Effect of protein-supplemented fasting on metabolic and hormonal responses to epinephrine infusion in obese subjects.

The present study aimed at investigating the effects of an epinephrine (EPI) intravenous infusion (10 micrograms/min for 30 min) in normal subjects and in obese patients before and after 13 days of protein-supplemented fasting (PSF, 70 g protein/day). Blood glucose, plasma free fatty acids (FFA), lactate, insulin (IRI) and glucagon were determined before, during (15, 30 min) and after (+30 and +60 min) the EPI infusion. 1. When compared to lean control subjects, obese patients exhibited a less marked rise in blood glucose and a more important increase in plasma FFA, EPI infusion decreased IRI plasma levels in normals but not in the obese. Plasma glucagon was lower in the obese under basal conditions and their A cell reactivity to EPI was clearly reduced. 2. Comparison of the results obtained in obese patients before and after PSF revealed that EPI-induced blood glucose rise was not altered despite lower basal values after PSF. Plasma lactate response was impaired, probably because of the depletion in muscle glycogen. Reduction in basal plasma IRI was associated with a significantly higher FFA mobilization. Abnormally low basal EPI-stimulated glucagon concentrations persisted after PSF despite concomitant reductions in blood glucose and plasma IRI.

[Decreased secretion of epinephrine during protein-supplemented fasting in obese subjects (author's transl)]. / Diminution de la sécrétion d'adrénaline au cours de la diète hypocalorique protélique chez l'obèse.

The protein-supplemented fasting induces a progressive but moderate decrease in blood glucose (-26%) and a marked rise in plasma free fatty acids levels (+ 43%). Nevertheless the secretion of epinephrine by the adrenal medulla, as indirectly estimated by the ratio of the basal urinary elimination to the recovery percentage from the urine of an epinephrine infusion, shows a significant decrease (- 36%) during the protein diet. Thus the enhanced lipolysis does not result from an adrenergic overactivity but merely depends upon the marked reduction in the plasma insulin level (- 38%).

Critical analysis of the "anaerobic threshold" during exercise at constant workloads.

The method described by Wasserman for anaerobic threshold (AT) determination, based on the recording of ventilatory parameters, was supported by the simultaneous appearance of hyperlactacidemia and hyperventilation during a standardized incremental work test. Our study aimed at testing the AT in another profile of exercise, viz., during exercises at constant workloads. A homogenous population of 66 healthy subjects performed on a treadmill a total of 100 exercises of 20 min duration at constant workloads (43, 48, 52, 57, 63, and 71% VO2 max). The VO2, V, and venous plasma lactic acid (LA) were determined every minute. LA showed an initial transient increase at 43% VO2 max and a steady-state elevated level above 48% VO2 max. In contrast, the hyperventilation threshold (HVT) was only observed above 57% VO2 max, simultaneously with a delayed steady-state VO2 and with a sustained increase of lactate until the end of exercise. The meaning of the simultaneity of these three events must still be studied. However, the dissociation between both early and steady-state lactate thresholds and HVT is not in keeping with the concept of AT. In these conditions, there is no evidence that HVT necessarily represents an AT, viz., a critical intensity of exercise inducing an insufficient oxygen delivery to the muscles. This conclusion does not imply that the measurement of HVT should be rejected as an empirical test of physical fitness.

[Endurance after propranolol in the human execution of a general dynamic exercise]. / Endurance après propranolol chez l'homme effectuant un exercice dynamique général.

The effects of a single oral dose of 40 mg propranolol on endurance time and on the maximum oxygen consumption were studied in eight healthy young men. They were running on a motor-driven treadmill (work rate from 80 to 150% VO2 max. The VO2 max and endurance time were decreased to an average of 10 and 30% of controls respectively. The relationship between the endurance time and the relative work load (VO2/VO2 max) remained unchanged after beta-adrenoceptor blockade. The reduction of the endurance time following beta-adrenoceptor blockade is a consequence of the reduction of the VO2 max.

[Independence of hyperlactacidemia and hyperventilation threshold work-load exercise in man]. / Indépendance du seuil d'hyperlactacidémie et du seuil d'hyperventilation dans l'exercice rectangulaire chez l'homme.

During exercises at constant workload, the hyperlactatemia threshold (continuous lactate production during the whole exercise) (48% VO2 max) and the hyperventilation threshold (57% VO2 max) are not simultaneous. This finding demonstrates that the hyperventilation threshold could not be regarded as an "anaerobic threshold".

[Intravenous perfusion of adrenaline and adaptation to muscular exercise in man]. / Perfusion intraveineuse d'adrénaline et adaptation à l'exercice musculaire chez l'homme.

Eleven normal subjects underwent epinephrine perfusions (1.9; 6.1; 11.8 ng/min) during a short (20 min) and mild (50% VO2 max) exercise. VO2 was not modified by epinephrine perfusion, while heart rate ventrilation and plasmatic lactate were increased proportionally to epinephrine doses.

[Urinary catecholamine excretion in aging]. / Excrétion urinaire des catécholamines au cours de la sénescence.

In ageing female subjects, the urinary noradrenaline excretion (UNA) is reduced with respect to the controls in young adults. On the other hand the ratio UNA/clearance of endogenous creatinine increases with ageing. This provides a confirmation of the fact that ageing is associated with an increase in plasma noradrenaline. The ratio UA/clearance of creatinine remains unaltered. So far the physiological meaning of these results remains unclear.

[Orthosympathetic stimulation after hypercapnia in the rat]. / Effets sympathico-stimulants de l'hypercapnie de brève durée chez le rat.

Inhalation of a gas mixture : CO2, 25% -- O2, 37.5% -- N2, 37.5%, provokes regularly in the light anaesthetized rat, an increase of catecholaminemia of central origin, associated with systemic arterial hypertension.

[Effect of pindolol on tachycardia and certain metabolic variations dependent of muscular exertion]. / Influence du pindolol sur la tachycardie et sur certaines variations métaboliques liées à l'exercice musculaire.

1. -- In young well trained adults, adrenergic beta receptors blockade by pindolol or propranolol causes a relative bradycardia during running on a threadmill during 10 to 20 min at 50% VO2 max. 2. -- Pindolol activity is maximum for 5-7.5 mg ingested one hour before starting. In two subjects, tachycardia reappears for 30 mg : this secondary increase may be explained by an intrinsic sympathetic activity of pindolol. 3. -- Propranolol is about 14 times less active than pindolol without any intrinsic sympathetic activity.

[Effect of horizontal immersion into water at 38 degrees C on the urinary elimination of catecholamines]. / Influence de l'immersion horizontale dans l'eau à 38 degrees C, sur l'élimination urinaire des catécholamines.

The urinary excretion of noradrenaline, adrenaline and creatinine has been studied in normal young individuals during a water bath at 38 degrees C for 40 minutes. The noradrenalinuria and the ratio noradrenalinuria/creatininuria are decreased, indicating an inhibition of the vasomotor activity of the orthosympathetic system. This inhibition is related to the consequence of the external hydrostatic pressure of the water filling the intrathoracic venous reservoirs and increasing the systemic blood pressure at the sino-baroreceptor level, hyperthermia playing a very limited role.

[Orthosympathetic reaction during paroxysmal asphyxia in the rat]. / Réaction orthosympathique lors de l'asphyxie paroxystique du rat.

Acute hypercapnic hypoxia provoked by the ligature of the trachea kills the rat in 3 to 5 minutes. Catecholaminemia is immediately increased by adrenaline release from the adrenal medulla for the largest part. Catecholamine contents of the suprarenal glands is not decreased at the time of death.