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Regular physical exercise corrects endothelial dysfunction and improves exercise capacity in patients with chronic heart failure.

BACKGROUND: The purpose of this study was to determine the effects of systemic exercise training on endothelium-mediated arteriolar vasodilation of the lower limb and its relation to exercise capacity in chronic heart failure (CHF). Endothelial dysfunction is a key feature of CHF, contributing to increased peripheral vasoconstriction and impaired exercise capacity. Local handgrip exercise has previously been shown to enhance endothelium-dependent vasodilation in conduit and resistance vessels in CHF. METHODS AND RESULTS: Twenty patients were prospectively randomized to a training group (n=10, left ventricular ejection fraction [LVEF] 24+/-4%) or a control group (n=10, LVEF 23+/-3%). At baseline and after 6 months, peak flow velocity was measured in the left femoral artery using a Doppler wire; vessel diameter was determined by quantitative angiography. Peripheral blood flow was calculated from average peak velocity (APV) and arterial cross-sectional area. After exercise training, nitroglycerin-induced endothelium-independent vasodilation remained unaltered (271% versus 281%, P=NS). Peripheral blood flow improved significantly in response to 90 microg/min acetylcholine by 203% (from 152+/-79 to 461+/-104 mL/min, P<0.05 versus control group) and the inhibiting effect of L-NMMA increased by 174% (from -46+/-25 to -126+/-19 mL/min, P<0.05 versus control group). Peak oxygen uptake increased by 26% (P<0.01 versus control group). The increase in peak oxygen uptake was correlated with the endothelium-dependent change in peripheral blood flow (r=0.64, P<0. 005). CONCLUSIONS: Regular physical exercise improves both basal endothelial nitric oxide (NO) formation and agonist-mediated endothelium-dependent vasodilation of the skeletal muscle vasculature in patients with CHF. The correction of endothelium dysfunction is associated with a significant increase in exercise capacity.

Blood Flow Velocity↗

Effects of exercise and time elapsed after exercise on VO2, VCO2 and R responses to norepinephrine in rats.

The effects of norepinephrine (NE) injection (300 microgram . kg-1 of body weight) on oxygen consumption (VO2), carbon dioxide production (VCO2) and respiratory exchange ratio (R) were investigated in female rats after 1 h of running on a treadmill (21.5 m . min-1) at 10% inclination. Six groups of animals were injected respectively at various times after the exercise (1, 3, 6, 9, 21, and 47 h), and were compared to six non-exercised groups injected at corresponding times. VO2 and VCO2 were monitored continuously during the 20 min preceding injection and for the 60 min following it. The increases in VO2 and VCO2, and the decrease in R were of similar magnitude in both exercised and non-exercised rats (about 30% and 20% for VO2 and VCO2, respectively, and -12% for R). Peak VO2 and R values attained after NE injection varied however with time of injection, specially in exercised animals 1 and 9 h after the run. Exercise significantly delayed time of response to NE for VO2 and VCO2 particularly 1 and 9 h after the running bout. It is concluded that time of day, exercise, and time elapsed after exercise are important factors to consider when studying metabolic responses to catecholamines. Furthermore, it is suggested that such experimental controls might be meaningful in human studies as well.

Animals↗

Effect of various types of acute exercise and exercise training on the insulin sensitivity of rat soleus muscle measured in vitro.

Effects of acute exercise varying in duration and intensity, as well as of two training regimes (endurance and sprint training) on the sensitivity of the soleus muscle of rat to insulin was measured in vitro and compared in rats. As an index of the muscle insulin sensitivity the hormone concentration in the incubation medium which would produce half maximum stimulation of lactate production (LA) and glycogen synthesis was determined. A single bout of moderate endurance exercise (60 min treadmill running at 20 m x min-1, 0 degrees inclination) increased the rate of LA production at the hormone concentrations used and increased the sensitivity of the process to insulin at 0.25 and 2 h but not 24 h after termination of exercise. Similar though less pronounced effects were found after heavy endurance exercise (30 min at 25 m x min-1, 10 degrees), but sprint exercise (6 x 10 s bouts at 43 m x min-1, 0 degrees) had no influence on the insulin sensitivity of the soleus muscle. The rate of glycogen synthesis in vitro was accelerated after endurance exercise, but the sensitivity of this process to insulin was unaffected by the preceding exercise. Endurance training for 5 weeks caused marked enhancement of sensitivity of both LA production and glycogen synthesis to insulin, which persisted for at least 48 h after the last training session. No changes in the soleus muscle sensitivity to insulin were found after sprint training. It is concluded that the increased insulin sensitivity of glucose utilization by skeletal muscle which occurs after endurance exercise and particularly during endurance training can substantially contribute to improved carbohydrate tolerance.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Effect of exercise duration during incremental exercise on the determination of anaerobic threshold and the onset of blood lactate accumulation.

To determine the effect of the duration of incremental exercise on the point at which arterial blood lactate concentration (HLa) increases above the resting value (anaerobic threshold: AT) and on the point at which HLa reaches a constant value of 4 mM (onset of blood lactate accumulation: OBLA), eight male students performed two different kinds of incremental exercise. A comparison of arterial HLa and venous HLa was made under both conditions of incremental exercise. The incremental bicycle exercise tests consisted of 25 W increase every minute (1-min test) and every 4 min (4-min test). At maximal exercise, there were no significant differences in either gas exchange parameters or HLa values for the two kinds of incremental exercise. However, the peak workloads attained during the two exercises were significantly different (P less than 0.01). At OBLA and AT, there were no significant differences in gas exchange parameters during the 1-min and 4-min tests except for the workload (at OBLA P less than 0.01; at AT P less than 0.05). When venous blood HLa was used instead of arterial HLa for a 4-min test, AT was not significantly different from that obtained by arterial HLa, but OBLA was significantly different from that obtained by arterial HLa (P less than 0.05). On the other hand, for the 1-min test, venous HLa values yielded significantly higher AT and OBLA compared with those obtained using arterial HLa (P less than 0.01). It was concluded that when arterial blood was used, there was no effect of duration of workload increase in an incremental exercise test on the determination of the AT and OBLA expressed in VO2.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Time pattern of exercise-induced changes in type I collagen turnover after prolonged endurance exercise in humans.

Type I collagen is known to adapt to physical activity, and biomarkers of collagen turnover indicate that synthesis can be influenced by a single intense exercise bout, but the exact time pattern of these latter changes are largely undescribed. In the present study, 17 healthy young males had their plasma concentrations of the carboxyterminal propeptide of type I procollagen (PICP), a marker of collagen formation, and the immunoactive carboxyterminal cross-linked telopeptide (ICTP), a marker of collagen resorption, measured before and immediately postexercise, as well as 1, 2, 3, 4, 5, and 6 days after completion of a marathon run (42 km). Serum concentrations of creatine kinase (S-CK) were measured as an indicator of muscular breakdown in response to the exercise bout. After a transient decrease in collagen formation immediately after exercise (plasma PICP concentration: 176 +/- 17 microg/liter to 156 +/- 9 microg/liter)(P < 0.05), concentrations rose in the days following the marathon, peaked 72 hours after exercise (197 +/- 8 microg/liter)(P < 0.05 versus basal), and returned to basal values similar to those 5 days postexercise (170 +/- 10 microg/liter). Apart from a short increase immediately after exercise, collagen resorption did not change from basal levels throughout the remaining period (P > 0.05). Muscle breakdown was elevated during the days following the exercise and peaked 24 hours after the exercise (S-CK concentration: 3,133 +/- 579 U/liter). The findings in the present study indicate that type I collagen synthesis is accelerated in response to prolonged strenuous exercise, reaching a peak after 3 days and returning to preexercising levels 5 days after the completion of a marathon run.

Adult↗

Prevalence and reproducibility of exercise-induced ventricular arrhythmias during maximal exercise testing in normal men.

The occurrence of ventricular arrhythmias at rest or during ordinary daily activities has been implicated as a risk factor for future coronary-related events and sudden death. However, the clerical significance of exercise-induced ventricular arrhythmias remains uncertain. To assess the prevalence and reproducibility of such arrhythmias, two serial maximal treadmill exercise tests were performed in a study population of 543 male Indian State policemen at an average interval of 2.9 years. Four hundred sixty-two subjects were clinically free of evidence of cardiovascular disease, and 81 had evidence of definite or suspected cardiovascular disease. The prevalence of exercise-induced ventricular arrhythmias during the first test was 30% in men aged 25 to 34 years, 32% in those aged 35 to 44 years and 36% in those aged 45 to 54 years. The prevalence rate in these age groups with repeat testing was 36, 38 and 42%, respectively. These differences were not statistically significant. The group with definite or suspected cardiovascular disease had a greater prevalence of exercise-induced ventricular arrhythmias than normal subjects during both tests but the prevalence rate with repeat testing remained constant. The occurrence of exercise-induced ventricular arrhythmias was reproducible in individual subjects during the second test in 55% of 25 to 34 year olds, 58% of 35 to 44 year olds and 62% of 45 to 54 year olds. Thus, individual reproducibility in two consecutive tests was only slightly greater than reproducibility by chance alone. The group with known or suspected cardiovascular disease demonstrated a trend toward greater reproducibility with repeat testing. Exercise-induced ventricular arrhythmias were not reproducible by type or complexity. The marked variability of exercise-induced ventricular arrhythmias during repeat maximal exercise testing in a clinically normal population appears to negate the usefulness of this finding during a single test as a marker of future cardiovascular disease. Nevertheless, subjects whose arrhythmias were reproducible may form a group destined to manifest clinical cardiovascular disease in long-term follow-up studies.

Adult↗

The prognostic value of normal exercise myocardial perfusion imaging and exercise echocardiography: a meta-analysis.

OBJECTIVES: The purpose of this work was to determine the prognostic value of normal exercise myocardial perfusion imaging (MPI) tests and exercise echocardiography tests, and to determine the prognostic value of these imaging modalities in women and men. BACKGROUND: Exercise MPI and exercise echocardiography provide prognostic information that is useful in the risk stratification of patients with suspected coronary artery disease (CAD). METHODS: We searched the PubMed, Cochrane, and DARE databases between January 1990 and May 2005, and reviewed bibliographies of articles obtained. We included prospective cohort studies of subjects who underwent exercise MPI or exercise echocardiography for known or suspected CAD, and provided data on primary outcomes of myocardial infarction (MI) and cardiac death with at least 3 months of follow-up. Secondary outcomes (unstable angina, revascularization procedures) were abstracted if provided. Studies performed exclusively in patients with CAD were excluded. RESULTS: The negative predictive value (NPV) for MI and cardiac death was 98.8% (95% confidence interval [CI] 98.5 to 99.0) over 36 months of follow-up for MPI, and 98.4% (95% CI 97.9 to 98.9) over 33 months for echocardiography. The corresponding annualized event rates were 0.45% per year for MPI and 0.54% per year for echocardiography. In subgroup analyses, annualized event rates were <1% for each MPI isotope, and were similar for women and men. For secondary events, MPI and echocardiography had annualized event rates of 1.25% and 0.95%, respectively. CONCLUSIONS: Both exercise MPI and exercise echocardiography have high NPVs for primary and secondary cardiac events. The prognostic utility of both modalities is similar for both men and women.

Age Factors↗

Acute and long-term effects of enalapril on the cardiovascular response to exercise and exercise tolerance in patients with congestive heart failure.

Enalapril is a recently developed angiotensin-converting enzyme inhibitor that improves cardiac function at rest in patients with congestive heart failure. This study investigated the acute effects of enalapril on the cardiovascular response to exercise, and then evaluated the long-term effects of enalapril on exercise capacity and functional status during a 12 week placebo-controlled trial in patients with heart failure. Ten patients underwent hemodynamic monitoring while at rest and during incremental bicycle exercise before and after 5 to 10 mg of enalapril orally. At rest, enalapril decreased mean blood pressure 13% (p less than 0.01) and systemic vascular resistance 20% (p less than 0.05) and increased stroke volume index 21% (p less than 0.01). During maximal exercise, enalapril decreased systemic vascular resistance and increased both cardiac and stroke volume indexes. Enalapril acutely increased exercise duration (p less than 0.05) and maximal oxygen consumption (p less than 0.001). These 10 patients and an additional 13 patients were then randomized to either placebo or enalapril treatment and followed up for 12 weeks. Of the 11 patients assigned to active treatment, 73% considered themselves improved compared with 25% of the patients assigned to placebo treatment (p less than 0.02). During long-term treatment, exercise capacity increased in patients receiving enalapril (p less than 0.001) but was unchanged in patients receiving placebo (intergroup difference, p less than 0.05). During long-term treatment, no adverse effects of enalapril occurred. Thus, enalapril improves cardiac function at rest and during exercise. Compared with placebo, maintenance therapy with enalapril results in symptomatic improvement and increased exercise capacity.

Adult↗

Pulmonary vascular resistance of horses decreases with moderate exercise and remains unchanged as workload is increased to maximal exercise.

This study was carried out to examine changes in pulmonary vascular resistance (PVR) induced by moderate and strenuous exercise; the objective being to understand why pulmonary artery blood pressure of exercising horses increases progressively as work intensity increases. Pulmonary arterial and wedge pressures (referenced at the point of the left shoulder) were determined simultaneously with cardiac output in 2 groups of healthy, sound, exercise-trained horses. Horses in Group 1 (n = 8) were studied at rest and during exercise performed at 8 and 13 m/s; the latter workload eliciting maximal heart rate (mean +/- s.e. 212 +/- 3 beats/min). Horses in Group 2 (n = 7 Thoroughbreds) were studied at rest and during galloping at 14.5 m/s on 5% uphill grade, a workload which elicited maximal heart rate (217 +/- 3 beats/min) and could not be sustained for > 90 s. Pulmonary vascular resistance was calculated by dividing pulmonary perfusion pressure gradient (i.e. mean pulmonary arterial pressure minus mean pulmonary wedge pressure) with cardiac output. Pulmonary arterial and wedge pressures, pulmonary perfusion pressure gradient and cardiac output increased significantly (P < 0.05) with exercise in both groups. There were no differences in PVR between the 2 groups of horses at rest. In Group 1 horses PVR decreased significantly (P < 0.05) with exercise at 8 m/s, but further pulmonary vasodilation did not occur as workload increased to 13 m/s. During exercise at 14.5 m/s on 5% grade, PVR of Group 2 horses also decreased significantly and was not different from values for 8 or 13 m/s in Group 1 horses. It is concluded that PVR reaches its nadir during moderate exercise, presumably due to upper limit of recruitment and distension having been reached. Therefore, in accordance with Ohm's law (P alpha Q x PVR), in going to higher workloads pulmonary blood flow (Q) remained the sole determinant of the rise in pulmonary arterial blood pressure (P). Our data also indicate that pulmonary artery wedge pressure is another variable that is important in determining the absolute value of pulmonary arterial blood pressure.

Animals↗

Regional vascular resistance during exercise: role of cardiac afferents and exercise training.

This study was designed to determine whether cardiac vagal afferents exert an inhibitory influence on increases in regional vascular resistance during exercise and to determine whether endurance exercise training enhances the inhibitory influence of cardiac vagal afferents. We measured changes in regional vascular resistance in 12 rabbits at rest and during running at 12.6 m/min, 20% grade, before and after reversible denervation of cardiac afferents (intrapericardial procainamide HCl, 2%). In addition, these procedures were repeated in five of these rabbits following an 8-wk endurance exercise training program. Because intrapericardial injections of procainamide anesthetize both the efferent as well as the afferent innervation to the heart, it was necessary to determine the effects of blocking the efferent innervation on the regulation of regional vascular resistance during exercise. Rabbits were instrumented with Doppler ultrasonic flow probes around the renal (R), mesenteric (M), ascending, and terminal aortic (TA) arteries. Catheters were positioned in the central ear artery and vein and pericardial sac. Mean arterial pressure, heart rate, cardiac output, R, M, TA, and systemic (S) resistances were determined. Exercise changed R (+37 +/- 4%), M (+88 +/- 9%), TA (-62 +/- 6%), and S (-34 +/- 3) resistances. Subsequent cardiac efferent blockade alone had no significant effect on regional vascular resistance during exercise. Combined efferent and afferent blockade resulted in significant increases in R (+62 +/- 6%) and M resistance (+134 +/- 13%) but did not alter TA (-51 +/- 4%) or S (-27 +/- 2%) resistance during exercise. Exercise training significantly enhanced the inhibitory influence of cardiac afferents on R and M regional vascular resistance.(ABSTRACT TRUNCATED AT 250 WORDS)

Afferent Pathways↗

Longitudinal changes in reproductive hormones and menstrual cyclicity in cynomolgus monkeys during strenuous exercise training: abrupt transition to exercise-induced amenorrhea.

Cross-sectional studies of exercise-induced reproductive dysfunction have documented a high proportion of menstrual cycle disturbances in women involved in strenuous exercise training. However, longitudinal studies have been needed to examine individual susceptibility to exercise-induced reproductive dysfunction and to elucidate the progression of changes in reproductive function that occur with strenuous exercise training. Using the female cynomolgus monkey (Macaca fascicularis), we documented changes in menstrual cyclicity and patterns of LH, FSH, estradiol, and progesterone secretion as the animals developed exercise-induced amenorrhea. As monkeys gradually increased running to 12.3 +/- 0.9 km/day, body weight did not change significantly although food intake remained constant. The time spent training until amenorrhea developed varied widely among animals (7-24 months; mean = 14.3 +/- 2.2 months) and was not correlated with initial body weight, training distance, or food intake. Consistent changes in function of the reproductive axis occurred abruptly, one to two menstrual cycles before the development of amenorrhea. These included significant declines in plasma reproductive hormone concentrations, an increase in follicular phase length, and a decrease in luteal phase progesterone secretion. These data document a high level of interindividual variability in the development of exercise-induced reproductive dysfunction, delineate the progression of changes in reproductive hormone secretion that occur with exercise training, and illustrate an abrupt transition from normal cyclicity to an amenorrheic state in exercising individuals, that is not necessarily associated with weight loss.

Amenorrhea↗

Increased muscle glucose uptake after exercise. No need for insulin during exercise.

It has recently been shown that insulin sensitivity of skeletal muscle glucose uptake and glycogen synthesis is increased after a single exercise session. The present study was designed to determine whether insulin is necessary during exercise for development of these changes found after exercise. Diabetic rats and controls ran on a treadmill and their isolated hindquarters were subsequently perfused at insulin concentrations of 0, 100, and 20,000 microU/ml. Exercise increased insulin sensitivity of glucose uptake and glycogen synthesis equally in diabetic and control rats, but insulin responsiveness of glucose uptake was noted only in controls. Analysis of intracellular glucose-6-phosphate, glucose, glycogen synthesis, and glucose transport suggested that the exercise effect on responsiveness might be due to enhancement of glucose disposal. After electrical stimulation of diabetic hindquarters in the presence of insulin antiserum, insulin sensitivity of 3-O-methylglucose transport was increased to the same extent as in muscle from healthy rats stimulated in the presence of insulin at 50 microU/ml. Furthermore, in muscle depleted of glycogen by contractions, transport of 3-O-methylglucose was increased in the presence of insulin antiserum and in the absence of increased regional perfusate flow. It is concluded that after exercise, increased sensitivity of muscle glucose metabolism to insulin can be found in the absence of insulin during exercise, but still involves increased membrane transport of glucose. At maximal insulin concentrations, the enhancing effect of exercise on glucose uptake may involve enhancement of glucose disposal, an effect that is probably less in muscle from diabetic rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Clenbuterol administration does not attenuate the exercise-induced pulmonary arterial, capillary or venous hypertension in strenuously exercising Thoroughbred horses.

The present study was carried out to ascertain whether beta2-adrenergic receptor stimulation with clenbuterol would attenuate the pulmonary arterial, capillary and venous hypertension in horses performing high-intensity exercise and, in turn, modify the occurrence of exercise-induced pulmonary haemorrhage (EIPH). Experiments were carried out on 6 healthy, sound, exercise-trained Thoroughbred horses. All horses were studied in the control (no medications) and the clenbuterol (0.8 pg/kg bwt, i.v.) treatments. The sequence of these treatments was randomised for every horse, and 7 days were allowed between them. Using catheter-tip-transducers whose in-vivo signals were referenced at the point of the left shoulder, right heart/pulmonary vascular pressures were determined at rest, sub-maximal exercise and during galloping at 14.2 m/s on a 3.5% uphill grade--a workload that elicited maximal heart rate and induced EIPH in all horses. In the control experiments, incremental exercise resulted in progressive significant increments in right atrial as well as pulmonary arterial, capillary and venous (wedge) pressures and all horses experienced EIPH. Clenbuterol administration to standing horses caused tachycardia, but significant changes in mean right atrial or pulmonary vascular pressures were not observed. During exercise performed after clenbuterol administration, heart rate as well as right atrial and pulmonary arterial, capillary and wedge pressures also increased progressively with increasing work intensity. However, these values were not found to be statistically significantly different from corresponding data in the control study and the incidence of EIPH remained unaffected. Since clenbuterol administration also does not affect the transpulmonary pressure during exercise, it is unlikely that the transmural force exerted onto the blood-gas barrier of exercising horses is altered following i.v. clenbuterol administration at the recommended dosage.

Adrenergic beta-Agonists↗

Exercise-induced increase of plasma lactate is abolished by a pre-exercise epinephrine infusion.

The purpose of this study was to determine the effect of a higher than normal epinephrine content in skeletal muscles, on metabolic and hormonal adjustments during a subsequent exercise. Four groups of 10 rats were studied: two control groups, one at rest and one after an exercise leading to exhaustion on a treadmill (28 m.min-1, 8% grade) and two epinephrine-infused groups (EI), one at rest and one after the same type of exercise. Epinephrine-infused rats (EI) received an infusion of epinephrine (5 nM.kg.min-1, i.v.) for 20 minutes, and were rested 20 minutes before the start of the exercise or rest period. In the soleus muscle, epinephrine content was shown to be multiplied by 15 and 8 times the control values, respectively following 20 and 60 min after the end of the infusion. Control rats received a corresponding volume of sterile saline with the same schedule. The exercise lasted 49 +/- 14 vs 54 +/- 6 minutes respectively for EI and control rats (not significant). At rest, plasma concentrations of epinephrine, norepinephrine, plasma free fatty acids, glycerol, glucose and lactate as well as the glycogen content of the liver, the soleus, gastrocnemius lateralis and superficial vastus lateralis muscles were not different between saline and epinephrine-infused rats. Immediately after exercise, plasma lactate concentration was not increased after exercise in EI vs (2.26 +/- 0.39 vs 4.53 +/- 0.73 mM). One possible explanation of this observation is that re-released epinephrine might induce a vasodilation in the splanchnic or the skeletal muscle vascular beds and thus favors lactate clearance during exercise.

Animals↗

Programming pre-exercise snacks to prevent post-exercise hypoglycemia in intensively treated insulin-dependent diabetics.

Five intensively treated, insulin-dependent diabetics exercised for 45 minutes after fasting while receiving basal insulin injections. Plasma glucose concentrations remained stable during exercise but then declined, resulting in clinical hypoglycemia 1 to 2 hours later. Efficacies of three pre-exercise snacks in preventing the hypoglycemia were compared in a randomized crossover design. Orange juice, whole milk, and skim milk, each containing 13 g of carbohydrate, all prevented postexercise hypoglycemia. However, the more rapidly absorbed snacks, orange juice and skim milk, caused a greater increase in plasma glucose concentrations and the area under the glucose curve during exercise. From the recognized glucose profiles that occur after consumption of different carbohydrates, snacks as well as exercise and insulin can now be programmed for intensively treated, insulin-dependent diabetics. Because plasma glucose levels remain stable during exercise done after fasting and only fall late after exercise, a "lente" carbohydrate snack, such as whole milk, is an appropriate pre-exercise snack.

Adult↗

Exercise performance and oxygen uptake efficiency slope in obese children performing standardized exercise.

Oxygen uptake efficiency slope (OUES) is an index meant to provide an objective measure of cardiopulmonary function at submaximal exercise. The aim was to study the exercise performance and OUES in obese children performing standardized exercise. Sixty children aged 6-17 years performed incremental treadmill exercise test. They were divided into two groups matched by age, sex and height: thirty obese subjects (15 girls/15 boys; BMI = 27.4+/-1.7 m x kg(-2)) and 30 controls (BMI = 18.8+/-1.0 m x kg(-2)). Perceived exertion was assessed by means of CR-10 Borg scale. The duration of the exercise for the obese children was significantly shorter than for controls (p = 0.010) but obese children had greater absolute values for oxygen uptake (VO2 peak mL x min(-1) = 1907+/-249 vs. 1495+/-208; p = 0.013) which, adjusted for body mass, decreased significantly (VO2/kg mL x min(-1) x kg(-1) = 29.2+/-1.4 vs. 33.6+/-1.3; p < 0.001). OUES correlated strongly with VO2 peak (r = 0.91) and oxygen pulse (r = 0.80), as well as with anthropometric variables height (r = 0.88) and age (r = 0.83). Extremely high correlation was found between OUES calculated for 100% of exercise duration and OUES at the anaerobic threshold (r = 0.979; p < 0.001). No significant differences were found between the studied groups concerning the absolute values of OUES. Obese children rated perceived exertion significantly higher than controls (Borg score 6.2+/-0.4 vs. 5.2+/-0.4; p = 0.001). In conclusion, the absolute metabolic cost of exercise and perceived exertion were higher in the obesity group. OUES is an objective measure of cardiopulmonary reserve that doesn't require a maximal effort but it is considerably dependent on anthropometric variables which impedes its interpretation as exercise index in childhood.

Adolescent↗

Relationships between oxygen consumption and heart rate in transitory and steady states of exercise and during recovery: influence of type of exercise.

Relationships between percentage of maximal oxygen consumption (%VO2max) and percentage of maximal heart rate reserve (%f(cr)) were compared during steady states of exercise (S), transitory states of exercise (T) and a 5-min recovery period (R). Male adults [mean age 27 (SD 10) years] were studied exercising on a treadmill (TR, n = 26), cycle ergometer (CE, n = 14) and arm traction bench (ATB, n = 14). The exercise intensity was adjusted according to the subjects in order to reach exhaustion in 4-5 steps of 2 min (ATB) or 3 min (TR, CE). The 1st min of each stage was considered as T and the last minute of each stage as S. The oxygen consumption (VO2) and heart rate (f(c)) were recorded simultaneously. Significant correlations were observed for each type of exercise and for each state between %f(cr) and %VO2max (r range 0.87-1.00). During T and R, the %VO2max versus %f(cr) relationships were laterally shifted, suggesting a resetting of f(c) control mechanisms. In S, the intercept was greater than in T and R; in T, the slope was greater than in S and R. The VO2 could be predicted from individual %VO2max versus %f(cr) relationships during T and R as is usually done in S using specific equations. Taking into consideration the average relationships established on the three ergometers, the standard error of the predicted VO2 during S and T reached 10%-20% and 22%-38% in R. During exercise, the higher the intensity the better was the prediction of VO2 from f(c) (r range 0.46-0.60, P < 0.001). Therefore except at high exercise intensities, it was found that individual relationships had to be used to obtain an accurate estimation of VO2.

Adult↗

Change in post-exercise vagal reactivation with exercise training and detraining in young men.

We studied the effects of aerobic exercise training and detraining in humans on post-exercise vagal reactivation. Ten healthy untrained men trained for 8 weeks using a cycle ergometer [70% of initial maximal oxygen uptake (VO2max) for 1 h, 3-4 days.week-1] and then did not exercise for the next 4 weeks. Post-exercise vagal reactivation was evaluated as the time constant of the beat-by-beat decrease in heart rate during the 30 s (t30) immediately following 4 min exercise at 80% of ventilatory threshold (VT). The VO2max and the oxygen uptake at VT had significantly increased after the 8 weeks training programme (P < 0.0001, P < 0.001, respectively). The t30 had shortened after training, and values after 4 weeks and 8 weeks of training were significantly shorter than the initial t30 (P < 0.05, P < 0.01, respectively). The change in the t30 after 8 weeks of training closely and inversely correlated with the initial t30 (r = -0.965, P < 0.0001). The reduced t30 was prolonged significantly after 2 weeks of detraining, and had returned almost to the baseline level after a further 2 weeks of detraining. These results suggest that aerobic exercise training of moderate intensity accelerates post-exercise vagal reactivation, but that the accelerated function regresses within a few weeks of detraining.

Adult↗