Central and regional circulatory adaptations to one-leg training.

Six young healthy male subjects performed submaximal and maximal exercise on bicycle ergometers with one leg and two legs before and after 8 wk of one-leg training with each of both legs. The following variables were measured during one- and two-leg exercise: oxygen uptake, heart rate, mean arterial blood pressure, cardiac output, leg blood flow, and iliac arteriovenous differences for oxygen and lactate. After training the maximal oxygen uptake during one- and two-leg exercise was increased by 19 and 11%, respectively. The corresponding cardiac outputs increased by 16 and 11%, respectively. During submaximal one-leg exercise, heart rate decreased by 11%, whereas a decrease of only 2% was seen during submaximal two-leg exercise. Mean blood pressure decreased by about 10 Torr in both types of exercise and during both submaximal and maximal exercise. Maximal leg blood flow increased only by 1.2 l/min during one-leg exercise. Leg blood flow and leg oxygen uptake were smaller during two-leg exercise than during one-leg exercise and more so after training. These findings indicate that one-leg exercise, compared with two-leg exercise, involves circulatory adaptations that respond differently to one-leg training. The findings further imply that oxygen supply to one large muscle group of exercising muscles may be limited by vasoconstriction when another large group of muscles is exercising simultaneously.

Immediate effects of labetalol on central, splanchnic-hepatic, and forearm haemodynamics during pleasant emotional stress in hypertensive patients.

The effects of intravenous administration of labetalol in a dose of 0.75 mg/kg body weight on central, splanchnic-hepatic and forearm haemodynamics were studied in 8 hypertensive patients resting in the supine position and during pleasant psychic stress induced by practice of a television-game of tennis. In the resting state labetalol caused immediate reduction of arterial blood pressures and of total vascular resistance, whereas heart rate, cardiac output and splanchnic-hepatic and forearm blood flow remained unchanged. After labetalol, the stress-induced increase in heart rate, cardiac output, estimated myocardial oxygen demand and forearm blood flow was significantly reduced, whereas total vascular resistance and splanchnic-hepatic vascular resistance remained unchanged. This is taken to indicate that the alpha-adrenoceptor blocking properties of labetalol may offer haemodynamic advantages as compared to the widely used non-selective beta-adrenoceptor blocking agents in the management of hypertension.

Regulation of gluconeogenesis and ketogenesis during rest and exercise in diabetic subjects and normal men.

The splanchnic-hepatic metabolism of glucose, lactate, pyruvate, alanine, glycerol, non-esterified fatty acids (NEFA), ketone bodies and oxygen were investigated in five normal men and six juvenile diabetic subjects at rest and during exercise after an overnight fast. A linear relationship was found between load (arterial concentration multiplied by hepatic blood flow) and splanchnic-hepatic uptake of lactate, pyruvate, glycerol and NEFA. The uptake of alanine was highly sensitive to load, but was also regulated by the concentration of hepatic venous glucagon. The uptake of pyruvate was high in exercising diabetic subjects, who had a high lactate/pyruvate concentration ratio in hepatic venous blood. The rate of uptake of the total measured gluconeogenic precursors was significantly higher in the diabetic group at a given load. The rate of ketogenesis was linearly related to the NEFA load in both groups; however, the rate of ketogenesis was twofold at a given load in the diabetic group. The highest rates of ketogenesis were found coincident with the highest concentrations of glucagon in hepatic venous blood. The observed antiketogenic effect of exercise was due to a decreased load of NEFA, mainly caused by a decrease in the hepatic blood flow.

Central and regional circulatory effects of adding arm exercise to leg exercise.

7 young, healthy, male subjects performed exercise on bicycle ergometers in two 20 min periods with an interval of 1 h. The first 10 min of each 20 min period consisted of arm exercise (38--62% of Vo2 max for arm exercise) or leg exercise (58--78% of Vo2 max for leg exercise). During the last 10 min the subjects performed combined arm and leg exercise (71--83% of Vo2 max for this type of exercise). The following variables were measured during each type of exercise: oxygen uptake, heart rate, mean arterial blood pressure, cardiac output, leg blood flow (only during leg exercise and combined exercise), arterio-venous concentration differences for O2 and lactate at the levels of the axillary and the external iliac vessels. Superimposing a sufficiently strenuous arm exercise (oxygen uptake for arm exercise greater than 40% of oxygen uptake for combined exercise) on leg exercise caused a reduction in blood flow and oxygen uptake in the exercising legs with unchanged mean arterial blood pressure. Superimposing leg exercise on arm exercise caused a decrease in mean arterial blood pressure and an increased axillary arterio-venous oxygen difference. These findings indicate that the oxygen supply to one large group of exercising muscles may be limited by vasoconstriction or by a fall in arterial pressure, when another large group of muscles is exercising simultaneously.

Heart rate and arterial blood pressure during exercise in patients with angina pectoris. Effects of training and of nitroglycerin.

In 29 patients with typical exertional angina pectoris, intra-arterial systolic blood pressure (SBP), heart rate (HR), and the rate-pressure product (RPP = HR X SBP X 10(-2) were continuously recorded during repeated bouts of leg or arm exercise. Development of chest pain was independent of the workload and occurred at a fairly constant value of RPP, of HR, and of SBP in each patient for a given type of exercise, but the pain threshold values for all three variables were consistently higher during arm exercise than during leg exercise. The reproducibility of the pain threshold values was assessed for leg exercise. The variation, based on individual coefficients of variation, ranged from 1.3% to 13% (group mean, about 6%). There was no significant difference between the SBP values obtained by the traditional, noninvasive cuff technique and the values during intra-arterial monitoring. In 25 patients a physical training program of an average of three months increased the maximal amount of work (watt X sec) performed before onset of pain by 100%. The most conspicuous effect of training on cardiac function was a 10% reduction of HR at a given workload, SBP being unchanged. Over-all, the data suggest that the increased exercise capacity caused by training could be accounted for by the reduction in the relation between RPP and external workload. The improvement in exercise capacity resulting from training was on the same level of magnitude as the 90% increase obtained in 11 untrained patients after administration of 0.25 to 0.50 mg of nitroglycerine sublingually prior to exercise. In contrast to the finding after training, nitroglycerin administered to subjects increased HR by 10%, but reduced SBP by 13%, RPP remaining unchanged. Therefore to explain the effect of nitroglycerin on exercise capacity additional economizing changes in myocardial performance (e.g., reduction of heart volume) are required.

Pulmonary ventilation, blood gases, and blood pH after training of the arms or the legs.

In two groups of young healthy subjects who performed arm training (N = 5) and leg training (N = 5), respectively, the respiratory adaptation to submaximal exercise with trained and nontrained muscle groups was compared by measurement of the ventilatory equivalent (Ve/Vo2, pH, and blood gases (Pco2, Po2, and So2) in arterial blood and in venous blood from exercising extremities. After training Ve/Vo2 was significantly reduced during exercise with trained muscles, but unchanged during exercise with nontrained muscles. The reduction in Ve/Vo2 was closely related to a less pronounced increase in heart rate and in arterial lactate content, but showed no quantitative correlation to changes in arterial adaptations in trained muscles are mainly responsible for the reduction in Ve/Vo2. After training during exercise with trained as well as nontrained muscles a shift to the right of the blood oxygen dissociation curve occurred as extremities was lower while corresponding Po2 was higher.

Utilization of acetate in the human forearm during exercise after ethanol ingestion.

The uptake of acetate in the human forearm was studied in five fasting (14 h) subjects during 10-min periods of ergometer work at 7 and 10 kilopond-meters per minute (kpm/min). A constant arterial acetate concentration was established by administration of a small quantity of alcohol (25 g) to the subjects after a control work period. Blood flow was measured by an indicator dilution technique. Acetate uptake varied linearly with the product of arterial acetate concentration and blood flow. Acetate metabolism was calculated to account for about 6.5% of the energy metabolism, assuming complete combustion to carbon dioxide and water. Oxygen uptake and blood flow did not change in the presence of acetate and ethanol. After administration of ethanol the arterial concentrations of FFA and glycerol decreased to about half, whereas the lactate concentration increased to about twice the control values, confirming other reports. Glucose utilization was increased and lactate output decreased during the ethanol periods, presumably a consequence of the changing arterial concentrations and increased insulin level. Measurements of the arterial and venous lactate/pyruvate concentration ratios indicate that the NAD-mediated cytoplasmic redox state in the muscle is not changed in the presence of acetate and ethanol.