmol/ml, LEX 2.89 (0.80) nmol/ml, HEX 2.99 (0.63) nmol/ml]. Serum total and non-protein (glutathione) thiols were higher in the LEX and HEX groups following training compared to CON (P < 0.05). These data suggest that RX can (1) reduce serum LIPOX, (2) provide protection against oxidizing agents in vitro, and (3) provide a "cross-protection" against the oxidative stress generated by aerobic exercise, perhaps mediated by improvements in the thiol portion of the antioxidant defense.

Aged↗

PubMed1993

Endurance exercise training augments diastolic filling at rest and during exercise in healthy young and older men.

BACKGROUND: Diastolic filling at rest is altered markedly with advancing age. Whether exercise training can improve diastolic filling at rest or during exercise in either healthy older or healthy young men has not been determined. The purpose of this study was to determine if 6 months of aerobic exercise training improves diastolic filling. METHODS AND RESULTS: Radionuclide diastolic filling parameters were measured at rest and during exercise in 14 older (age, 60 to 82 years) and 17 young (age, 24 to 32 years) rigorously screened healthy males before exercise training and in 13 older and 11 young men after 6 months of endurance exercise training. Diastolic filling rates were expressed in two ways, as absolute milliliters of blood (mL.s-1.m-2) and normalized to the end-diastolic volume. At baseline, the peak early filling rates were lower in the older group compared with the young group as expressed in absolute milliliters of blood (older, 85 +/- 7 mL.s-1.m-2; young, 173 +/- 10 mL.s-1.m-2; P < or = .0001) and in end-diastolic volume per second (1.66 +/- 0.11 versus 2.55 +/- 0.08, P < .0001), whereas the peak atrial filling rates were greater in absolute milliliters of blood (85 +/- 5 versus 56 +/- 7 mL.s-1.m-2, P = .003) and in end-diastolic volume per second (1.70 +/- 0.12 versus 0.80 +/- 0.06, P < .0001). During exercise, at any given heart rate, the older group had a lower peak filling rate than the young group. Also, at peak exercise, the single peak filling rate was decreased in the older group in mL.s-1.m-2 (384 +/- 19 versus 565 +/- 36 mL.s-1.m-2, P = .0002) and in end-diastolic volume per second (6.01 +/- 0.25 versus 7.91 +/- 0.28 end-diastolic volume per second, P < .0001). Six months of intensive aerobic exercise training had similar effects in the old and young groups overall. Maximal oxygen consumption increased 19% (ANOVA training effect, P < or = .0001) and echocardiographic left ventricular mass increased 8% (ANOVA training effect, P = .002). Training increased the resting peak early filling rate in absolute milliliters of blood by +14% (ANOVA training effect, P = .02). During exercise, the peak early or single peak filling rate at any given heart rate was increased. At peak exercise, the single peak filling rate was increased by 14% in mL.s-1.m-2 (ANOVA training effect, P = .0004). The only age-related differential effect of training was on the peak atrial filling rate in end-diastolic volume per second, which decreased by 27% in the older group but was unchanged in the young (+5%) (ANOVA young versus older, P = .001). The independent predictors of a greater maximal oxygen consumption by multivariate analysis were a higher peak exercise heart rate, a greater resting peak early filling rate, the exercise trained state, and a younger age. CONCLUSIONS: Healthy older men have reduced early diastolic filling at rest and during exercise compared with young men. Endurance exercise training enhances early diastolic filling at rest and during exercise in both the old and the young. Training reduces the elevated resting atrial filling rate in the old, whereas the young were unchanged. The training-induced augmentation of early diastolic filling at rest and during exercise may be an important adaptation to allow an increase in stroke volume at rest and an increase in stroke volume, cardiac output, and maximal oxygen consumption during exercise.

Adult↗

PubMed2005

Short-term exercise training in humans reduces AMPK signalling during prolonged exercise independent of muscle glycogen.

We examined the effect of short-term exercise training on skeletal muscle AMP-activated protein kinase (AMPK) signalling and muscle metabolism during prolonged exercise in humans. Eight sedentary males completed 120 min of cycling at 66 +/- 1% , then exercise trained for 10 days, before repeating the exercise bout at the same absolute workload. Participants rested for 72 h before each trial while ingesting a high carbohydrate diet (HCHO). Exercise training significantly (P < 0.05) attenuated exercise-induced increases in skeletal muscle free AMP: ATP ratio and glucose disposal and increased fat oxidation. Exercise training abolished the 9-fold increase in AMPK alpha2 activity observed during pretraining exercise. Since training increased muscle glycogen content by 93 +/- 12% (P < 0.01), we conducted a second experiment in seven sedentary male participants where muscle glycogen content was essentially matched pre- and post-training by exercise and a low CHO diet (LCHO; post-training muscle glycogen 52 +/- 7% less than in HCHO, P < 0.001). Despite the difference in muscle glycogen levels in the two studies we obtained very similar results. In both studies the increase in ACCbeta Ser(221) phosphorylation was reduced during exercise after training. In conclusion, there is little activation of AMPK signalling during prolonged exercise following short-term exercise training suggesting that other factors are important in the regulation of glucose disposal and fat oxidation under these circumstances. It appears that muscle glycogen is not an important regulator of AMPK activation during exercise in humans when exercise is begun with normal or high muscle glycogen levels.

AMP-Activated Protein Kinases↗

PubMed1992

Effects of chronic intense exercise training on the leukocyte response to acute exercise.

Circulatory leukocytes vary significantly in response to acute bouts of exercise. However, little is known concerning the adaptability of this response to chronic intense exercise training. We investigated the circulating leukocytic response to acute exercise in trained athletes during a 28-day intense exercise training program. On day 0, 14, 28 and two days after cessation of the increased training, eight trained male athletes (VO2max greater than 60 ml.kg-1.min-1) were subjected to a 20-km bicycle ergometer time trial. Blood samples were drawn before (PRE, for resting baseline values) and five minutes after (POST, response to acute exercise) the time trial. Beginning on day 0, athletes were instructed to increase the duration of their training 50%. The intense exercise training, which lasted 28 days, was verified weekly. Acute bouts of exercise caused a significant increase (p less than 0.05) in circulating white blood cells, lymphocytes, polymorphonuclear neutrophils and monocytes. The baseline resting values and the magnitude of the response to the acute bouts of exercise in the above parameters were not different during the 28 days of chronic intense exercise training or 2 days after cessation of training as compared to the values observed on day 0. Similarly there was a significant increase (p less than 0.05) in cortisol levels in response to the acute bouts of exercise during the chronic intense exercise training, but the increases were not different from that observed under baseline conditions. These results lead to the conclusion that chronic intense exercise training does not alter the circulating leukocytic response to acute exercise.

Analysis of Variance↗

PubMed2006

Long-term versus intermediate-term supervised exercise training in advanced heart failure: effects on exercise tolerance and mortality.

AIM: To date there have been no studies exploring the effects of long-term versus intermediate-term and short-term supervised exercise training program in patients with severe chronic heart failure (CHF) on optimal medical therapy. We assessed exercise tolerance and mortality in CHF patients undergoing long- versus intermediate-term exercise training (ET). METHODS: Forty-two consecutive severe CHF patients (New York Heart Association functional class III) were referred for a supervised exercise and cardiac rehabilitation program and were followed-up for 3 years: 20/42 (48%) patients discontinued ET after intermediate-term period of 1.6+/-0.8 years (Group A, intermediate-term ET), and 22/42 (52%) remained on the ET program for 3.0+/-0.3 years (Group B, long-term ET). Exercise duration, 6-min walked distance and metabolic equivalents (METs) assessed by modified Bruce protocol were recorded before, 4.5 months after, and 3 years after initiation of ET. RESULTS: Both groups were comparable regarding age, gender, prevalence of ischemic etiology, mean ejection fraction and medications. Risk factors for ischemic heart disease were similar, except for the prevalence of diabetes, which was higher in Group A compared to Group B (11/20 versus 5/22, p=0.03). Significantly more Group A patients died after ET discontinuation (4/20 versus 0/22, p=0.01). At the end of follow-up a significant improvement could be seen in Group B patients compared to A in exercise duration, 6-min walked distance and metabolic equivalents (p<0.01 for all). CONCLUSIONS: Higher survival rate was observed in severe CHF patients undergoing long-term versus intermediate-term exercise training. Long-term supervised exercise training is safe and improves exercise tolerance in these patients.

Exercise Therapy↗

PubMed1988

Smoking cessation after acute myocardial infarction: the effects of exercise training.

To determine the influence of exercise training on smoking after acute myocardial infarction (AMI), smoking rates in 42 pre-AMI smokers assigned to exercise training were compared with 26 pre-AMI smokers assigned to no training. Exercise training occurred 3-26 weeks after AMI. The increase in functional capacity in 3-26 weeks was significantly greater in training than in no-training patients: 1.8 vs. 1.2 METs respectively (p less than 0.05). Adherence to exercise training was higher in non-smokers and former smokers than in those who continued to smoke: 89% and 88% vs. 80% respectively (NS). The prevalence of smoking 6 months post-AMI was lower in training than in no-training patients: 31% vs. 39% respectively (NS). Plasma thiocyanates collected on a random sample of 42 patients suggested that 19% of patients who are smoking after MI fail to report doing so. Self-reported cigarette consumption at 28 weeks was half as great in training as in no-training patients: 11 +/- 7 vs. 22 +/- 16 cigarettes per day (p less than 0.03). Firm advice to stop smoking followed by medically supervised exercise training with frequent followup reduces self-reported cigarette consumption in patients after AMI.

Aged↗

PubMed2005

Exercise training decreases ventilatory requirements and exercise-induced hyperinflation at submaximal intensities in patients with COPD.

STUDY OBJECTIVES: We hypothesized that endurance exercise training would reduce the degree of hyperinflation for a given level of exercise and thereby improve submaximal exercise endurance. METHODS: Twenty-four patients with COPD (mean FEV(1), 36.4 +/- 8.5% of predicted [+/- SD]) undertook a high-intensity cycle ergometer exercise training program for 45 min, three times a week for 7 weeks. Before and after training, the patients performed both an incremental exercise test to maximum and a constant work rate (CWR) test on a cycle ergometer at 75% of the peak work rate obtained in the pretraining incremental test. Ventilatory variables were measured breath-by-breath, and inspiratory capacity (IC) was measured every 2 min to assess changes in end-expiratory lung volume. RESULTS: After training, the increase in peak oxygen uptake was not statistically significant; however, the peak work rate increased by 12.9 +/- 10.3 W (p < 0.01). For the CWR test performed at the same work rate both before and after training, ventilation and breathing frequency (f) were lower after training (average, 1.97 L/min and 3.2 breaths/min, respectively; p < 0.01) and IC was greater (by an average of 133 mL, p < 0.05), signifying decreased hyperinflation. The increase in IC at the point of termination in the shortest CWR test for each individual (defined as isotime) correlated well with both the decreased f (r = 0.63, p = 0.001) and with the increase in CWR exercise endurance (average, 13.1 min, r = 0.46, p = 0.023). CONCLUSIONS: Exercise training in patients with severe COPD dramatically improves submaximal exercise endurance. Decreased dynamic hyperinflation may, in part, mediate the improvement in exercise endurance by delaying the attainment of a critically high inspiratory lung volume.

Aged↗

PubMed2004

Exercise training increases oxidative capacity and attenuates exercise-induced ultrastructural damage in skeletal muscle of aged horses.

Exercise training improves functional capacity in aged individuals. Whether such training reduces the severity of exercise-induced muscle damage is unknown. The purpose of the present study was to determine the effect of 10 wk of treadmill exercise training on skeletal muscle oxidative capacity and exercise-induced ultrastructural damage in six aged female Quarter horses (>23 yr of age). The magnitude of ultrastructural muscle damage induced by an incremental exercise test before and after training was determined by electron microscopic examination of samples of triceps, semimembranosus, and masseter (control) muscles. Maximal aerobic capacity increased 22% after 10 wk of exercise training. The percentage of type IIa myosin heavy chain increased in semimembranosus muscle, whereas the percentage of type IIx myosin heavy chain decreased in triceps muscle. After training, triceps muscle showed significant increases in activities of both citrate synthase and 3-hydroxyacyl-CoA-dehydrogenase. Attenuation of exercise-induced ultrastructural muscle damage occurred in the semimembranosus muscle at both the same absolute and the same relative workloads after the 10-wk conditioning period. We conclude that aged horses adapt readily to intense aerobic exercise training with improvements in endurance, whole body aerobic capacity, and muscle oxidative capacity, and heightened resistance to exercise-induced ultrastructural muscle cell damage. However, adaptations may be muscle-group specific.

Adaptation, Physiological↗

PubMed1994

Muscle torque changes caused by inertial exercise training.

Inertial exercise is a unique form of muscle loading with minimal data available regarding its use or efficacy. The purpose of this study was to describe a standardized clinical training program for inertial exercise using the Impulse system and to experimentally examine the influence of an inertial training program on muscle torque performance. The biceps brachii of 40 healthy subjects were pretested and posttested on the Lido Active dynamometer at 60 and 120 degrees/sec using the continuous passive motion mode. Subjects were randomly assigned to a control or training group. The training group exercised only the nondominant arm three times per week for 5 weeks on the Impulse system. Statistical analysis of peak torque measures between pretests and posttests of muscle torque was performed using a repeated measures analysis of variance design of one between-group (control vs. trained group) and three-within group (speed, arm, and movement; eccentric vs. concentric) factors. Posttraining peak torque measures for both the concentric and eccentric modes of exercise at 60 degrees/sec and for the eccentric mode at 120 degrees/sec were statistically significant at the p < .05 level. Complaints of muscle fatigue occurred during early training sessions, with no injuries and only minimal soreness reported. Inertial training appears to be an effective form of clinical muscular training that is measurable by muscle torque assessment.

Adult↗

PubMed1995

Low-intensity exercise training attenuates cardiac beta-adrenergic tone during exercise in spontaneously hypertensive rats.

Acute and chronic exercise decrease peripheral sympathetic nerve activity, but the effect of exercise training of varying intensity on the sympathetic control of heart rate of spontaneously hypertensive rats has not yet been described. The effect of low and high intensities of exercise training on the vagal and sympathetic activities that control heart rate at rest and during dynamic exercise at 0.5, 0.8, and 1.0 mph for 4 minutes per stage was investigated in sedentary (SED, n = 11), high-intensity (HT, n = 12), and low-intensity exercise-trained (LT, n = 13) spontaneously hypertensive rats. Exercise training was performed on a treadmill for 60 minutes, 5 days per week for 18 weeks, at 55% maximum oxygen consumption for the LT group and 85% for the HT group. Vagal and sympathetic activities were studied after administration of methylatropine (3 mg/kg) and propranolol (4 mg/kg), respectively. The LT group had a significantly lower heart rate (at 0.5, 0.8, 1.0 mph versus rest: 410 +/- 7, 464 +/- 9, and 295 +/- 6 beats per minute [bpm], respectively) than the HT (440 +/- 6, 453 +/- 7, 474 +/- 5, and 315 +/- 4 bpm) and the SED (474 +/- 11, 500 +/- 11, 523 +/- 10, and 327 +/- 3 bpm) groups. Sympathetic effect (LT: 84 +/- 10, 88 +/- 12, 105 +/- 12, and 9 +/- 4; HT: 123 +/- 8, 125 +/- 7, 133 +/- 7, and 34 +/- 7; SED: 130 +/- 13, 143 +/- 12, 150 +/- 10, and 38 +/- 7 bpm) and sympathetic tonus (LT: 125 +/- 6, 121 +/- 5, 112 +/- 6, and 91 +/- 6; HT: 145 +/- 9, 136 +/- 6, 142 +/- 8, and 118 +/- 7; SED: 136 +/- 6, 129 +/- 6, 132 +/- 7, and 118 +/- 8 bpm) were significantly decreased by low-intensity exercise training. In conclusion, low- but not high-intensity exercise training causes resting bradycardia and attenuation of tachycardiac response during progressive dynamic exercise in spontaneously hypertensive rats. This effect can be attributed to a significantly decreased beta-adrenergic tone that controls heart rate.

Animals↗

PubMed1992

Principles of exercise training.

Design of exercise programs that are part of pulmonary rehabilitation programs should be founded on an appreciation of the principles of exercise training of healthy subjects. Training produces structural and biochemical changes in the muscles that exercise which increase the ability of the trained muscle to perform aerobic exercise. After training, a given level of heavy exercise engenders lower levels of blood lactate. This is associated with a lower requirement for oxygen uptake, carbon dioxide output, and ventilation. Although the precise mechanism by which training produces changes in the exercising muscles is unknown, characteristics of an effective training program have been defined. Healthy subjects must train for at least 30 min per day, 3 to 5 days per week for 4 to 8 weeks to achieve a physiologic training effect. More controversial is whether a critical training intensity exists. Further, it is not clear which yardstick to apply to quantitate training intensity. Finally, after a training effect has been achieved, regular exercise must be continued or the gains will be lost.

Exercise↗

PubMed1980

Mechanism of enhanced lipolysis in adipose tissue of exercise-trained rats.

The effects of exercise training and food restriction on the regulation of lipolysis were studied comparatively in adipocytes isolated from male and female rats. Exercise training inhibited cell proliferation in parametrial, but not in epididymal adipose tissue, whereas it significantly reduced adipocyte size in both fat depots. Adipocyte capacity for responding lipolytically to epinephrine (10 microns) or to ACTH (1 micron) was markedly increased by exercise training. Enhanced lipolysis was also observed when cells isolated from exercise-trained animals were stimulated by bypassing with dibutyryl cyclic AMP (5 mM) or theophylline (5 mM) the early metabolic steps associated with hormonal activation of the adenylate cyclase complex. Significantly, binding of (-)-[3H]dihydroalprenolol to cellular receptor sites was not affected by exercise training. It is therefore concluded that exercise training increases adipocyte responsiveness to lipolytic hormones at a metabolic step distal to stimulus recognition by adrenoreceptors, possibly at the level of protein kinases or lipases. Food restriction markedly reduced adipocyte size and partially mimicked the effects of exercise training on adipocyte proliferation and lipolysis.

Adipose Tissue↗

PubMed2000

Collagen gene expression in rat left ventricle: interactive effect of age and exercise training.

Whether or not exercise training of sufficient intensity and duration to produce left ventricle (LV) hypertrophy also regulates deposition of interstitial collagen and cross-linking at the pretranslational level is unknown. Therefore, the effects of exercise training on gene expression for the two principal fibrillar collagens in LV, types I and III, were assessed in young adult (5 mo), middle-aged (15 mo), and old (26 mo) rats. We also evaluated the potential interaction of changes in mRNA for these procollagens with alterations in LV extracellular matrix characteristics by simultaneously measuring collagen concentration (hydroxyproline) and extent of mature collagen cross-linking (hydroxylysylpyridinoline, HP). Ten weeks of treadmill running resulted in LV hypertrophy and an increased maximal oxygen uptake in all three age groups of trained rats compared with sedentary controls. Percent collagen in rat LV almost doubled (P < 0.0001) from 5 to 26 mo of age, an increase unaffected by exercise training. With aging, a significant decline in expression of mRNAs for both collagen type I (P < 0.005) and type III (P < 0.001) was observed in LV free wall (LVF) but not septum (LVS). Training prevented this decline in LVF mRNAs for the two principal fibrillar collagens in middle-aged rats whereas it attenuated the decline in senescent animals. HP concentration increased significantly with aging in both LVF (P < 0.005) and LVS (P < 0.01). Training modulated this effect, but again only in LVF, so that HP was significantly lower (P < 0.05) in this region of the LV in old trained rats compared with sedentary counterparts. We conclude that exercise training modulates the effects of aging on collagen gene mRNAs and HP cross-linking regionally within the LV.

Aging↗

PubMed2003

A practical guide to exercise training for heart failure patients.

BACKGROUND: Exercise training has been shown to improve exercise capacity in patients with heart failure. We sought to examine the optimal strategy of exercise training for patients with heart failure. METHODS: Review of the published data on the characteristics of the training program, with comparison of physiologic markers of exercise capacity in heart failure patients and healthy individuals and comparison of the change in these characteristics after an exercise training program. RESULTS: Many factors, including the duration, supervision, and venue of exercise training; the volume of working muscle; the delivery mode (eg, continuous vs. intermittent exercise), training intensity; and the concurrent effects of medical treatments may influence the results of exercise training in heart failure. Starting in an individually prescribed and safely monitored hospital-based program, followed by progression to an ongoing and progressive home program of exercise appears to be the best solution to the barriers of anxiety, adherence, and "ease of access" encountered by the heart failure patient. CONCLUSIONS: Various exercise training programs have been shown to improve exercise capacity and symptom status in heart failure, but these improvements may only be preserved with an ongoing maintenance program.

Exercise Therapy↗

PubMedDate not supplied

Effects of exercise training on abnormal ventilatory responses to exercise in patients with chronic heart failure.

Patients with chronic heart failure frequently report shortness of breath during daily activities as their primary symptom. In recent years, many efforts have been made by researchers to explain the mechanisms that underlie the characteristic heightened ventilatory response to activity in patients with chronic heart failure. The degree to which the ventilatory response to exercise is heightened parallels the severity of the disease, and measuring the ventilatory gas exchange response to exercise can help quantify the patient's response to therapy. Prior to the 1990s, patients with chronic heart failure were generally discouraged from participating in programs of exercise training. However, in the last decade, studies have demonstrated that exercise training is quite safe for these patients, and a multitude of benefits have been reported. Among the benefits of training are improvements in the abnormal ventilatory response to exercise. Although many mechanisms could potentially explain this response, it appears most likely that this improvement after training is due to a reduction in lactate accumulation and an attenuation of the heightened muscle receptor reflex response that occurs in chronic heart failure. This article reviews the mechanisms of dyspnea in chronic heart failure, along with recent studies assessing the effects of training on abnormal ventilatory responses to exercise in these patients. (c)2000 by CHF, Inc.

Journal Article↗

PubMed1998

Effects of intense exercise training on endothelium-dependent exercise-induced vasodilatation.

To determine whether intense exercise training affects exercise-induced vasodilatation, six subjects underwent 4 weeks of handgrip training at 70% of maximal voluntary contraction. Exercise forearm vascular conductance (FVC) responses to an endothelium-dependent vasodilator (acetylcholine, ACH; 15, 30, 60 micrograms min-1) and an endothelium-independent vasodilator (sodium nitroprusside, SNP; 1.6, 3.2, 6.4 micrograms min-1) and FVC after 10 min of forearm ischaemia were determined before and after training. Training elicited significant (P < 0.001) increases in grip strength (43.4 +/- 2.3 vs. 64.1 +/- 3.5 kg, before vs. after, mean +/- SEM), forearm circumference (26.7 +/- 0.4 vs. 27.9 +/- 0.4 cm) and maximal FVC (0.4630 +/- 0.0387 vs. 0.6258 +/- 0.0389 units, P < 0.05). Resting FVC did not change significantly with training (0.0723 +/- 0.0162 vs. 0.0985 +/- 0.0171 units, P > 0.4), but exercise FVC increased (0.1330 +/- 0.0190 vs. 0.2534 +/- 0.0387 units, P < 0.05). Before and after the training, ACH increased exercise FVC above the control (no drug) exercise FVC, whereas SNP did not. Training increased (P < 0.05) the exercise FVC responses to ACH (0.3344 +/- 0.1208 vs. 0.4303 +/- 0.0858 units, before vs. after training, 60 micrograms min-1) and SNP (0.2066 +/- 0.0849 vs. 0.3172 +/- 0.0628 units, 6.4 micrograms min-1). However, these increases were due to the increase in control (no drug) exercise FVC, as the drug-associated increase in exercise FVC above control did not differ between trials (P > 0.6). These results suggest that exercise FVC is increased by both exercise training and stimulating the release of endothelium-dependent vasodilators. However, training does not affect the vascular response to these vasodilators.

Acetylcholine↗