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Supervised exercise training improves aerobic capacity and muscle strength in older women with heart failure.

BACKGROUND: The effect that supervised or unsupervised exercise training has on aerobic capacity (peak oxygen consumption [VO2peak]), muscle strength and quality of life in older women with heart failure remains unknown. OBJECTIVE: To examine the effect of six months (three months supervised followed by three months unsupervised) of aerobic training (AT) or combined aerobic and strength training (CAST) on VO2peak, muscle strength and quality of life in older women with heart failure. METHODS: Twenty older women (mean age +/- SD, 72+/-8 years) with clinically stable heart failure were randomly assigned to AT (n=10) or CAST (n=10). Supervised AT was performed two days per week at 60% to 70% heart rate reserve, whereas unsupervised training was performed two days per week at a rate of perceived exertion of 12 to 14 on the Borg scale. The CAST group also performed one to two sets of low-to-moderate intensity strength training two days per week. RESULTS: Supervised AT or CAST resulted in an increase in VO2peak (12%; P<0.05) and leg press strength (13%; P<0.05) that returned to baseline after unsupervised training. Vertical row strength was greater (+23%; P<0.05) after supervised CAST and remained unchanged after supervised or unsupervised AT. Supervised or unsupervised exercise training was not associated with a significant change in quality of life. CONCLUSIONS: Supervised AT or CAST are effective modes of exercise to improve VO2peak and muscle strength in older women with heart failure. However, the improvements in VO2peak and muscle strength are not maintained with unsupervised exercise training.

Age Factors↗

Endothelin-1 sensitivity of porcine coronary arteries is reduced by exercise training and is gender dependent.

We tested the hypothesis that exercise training reduces the sensitivity of coronary smooth muscle to endothelin-1 (ET-1), with the adaptation being greater in male than in female miniature swine. The efficacy of training was similar in males and females. Cumulative ET-1 contractile responses of coronary branches and left circumflex artery were significantly shifted to the right in exercise-trained (Ex) males but not in Ex females. Analyses of the excitatory concentration causing a 50% response (EC(50)) showed a 1.7- to 2.2-fold shift in Ex males with no change in maximum tension. Nonselective blockade of K-channel activity with tetraethylammonium (TEA; 30-50 mM) significantly shifted the EC(50) to a lower concentration in both Ex males (1.25-fold) and Ex females (2.2-fold) but not in sedentary (Sed) groups. Females (combined Sed and Ex) exhibited a greater response to TEA than did combined Sed and Ex males. Changes in [(32)P]phosphatidic acid ([(32)P]PA) provided an indicator of ET-1-induced phospholipase activity. The magnitude of the [(32)P]PA response was reduced by Ex in both males and females without affecting the EC(50). It is concluded that the contractile sensitivity of coronary arteries to ET-1 is influenced by physical activity in a gender-dependent manner. It is unclear why the contractile sensitivity in females was not reduced by Ex as in the males, because Ex significantly affected responses to TEA and ET-1 stimulation of [(32)P]PA production in both males and females. A potential gender difference in K-channel function may contribute to this discrepancy.

Adaptation, Physiological↗

Exercise training protects the renal circulation against high glucose challenge.

It has been shown previously that high glucose causes direct and acute endothelial dysfunction in non-diabetic isolated rabbit kidney. This study assessed whether exercise training is able to maintain normal renal vascular endothelial function despite high glucose exposure. Animals were pen confined (SED) or treadmill trained over a 12-week period (ExT). Kidneys isolated from SED and ExT rabbits were continuously perfused ex vivo during 3 h with Krebs-Henseleit solutions containing normal (5.5 mm) or high (15 mm) concentrations of d-glucose. In the SED 5.5 group, acetylcholine (ACh) induced dose-related vasodilator responses, reaching the maximum of 41+/- 2% (n=10; P<0.05). In the kidneys perfused with high concentrations of glucose (SED 15), endothelium-dependent vasodilation was significantly blunted. Maximal relaxation in the presence of 15 mm glucose was of 19 +/- 2%, which was significantly different from the SED 5.5 group (41+/- 2%, n=10, P<0.01). In the ExT 5.5 group, ACh-induced vasodilation was significantly enhanced when compared with the SED 5.5 group, reaching the maximum of (52+/- 2%, n=10, P<0.05). Moreover, the exposure of the renal circulation of ExT animals to high glucose did not change endothelium-dependent vasodilation induced by ACh (46+/- 3%, n=6), when compared with the ExT 5.5 group. Finally, exercise training prevented the deleterious effects of high glucose on endothelial-dependent renal vasodilation (SED 15: 19+/- 2% vs. ExT 15: 46+/- 3%; P<0.05). It is concluded that exercise training protects the rabbit renal circulation against endothelial dysfunction elicited by acute exposure to moderately elevated glucose levels, corresponding to the postprandial glycemia of diabetes type 2 patients under treatment. The enhanced renal vasodilator reserve elicited by exercise training turns out to be a response that protects the kidney from the deleterious effects of glycemic peaks.

Acetylcholine↗

5'-AMP-activated protein kinase activity and subunit expression in exercise-trained human skeletal muscle.

5'-AMP-activated protein kinase (AMPK) has been proposed to be a pivotal factor in cellular responses to both acute exercise and exercise training. To investigate whether protein levels and gene expression of catalytic (alpha(1), alpha(2)) and regulatory (beta(1), beta(2), gamma(1), gamma(2), gamma(3)) AMPK subunits and exercise-induced AMPK activity are influenced by exercise training status, muscle biopsies were obtained from seven endurance exercise-trained and seven sedentary young healthy men. The alpha(1)- and alpha(2)-AMPK mRNA contents in trained subjects were both 117 +/- 2% of that in sedentary subjects (not significant), whereas mRNA for gamma(3) was 61 +/- 1% of that in sedentary subjects (not significant). The level of alpha(1)-AMPK protein in trained subjects was 185 +/- 34% of that in sedentary subjects (P < 0.05), whereas the levels of the remaining subunits (alpha(2), beta(1), beta(2), gamma(1), gamma(2), gamma(3)) were similar in trained and sedentary subjects. At the end of 20 min of cycle exercise at 80% of peak O(2) uptake, the increase in phosphorylation of alpha-AMPK (Thr(172)) was blunted in the trained group (138 +/- 38% above rest) compared with the sedentary group (353 +/- 63% above rest) (P < 0.05). Acetyl CoA-carboxylase beta-phosphorylation (Ser(221)), which is a marker for in vivo AMPK activity, was increased by exercise in both groups but to a lower level in trained subjects (32 +/- 5 arbitrary units) than in sedentary controls (45 +/- 1 arbitrary units) (P < 0.01). In conclusion, trained human skeletal muscle has increased alpha(1)-AMPK protein levels and blunted AMPK activation during exercise.

AMP-Activated Protein Kinases↗

Exercise training and tumour metastasis in mice: influence of time of exercise onset.

The present study was designed to investigate the factor of timing of activity onset in determining the effects of exercise on experimental metastases. After 9 weeks of wheel running activity (W) or remaining sedentary (S), male C3H/He mice received an i.v. injection of CIRAS 1 tumor cells. Mice were then randomized into sedentary and wheel running groups (SS, SW, WS, WW) for a further 3 weeks. Although the average number of lung tumours did not differ by activity condition, the groups exercised prior to tumour injection had a greater incidence in the lowest tertile of tumour distribution relative to sedentary controls (SS = 8/20 vs. WS = 16/19, p < 0.005; SS vs. WW = 14/18, p < 0.05). In a replication trial, a similar outcome was present in the lowest tertile: increased incidence of animals exercised prior to injection (SS = 3/9 vs. WW = 7/9: p < 0.05). These data suggest that exercise training before, but not after, i.v. exposure to tumour reduces the number of lung metastases and that the timing of exercise onset influences the extent of experimental metastasis in this model.

Animals↗

Resistance exercise training is associated with decreases in serum low-density lipoprotein cholesterol levels in premenopausal women.

BACKGROUND: Aerobic exercise training is associated with reduced serum concentrations of triglycerides, increased concentrations of high-density lipoprotein cholesterol, and minimal changes in serum levels of total cholesterol or low-density lipoprotein cholesterol. There are few data on the effects of resistance exercise on blood lipid levels. METHODS: Premenopausal women were randomly assigned to a supervised resistance exercise training program (n = 46) or a control group (n = 42) for 5 months. Serum was analyzed for levels of total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, and triglycerides. Body composition and dietary intake were also measured. RESULTS: The exercise group showed a 0.33 +/- 0.03-mmol/L (mean +/- SE) decrease in total cholesterol level and a 0.36 +/- 0.001-mmol/L decrease in low-density lipoprotein cholesterol level that was significantly different from the control group. No significant changes were noted in serum high-density lipoprotein cholesterol or triglyceride levels in either group. Changes in body composition showed no significant correlations with changes in total cholesterol or low-density lipoprotein cholesterol. There were no significant differences in nutrient intake between the groups. CONCLUSION: In healthy, premenopausal women, with normal baseline lipid profiles, 5 months of resistance exercise training was associated with significant decreases in serum total cholesterol and low-density lipoprotein cholesterol concentrations.

Adult↗

Effect of high-intensity exercise training on lactate/H+ transport capacity in human skeletal muscle.

The present study examined the effect of high-intensity exercise training on muscle sarcolemmal lactate/H+ transport and the monocarboxylate transporters (MCT1 and MCT4) as well as lactate and H+ release during intense exercise in humans. One-legged knee-extensor exercise training was performed for 8 wk, and biopsies were obtained from untrained and trained vastus lateralis muscle. The rate of lactate/H+ transport determined in sarcolemmal giant vesicles was 12% higher (P < 0.05) in the trained than in untrained muscle (n = 7). The content of MCT1 and MCT4 protein was also higher (76 and 32%, respectively; n = 4) in trained muscle. Release of lactate and H+ from the quadriceps muscle at the end of intense exhaustive knee-extensor exercise was similar in the trained and untrained leg, although the estimated muscle intracellular-to-interstitial gradients of lactate and H+ were lower (P < 0.05) in the trained than in the untrained muscle. The present data show that intense exercise training can increase lactate/H+ transport capacity in human skeletal muscle as well as improve the ability of the muscle to release lactate and H+ during contractions.

Acid-Base Equilibrium↗

Familiality of triglyceride and LPL response to exercise training: the HERITAGE study.

PURPOSE: The main purpose of the present investigation was to test whether and to what extent familial/genetic factors are involved in the changes of postheparin lipoprotein lipase (deltaPH-LPL) activity and triglyceride (deltaTG) levels in response to exercise training. Additional hypotheses were also tested as to whether there were familial/genetic factors shared by baseline and the corresponding response to exercise training (i.e., by baseline triglyceride (TG(B)) and deltaTG and by baseline postheparin lipoprotein lipase (PH-LPL(B)) and deltaPH-LPL activity). METHODS: Serum TG and PH-LPL were measured in 459 subjects from 99 sedentary Caucasian families of the HERITAGE Family study before (baseline) and after completing a 20 wk (3 times per week) exercise training protocol. The training protocol had a target intensity of 75% of the heart rate associated with baseline VO2max during the last 6 wk. PH-LPL activity was measured in the study subjects. Both univariate and bivariate familial correlation analyses were applied to the baseline and response data. RESULTS: The maximal heritabilities for deltaTG and deltaPH-LPL activity were 22% and 15%, respectively. There were no common familial factors for TG(B) and deltaTG, nor were there any for PH-LPL(B) and deltaPH-LPL. However, we found that there were common familial factors underlying deltaTG and deltaPH-LPL; these familial factors seemed to differ across sex and generation groups. CONCLUSION: Although there were no common familial factors underlying the covariation between the baseline triglyceride and PH-LPL activity and the corresponding responses to exercise training (i.e., TG(B) with deltaTG or PH-LPL(B) with deltaPH-LPL), the deltaTG and deltaPH-LPL covariation apparently share some common familial determinants.

Adolescent↗

Exercise training restores abnormal myocardial glucose utilization and cardiac function in diabetes.

BACKGROUND: Clinical and experimental studies have shown that a reduction in myocardial glucose utilization is a factor contributing to diabetic cardiomyopathy. This study determined whether exercise training could prevent the depression in glucose utilization observed in the diabetic rat heart. METHODS: Diabetes was induced in Sprague-Dawley rats by an intravenous injection of streptozotocin (60 mg/kg). After 10 weeks of treadmill running, exogenous myocardial glucose utilization and cardiac function were determined in isolated working hearts perfused under aerobic conditions and then subjected to a 60-min period of low-flow ischemia followed by reperfusion. RESULTS: Compared to aerobically perfused sedentary control hearts, rates of myocardial glucose oxidation and glycolysis were lower in diabetic hearts. Diabetes was also characterized by a pronounced decrease in cardiac function. Following exercise training, rates of myocardial glucose oxidation and glycolysis were restored and cardiac performance was improved compared to sedentary diabetic hearts. During low-flow ischemia, the decrease in glycolysis observed in hearts of sedentary diabetic rats was attenuated following exercise training. Following ischemia, glucose oxidation and glycolysis returned to preischemic levels in all groups. However, hearts from trained diabetic animals had higher rates of glucose oxidation compared to their respective sedentary group. This was accompanied by an enhanced recovery of heart function following ischemia. CONCLUSIONS: Our results indicate that exercise training is effective in preventing the depression in myocardial glucose metabolism observed in the diabetic rat. This may explain the benefits of exercise in preventing cardiac dysfunction in diabetes.

Animals↗

Differential effects of high-frequency versus low-frequency exercise training in rehabilitation of patients with coronary artery disease.

OBJECTIVES: We sought to study the influence of frequency of exercise training during cardiac rehabilitation on functional capacity (i.e., peak oxygen consumption [VO2] and ventilatory anaerobic threshold [VAT]) and quality of life (QoL). BACKGROUND: Although the value of cardiac rehabilitation is now well established, the influence of the different program characteristics on outcome has received little attention, and the effect of frequency of exercise training is unclear. Functional capacity is regularly evaluated by peak VO2 but parameters of submaximal exercise capacity such as VAT should also be considered because submaximal exercise capacity is especially important in daily living. METHODS: Patients with coronary artery disease (n = 130, 114 men; mean age 52 +/- 9 years) were randomized to either a high- or low-frequency program of six weeks (10 or 2 exercise sessions per week of 2 h, respectively). Functional capacity and QoL were assessed before and after cardiac rehabilitation. Global costs were also compared. RESULTS: Compared with baseline, mean exercise capacity increased in both programs: for high- and low-frequency, respectively: peak VO2 = 15% and 12%, Wmax = 18% and 12%, VAT = 35% and 12% (all p < 0.001). However, when the programs were compared, only VAT increased significantly more during the high-frequency program (p = 0.002). During the high-frequency program, QoL increased slightly more, and more individuals improved in subjective physical functioning (p = 0.014). We observed superiority of the high-frequency program, especially in younger patients. Mean costs were estimated at 4,455 and 2,273 Euro, respectively, for the high- and low-frequency programs. CONCLUSIONS: High-frequency exercise training is more effective in terms of VAT and QoL, but peak VO2 improves equally in both programs. Younger patients seem to benefit more from the high-frequency training.

Adult↗

Implications of exercise training in mtDNA defects--use it or lose it?

Whether regular exercise is beneficial or should be avoided is a question currently unsettled in patients with heteroplasmic mitochondrial DNA (mtDNA) disorders of skeletal muscle. Deleterious effects of habitual physical inactivity superimposed upon impaired mitochondrial oxidative phosphorylation may contribute to varying degrees of exercise intolerance in these patients. Endurance exercise training is widely known to improve exercise capacity in healthy subjects and various chronic-disease patient populations. Although we have shown that beneficial physiological and biochemical responses to training increase exercise tolerance in patients with mtDNA defects, knowledge of the muscle adaptive response to endurance training within the setting of mitochondrial heteroplasmy remains limited. In order to determine advisability of endurance training as therapy, it remains to be established whether potential endurance training-induced increases in mutant mtDNA levels may be offset by increases in absolute wild-type mtDNA levels, and whether chronic inactivity leads to a selective down-regulation of wild-type mtDNA. Resistance training utilizes a different adaptive exercise approach to induce the transfer of normal mitochondrial templates from satellite cells to mature muscle fibers of patients with sporadic mtDNA disorders. The efficacy and safety of this approach needs to be further established. Our current inability to clearly advise patients to "use it or lose it" underscores the immediate urgency of studying the effects of exercise on skeletal muscle of patients with heteroplasmic mtDNA defects.

DNA, Mitochondrial↗

Low-grade systemic inflammation and the response to exercise training in patients with advanced COPD.

STUDY OBJECTIVE: Low-grade systemic inflammation may cause a chronic catabolic state that may affect trainability in patients with COPD as has been seen previously in healthy elderly. Therefore, the aim of the present study was to study the relationship between baseline circulating levels of inflammatory markers and the response to exercise training in clinically stable patients with COPD. DESIGN: An open prospective intervention study. SETTING: Tertiary care setting, University Hospital Gasthuisberg, Leuven, Belgium. PATIENTS: Seventy-eight clinically stable outpatients with COPD. INTERVENTION: A 12-week outpatient exercise-training program consisting of strengthening and endurance types of exercises. MEASUREMENTS AND RESULTS: Circulating levels of inflammatory markers were assessed at baseline. Moreover, lung function, quadriceps force (QF), peak and functional exercise capacity, and health-related quality of life were determined at baseline and after the intervention. Sixty-five of the 78 consecutive outpatients completed the study protocol. QF, peak and functional exercise capacity and health-related quality of life improved significantly compared to baseline. The absolute changes in health-related quality of life showed weak relationships with baseline circulating levels of interleukin-8 (CXCL8) in the whole group (n = 65; r= -0.26; p = 0.04). In addition, soluble tumor necrosis factor receptor p55 was strongly and positively related to the absolute changes in QF in the female patients only (n = 18; r = 0.81; p = 0.0001), while CXCL8 was inversely related to the absolute change in the total score of the Chronic Respiratory Disease Questionnaire (r= -0.65; p = 0.004). CONCLUSION: Baseline markers of low-grade systemic inflammation did not clearly explain the variances in absolute changes in QF, the distance walked in 6 min, peak external load, or health-related quality of life following a 12-week exercise-training program. Hence, they seem not very constructive in the characterization of patients with advanced COPD who do or do not respond to exercise training.

Aged↗

Increased expression of VEGF following exercise training in patients with heart failure.

BACKGROUND AND AIMS: During the last decades several angiogenic factors have been characterized but so far it is unknown whether local muscle exercise training increases the expression of these factors in patients with moderate heart failure. Expression of the major putative angiogenic factor vascular endothelial growth factor (VEGF) at the level of messenger RNA (mRNA) and/or protein was therefore studied before and after 8 weeks of training in patient with chronic heart failure. METHODS: VEGF mRNA and protein concentrations were determined in skeletal muscle biopsies before and after 8 weeks of one-legged knee extension training in patients with chronic heart failure (New York Heart Association II-III). RESULTS: Exercise training increased the citrate synthase activity and peripheral exercise capacity by 46% and 36%, respectively, in parallel with a two-fold increase in VEGF at both the mRNA (P = 0.03) and protein (P = 0.02) levels CONCLUSION: The increase in VEGF gene expression in response to exercise training indicates VEGF to be one possible mediator in exercise-induced angiogenesis and may therefore regulate an important and early step in adaptation to increased muscle activity in patient with chronic heart failure.

Aged↗

Cardiovascular and behavioral effects of aerobic exercise training in healthy older men and women.

The cardiovascular and behavioral adaptations associated with a 4-month program of aerobic exercise training were examined in 101 older men and women (mean age = 67 years). Subjects were randomly assigned to an Aerobic Exercise group, a Yoga and Flexibility control group, or a Waiting List control group. Prior to and following the 4-month program, subjects underwent comprehensive physiological and psychological evaluations. Physiological measures included measurement of blood pressure, lipids, bone density, and cardiorespiratory fitness including direct measurements of peak oxygen consumption (VO2) and anaerobic threshold. Psychological measures included measures of mood, psychiatric symptoms, and neuropsychological functioning. This study demonstrated that 4 months of aerobic exercise training produced an overall 11.6% improvement in peak VO2 and a 13% increase in anaerobic threshold. In contrast, the Yoga and Waiting List control groups experienced no change in cardiorespiratory fitness. Other favorable physiological changes observed among aerobic exercise participants included lower cholesterol levels, diastolic blood pressure levels, and for subjects at risk for bone fracture, a trend toward an increase in bone mineral content. Although few significant psychological changes could be attributed to aerobic exercise training, participants in the two active treatment groups perceived themselves as improving on a number of psychological and behavioral dimensions.

Aged↗

Ventilatory and metabolic changes as a result of exercise training in COPD patients.

Patients with COPD feel better and are able to sustain a given level of activity longer after a program of exercise training, but the underlying physiologic mechanisms have not been completely elucidated. Since the physical performance of patients with COPD is limited mainly by pathophysiologic derangements of the ventilatory system, the exercise performance can be ameliorated by increasing the level of ventilation that they can sustain or by reducing the ventilatory requirement for a given level of activity. Almost all studies have yielded negative results in patients with COPD in terms of exercise training having the ability to improve VEmax. The only way to reduce the ventilatory requirement is to reduce CO2 output. Lower levels of lactate result in less nonmetabolic CO2 produced by bicarbonate buffering and this is the likely mechanism responsible for a lower ventilatory requirement for work rates above the pretraining anaerobic threshold. We specifically wished to determine whether a program of intensity, frequency, and duration known capable of producing a physiologic training effect in healthy subjects would do so in patients with COPD. Further, we sought to determine whether exercise training at a work rate associated with lactic acidosis is more effective in inducing a training effect in patients with COPD than a work rate not associated with lactic acidosis. Nineteen patients with COPD were selected and performed an incremental test as well as 2 square wave tests at a low and a high work rate. Identical tests were performed after an 8-week program of cycle ergometer training either for 45 min/day at a high work rate or for a proportionally longer time at a low work rate. For the high work rate training group, identical work rates engendered less lactate (4.5 vs 7.2 mEq/L) and less VE (48 vs 55 L/min) after training; the low work rate training group had significantly less lactate and VE decrease (p less than 0.01). Further, in the first group, there was an increase in exercise tolerance averaging 71% in the high constant work rate test. There was a good correlation (r = 0.73, p less than 0.005) between the decrease in blood lactate and the decrease in ventilation. The major findings of this study are that patients with COPD who experience lactic acidosis during exercise can achieve physiologic training responses from a program of endurance training and that training work rates engendering high levels of blood lactate are more effective than work rates eliciting low lactate levels.

Acidosis, Lactic↗

[Possibilities and perspectives of home-based exercise training in patients with chronic obstructive pulmonary diseases].

In Germany there is a long tradition of rehabilitation and exercise training programs to improve the clinical state and physical function of patients with chronic obstructive pulmonary diseases. This is particularly true regarding inpatient rehabilitation. Based on experiences gained in other countries, outpatient and home-based programs are currently getting more attention. One of the key components of pulmonary rehabilitation is exercise training which can be expected to exert direct and indirect beneficial effects on physical performance, health-related quality of life and even the progress of the disease. Most of the available experience refers to patients with COPD -- besides those with bronchial asthma. The data available so far suggest that exercise training programs can reduce exacerbation rates and that this effect is achievable by minimal personal assistance. Thus the most important aim of future studies seems to be the development and evaluation of training programs which are efficient but also easy to implement and minimally expensive. Furthermore it needs to be studied whether such programs can be transferred to pulmonary disorders other than obstructive airway diseases.

Disease Progression↗

Effects of exercise training on resting energy expenditure during caloric restriction.

Resting energy expenditure (REE), maximum oxygen uptake (VO2max), and body composition were measured in seven moderately obese women during 9 wk of dietary restriction (800 kcal/d). During weeks 4-6, subjects underwent exercise training (30 min cycling/d, 5 d/wk, at 70% VO2max). The first 3 wk of caloric restriction decreased REE by 13% (from 1437 +/- 76 to 1254 +/- 66 kcal/24 h, means +/- SEM, p less than 0.05). Exercise training increased VO2max (from 1717 +/- 108 to 1960 +/- 120 mL/min, means +/- SEM, p less than 0.05) but did not elevate the dietary-depressed REE (from 1254 +/- 66 to 1262 +/- 62 kcal/24 h). The greatest decrease in body fat (3.7 +/- 0.4 kg) occurred during exercise training, resulting in a small apparent increase in REE when expressed per kilogram total body weight. However, expressed per unit lean body mass, REE remained suppressed throughout the period of caloric restriction. We conclude that exercise training of sufficient intensity to substantially increase VO2max does not reverse the dietary-induced depression of REE.

Adult↗

Increase in myocardial oxygen consumption indexes by exercise training at onset of ischemia in patients with coronary artery disease.

It has been unclear whether exercise training of patients with coronary artery disease increases the level of myocardial oxygen consumption, as indicated by heart rate and double product of heart rate and systolic blood pressure, at which electrocardiographic evidence of myocardial ischemia develops. To assess this question we evaluated the experience of 10 patients with coronary artery disease who underwent a modest-level exercise training program for 6 months. All of these subjects had achieved a training effect, had developed electrocardiographic evidence of ischemia during initial exercise testing, had not increased the amount of cardiac medication taken, and had not been taking digoxin. After completion of the training period, the mean heart rate at which electrocardiographic evidence of ischemia developed increased from 107 +/- 19 to 119 +/- 23 beats/min (p less than .05) and the mean double product increased from 166 +/- 18 to 209 +/- 51 X 10(2) mm Hg X beats/min (p less than .05). Eight of the 10 patients demonstrated an increase in heart rate at onset of ischemia (p less than .02), and seven of the eight in whom double product could be assessed manifested an increase in this parameter at onset of ischemia (p less than .05). Thus the rate of myocardial oxygen consumption at which myocardial ischemia develops, as indirectly assessed by heart rate and double product, can be favorably altered by 6 months of moderate-level exercise training.

Adult↗