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Reduced exercise capacity of chronic obstructive pulmonary disease patients exercising with noseclip/mouthpiece.

A noseclip and low resistance mouthpiece are often used to monitor exhaled gases during exercise. Because otolaryngologic studies suggest that 50% of airway resistance is in the nose and mouth, it was hypothesized that patients with advanced chronic obstructive pulmonary disease might be artifactually limited by exercise testing with a noseclip and mouthpiece. Accordingly, 12 patients with stable chronic obstructive pulmonary disease performed identical symptom-limited supine bicycle exercise tests with and without noseclip and mouthpiece. Right-sided cardiac hemodynamic measurements, radionuclide ventriculography and arterial and mixed venous gas sampling were performed during each exercise test. Exhaled gases were analyzed during the noseclip/mouthpiece exercise. The order of exercise tests was alternated. Comparing exercises with and without a noseclip, there were significant reductions in exercise duration (397 +/- 270 vs 300 +/- 230 seconds, p less than 0.01), exercise oxygen consumption (780 +/- 279 vs 638 +/- 200 ml/min, p less than 0.01) and exercise cardiac output (8.4 +/- 2.7 vs 7.3 +/- 2.0 liters/min, p less than 0.05), an increase in right ventricular ejection fraction (0.39 +/- 0.08 vs 0.43 +/- 0.08, p less than 0.01) and no change in exercise heart rate (106 +/- 14 vs 106 +/- 14), right-sided cardiac pressures or arterial and mixed venous blood gases. These data suggest that a noseclip/mouthpiece can limit exercise tolerance in advanced chronic obstructive pulmonary disease patients. This limitation may result from decreased right-sided cardiac preload (venous return).

Adult

Pre-exercise carbohydrate ingestion: effect of the glycemic index on endurance exercise performance.

PURPOSE: This study aimed to examine the effect of glycemic index of pre-exercise carbohydrate (CHO) ingestion on exercise metabolism and performance. METHODS: Eight endurance trained men ingested a high glycemic index (HGI), low glycemic index (LGI), or a placebo (CON) meal 45 min before exercise and then cycled for 50 min at 67% VO2max. Subjects subsequently performed a 15-min self-paced performance ride in which total work (kJ) was recorded. RESULTS: Plasma glucose concentrations were higher (P < 0.01) after ingestion in HGI compared with LGI and CON (7.53 +/- 0.64 vs 5.55 +/- 0.21 and 4.65 +/- 0.14 mmol.L-1 for HGI, LGI, and CON, respectively, 30 min postprandial; mean +/- SE) but declined at the onset of exercise and were lower (P < 0.01) compared with LGI and CON (4.03 +/- 0.31 vs 4.64 +/- 0.24 and 5.09 +/- 0.16 mmol.L-1 for HGI, LGI, and CON respectively; mean +/- SE) at 10 min of exercise. Plasma glucose remained depressed (P < 0.01) until 30 min into exercise in HGI compared with other trials. Plasma insulin concentrations were higher (P < 0.01) following ingestion during rest and exercise in HGI compared with LGI and CON. Plasma FFA concentrations were lower (P < 0.05) following ingestion in HGI and LGI compared with CON and higher (P < 0.05) in LGI compared with HGI at the start and end of exercise. RER and CHO oxidation was higher (P < 0.01) in HGI compared with LGI and CON during submaximal exercise. There were no differences in work output during the performance cycle. CONCLUSIONS: These data indicate that pre-exercise CHO feedings with varying glycemic indexes do not affect exercise performance following short term submaximal exercise despite alterations in metabolism.

Adult

Norepinephrine response to exercise at the same relative intensity before and after endurance exercise training.

It is well documented that endurance exercise training results in a blunted norepinephrine (NE) response to exercise of a given absolute exercise intensity. However, it is not clear what effect training has on the catecholamine response to exercise of the same relative intensity because previous studies have provided conflicting results. The purpose of the present study was, therefore, to determine the catecholamine response to exercise of the same relative exercise intensity before and after endurance exercise training. Six women and three men [age 28 +/- 8 (SD) yr] performed 10 wk of training. Maximal O2 uptake (VO2 max) was determined during treadmill exercise. Fifteen-minute treadmill exercise bouts were performed at 60, 65, 70, 75, 80, and 85% of VO2 max before and after training. VO2 max was increased by 20% (from 39.2 +/- 7.7 to 46.9 +/- 8.1 ml. kg-1. min-1; P < 0.05) in response to training. Plasma NE concentrations were higher (P < 0.05) during exercise at the same relative intensity after, compared with before, training at 65-85% of VO2 max. Differences between heart rates and plasma epinephrine concentrations after, compared with before, training were not statistically significant. These results provide evidence that the NE response to exercise is dependent on the absolute as well as the relative intensity of the exercise.

Adult

Long-term prognostic value of exercise echocardiography compared with exercise 201Tl, ECG, and clinical variables in patients evaluated for coronary artery disease.

BACKGROUND: The accuracy of exercise echocardiography and 201Tl single photon emission computed tomography (SPECT) is similar in the diagnosis of coronary artery disease (CAD). However, comparative data on long-term prognosis are lacking. METHODS AND RESULTS: Clinical variables and exercise, echocardiographic, and 201Tl tomographic parameters were studied in 248 patients (age, 56+/-12 years [mean+/-SD]; 189 men) who underwent simultaneous treadmill exercise 201Tl SPECT and echocardiography. Follow-up was obtained in 225 patients (91%) at a mean of 3.7+/-2.0 years. A total of 64 cardiac events occurred. With the use of stepwise logistic regression, 4 models simulating clinical stress testing scenarios were evaluated in the prediction of all cardiac events, ischemic events, and/or cardiac death. The best clinical models were exercise echocardiography with exercise ECG and exercise 201Tl SPECT with exercise ECG. Both models were comparable in the prediction of cardiac events. For the exercise echocardiography model, exercise wall motion score index and induction of ischemia were the strongest predictors of events with ORs of 2.63 per unit increment (95% CI, 1. 34 to 5.17; P=0.005) and 4.1 (95% CI, 1.32 to 12.79; P=0.015), respectively. For the model with exercise 201Tl SPECT, the strongest predictor was ischemic perfusion defect (OR, 4.93; 95% CI, 1.72 to 14.08; P=0.003). The absence of ST changes during exercise decreased the risk of events. For the prediction of ischemic events and/or cardiac death, echocardiographic and 201Tl parameters were the only predictive variables. CONCLUSIONS: In patients evaluated for CAD, exercise echocardiography and 201Tl combined with ECG variables provide comparable prognostic information and can be used interchangeably for risk stratification.

Adult

Exercise habits and exercise relapse in persons with non-insulin-dependent diabetes mellitus.

Exercise is widely recognized as a crucial component in the management of non-insulin-dependent diabetes mellitus (NIDDM), but little is known about actual exercise practices in this group. This study investigated exercise habits in 60 persons with NIDDM and 60 nondiabetic significant others. Despite the importance of exercise, most of the persons with NIDDM in our study were not exercising regularly, and the percent of persons exercising regularly was no greater in the diabetic group than in the group of significant others. Although those with NIDDM reported more frequent discussion about exercise with health care professionals, only 25% reported receiving specific guidelines for exercise. Diabetic respondents reported a greater number of relapse or dropout episodes than did the nondiabetic significant others, and relapse was associated with increased guilt. Persons with NIDDM appear to receive recommendations to exercise without instruction on exercise maintenance strategies, resulting in more failed attempts to exercise, and increased guilt. Interventions shown to be effective for increasing exercise maintenance need to be incorporated into the diabetic regimen.

Diabetes Mellitus, Type 2

[Effect of exercise duration on the magnitude and duration of post-exercise hypotension].

PURPOSE: Considering that exercise duration may play a role in post-exercise hypotension, we tested the hypothesis that a prolonged submaximal exercise would lead to a greater and longer blood pressure fall after exercise than a shorter exercise bout. METHODS: Experimental protocol-10 subjects were submitted to two cycle ergometer exercise trials (25 and 45 min) at 50% of VO2 peak. Control protocol-12 subjects rested in the sitting position for 45 min. Blood pressure (BP) was measured before (20 min) and after (90 min) rest or exercise bouts. RESULTS: Systolic BP decreased significantly after exercise and this reduction was greater and lasted longer after 45 min of exercise. Mean and diastolic BP decreased after exercise and they were significantly lower during the 45 min session. Control protocol--no change in BP was observed after resting condition. CONCLUSION: A longer exercise bout leads to a greater and longer post-exercise hypotension.

Adult

[Hypertensive reaction to exercise. Retrospective studies of 1363 consecutive exercise tests].

OBJECTIVE: To study exercise hypertensive reaction and its relation with rest blood pressure, hypertension type and hypertensive cardiac disease. DESIGN: Retrospective study of treadmill exercise testes (ET) performed from January/89 to June/91: (n: 1703). SETTING: Stress tests Laboratory of Cardiology Service of a Military Hospital. METHODS: 1363 consecutive ET of male subjects, performing at least the 3rd stage of the Bruce protocol, were studied. From each ET record were obtained general data, including the reason for test, medication and the rest and exercise blood pressure. Exercise hypertensive reaction was defined as a Bruce protocol 3rd stage systolic blood pressure above 187 mmHg, which corresponds to mean +2SD of 130 normal male subjects previously studied. The Echocardiograms of non-treated hypertensives, obtained less than a month from ET, were reviewed. The diagnosis of borderline or moderate hypertension was base on the clinical records. RESULTS: 1) The 1363 ET included 132 (9.7%) ET to study hypertensive subjects, and 68 of these had hypertensive reaction. 86 ET were performed by non-treated hypertensive subjects, of whom 73 had Echocardiogram. 43 (3.5%) from 1231 ET performed by non-hypertensive subjects also had exercise hypertensive reaction. 2) The left ventricular (LV) mass index of non-treated hypertensive patients had a positive correlation with exercise systolic pressure (r: 0.45; p < 0.001), more important than with rest blood pressure or exercise systolic pressure response; there was a relation with LV wall thickness, but not with internal ventricular dimensions, that was only observed in hypertensive subjects that also had hypertensive reaction to exercise. 3) Exercise systolic blood pressure was usually normal in borderline and elevated in moderate hypertensives (Qui2: 27.249; p < 0.001). 4) Subjects with exercise hypertensive reaction, but not previously diagnosed as hypertensives, were usually true hypertensives. CONCLUSIONS: 1) Hypertensive peaks seem to be an important determinant factor in LV hypertrophy of hypertension, but its influence is felt only above a certain blood pressure threshold; it results on LV concentric type hypertrophy. 2) Exercise systolic blood pressure had a discrimination power of about 80% to separate borderline and moderate hypertensive subjects. 3) All subjects having an exercise hypertensive reaction must be carefully observed, even if their blood pressure at rest is normal, because most of them are true hypertensive patients.

Adult

Exhausting handgrip exercise reduces the blood flow in the active calf muscle exercising at low intensity.

The calf and forearm blood flows (Qcalf and Qforearm respectively), blood pressure, heart rate and oxygen uptake of six men and women were studied during combined leg and handgrip exercise to determine whether a reduction of exercise-induced hyperaemia would occur in the active leg when exhausting rhythmic handgrip exercise at 50% maximal voluntary contraction (MVC) was superimposed upon rhythmic plantar flexion lasting for 10 min at 10% MVC (P10) prior to this combined exercise. The Qcalf and Qforearm were measured by venous occlusion plethysmography during 5-s rests interposed during every minute of P10 exercise and immediately after combined exercise. The muscle sympathetic nerve activity (MSNA) changes were also recorded during leg exercise alone and combined exercise. During plantar flexion performed 60 times.min-1 with a load equal to 10% MVC (P10), Qcalf was maintained at a constant level, which was significantly higher than the resting value (P < 0.001). When rhythmic handgrip contraction at 50% MVC (H50) and P10 were performed simultaneously, the combined exercise was concluded due to forearm exhaustion after a mean of 51.2 (SEM 5.5) s. At exhaustion, Qcalf had decreased significantly from 20.6 (SEM 3.0) ml.100 ml-1.min-1 (10th min during P10 exercise) to 15.3 (SEM) ml.100 ml-1.min-1 (P = 0.001), whereas Qforearm had increased significantly (0.001 < P < 0.01) from 8.6 (SEM 1.9) ml.100 ml-1.min-1 (10th min of P10 exercise) to 26.2 (SEM 3.2) ml.100 ml-1.min-1. The mean blood pressure remained at an almost constant level during the 3rd to 10th min of P10 exercise and increased markedly when H50 was added.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult

Cardiovascular adjustments to rhythmic handgrip exercise: relationship to electromyographic activity and post-exercise hyperemia.

The purpose of this study was to examine the association among electromyographic (EMG) activity, recovery blood flow, and the magnitude of the autonomic adjustments to rhythmic exercise in humans. To accomplish this, 10 healthy subjects (aged 23-37 y) performed rhythmic handgrip exercise for 2 min at 5, 15, 25, 40, and 60% of maximal voluntary force. Heart rate and arterial blood pressure were measured at rest (control), during each level of exercise, and for 2 min following exercise (recovery). The rectified, filtered EMG activity of the exercising forearm was measured continuously during each level of exercise and was used as an index of the level of central command. Post-exercise hyperemia was calculated as the difference between the control and the average recovery (2 min) forearm blood flows (venous occlusion plethysmography) and was examined as a possible index of the stimulus for muscle chemoreflex activation. Heart rate, arterial pressure, forearm EMG activity, and post-exercise hyperemia all increased progressively with increasing exercise intensity. The magnitudes of the increases in heart rate and arterial pressure from control to exercise were directly related to both the level of EMG activity and the degree of post-exercise hyperemia across the five exercise intensities (delta heart rate vs EMG activity: r = 0.99; delta arterial pressure vs EMG activity: r = 0.99; delta heart rate vs hyperemia: r = 0.99; and delta arterial pressure vs hyperemia: r = 0.98; all p less than 0.01). Furthermore, the level of EMG activity was directly related (r = 0.99) to the corresponding degree of hyperemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Adaptation, Physiological

Exercise and hypoxia increase sickling in venous blood from an exercising limb in individuals with sickle cell trait.

PURPOSE: The association between sickle cell trait (SCT) and complications related to exercise may be explained if exercise-induced sickling interferes with capillary blood flow and causes tissue ischemia and functional abnormalities. To test this hypothesis, we measured sickling and blood gas values in venous and arterial blood of an exercising limb in subjects with SCT and in controls. SUBJECTS AND METHODS: The study consisted of 15 subjects with hemoglobin AS (SCT group) and 15 subjects with hemoglobin AA (control group). Each performed two maximal arm crank exercise tests, one at 1,270 meters and one at simulated 4,000 meters. RESULTS: At 1,270 meters, axillary venous sickling increased significantly (p less than 0.05) from (mean +/- SD) 1.0 +/- 1.0% at rest to 2.3 +/- 2.6% during peak exercise. At simulated 4,000 meters, sickling increased significantly (p less than 0.001) from 1.5 +/- 1.2% to 8.5 +/- 7.1%. A wide range of sickling during peak exercise was observed (1% to 25%). One minute after exercise at simulated 4,000 meters, venous sickling remained elevated (7.2 +/- 7.8%) despite high levels of oxygen saturation. Arterial sickling (less than 1%) was present in only two subjects. There was no significant difference in oxygen consumption (29.4 +/- 3 versus 30.7 +/- 4 mL/kg/minute) between the subjects with SCT and the controls, nor was there a correlation between exercise performance and sickling (r less than 0.2). CONCLUSION: We conclude that exercise at 1,270 meters slightly, albeit significantly, increased sickling in blood from an exercising limb and that simulated 4,000 meters dramatically potentiated this effect. Sickling in the effluent blood of an exercising limb does not appear to measurably affect overall maximal arm crank exercise performance.

Adult

Exercise haemodynamics and maximal exercise capacity during beta-adrenoceptor blockade in normotensive and hypertensive subjects.

1. The effects of atenolol administration on maximal exercise capacity and exercise haemodynamics have been compared in eight normotensive and eight mildly hypertensive subjects, matched for sex, age, body weight, and maximal oxygen uptake, and familiar with maximal exercise testing. 2. Supine and exercise blood pressure, and exercise total peripheral resistance were significantly higher, and exercise cardiac output was significantly lower in the hypertensive than in the normotensive subjects. 3. Administration of atenolol (1 X 100 mg day-1) for 3 days reduced supine and exercise systolic blood pressure, heart rate, and cardiac output, and increased exercise stroke volume. Supine and exercise diastolic blood pressure and exercise total peripheral resistance were unaffected by atenolol. The effects of atenolol did not differ in the normotensive and the hypertensive subjects. 4. Maximal work load, maximal oxygen uptake, and maximal heart rate were reduced to a similar extent in normotensive and hypertensive subjects during atenolol treatment. 5. It is concluded that there is no difference in the effects of short-term atenolol administration on exercise haemodynamics and maximal exercise capacity in normotensive and mildly hypertensive subjects.

Adrenergic beta-Antagonists

Exercise, performance and temperature control: temperature regulation during exercise and implications for sports performance and training.

Thermoregulation is an important consideration not only for athletic performance but also for the safety of the athlete. This article presents a broad overview of the mechanisms by which body heat is dissipated in an individual exercising in a hot environment. Particularly emphasised are more recent views of body heat loss mechanisms and the influences of non-thermal inputs, such as effects due to changing blood volume or blood flow distribution. During exercise in a hot environment, metabolic heat produced by the exercising muscles is transported by the circulating blood to the surface of the body where it is released to the environment, either by radiation and convection or by evaporation of sweat. The primary drives for both the increased skin blood flow and increased body sweating are the thermal inputs which are sensed by receptors in the deep body core, with a lesser drive from skin receptors. These thermal signals are integrated in the hypothalamus and proper heat loss responses are effected. When exercise is prolonged, however, and body rehydration is not adequate, the total blood volume may be compromised. In addition, as the core temperature increases during exercise, larger proportions of the blood volume are distributed to the cutaneous vessels, thus effectively reducing cardiac return and central blood volume. During severe exercise, a reduction in cardiac filling may result in a fall in central venous pressure and stimulate baroreceptor vasoconstrictor reflexes. As discussed below, the outputs from these baroreceptors compete with and modify the thermal drives for both the control of the skin blood flow and control of the sweat glands. The effect of high ambient temperatures on exercise performance is most evident in prolonged submaximal exercise. Normally, maximal exercise performance is not altered by high temperatures unless the individual has an elevated deep body temperature before the start of the exercise task. However, submaximal exercise performance is often impaired by high ambient temperatures, but may be improved by programmes of physical training and heat acclimatisation. Both training and heat acclimatisation significantly modify the control systems which regulate skin blood flow and sweating. Only acclimatisation programmes, however, are effective in preventing heat stress during prolonged exercise in hot environments.

Animals

Duration of ST segment depression after exercise-induced myocardial ischemia is influenced by body position during recovery but not by type of exercise.

To assess whether the duration of ischemic ST segment depression after exercise can be modified by changes in body position during recovery or with different types of exercise, 18 patients with chronic stable angina, positive exercise test results, and documented coronary artery disease were prospectively studied. Every patient underwent testing with three different exercise protocols: (1) Bruce (Bruce-standing recovery), (2) abrupt onset of exercise (abrupt), and (3) modified Bruce protocol preceded by a 10-minute warm-up period (warm-up). After exercise test patients recovered in a sitting position. In addition, all patients performed a fourth exercise (Bruce protocol), but this time they recovered in the supine position (Bruce-supine recovery). Time and heart rate-blood pressure product at 1 mm ST segment depression were similar for Bruce-standing recovery, abrupt, and Bruce-supine recovery protocols (5.1 +/- 2, 4.4 +/- 2, and 5.2 +/- 2 minutes and 20.8 +/- 4, 21.3 +/- 4, and 20.4 +/- 4 beats/min x mm Hg x 10(-3), respectively. Heart rate and heart rate-blood pressure product at peak exercise did not differ in Bruce-standing recovery, abrupt, and Bruce-supine recovery. Maximal ST segment depression was -2.0, -1.9, and -2.0 mm with Bruce-standing recovery, abrupt, and Bruce-supine recovery exercise, respectively, and -1.5 mm with warm-up exercise (p less than 0.05). Duration of ST segment depression into recovery was significantly prolonged after Bruce-supine recovery exercise (9.4 + 5 minutes) compared with Bruce-standing recovery, abrupt, and warm-up protocols (6.8 + 3, 5.9 + 4, and 5.0 + 3 minutes, respectively; p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult

Exercise training in patients with chronic heart failure delays ventilatory anaerobic threshold and improves submaximal exercise performance.

We have recently demonstrated that exercise training can induce important hemodynamic and metabolic adaptations in patients with chronic heart failure due to severe left ventricular dysfunction. This study examines the accompanying changes in submaximal exercise performance and the ventilatory response to exercise in these patients. Before and after 16-24 weeks of exercise training, subjects underwent two symptom-limited bicycle exercise tests, one with an incremental graded workload, and one with a constant workload that represented 79 +/- 11% of the pretraining peak oxygen consumption. Breath-by-breath expired gas analysis was performed continuously during each test, and central hemodynamic, leg blood flow, and blood lactate measurements were obtained during the incremental protocol. The ventilatory anaerobic threshold was determined during the incremental exercise study from coplotted breath-by-breath ventilatory data with standard criteria by observers who were unaware of patient identity or training status. As previously reported, exercise training increased peak oxygen consumption by 23% from 16.8 +/- 3.8 to 20.6 +/- 4.7 ml/kg/min and reduced blood lactate levels during submaximal exercise. The training-induced decrease in lactate accumulation was accompanied by a decrease in carbon dioxide production, respiratory exchange ratio, and ventilation during submaximal exercise. The ventilatory anaerobic threshold was delayed from 284 +/- 43 to 352 +/- 91 seconds of exercise (p = 0.02), and it occurred at an increased oxygen consumption (10.1 +/- 1.2 vs. 12.1 +/- 2.6 ml/kg/min, p = 0.01). Exercise duration during the constant workload protocol increased from 938 +/- 410 to 1,429 +/- 691 seconds (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged

Effects of arotinolol on exercise capacity and humoral factors during exercise in normal subjects.

A placebo-controlled, double-blind crossover study was undertaken in 10 normal subjects to examine the effects of arotinolol (10 mg bid), a nonselective beta blocker with alpha-blocking activity, on exercise capacity and hormone levels during exercise after a 2-week treatment period. Maximal oxygen uptake (VO2 max) and blood lactic acid concentration (LA) were measured during progressive exercise testing. An exercise intensity equivalent to 4 mmol/l of LA was used for the constant workload exercise test. Humoral factors were measured after 20 minutes of constant workload exercise. The administration of arotinolol significantly decreased systolic blood pressure and heart rate at rest and during exercise, but diastolic blood pressure did not change. No significant difference was found between arotinolol and placebo with regard to VO2 max and maximal workload. Plasma renin activity (PRA), aldosterone (PAC), and norepinephrine (NE) levels at rest and during exercise did not differ between the two treatments. In contrast, plasma epinephrine (EN) levels at rest and during exercise were significantly greater with arotinolol. Atrial natriuretic peptide (ANP) at rest did not differ between the two treatments. However, exercise caused a significant increase in ANP after arotinolol treatment. These findings suggest that arotinolol decreases blood pressure and heart rate without affecting exercise capacity.

Adrenergic beta-Antagonists

Differential cardiorespiratory response to combined exercise with different combinations of forearm and calf exercise.

The purpose of this study was to examine whether cardiorespiratory responses to combined rhythmic exercise (60 contractions.min-1) was affected by different combinations of upper and lower limb exercise in seven healthy women. Six different rhythmic exercises were compared: 6-min rhythmic handgrip at 10% of isometric maximal voluntary contraction (MVC) (H10); 6-min rhythmic plantar flexion at 10% MVC (P10); exhausting rhythmic handgrip at 50% MVC (H50); exhausting rhythmic plantar flexion at 50% MVC (P50); H50 was added to P10 (P10H50); and P50 was added to H10 (H10P50). Exercise duration, after handgrip was combined with plantar flexion (P10H50), was shorter than that of H50, although the exercise duration of H10P50 was not significantly different from P50. No significant difference was found between the difference from rest in oxygen uptake (delta VO2) during H10P50 and the sum of delta VO2 during H10 and P50. Also, the differences from rest in forearm blood flow (delta FBF) and calf blood flow (delta CBF) during H10P50 were not significantly different from delta FBF in H10 and from delta CBF in P50. In contrast, delta VO2 in P10H50 was lower than the sum of delta VO2 in P10 and H50 (P < 0.05), and delta FBF in P10H50 was lower than that in H50 (P < 0.05), while delta CBF was not significantly different between P10H50 and P10. The changes in heart rate from rest (delta HR) during the combined exercises were lower than the sums of delta HR in the corresponding single exercises (P < 0.05). These results demonstrated an inhibitory summation of several cardiorespiratory responses to combined exercise resulting in a reduction in exercise performance which would seem to occur easily when upperlimb exercise is added to lower limb exercise.

Adult

Gentle exercise with a previously inactive muscle group hastens the decline of blood lactate concentration after strenuous exercise.

The aim of this study was to elucidate the mechanism by which the disappearance of blood lactate following severe exercise is enhanced during active recovery in comparison with recovery at rest. Rates of decline of arterialised venous blood lactate concentrations in man after maximal one-leg exercise were compared during four different modes of recovery: passive (PR), exercise of the muscles involved in the initial exercise (SL), exercise of the corresponding muscles in the hitherto-inactive leg (OL), or exercise of one arm (RA). Recovery exercise workloads were each 40% of the onset of blood lactate accumulation (OBLA) for the limb used. In comparison with PR, SL and OL accelerated the fall in blood lactate to similar extents whereas RA was without effect. The first-order rate constant (min-1) for decline of arterialised venous blood lactate concentration after the intense exercise was 0.027 (0.003) in PR, 0.058 (0.025) in SL, 0.034 (0.002) in OL, and in RA was 0.028 (0.002) [mean (SEM), n = 6 subjects]. Preliminary studies had shown that RA in isolation elevated blood lactate whereas SL and OL did not. Thus, with appropriate workloads, exercise of either hitherto active or passive muscles enhanced blood lactate decline during recovery from intense exercise. This suggests that the effect resulted principally from the uptake and utilisation of lactate in the circulation by those exercising muscles rather than from increased transport of lactate to other sites of clearance by sustained high blood flow through the previously active muscles.

Adult

Acute and long-term effects of captopril on exercise cardiac performance and exercise capacity in congestive heart failure.

Although many studies have shown that captopril (CPT) provides acute hemodynamic improvement in patients with severe congestive heart failure (CHF) at rest, little information is available concerning exercise hemodynamic responses to CPT or the effect of this drug on exercise tolerance in CHF. Therefore, we evaluated the hemodynamic effects of CPT at rest and during upright bicycle exercise in 15 patients with stable CHF. CPT (25 to 50 mg) reduces both resting heart rate and mean arterial pressure (84 +/- 11 to 78 +/- 7 bpm, p less than 0.025 and 85 +/- 9 to 64 +/- mm Hg, p less than 0.001). Concomitantly, left ventricular filling pressure dropped dramatically (26 +/- 9 to 15 +/- 7 mm Hg, p less than 0.001), while cardiac and stroke indices rose (2.0 +/- 0.5 to 2.5 +/- 0.6 L/min/m2, p less than 0.001, and 25 +/- 8 to 33 +/- 7 ml/m2, p less than 0.001). Similar directional changes occurred during exercise, with heart rate, mean arterial pressure, and left ventricular filling pressure at maximum exercise being less (123 +/- 15 to 115 +/- 16 bpm, p less than 0.01; 93 +/- 17 to 86 +/- 14 mm Hg, p less than 0.05; and 35 +/- 10 to 30 11 mm Hg, p less than 0.001, respectively) after CPT ingestion. Peak exercise cardiac index rose slightly (3.6 +/- 0.7 to 3.9 +/- 0.6 L/min/m2) but not significantly. Six patients followed long term on CPT underwent elective recatheterization after 3 months. In these, the beneficial hemodynamic changes seen acutely persisted or further improvement was noted, both at rest and during exercise. Most impressively, peak exercise cardiac index rose from 3.6 +/- 0.7 to 4.6 +/- 1.0 L/min/m2 (p less than 0.05), and this was associated with an increase in exercise duration (8.0 +/- 2.2 to 11.5 +/- 1.4 minutes, p less than 0.05) and exercise work load (332 +/- 32 to 468 +/- 52 kp-m/min, p less than 0.05). These findings indicate that in patients with severe CHF, oral CPT provides markedly beneficial augmentation of cardiac function during activity as well as at rest; moreover, chronic CPT therapy substantially increases exercise capacity in this setting.

Aged