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In addition to its well-known ventilatory effect, a small rise in pulmonary arterial pressure or pulmonary vascular resistance is occasionally observed with chronic administration of almitrine. In order to test the hypothesis of enhancement of exercise pulmonary vasoconstriction by almitrine, mongrel dogs were studied at rest and during submaximal exercise before and after 4 weeks of chronic ingestion of almitrine (10 mg/kg). It was shown that resting pulmonary arterial pressure (PAP) remained unchanged by almitrine treatment. However, when exercise was superimposed on almitrine medication, PAP was significantly increased throughout the exercise bout. Thus the rise in PAP during the 20th min of exercise averaged 8.7 ± 3.4 mm Hg after almitrine treatment while PAP increased by only 1.3 ± 1.7 mm Hg before medication. The exaggerated exercise-induced PAP response in conjunction with the enhanced secretion of norepinephrine that we observed during almitrine treatment suggests that catecholamine could be involved in the pulmonary haemodynamic adjustments. Furthermore, mixed-venous PO2 (P v O2) both during rest and exercise declined with prolongation of almitrine ingestion, suggesting that P v O2 might possibly be implicated in the pulmonary haemodynamic response to almitrine, in the same way as it is involved in the hypoxia-induced pulmonary vasoconstriction. These findings demonstrate that almitrine condition, even at a high dose, does not have any deleterious effect on pulmonary vasculature in resting conditions, but prolonged submaximal exercise should be proscribed in patients on a long-term therapy.

Male Wistar rats were subjected to 12.5 days of weightlessness aboard Cosmos 1887. Histomorphometric and biochemical analyses were investigated in soleus (SOL), plantaris (PL) and extensor digitorum longus (EDL) muscles of flight rats (group F) and compared with data from two groups of terrestrial controls: one group living free in a vivarium (group V) and another subjected to a flight simulation except for the state of weightlessness (group S). Relative to groups V and S, no alteration in the percentage distribution of fibres had occurred in SOL, PL or EDL, after the flight. In SOL muscles from group F animals, cross-sectional areas of all fibre types were reduced to a greater extent (-40%) than capillary to fibre ratio (-24%) leading to a higher capillary density (+33%) than in V and S groups. In PL, type I, IIA and IIB fibre cross-sectional areas were less decreased (-25%). In EDL, only fast-twitch fibre cross-sectional areas showed an average decrease of 30%. Capillary per fibre ratio was reduced by 15% and 28% respectively in PT and EDL muscles from group F rats compared to control groups V and S. Citrate synthase and 3-hydroxyacyl-coenzyme A dehydrogenase activities remained unchanged in SOL, PL and EDL following spaceflight. These findings indicate greater atrophy and functional alterations (capillarity) compared to those observed after 7 days of microgravity on Cosmos 1667.

The aim of the present investigation was to determine, by quantitative electron microscopy, the effects of a 5-wk tail-suspension period on rat soleus muscle ultrastructure. A marked decline (-60%) in muscle mass occurred. The mean fiber cross-sectional area decreased to a greater extent (-75%) than the capillary-to-fiber ratio (-37%), leading to a higher capillary density (+148%) after hypokinesia. The total mitochondrial volume density remained unchanged, whereas the volume density of myofibrils was slightly but significantly reduced (-6%). A shift from subsarcolemmal to interfibrillar mitochondria occurred. Interfibrillar mitochondrial volume density was highest near the fiber border and decreased toward the fiber center. An increase in volume density of satellite cells suggested muscle regenerative events. Soleus atrophy with tail suspension greatly decreases the muscular volume but leaves the ultrastructural composition of muscle fibers relatively unaffected.

Seven male Wistar rats were subjected to 7 days of weightlessness on the Soviet biosatellite Cosmos 1667. Muscle histomorphometry and biochemical analyses were performed on the soleus (SOL) and extensor digitorum longus (EDL) of flight rats (group F) and compared with data from three groups of terrestrial controls: one subjected to conditions similar to group F in space except for the state of weightlessness (group S) and the others living free in a vivarium (V1, V2). Relative to group V2 (its age and weight-matched control group), group F showed a greater decrease of muscle mass in SOL (23%) than in EDL (11%). In SOL a decrease in the percentage of type I fibers was counterbalanced by a simultaneous increase in type IIa fibers. The cross-sectional area of type I fiber was reduced by 24%. No statistically significant difference in capillarization and enzymatic activities was observed between the groups. In EDL a reduction in type I fiber distribution and 3-hydroxyacyl-CoA-dehydrogenase activity (27%) occurred after the flight. The small histochemical and biochemical changes reported suggest the interest in studying muscular adaptation during a flight of longer duration.

Thermal balance was studied in 11 boys, aged 10-12 years, with various values for maximal oxygen uptake (VO2max), during two standardized sweating tests performed in a climatic chamber in randomized order. One of the tests consisted in a 90-min passive heat exposure [dry bulb temperature (Tdb) 45 degrees C] at rest. The second test was represented by a 60-min ergocycle exercise at 60% of individual VO2max (Tdb 20 degrees C). At rest, rectal temperature increased during heat exposure similar to observations made in adults, but the combined heat transfer coefficient reached higher values, reflecting greater radiative and convective heat gains in the children. Children also exhibited a greater increase in mean skin temperature, and a greater heat dissipation through sweating. Conversely, during the exercise sweating-test, although the increase in rectal temperature did not differ from that of adults for similar levels of exercise, evaporative heat loss was much lower in children, suggesting a greater radiative and convective heat loss due to the relatively greater body surface area. Thermophysiological reactions were not related to VO2max in children, in contrast to adults.

The purpose of this study was to consider which characteristics are related to a high velocity in water during swimming. The study was performed on 13 of the best competition swimmers of the region of Lyon (France). The collected data were:\(\dot V_{O_2 } \) max, measured during leg-work (\(\dot V_{O_2 } \) max LW), during arm-work (\(\dot V_{O_2 } \) max AW), and the hydrodynamic resistances measured when the swimmers were towed at the speed of 1.80 m/sec. The cardiac output was measured for four of the subjects. The swimmers were characterized by a mean\(\dot V_{O_2 } \) max LW of 56 ml/kg/min and by a high value of the ratio\(\frac{{\dot V_{O_2 } \max {\text{ }}AW}}{{\dot V_{O_2 } \max {\text{ }}LW}}\) which reached 99% for three of them. There was a very high correlation (r = 0.90 and 0.91) between the mean speed calculated from the best performances in competition swims of 400 m and 1500 m and a value which is thought to express the aerobic energy available to the swimmer: $$\dot V_{O_2 } \max water:\dot V_{O_2 } \max {\text{ }}AW + \frac{{\dot V_{O_2 } \max {\text{ }}LW - \dot V_{O_2 } \max {\text{ }}AW}}{6}$$

Thirteen human subjects were submitted to a moderate muscular work on ergometric bicycle (at intensity corresponding to 80% of maximal oxygen uptake during 10 min). No modifications were observed in the urinary amounts of the three catecholamines (A, NA, DA), DOPA, DOPAC and 3-MT. On the contrary, the excretion of metadrenaline (MN) and normetadrenaline (NMN) was slightly increased, showing a mild stimulation of adrenergic system. Our result point out the interest of urinary methoxyamines as useful index of adrenergic activity in man. For experimental and physiopathological use, the metabolic alteration induced by a short submaximal muscular work is negligible for most adrenergic compounds, except for MN and NMN, the amounts of which are slightly modified.

The purpose of this study was to investigate alterations in structural and functional properties in the soleus (SOL) and extensor digitorum longus (EDL) muscles of rats after 1, 2, and 5 wk of tail suspension. Maximal O2 uptake was 19% lower after 5 wk suspension. Loss of muscle mass was greater in SOL (63%) than in EDL (22%) muscle. A reduction of type I distribution was accompanied by an increase of intermediate fiber subgroups (int I in SOL, int II in EDL). The cross-sectional area of all three fiber types was reduced by hypokinesia. The decrease in capillaries per fiber in SOL was greater than the decrease in citrate synthase and 3-hydroxyacyl-CoA dehydrogenase activities after 5 wk. No alteration in lactate dehydrogenase activity was noted. In EDL, no changes in fiber area, capillarization, and enzymatic activities occurred. Energy charge remained unchanged (0.91) whatever the muscle. These results suggest that type I fibers showed an earlier and greater susceptibility than type II fibers to suspension which is also accompanied by a decreased aerobic capacity.

The purpose of this study was to compare the effects of spontaneous recovery or recovery by treadmill training (180 min/day, 5 days/wk, 30 m/min for 8 wk) on maximal O2 uptake (VO2max), histochemical and biochemical muscular properties (soleus), of rats subsequent to 5 wk of hindlimb suspension. Spontaneous recovery reversed the 15% reduction in VO2max, whereas training posthypokinesia induced a 20% increase over control values. In the spontaneous recovery group, both citrate synthase and 3-hydroxyacyl-CoA dehydrogenase activities, decreased by hypokinesia (-40%), increased but remained 20% below the control level. In the training posthypokinesia group, an increase of these activities over control occurred (+50 and +20%, respectively). Recovery or training led to a 100% type I distribution in soleus muscle and to a recovery of all fibers' cross-sectional areas. In the spontaneous recovery group, capillaries per fiber, decreased by 46%, returned to the normal range. In the training posthypokinesia group, training induced an increase in capillaries per fiber above their control values (+23%). These results point to the plasticity of the muscle and indicate the necessity of a posthypokinesia training program for recovery of the total oxidative enzyme capacity.

O2 chemoreflex drive of ventilation was studied before and after an intravenous infusion of L-norepinephrine (9μg/min), inducing a plasmatic hormone concentration similar to that obtained during submaximal exercise.The ventilation increasing rapidly at the beginning of the infusion was stabilized after 30 min: the ventilation was two times the reference value.The O2 chemoreflex drive of ventilation increased during norepinephrine infusion. When man was transiently switched from hypoxia to pure O2 (O2 test) the maximal fall of ventilation was two times the reference response. This increase in the chemoreflex drive, although the physico-chemical blood state was unchanged, may be explained by a norepinephrine chemoreceptor sensitization. Such a mechanism could partly explain the increase of O2 chemoreflex drive observed during muscular exercise.

The influence of vagal fibers from the lung on ventilatory responses to hypercapnica, hypoxia and exercise was studied in two infact dogs (C) and two chronically lung denervated dogs (C.L.D.). In intact dogs, inspiration duration did not change as tidal volume increased in response to increased chemical drives. Chronic lung denervation did not affect the hypercapnia- or hypoxia-induced elevations in V, despite significant changes in the breathing pattern. During exercise, oxygen consumption was similar for C and C.L.D. animals. V for a given oxygen uptake was the same in C and C.L.D. dogs, but V t was higher in C.L.D. animals at all levels of exercise. It si concluded that vagal fibers from the lung play a role in determining the breathing patter, but are not required for a normal ventilatory response to hypercapnia, hypoxia and exercise. Interaction between vagal sensory input and specific structures sensitive to chemical or physical stimuli is discussed.

Awake dogs were studied before (control) and after chronic bilateral carotid denervation (denervated) at rest and running for 3 min on a treadmill, at 8 km · h−1 and at various grades, in an altitude chamber operated either at 140 m or at 4000 m for 3 h. Steady-state pulmonary ventilation (Vg) and breathing pattern (V T , f R ), oxygen consumption (ṀO2), O2 concentrations (C) pressures (P) in the arterial (a) and mixed venous blood ( v ), hematocrit (Ht) and acid-base status in arterial blood, and heart frequency (f H ) were measured. From these data cardiac output (Vb) and stroke volume (Vs), ventilatory and circulatory requirements (Vg/ṀO2, Vb/ṀO2), extraction of O2 from inspired gas (EairO2) and blood (EbO2), and capacitance coefficient of blood for oxygen (βbO2) were calculated. Ventilatory responses to transient O2-inhalation were also studied and the aortic (AP) and pulmonary (PP) blood pressures measured in resting conditions. 1. 1. After chronic carotid denervation the hypoxic chemoreflex drive of ventilation was reduced by about half, maximal ṀO2 remained unaffected at 140 m, but at 4000 m decreased 50% compared to 30% in controls. 2. 2. In all experimental conditions, Vg/ṀO2, PaO2 and CaO2 were less in denervated animals than in controls, and EairO2, PaCO2 and H+ ion concentration were higher. 3. 3. At 140 m, circulatory O2 convective transport was identical in the two groups of dogs. At 4000 m, βbO2 increased similarly in both groups, but Vb and Vb/ṀO2 were higher in denervated dogs than in controls, in relation with reduced Ca O 2 − C v O 2 difference which contributed to restore P v O 2 towards higher values. 4. 4. At 140 m, mean resting AP and PP were similar in both groups of dogs. At 4000 m, AP increased not significantly in controls, and decreased in denervated animals; PP increased in controls, but not in denervated dogs. It is concluded that integrity of the arterial chemoreceptor drive is essential in determining the eupneic level of ventilation and normal acid-base status of the blood in both resting and exercising dogs, at low and at high altitude, and in reducing the O2 circulatory requirement at high altitude. At 4000 m, the lack of carotid chemosensitivity is accompanied by severe hypoxemia, in association with hypercapnia and acidosis, and by increased cardiac blood flow, most presumably due to decreased peripheral resistance and increased venous return; despite these compensatory changes in circulatory O2 convective transport, denervated animals reach a maximum O2 uptake at lower work load than controls.

Pulmonary gas exchanges, alveolar Pco2, ventilatory output, adrenaline and noradrenaline plasma concentrations were studied in awake dogs at rest and during exercise, before and after adrenal medullectomy. In the plasma of intact resting dogs, adrenaline varied between 0.07 and 0.21 μg/1 and noradrenaline between 0.11 and 0.16 μg/1. With near-maximal exercise, the concentration of the two hormones rose significantly. Noradrenaline concentration was little affected by medullectomy; in contrast, adrenaline disappeared at rest and in exercise. The lack of adrenaline in the plasma had no effect on the capacity to perform maximal exercise but did markedly alter the breathing pattern: minute volume and respiratory frequency were lower, tidal volume was higher but alveolar ventilation requirements did not change. The altered breathing pattern persisted during exercise at all intensities. It is concluded that adrenaline is a factor of ventilatory control not only during exercise but also at rest. The effect concerns minute volume and the relation tidal volume-respiratory period; it is not due to action of adrenaline on the bronchomotricity since the total pulmonary resistance is not modified significantly when a normal adrenaline plasma concentration is restored by intravenous infusion of this hormone. A diminution of chemoreceptor activity secondary to a lack of adrenaline in the plasma is doubtful. A reflex from peripheral receptors is possible but still unknown. A direct central action of adrenaline is also discussed.

The urinary excretion of dihydroxyphenylalanine (DOPA), catecholamines (CA) [dopamine (DA), norepinephrine (NE), and epinephrine (e)], their 3-O-methylated derivatives [3-O-methyldopamine (3-MT), normetanephrine (NMN), and metanephrine (MN)], and their deaminated metabolites [dihydroxyphenylacetic acid (DOPAC) and vanilmandelic acid (VMA)] was studied in six healthy men, at rest during short-term (15 min) or exhaustive submaximal exercise, and in the 2-h postexercise recovery period. During short-term exercise only NE and VMA excretions increased, whereas in postexercise period only DA output was enhanced. Exhaustive muscular work induced a rise in NE and E excretion during the test, and an increase in DA, NE, and NMN urinary levels during postexercise recovery, while the output of deaminated metabolites was unaltered. It is concluded that both release and synthesis of CA are stimulated by submaximal exercise, which induces, in addition to NE, a specific release of DA. A possible role of NE in lipid mobilization during recovery from exhaustive muscular work is evoked. The origin and role of released DA are also discussed.

Sweating sensitivity has been evaluated at rest in 10 competitive athletes (cross-country skiers and swimmers). Three sedentary men underwent a 3-mo period of endurance training in a temperate climate, (dry bulb temperature (Tdb): 18 degrees C) and had their sweating sensitivity measured before and after the training period. Mean maximum oxygen uptake (Vo2max, ml.min(-1).kg(-1)) was: skiers: 66.5; swimmers 65.8; sedentary men, pretraining 40.9; posttraining: 48.3 (+18%). Sweat output of athletes under a given stress (passive heating) was markedly higher than that of sedentary men. Skiers exhibited a high level of heat tolerance and were better acclimatized than swimmers, although they had never experienced exposure to heat. The increase in Vo2max of sedentary men was accompanied by 1) an increase in sweating sensitivity with a decrease of body heat storage at steady state (pretraining: 5.4 kJ.kg(-1); posttraining: 3.5 kJ.kg(-1); P less than 0.05); 2) significant shift down the temperature scale with reduced rectal temperature (Tre) for sweat onset; 3) an increase of gain constants of sweating (W.m-2 degrees C(-1) (pretraining: 168; posttraining: 269; gain constant of swimmers: 222). It was suggested that endurance training in cold or temperate conditions with significant increase of Vo2max could act on the thermoregulatory function in a way similar to body heating procedures, such as work in heat, and could contribute to heat acclimatization.

The importance of gluconeogenic substrates (i.e., lactate, glycerol, and alanine) in the glycogen resynthesis observed in fasting rats after exhausting submaximal exercise [R.D. Fell et al. Am. J. Physiol. 238 (Regulatory Integrative Comp. Physiol. 7): R328-R332, 1980] was examined in muscles and liver in response to pharmacological alterations of gluconeogenic precursor flux. The minor role of lactate for glycogen resynthesis after prolonged submaximal exercise was confirmed by the insignificant accumulation of lactate neither in muscles nor in plasma. When the rate of lipolysis is reduced either by beta-blockade or by nicotinic acid injection, the replenishment of muscle glycogen persisted, suggesting that glycerol released by triglycerides hydrolysis did not play an important role in glycogen resynthesis. On the other hand, when pyruvate oxidation is enhanced by dichloroacetate (DCA), thus reducing plasma levels of lactate and alanine, glycogen resynthesis was completely blocked in liver and partly in some but not all muscles. This failure in total inhibition of glycogen resynthesis associated with the significant reduction of the plasma alanine level could be attributed to the possible stimulation of gluconeogenesis from alanine by DCA (R.A. Harris and D.W. Crabb. Arch. Biochem. Biophys. 189: 364–371, 1978). The results could point out alanine as the major gluconeogenic substrate during recovery from exhaustive exercise in fasting conditions.

To determine adaptation to prolonged exercise in paraplegics, maximal O2 uptake (VO2max) and lactate threshold (LT) were evaluated during an arm cranking exercise in nine patients (P) and nine able-bodied (AB) subjects. Mean VO2max averaged 25.1 and 31.6 ml X min-1 X kg-1 in P and AB groups respectively. VO2max in P was found to be directly related to the level of spinal injury: the higher the lesion the lower the uptake. Lactate threshold expressed as a percentage of VO2max was higher in P (59%) than in AB (43%), and close to that observed in arm-trained athletes. Since training has less effect on VO2max in paraplegics than in able-bodied subjects, attributable to a deficiency in the circulatory adaptation of paraplegics to exercise, the observed differences between AB and P in lactate threshold and submaximal exercise indicate that the possible effect of training in paraplegics is located at the level of intracellular chemistry, with a diminution in glycogenolysis (higher LT) and a higher rate of lipid utilization (lower RQ).

Sept sujets masculins sedentaires ont effectue sur une bicyclette ergometrique des exercices musculaires intenses (80% de la consommation maximale d'oxygene), soit d'une courte duree (15 min), soit pendant le temps necessaire pour atteindre l'epuisement (duree moyenne egale a 47±2 min).

The ventilatory response to exercise was studied on awake dogs trained to run on a treadmill. The exercise were performed at a grade and speed inducing an increase in the energy metabolic level up to 7 times the resting value. The roles of nervous and humoral stimuli in ventilatory control were analyzed by measuring ventilatory flow rate, tidal volume and respiratory frequency during exercise in three gaseous environments (air, hypoxia and hypercapnia) before and after carotid chemodenervation. At the start of exercise, the marked early rapid change of ventilation was unaffected by the gaseous environment. The terminal fall of ventilation was smaller than the early increase and its magnitude was decreased by hypoxia and hypercapnia. The 02 stimulus was lessened by exercise. For given levels of energy metabolism and of rectal temperature, hypoxia and hypercapnia altered the ventilatory pattern: the ventilatory frequency was decreased while the ventilatory flow rate and tidal volume were increased, inducing then an increase in alveolar ventilation. Hyperpnea related to hyperthermia was unaffected by the gaseous environment. Sinocarotid chemodenervation altered the exercise ventilatory pattern: for a given energy metabolism level, tidal volume was decreased and respiratory frequency increased. The transient rapid changes of ventilation of both the beginning and the end of exercise were altered.

The ventilatory response to exercise was studied on awake dogs trained to run on a treadmill. Various combinations of speed and grade produced metabolic increases up to 6.5 times the resting value. Ventilatory flow, tidal volume and respiratory frequency were measured cycle by cycle for the purpose of analyzing the roles of nervous and humoral stimuli in ventilatory control. In light work, neurogenic stimuli play an important role in ventilatory control and are responsible for almost all the increase in ventilation. Some minutes after the beginning of exercise a delayed humoral stimulation comes into play. Thermal polypnea develops progressively; its intensity depends on the metabolic level. The respiratory centers are organised in such a way that the dog provides for both its metabolic and thermolytic needs. Thus, in light exercise performed at 19 °C ambiant temperature, PaO2, PaCO2 and arterial pH are not modified by thermal panting. Thermal polypnea induces no relative alveolar hyperventilation unless the work load is high or the environment does not allow an important heat loss.

The neurogenic ventilatory stimulus has been studied in lightly anesthetized dogs by measuring the ventilatory responses induced by passive motion of their hindlimbs or by the reflex conti action of their quadriceps. The drug 28882 Ba [2,4-di(diethylamino)-6-(2-phenylacetylhydrazino)-1,3,5-triazine] inhibits muscle spindle activity. It likewise reduces the magnitude of the ventilatory increase induced by passive motion, chiefly by affecting the increase of tidal volume. Local procain anesthesia, which depresses activity of articular mechanoreceptors, or mechanical block of the knee articulations also leads to reduction of the magnitude of the ventilatory increase induced by passive motion or by the reflex contraction of the quadriceps. The increase of ventilatory frequency is mainly altered. In animals whose articular receptors are anesthetized, the injection of 28882 Ba decreases but does not completely suppress the ventilatory reaction to passive movement. Perhaps muscle spindle receptors and articular receptors are incompletely inhibited by the drugs; alternatively other types of limb mechanoreceptors may also be involved in the reflex hyperpnea. These experimental results show that in the dog a neurogenic ventilatory stimulus originates in muscles spindle and articular receptors.

The influence of exercise on blood borne substrates in relation to plasma catecholamine (CA) levels has been studied in untrained subjects (eight men and eight women). Subjects pedalled a bicycle ergometer for 20 min at a workload approximating to 80% maximal aerobic power. During exercise women reacted similarly to men except that their weight loss and hematocrit were significantly lower. At the end of the bicycling test, plasma dopamine (DA), norepinephrine (NE) and epinephrine (E) concentrations increased similarly in both groups. There was no significant difference in blood energy substrates between men and women except that the plasma free fatty acid (FFA) level was significantly higher in the female. When fitness levels were similar, the previously reported sex-related difference in response to exercise seemed to disappear. The lack of correlation between blood borne substrates variations and CA changes raised the question whether other hormonal factors combined with CA could play a role in the mobilization of energy substrates during exercise.

1. Maximal oxygen uptake (VO2 max) was determined in 451 boys and girls ranging from 11 to 16 years and divided in two groups. Group I (n = 287) was considered as an untrained reference group. Group II (n = 174) was regularly trained. This group concerned school-children affiliated to a swimming club and trained 5 to 10 h per week. Body growth is nearly the same in the two groups until puberty but, at 15-16 years in the boys, 14-16 years in the girls, height and weight are higher in group II. 2. In group I, between 11 and 16 years, VO2 max increases by 50% in boys against only 25% in girls. For the same age, VO2 max remained smaller in girls, even before puberty although there is no difference in body growth. At 11 years, specific VO2 max averaged 47 ml . min-1 . kg-1 in boys and 40 ml . min-1 . kg-1 in girls and decreases with age only in sedentary girls down to 37 ml . min-1 . kg-1. From the results presented here it appears that maximal oxygen uptake in the average french schoolchild is similar to those of subjects from different countries with same cultural and socio-economical level. 3. In group II, VO2 max is similar in both sexes at 11-12 years old, and then up to 16 years of age increases more rapidly in boys (+100%) than in girls (+50%). Specific VO2 max ranges between 57 and 62 m. min-1 . kg-1 in boy swimmers and averages 53 ml . min-1 . kg-1 in girl swimmers. The influence of physical training on aptitude development is discussed and compared with previously published data.

To investigate the relationship between dopamine (DA) released into the bloodstream and sympathoadrenal activity, levels of free DA, norepinephrine (NE), and epinephrine (E) in plasma were recorded in four dogs subjected to three tests: treadmill exercise at two work levels [55 and 75% maximal O2 uptake; 15 min], normobaric hypoxia (12% O2; 1 h), combined exercise and hypoxia. Normoxic exercise induced slight nonsignificant decreases in the arterial partial pressure of O2 (PaO2), increases in NE [median values and ranges during submaximal work vs. rest: 1086 (457–1,637) vs. 360 (221–646) pg/ml; P less than 0.01] and E [277 (151–461) vs. 166 (95–257) pg/ml; P less than 0.05], but it failed to alter the DA level. Hypoxia elicited large decreases in PaO2 [hypoxia vs. normoxia: 42.8 (40.3–50.0) vs. 97.6 (83.2–117.6) Torr; P less than 0.01], increases in DA [230 (105–352) vs. 150 (85–229) pg/ml; P less than 0.01] and NE [383 (219–1,165) vs. 358 (210–784) pg/ml; P less than 0.05], but it failed to alter the E level. Combined exercise and hypoxia further increased NE levels but did not alter the DA response to hypoxia alone. The data indicate that free DA in plasma may vary independently of the sympathoadrenal activity.

The sympathoadrenal contribution to cardiorespiratory response elicited by hypoxia and/or exercise was assessed in the dog. The increased plasma norepinephrine (NE) and dopamine (DA) levels which follow hypoxia (fraction of inspired O2 equals 0.12) while epinephrine (E) remained unchanged ruled out the possibility of a primacy of the adrenal medulla in the response to hypoxia. In contrast to the lack of effect of hypoxic exposure, the adrenal medulla was substantially stimulated during exercise. The exercise-induced sympathoadrenal response remained unchanged during hypoxia as compared to normoxia when expressed as function of relative work intensity. Nevertheless at a given oxygen uptake, all plasma catecholamines were increased by hypoxia. These modifications in hormonal milieu failed, however, to alter the cardiac responses to exercise but were associated with a change in breathing pattern.

Seven male sedentary human subjects were studied during intense muscular work (80% of maximal oxygen uptake) performed either for 15 min or until exhaustion (mean duration: 47 +/- 2 min). Plasma catecholamines were estimated before and after the experiment by means of an original fluorimetric assay. Epinephrine or norepinephrine were individually isolated from plasma and assayed in single extracts by a highly sensitive fluorimetric method. Epinephrine and norepinephrine levels as low as 15 ng per liter were detectable by this procedure in human plasma. The adrenergic pattern was found to be greatly different from one subject to another and related to emotivity: the effect of this factor was revealed by the predominance of epinephrine in plasma at rest or under exercise (ratio NA/A less than 1). In nonemotive subjects (ratio NA/A greater than 1 at rest) plasma epinephrine and norepinephrine increased progressively during exercise. Increments after exercise were higher for norepinephrine changes; however, the fact that epinephrine concentrations correlated significantly with norepinephrine suggests a simulataneous and coordinated stimulation of adrenal glands and orthosympathetic nervous system. In emotive subjects (ratio NA/A less than 1 at rest) the apprehension of muscular work promoted a difference in catecholamine responses: norepinephrine release was not affected by subject's anxiety, while epinephrine secretion, already elevated before the test, reached a high degree of magnitude in the first minutes of muscular work, remaining nearly constant until exhaustion. Physical training of nonemotive subjects, during 2 months with two intense exercises by a week, reduced strongly norepinephrine release after exhaustive muscular work. In the same conditions, the adrenal-medullary response was not significantly modified when compared with untrained subjects. Our results suggest that the adrenergic behaviour during exercise is a function of effort intensity to be supplied; catecholamines seem to be important factors in regulating body homeostasy during muscular work in man. In addition, emotive subjects exhibit amplified adrenal-medullary response, which may be related to psychological stimuli.

The purpose of this review is to analyze the different factors which intervene with respect to the ability to perform intense exercises of long duration. This ability implies : (a) a high level of maximal oxygen uptake (Vo 2 max) and (b) a great endurance, i.e. the capacity of maintaining for a long time a high percentage of this Vo2 max. First of all, the values Vo2 max usually recorded on normal subjects are given, as well as those of subjects specially trained for endurance events ; then the factors which condition a high level of Vo2 max are described. These factors consist on great capacity in all of the links of the oxygen transport system. These capacities appear to be essentially dependant on the genetic endowment, but their maximal size can only by attained through intensive training. Endurance can be defined as the maximal period of time during which a given percentage of the Vo2 max can be sustained. The values recorded on normal subjects and on those specially trained for endurance events are given, and then the factors conditioning a high level of endurance are studied. Endurance appears to depend on the feeding of muscular fibers with energentic substrates. Training permits the muscles to store large quantities of glycogen. It also seems to enable the organism to increase the percentage of energetic substrates made up by lipids. This latter ability in associated with an alteration of the endocrine reactions induced by exercise. Finally, endurance is accompanied by an ability of the body to store and to eliminate the heat produced during exercise.

O2 chemoreflex drive of ventilation was studied before and after an intravenous infusion of L-norepinephrine (9 microgram/min), inducing a plasmatic hormone concentration similar to that obtained during submaximal exercise. The ventilation increasing rapidly at the beginning of the infusion was stabilized after 30 min : the ventilation was two times the reference value. The O2 chemoreflex drive of ventilation increased during norepinephrine infusion. When man was transiently switched from hypoxia to pure O2 (O2 test) the maximal fall of ventilation was two times the reference response. This increase in the chemoreflex drive, although the physico-chemical blood state was unchanged, may be explained by a norepinephrine chemoreceptor sensitization. Such a mechanism could partly explain the increase of O2 chemoreflex drive observed during muscular exercise.

During the last two decades, numerous investigations have been conducted to determine the degree of involvement and mechanism of action of various factors responsible for ventilatory adaptation to exercise in human. The neuromechanical ventilatory system plays a role, exercise ventilation representing a compromise between the necessity of maintaining an adequate level of chemical arterial stimulus and of avoiding mechanical overload and, consequently, respiratory fatigue. The role of arterial chemoreceptors is essential and that of muscular chemoreceptors likely. The limb mechanoreceptors also play a role essentially via small nerve fibers on the other hand. To date, there is no experimental evidence of ventilatory reflexes elicited by pulmonary chemoreceptors. Further, the action of cardiopulmonary baroreceptors was proved only in extraphysiological conditions in animals. It is also possible that a feed-forward mechanism originating in the central nervous system plays an important role. In conclusion, the time course of pulmonary ventilation during exercise could be explained by the action of humoral and neurogenic stimuli.

The effects of training alone or in combination with long-term, non-selective, beta-adrenergic blockade on histochemical and biochemical properties of fast-twitch [extensor digitorum longus muscle (EDL)] and slow-twitch [soleus muscle (Sol)] muscle were analyzed in spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto strain rats (WKY). Fiber type distribution of Sol was drastically modified in SHR with fewer type I fibers and more type IIA fibers. No such histochemical alterations were observed in EDL. While prolonged swimming training remained ineffective in inducing both histochemical and biochemical improvement in WKY, SHR displayed a significant enhancement of capillarization and oxidative capacity in both Sol and EDL. However, in long-term beta-blocks rats training failed to improve significantly the oxidative capacity of SHR muscles, suggesting that beta-adrenoreceptor stimulation is necessary for a fully efficient adaptation of muscular metabolism to physical training.

The fast component of the ventilatory changes that occur at the transition phases of exercise was studied in awake dogs trained to run on a treadmill. Two questions were examined: firstly, is the fast ventilatory component modified by changes in venous return to the lungs, such as those consecutive either to increased work loads or to beta adrenergic blockade?, and secondly, is this component altered by central ventilatory depressants? The results showed that at the onset of exercise, there is no correlation between the instantaneous increment in ventilation and the intensity of exercise, but at the end of the treadmill run, the fall in ventilation is closely linked to the power of the work performed. Ventilatory transients observed either at the start or at the end of exercise remain unaffected by administration of a beta-adrenergic blocking agent. But central depressant effects on ventilation caused by narcotic analgesics or hypnotic drugs altered the breathing pattern of the fast component of exercise-induced ventilatory changes. It is concluded that the instantaneous changes in ventilation occurring at the transition phases of exercise are controlled by mechanoreceptor mechanisms, but cerebral control is superimposed on the reflex control in regulating both tidal volume and breathing rate.

The ventilatory changes as function of time or power depend on the type of exercise. However, in any case, two kinds of factors are involved in these changes : fast, neurogenic, factors and other factors, slower, which are thought to be humoral. Neurogenic stimuli arise from the periphery and from the central nervous system. Peripheral stimuli are induced by the repetitive changes of muscle length and by the motion of articulations. Ventilatory output is also increased by stimuli coming from motor centers. These two kinds of factors induce a ventilatory increase at the start of exercise ("accrochage ventilatoire"). Both chemical and physical stimuli act as humoral factors. The arterial PO2 is scarcely reduced even during maximal exercise, but the increased blood level of norepinephrine may account for the enhanced sensitivity of the centers to the oxygen drive. The sensitivity of the respiratory centers to PaCO2 is not increased. The pH is lowered and can reach 7.15 during very intense exercise. tthis acidity may account for the increased ventillatoy output under these circumstances. The increased body temperature may partly explain the progressive increase of ventilatory output during long lasting exercise, but it does not change the alveolar ventilation. It thus appears that the exercise ventilatory behaviour meets the metabolic, acid-base balance and thermolytic requirements.