Cardiopulmonary exercise test for evaluating cardiac reserve in chronic congestive heart failure]

To evaluate whether maximal oxygen consumption (VO2 max) measured by cardiopulmonary exercise test (CAR-PET) reflects cardiac reserve in patients with congestive heart failure (CHF), supine bicycle CAR-PET and exercise hemodynamic measurements were performed simultaneously in 12 patients with CHF of NYHA II-IV. With increasing workload, VO2 and cardiac output elevated gradually, then plateaued, demonstrating that patients with CHF could reach VO2max. According to VO2max, patients were divided into 4 classes: including 2 patients of class A (VO2max: 24.5 +/- 2.29 ml.min-1/kg, mean +/- s mean), 3 of B (17.6 +/- 1.37 ml.min-1/kg), 5 of C (13.6 +/- 0.66 ml.min-1/kg) and 2 of D (6.5 +/- 1.64 ml.min-1/kg). Maximal cardiac indices were 8.79 +/- 2.35 L.min-1/m2 in class A, 5.82 +/- 0.97 L.min-1/m2 in B, 3.53 +/- 0.95 L.min-1/m2 in C and 2.21 +/- 1.56 L.min-1/m2 in D. No significant correlation between supine resting hemodynamic parameters and VO2max/kg was found, suggesting that exercise tolerance could not be predicted by the measurement of resting cardiac performance. Furthermore, VO2max correlated poorly with NYHA classification in these patients. However, cardiac output correlated linearly with VO2 during exercise, suggesting that VO2 max/kg is a good predictor for cardiac reserve in CHF(CI = 0.6809 +/- 0.2748 VO2/kg, n = 40, r = 0.84, P < 0.0001; CO = 1.1618 +/- 7.9065 VO2, n = 40, r = 0.84, P < 0.0001). The results also showed that VO2max/kg did not correlate with the changes of pulmonary capillary wedge pressure (PCWP), indicating that exercise tolerance in CHF depends more on cardiac output than on ventilatory consequence of pulmonary congestion.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of exercise on postprandial insulin responses in Mexican American and non-Hispanic women.

Postprandial insulin responses (integrated area under the curve) to an oral glucose load after a period of aerobic exercise and no exercise (control) were compared in sedentary normoglycemic Mexican American and non-Hispanic women pair-matched (n = 9) on total body fat mass (21.8 +/- 3.5 kg). The age (27.4 +/- 3.0 years), body mass index (BMI) (23.6 +/- 1.4 kg/m2), waist to hip ratio (WHR) (0.85 +/- .02), waist circumference (83.5 +/- 4.5 cm), lean mass (36.2 +/- 1.5 kg), and maximal O2 consumption ([VO2 max] 32.9 +/- 1.6 mL x kg(-1) x min(-1)) were similar, although the centrality index (subscapular/triceps skinfolds) was significantly greater in Mexican Americans (0.88 +/- 0.06 v 0.70 +/- 0.05, P < .01). Exercise (treadmill walking for 50 minutes at 70% VO2 max) and control trials were performed 4 weeks apart and 5 to 12 days after the onset of menstruation. A 75-g oral glucose load was administered 15 hours after the completion of each trial, with the subjects 12 hours postprandial. Blood samples were drawn prior to glucose ingestion (fasting, 0 minutes) and at minutes 15, 30, 60, 90, 120, and 150 postingestion. The postprandial insulin response was calculated using a trapezoidal method. In Mexican Americans, significant (P < .02) reductions in the postprandial insulin response (exercise v control, 6.5 +/- 1.0 v 8.5 +/- 1.4 pmol/L x min x 10(4)) and fasting insulin (exercise v control, 77.4 +/- 7.0 v 88.5 +/- 10.3 pmol/L) occurred after exercise compared with the control condition. In non-Hispanics, neither the postprandial insulin response (exercise v control, 7.2 +/- 1.0 v 6.2 +/- 0.9 pmol/L x min x 10(4)) nor fasting insulin (exercise v control, 77.0 +/- 8.2 v 82.9 +/- 8.9 pmol/L) were significantly different between trials. The postprandial insulin response in the control trial was significantly correlated with the change in the insulin response (control minus exercise) in the 18 women (r = .56, P = .01). No trial or group differences were found for postprandial glucose and C-peptide responses. Mexican American women have a high risk of developing type 2 diabetes, and aerobic exercise may be valuable in the prevention or delay of onset of diabetes by reducing peripheral insulin resistance.     

Effects of exercise rehabilitation program on heart rate recovery in patients with chronic heart failure.

BACKGROUND: Heart rate recovery (HRR1) immediately after exercise reflects parasympathetic activity, which is markedly attenuated in chronic heart failure (CHF) patients. The aim of our study was to examine both continuous and interval exercise training effects on HRR1 in these patients. DESIGN: The population study consisted of 29 stable CHF patients that participated at a rehabilitation program of 36 sessions, three times per week. Of the 29 patients, 24 completed the program. Patients were randomly assigned to interval {n=10 [100% peak work rate (WRp) for 30 s, alternating with rest for 30 s]} and to continuous training [n=14 (50%WRp)]. METHODS: All patients performed a symptom-limited cardiopulmonary exercise test on a cycle ergometer before and after the completion of the program. Measurements included peak oxygen uptake (VO2p), anaerobic threshold (AT), WRp, first degree slope of VO2 during the first minute of recovery (VO2/t-slope), chronotropic response [% chronotropic reserve (CR)=(peak HR - resting HR)x100/(220 - age - resting HR)], HRR1 (HR difference from peak exercise to one minute after). RESULTS: After the completion of the rehabilitation program there was a significant increase of WRp, VO2p, AT and VO2/t-slope (by 30%, P=0.01; 6%, P=0.01; 10%, P=0.02; and 27%, P=0.03 respectively for continuous training and by 21%, P<0.05; 8%, P=0.01; 6%, P=NS; and 48%, P=0.02 respectively for interval training). However, only patients exercised under the continuous training regime had a significant increase in HRR1 (15.0+/-9.0 to 24.0+/-12 bpm; P=0.02) and CR (57+/-19 to 72+/-21%, P=0.02), in contrast with those assigned to interval training (HRR1: 21+/-11 to 21+/-8 bpm; P=NS and CR: 57+/-18 to 59+/-21%, P=NS). CONCLUSIONS: Both continuous and interval exercise training program improves exercise capacity in CHF patients. However, continuous rather than interval exercise training improves early HRR1, a marker of parasympathetic activity, suggesting a greater contribution to the autonomic nervous system.     

Exercise training increases basal nitric oxide production from the forearm in hypercholesterolemic patients

The objective of this study was to investigate the effects of cycle training on basal nitric oxide (NO) production and endothelium-dependent dilator capacity in hypercholesterolemic patients in whom acetylcholine responsiveness is impaired. Nine sedentary hypercholesterolemic volunteers (total plasma cholesterol >6.0 mmol/L; 2 female) aged 44+/-3 years (mean+/-SEM) participated in the study. Subjects remained sedentary for 4 weeks and performed 4 weeks of home-based cycle training (3 x 30 minutes/week at 65% maximum oxygen consumption [VO(2)max]) in a randomized order. Arteriovenous nitrate/nitrite (NO(x)) gradient was assessed and plethysmography was used to measure the forearm blood flow responses to arterial infusions of acetylcholine, sodium nitroprusside, and N(G)mono methyl L-arginine. Training increased VO(2)max from 30.4+/-1.9 to 34.3+/-1.4 mL x kg(-1) x min(-1) (P=0.01). Intrabrachial diastolic blood pressure was reduced from 70+/-3 to 68+/-3 mm Hg (P=0.02) with training, whereas systolic pressure did not change. Plasma triglycerides and total, LDL, and HDL cholesterol were not different between interventions. In the sedentary state, there was a positive forearm arteriovenous difference in plasma NO(x) indicating net extraction (6.8+/-4.0 nmol x 100 mL(-1) x min(-1)), whereas in the trained state this difference was negative, indicating net production (-5.8+/-5.8 nmol x 100 mL(-1) x min(-1); P=0.03). N(G)mono methyl L-arginine, at a dose of 4 micromol/min, caused a greater vasoconstriction after training (79.6+/-3.4% versus 69.9+/-6.8%; P=0.05). Acetylcholine and sodium nitroprusside induced dose-dependent elevations in forearm blood flow that were unaffected by training. These data suggest that basal release of endothelium-derived NO is increased with 4 weeks of home based training in hypercholesterolemic patients, independently of lipid profile modification. This may contribute to the cardiovascular protective effects of exercise training, including reduced blood pressure.     

Maximal functional capacity in patients with Chagas' cardiomyopathy without congestive heart failure

BACKGROUND: Chagas' disease is a known dilated form of cardiomyopathy. However, a great number of patients, although showing electrocardiographic (ECG) well-recognized changes, maintain normal ventricular chamber dimensions and are asymptomatic. The aim of the present study was to objectively characterize functional capacity in asymptomatic patients with Chagas' disease and normal left ventricular function. METHODS AND RESULTS: Eighteen asymptomatic male patients with Chagas' disease, aged 33+/-6 years, were selected for the study. All showed ECG changes typical of the disease, as well as left ventricular fractional shortening (LVFS) greater than 0.30 on M-mode 2-dimensionally guided echocardiography. Twenty sedentary normal male patients, aged 29+/-6 years, served as controls. Both groups were submitted to ergoespirometry testing for assessment of exercise functional capacity. Patients with Chagas' disease, when compared with controls, showed lower (P < .001) maximal O2 consumption (VO2max, 24.3+/-4.2 v 37.0+/-5.4 mL x kg(-1) x min(-1) respectively); O2 pulse rate (PO2max, 10.5+/-1.4 v 15.1+/-2.5 mL/beat, respectively); maximal ventilation (VEmax, 50.1+/-13.5 v 113.0+/-17.6 L x min(-1), respectively); anaerobic threshold of maximal O2 consumption (VO2-AT, 15.8+/-3.6 v 24.6+/-4.7 mL x kg(-1) x min(-1), respectively); and maximal heart rate (HRmax, 154+/-21 v 186+/-7 beat x min(-1), respectively). CONCLUSIONS: Asymptomatic patients with Chagas' disease, although presenting normal left ventricular systolic function at rest, display a substantial impairment of exercise functional capacity.     

Comparison of effects of supervised versus self-monitored training programmes in patients with chronic obstructive pulmonary disease.

The effects of two 8 week programmes of reconditioning in chronic obstructive pulmonary disease (COPD) patients were studied. Forty one subjects (mean+/-SD) 644.5) yrs; forced expiratory volume in one second (FEV1) 1.09+/-0.16 L; 40.6+/-6.2% predicted were randomly assigned either to supervised training on a treadmill, 4 days x week(-1) (group S; n=21) or walking 3 or 4 km in 1 h 4 days x week(-1), self-monitored with a pedometer, with weekly visits to encourage adherence (group SM; n=20). Patients were evaluated with the chronic respiratory diseases questionnaire (CRQ) and two exercise tests on a treadmill: incremental (IT) and constant (CT), above lactic threshold or 70% of maximal oxygen uptake (VO2, max) with arterial blood lactate determinations. Estimated mean work rate of training was 69+/-27 W and 25+/-5 W respectively for groups S and SM. Both types of training produced similar changes in the four dimensions of the CRQ. In group S reconditioning yielded significant (p<0.05) increases in VO2, max and increases in duration, with decreased lactate accumulation, ventilation, CO2 output (VCO2), heart rate (HR) and diastolic blood pressure (DBP) at the end of CT. They also adopted a deeper slower pattern of breathing during exercise. The SM group showed significant (p<0.05) increases in duration, lower HR and DBP at the end of CT. Significantly (p<0.05) different effects between S and SM programmes were changes in VO2, max 100+/-101 mL x min(-1) versus 5+/-101 mL x min(-1)), duration of the CT (8.1+/-4.4 min versus 3.9+/-4.7 min), VCO2 (-94+/-153 mL x min(-1) versus 48+/-252 mL x min(-1)), lactate accumulation (-1.3+/-2.2 mmol x L(-1) versus 0+/-1.2 mmol x L(-1) and respiratory rate at the end of CT (4.3+/-3.4 min(-1) versus -1+/-4.2 min(-1)). Supervised, intense training yields physiological improvements in severe chronic obstructive pulmonary disease patients not induced by self-monitored training. The self-monitored, less intense training, increases submaximal exercise endurance, although to a lesser degree.     

Fat metabolism during high-intensity exercise in endurance-trained and untrained men

To determine whether trained individuals rely more on fat than untrained persons during high-intensity exercise, six endurance-trained men and six untrained men were studied during 30 minutes of exercise at 75% to 80% maximal oxygen consumption (VO2max). The rates of appearance (Ra) and disappearance (Rd) of glycerol and free fatty acids (FFAs) were determined using [1,1,2,3,3-2H]glycerol and [1-13C]palmitate, respectively, whereas the overall rate of fatty acid oxidation was determined using indirect calorimetry. During exercise, the whole-body rate of lipolysis (ie, glycerol Ra) was higher in the trained group (7.1 +/- 1.2 v 4.5 +/- 0.7 micromol x min(-1) x kg(-1), P < .05), as was the Ra (approximately Rd) of FFA (9.0 +/- 0.9 v 5.0 +/- 1.0 micromol x min(-1) x kg(-1), P < .001). FFA utilization was higher in trained subjects even when expressed as a percentage of total energy expenditure (10% +/- 1% v 7% +/- 1%, P < .05). However, this difference in plasma FFA flux could not account for all of the difference in fatty acid oxidation between trained and untrained subjects (20.8 +/- 3.3 v 7.9 +/- 1.6 micromol x min(-1) x kg(-1), or 23% +/- 3% v 13% +/- 2% of total energy expenditure, both P < .05). Thus, the oxidation of fatty acids derived from some other source also must have been greater in the trained men. We conclude that trained athletes use more fat than untrained individuals even during intense exercise performed at the same percentage of VO2max. The additional fatty acids appear to be derived from both adipose tissue and, presumably, intramuscular triglyceride stores.     

Do hemodynamic indices correlate with maximum exercise capacity and oxygen consumption in chronic congestive heart failure?

The mechanism of exercise intolerance in chronic congestive heart failure remains unclear. We correlated resting haemodynamic variables with the peak exercise capacity and maximum oxygen consumption (VO2 max) in patients with congestive heart failure in 27 studies on treadmill exercise testing using the modified Bruce protocol. VO2 max was measured using breath by breath expiratory gas analysis. The patients were in severe congestive heart failure (NYHA class II and III, pulmonary artery wedge pressure 23 +/- 2 mmHg, cardiac index 2.4 +/- 0.21 l/min/m2). VO2 max was 23 +/- 2 ml/kg/min. Fatigue was the commonest symptom limiting the exercise. None of the hemodynamic variables correlated well with VO2 max. [right atrial pressure (r = 0.08), pulmonary artery pressure (r = 0.05), pulmonary artery wedge pressure (r = 0.08), aortic pressure (r = -0.3) & cardiac index (r = 0.29)]. Both uni- and multi-variate analysis failed to show any relation between VO2 max and resting hemodynamic variables. We conclude that unlike the acute heart failure syndromes, resting hemodynamic variables do not correlate with exercise capacity in patients with chronic congestive heart failure. The abnormal resting haemodynamics do not limit exercise in these patients. Peripheral mechanisms may thus be more important.     

Adiponectin and stress hormone responses to maximal sculling after volume-extended training season in elite rowers

The purpose of this study was to investigate the resting and short-duration exercise-induced hormone responses of male rowers as a result of 6 months of volume-extended training season. Body composition, maximal aerobic capacity, and on-water 2000-m sculling performance were assessed before and after a 24-week training in elite rowers (n = 11; 193.1 +/- 5.2 cm; 91.6 +/- 5.8 kg; maximum oxygen consumption [VO2max], 6.2 +/- 0.5 L x min(-1)). Six rowers were selected (SEL; 192.0 +/- 6.3 cm; 93.5 +/- 7.1 kg; VO2max, 6.4 +/- 0.4 L x min(-1)) and 5 were not selected (N-SEL; 194.8 +/- 4.1 cm; 89.6 +/- 4.0 kg; VO2max, 6.0 +/- 0.5 L x min(-1)) for the national team. Resting adiponectin did not change as a result of prolonged training. Adiponectin did not change after 2000-m rowing at baseline either. No responses were also observed 24 weeks later in SEL rowers, whereas a significant decrease (P < .05) was observed in N-SEL rowers. At the same time, leptin also decreased after the first 30 minutes of recovery in N-SEL rowers. After the training period, immediate postexercise increases in growth hormone and testosterone were significantly higher in the whole group of rowers. No differences in cortisol responses were observed before and after the training period in SEL and N-SEL rowers. In conclusion, it appears that resting adiponectin does not change as a result of prolonged training. Training may modify adiponectin response to an short-duration exercise depending on the performance level of athletes. Decreased postexercise adiponectin and leptin values in rowers with lower performance capacity may be indicative of the inadequate recovery of these athletes.     

轻中度哮喘患者提高运动耐量可行性研究

目的 比较同等日常运动水平的轻、中度哮喘患者与健康志愿者的运动心肺功能;探讨静息深吸气量与大运动功率的关系。方法 轻、中度哮喘患者１９例和健康志愿者１９例接受了运动心肺功能试验。试验采用负荷递增运动方案,运动前测一秒钟用力呼气容积（ＦＥＶ１）、深吸气量（ＩＣ）,运动后监测ＦＥＶ１。运动中监测心率、氧耗量（ＶＯ２）、每分钟通气量（ＶＥ）、氧脉搏（Ｏ２－ｐｕｌｓｅ）、呼吸频率等。结果 哮喘患者运动后Ｆ     

Alcohol and glucose counterregulation during acute insulin-induced hypoglycemia in type 2 diabetic subjects

To investigate the influence of alcohol on glucose counterregulation and recovery during acute insulin-induced hypoglycemia in type 2 diabetic subjects, 8 diet-treated type 2 diabetic subjects were examined twice after an overnight fast. A graded hyperinsulinemic (1 mU/kg/min, 60 to 195 minutes) euglycemic/hypoglycemic clamp was performed with concomitant infusion of 3-(3)H-glucose to assess glucose turnover. After a euglycemic baseline period (150 to 180 minutes), 200 mL of water was taken either alone or with alcohol (0.4 g/kg body weight). Hypoglycemia (plasma glucose nadir, 2.8 mmol/L) was subsequently induced, and the recovery period followed after discontinuation of insulin and the variable glucose infusion. On both study days, circulating concentrations of insulin and glucose were comparable. Alcohol intake markedly increased plasma lactate (area under the curve [AUC], recovery period) (244 +/- 30 v 12 +/- 4 mmol/L x 240 minutes; P = .00009) and suppressed plasma nonesterified fatty acids (NEFA) (AUC, recovery period) (95 +/- 13 v 161 +/- 18 mmol/L x 240 minutes; P = .0008). No differences were found in the counterregulatory response of catecholamines, cortisol, and growth hormone (GH). However, alcohol intake decreased peak glucagon significantly (155 +/- 12 v 200 +/- 17 pg/mL; P = .038). In diet-treated, mild type 2 diabetic subjects, alcohol does not modify recovery from insulin-induced hypoglycemia.     

Effects of moderate and high glycemic index meals on metabolism and exercise performance.

The purpose of this study was to determine whether pre-exercise ingestion of meals with moderate and high glycemic indexes (GI) affects glucose availability during exercise and exercise performance time. Six male volunteers (22 +/- 1 years; 80.4 +/- 3.7 kg; VO(2peak), 54.3 +/- 1.2 ml. kg(-1). min(-1)) ingested 75 g of carbohydrate in the form of 2 different breakfast cereals, rolled oats (moderate GI, approximately 61; MOD-GI) or puffed rice (high GI, approximately 82; HI-GI), combined with 300 mL of water; or water alone (control). The trials were randomized, and the meals were ingested 45 minutes before the subjects performed cycling exercise (60% VO(2peak)) to exhaustion. Venous blood samples were drawn to measure glucose, free fatty acids (FFAs), glycerol, insulin (INS), epinephrine (EPI) and norepinephrine (NE) concentrations. A muscle biopsy specimen was obtained from the vastus lateralis before the meal and immediately after exercise for glycogen determination. Before exercise, both test meals elicited significant (P <.05) hyperglycemia and hyperinsulinemia compared with control. The glycemic response was higher (P <.05) at the start of exercise after the HI-GI meal than after the control. During exercise, plasma glucose levels were higher (P <.05) at 60 (5.2 +/- 0.1, 4.2 +/- 0.2, and 4.6 +/- 0.1 mmol. L(-1)) and 90 (4.8 +/- 0.1, 4.1 +/- 0.1, and 4.3 +/- 0.1 mmol. L(-1)) minutes after the MOD-GI meal than after either the HI-GI or control. Total carbohydrate oxidation was greater (P <.05) during the MOD-GI trial than in control and was directly correlated with exercise performance time (r =.95, P <.0001). Pre-exercise plasma FFA levels were suppressed (P <.05) 30 and 45 minutes after ingestion of the HI-GI meal and 45 minutes after the MOD-GI meal compared with control. At 30, 60, and 120 minutes of exercise, FFAs remained suppressed (P <.05) for both test meals compared with control. At exhaustion, plasma glucose, INS, FFA, glycerol, EPI, and NE levels and muscle glycogen use were not different for all trials. Exercise time was prolonged (P <.05) after the MOD-GI meal compared with control, but the HI-GI trial was not different from control (MOD-GI, 165 +/- 11; HI-GI, 141 +/- 8; control, 134 +/- 13 minutes). Thus, in contrast to the HI-GI meal or control, the MOD-GI breakfast cereal ingested 45 minutes before exercise enhanced performance time, maintained euglycemia for a longer period during exercise, and resulted in greater total carbohydrate oxidation during the exercise bout. We conclude that a MOD-GI meal provides a significant performance and metabolic advantage when consumed 45 minutes before exercise.     

The pressor effect of sodium-volume expansion is calcium mediated.

To investigate the calcium dependence of salt-induced hypertension we concurrently measured blood pressure and serum ionized calcium in conscious normotensive female dogs undergoing five infusions: 1) sodium chloride (0.9%) 2) calcium chloride (10 mg/kg), 3) combined sodium chloride and calcium chloride, 4) nicardipine (1 micrograms/kg/min), and 5) combined sodium chloride and calcium chloride in the presence of nicardipine. While saline and calcium chloride infusions individually did not affect blood pressure, saline combined with calcium chloride significantly and consistently raised mean arterial pressure (MAP) (delta MAP = 7 +/- 2 mm Hg, P less than .001 v baseline). Serum ionized calcium (Caio) levels increased within the normal range with the infusion of calcium alone (1.32 +/- 0.03 to 1.48 +/- 0.01 mmol/L, P less than .005). Extracellular Caio rose less with the combined NaCl-CaCl2 infusion (delta Caio 0.10 +/- 0.01 v 0.16 +/- 0.02 mmol/L, P less than .02). The difference in calcium elevations could not be attributed to volume expansion alone, since saline infusion itself did not affect serum ionized calcium (1.32 +/- 0.3 to 1.31 +/- 0.01 mmol/L, P = NS). Furthermore, nicardipine prevented the pressor effect of the combined saline-calcium infusion. (delta MAP = -2 +/- 3 v 7 +/- 2 mm Hg, P less than .001), and restored the rise in extracellular Caio to that seen with the nonpressor calcium infusion (delta Caio 0.15 +/- 0.01 mmol/L v 0.16 +/- 0.02 mmol/L, P = NS). Altogether, these data demonstrate that the rise in blood pressure and ionized calcium following an acute infusion of sodium and calcium chloride are interdependent.(ABSTRACT TRUNCATED AT 250 WORDS)     

Right ventricular performance and central circulatory hemodynamics during upright exercise in patients with chronic obstructive pulmonary disease

A combined hemodynamic and radionuclide approach was used to evaluate right ventricular performance during upright exercise in 12 male patients with chronic obstructive pulmonary disease. To assess the influence of intrathoracic pressure on hemodynamic parameters, pleural pressure was measured using an esophageal balloon. Mean age was 58.5 +/- 6.7 yr (+/- SD), and all had dyspnea on physical exertion. For the group, forced expiratory volume in one second (FEV1) was 1.04 +/- 0.40 L and arterial oxygen-tension (PaO2) was 77 +/- 11 mmHg. During steady-state, upright exercise on the bicycle ergometer at 58% of maximal oxygen consumption (VO2 max): (1) mean pulmonary artery pressure (Ppa) and pulmonary vascular resistance index (PVRI) increased significantly; (2) right ventricular ejection fraction (RVEF) failed to augment appropriately (less than 5% increase); and (3) right ventricular end-diastolic volume index (RVEDVI) increased significantly, whereas right ventricular end-systolic volume index (RVESVI) did not change. A diminished pulmonary vascular bed, the change in PaO2, and possibly increased alveolar pressure appeared to contribute to the increased load placed on the right ventricle. Both RVEDVI and RVESVI were significantly correlated with Ppa at rest and during exercise. In 2 of the 12 patients, stroke volume index and left ventricular end-diastolic volume index showed minimal change with exercise. VO2max was correlated with the FEV1 (r = 0.75; p = 0.01) as well as resting (r = -0.60; p = 0.02) and exercise (r = -0.61; p = 0.02) PVRI. These results suggest that exercise performance may be limited by right ventricular dysfunction in addition to respiratory impairment in some patients with chronic airway disease.     

Anaerobic threshold and maximal oxygen uptake in patients with coronary artery disease and stable angina before and after percutaneous transluminal coronary angioplasty

In this study, we investigated the effect of percutaneous transluminal coronary angioplasty (PTCA) on functional exercise capacity, oxygen uptake at anaerobic threshold (VO(2 AT)) and maximal oxygen uptake (VO(2 max)) in patients with coronary artery disease (CAD). Twenty-five patients with CAD and stable angina pectoris underwent spiroergometry before and after PTCA. All patients had reduced functional capacity with Weber class B in 5, class C in 16 and class D in 4 patients with mean VO(2 AT) of 9.4 +/- 1.5 ml.kg(-1).min(-1) and mean VO(2 max) of 13.3 +/- 3.3 ml. kg(-1).min(-1). After PTCA, VO(2 max) (15.8 +/- 3.1 ml.kg(-1). min(-1)) increased significantly (p < 0.001) compared to before PTCA. Subgroup analysis revealed that patients with low functional capacity before PTCA (VO(2 max) <15 ml x kg(-1) x min(-1)) had the most benefit from PTCA with an increase in VO(2 AT) from 8.7 +/- 1.0 to 9.6 +/- 1.4 ml x kg(-1) x min(-1) (p < 0.05) and of VO(2 max) from 11.3 +/- 2.2 to 14.8 +/- 3.5 ml x kg(-1) x min(-1) (p < 0.001) whereas in patients with VO(2 max) >15 ml x kg(-1) x min(-1), VO(2 AT) (p = 0.9) and VO(2 max) (p = 0.2) did not improve significantly. In conclusion, there is reduced functional capacity and VO(2 max) which improved after PTCA in CAD patients. In patients with low VO(2 max) before PTCA, functional capacity, VO(2 AT) and VO(2 max) significantly improved after PTCA, suggesting reversible myocardial impairment induced by intermittent myocardial ischemia. Patients with higher VO(2 max) had no significant benefit from PTCA with respect to functional capacity, VO(2 max) and VO(2 AT).     

Effects of severity of long-standing congestive heart failure on pulmonary function

To investigate the effects of severity of long-standing congestive heart failure (CHF) on pulmonary function, we studied 53 (47 men) consecutive patients, all heart transplant candidates. Their mean (+/- SD) age and ejection fraction were 47 +/- 12 years and 23 +/- 7%, respectively. All patients underwent spirometry, lung volume, diffusion capacity (DLCO), maximum inspiratory (PImax) and expiratory pressure (PEmax) measurement. Maximum cardiopulmonary exercise test on a treadmill was also performed to determine maximum oxygen consumption (VO2max). On the basis of VO2max, the patients were then divided into those with a VO2max > 14 ml min-1 kg-1 (group 1, n = 30) and those with a VO2max < or = 14 ml min-1 kg-1 (group 2, n = 23). In comparison with group 1, group 2 patients had lower FEV1/FVC (70 +/- 8% vs 75 +/- 7%, P = 0.008), lower FEF25-75 (46 +/- 21 vs 70 +/- 26%pred, P < 0.001), lower TLC (76 +/- 15 vs 85 +/- 13%pred, P = 0.02) and lower PImax (68 +/- 20 vs 87 +/- 22 cmH2O, P = 0.003), but comparable DLCO (84 +/- 15 vs 88 +/- 20%pred, P = N.S.), and PEmax (99 +/- 25 vs 96 +/- 22 cmH2O, P = N.S.). In conclusion, our data suggest that respiratory abnormalities, such as restrictive defects, airway obstruction, and inspiratory muscle weakness, are more pronounced in patients with severe CHF than in those with mild-to-moderate disease. Further studies are required to investigate the extent to which these abnormalities contribute to dyspnoea during daily activities in patients with heart failure.     

Norepinephrine infusion during moderate-intensity exercise increases glucose production and uptake

A role for the increase in circulating norepinephrine (NE) during intense exercise [IE; > or = 80% maximum O(2) uptake (VO(2max))] in the marked increment in glucose rate of production (Ra) during IE is hypothesized. Seven fit male subjects (27 +/- 2 yr old; body mass index, 23 +/- 1 kg/m(2); VO(2max), 63 +/- 5 mL/kg.min) underwent 40 min of postabsorptive moderate-intensity (53% VO(2max)) cycle ergometer exercise (126 +/- 14 W), once without [control (CON)] and once with NE infusion (0.1 microg/kg.min) from 30-40 min (NE). With infusion, plasma NE reached 15.9 +/- 1.0 nM (8-fold rest, 2-fold CON). Ra doubled to 4.40 +/- 0.44 in CON, but rose to 7.55 +/- 0.68 mg/kg.min with NE infusion (P = 0.003). Ra correlated strongly (r(2) = 0.92, P < 0.02) with plasma NE during and immediately after infusion. With NE infusion, peak glucose uptake [rate of disappearance (Rd), 6.57 +/- 0.59 vs. 4.53 +/- 0.55 mg/kg.min, P < 0.02] and glucose metabolic clearance rate (P < 0.05) were higher than in CON. Glycemia rose minimally during the NE infusion but did not differ between groups at any time during exercise. Glucagon-to-insulin ratio increased minimally, and epinephrine increased approximately 2.5- to 3-fold at peak but did not differ between groups. Thus, NE infusion during moderate exercise led to increments in Ra and Rd in fit individuals, supporting a possible contributory role for the increase of plasma NE in IE. NE effects on Rd and metabolic clearance rate during exercise may differ from its effects at rest.     

Effect of physical exercise on lipoprotein(a) and low-density lipoprotein modifications in type 1 and type 2 diabetic patients

To evaluate the effect of physical exercise on blood pressure, the lipid profile, lipoprotein(a) (Lp(a)), and low-density lipoprotein (LDL) modifications in untrained diabetics, 27 diabetic patients (14 type 1 and 13 type 2) under acceptable and stable glycemic control were studied before and after a supervised 3-month physical exercise program. Anthropometric parameters, insulin requirements, blood pressure, the lipid profile, Lp(a), LDL composition, size, and susceptibility to oxidation, and the proportion of electronegative LDL (LDL(-)) were measured. After 3 months of physical exercise, physical fitness improved (maximal O2 consumption [VO2max], 29.6 +/- 6.8 v 33.0 +/- 8.4 mL/kg/min, P < .01). The body mass index (BMI) did not change, but the waist circumference (83.2 +/- 11.8 to 81.4 +/- 11.2 cm, P < .05) decreased significantly. An increase in the subscapular to triceps skinfold ratio (0.91 +/- 0.37 v 1.12 +/- 0.47 cm, P < .01) and midarm muscle circumference ([MMC], 23.1 +/- 3.4 v 24.4 +/- 3.7 cm, P < .001) were observed after exercise. Insulin requirements (0.40 +/- 0.18 v 0.31 +/- 0.19 U/kg/d, P < .05) and diastolic blood pressure (80.2 +/- 10 v 73.8 +/- 5 mm Hg, P < .01) decreased in type 2 diabetic patients. High-density lipoprotein cholesterol (HDL-C) increased in type 1 patients (1.48 +/- 0.45 v1.66 +/- 0.6 mmol/L, P < .05), while LDL cholesterol (LDL-C) decreased in type 2 patients (3.6 +/- 1.0 v3.4 +/- 0.9 mmol/L, P < .01). Although Lp(a) levels did not vary in the whole group, a significant decrease was noted in patients with baseline Lp(a) above 300 mg/L (mean decrease, -13%). A relationship between baseline Lp(a) and the change in Lp(a) (r = -.718, P < .0001) was also observed. After the exercise program, 3 of 4 patients with LDL phenotype B changed to LDL phenotype A, and the proportion of LDL(-) tended to decrease (16.5% +/- 7.4% v 14.0% +/- 5.1%, P = .06). No changes were observed for LDL composition or susceptibility to oxidation. In addition to its known beneficial effects on the classic cardiovascular risk factors, regular physical exercise may reduce the risk of cardiovascular disease in diabetic patients by reducing Lp(a) levels in those with elevated Lp(a) and producing favorable qualitative LDL modifications.     

The reduction in postprandial lipemia after exercise is independent of the relative contributions of fat and carbohydrate to energy metabolism during exercise

A single session of exercise several hours before a high-fat meal reduces postprandial lipemia. The purpose of the present study was to test the hypothesis that this effect is independent of substrate metabolism during exercise. Twelve men aged 21 to 36 years underwent three oral fat tolerance tests with intervals of at least 1 week. On one occasion, only activities of daily living were allowed the preceding day (control). On the other two occasions, subjects ran on a treadmill for 90 minutes on the afternoon preceding the fat tolerance test; 90 minutes before running, they ingested either acipimox, an inhibitor of lipolysis in adipose tissue, or placebo. Acipimox abolished the increase in the nonesterified fatty acid (NEFA) concentration observed during the run after placebo and reduced lipid oxidation (placebo, 37 +/- 7 g; acipimox, 21 +/- 3 g; P < .05, mean +/- SEM), but had no effect on gross energy expenditure (placebo, 4.86 +/- 0.20 MJ; acipimox, 4.83 +/- 0.18 MJ). Before each of the three fat tolerance tests, subjects reported to the laboratory after an overnight fast. Blood samples were obtained in the fasted state and for 6 hours after consumption of a high-fat meal (per kilogram of body mass: 1.2 g fat, 1.2 g carbohydrate, and 61 kJ energy). Plasma concentrations of NEFA were higher postprandially with acipimox, compared with control and placebo (P < .05), as were glucose concentrations measured over the first 4 hours. The insulin response to the meal was lower in placebo compared with control and acipimox (P < .05). Despite these counterregulatory responses, postprandial lipemia was reduced to the same degree (compared with control, P < .05) by exercise preceded by acipimox and by exercise preceded by placebo (area under the plasma triacylglycerol concentration v time curve: control, 8.77 +/- 1.17 mmol/L x 6 h; placebo, 6.95 +/- 0.97 mmol/L x 6 h; acipimox, 6.81 +/- 0.81 mmol/L x 6 h). These findings suggest that some factor other than the nature of the metabolic substrate used during exercise determines the attenuating effect of prior exercise on postprandial lipemia.