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The aim of the study was to investigate peak anaerobic power during all-out exercise in patients with COPD. Twenty patients (ten women, ten men) [FEV1=50.5 (7.6)% of predicted] and 11 healthy subjects (six women, five men) performed: (1) three maximal sprints on a cycle ergometer to measure peak anaerobic power (Pmax) and optimal velocity (Vopt), (2) assessment of whole-body composition by dual-energy X-ray absorptiometry (DEXA) and (3) assessment of mean habitual daily energy expenditure (MHDEE). Pmax was 30% lower in COPD than in healthy subjects [22.9 (7.1) vs. 32.8 (5.6) W kg-1 (legs FFM), P<0.001]. Nevertheless, Vopt was similar in both series. In COPD, Pmax was lower in women than in men [21.4 (7.7) vs. 23.8(6.4) W kg-1 (legs FFM), P<0.05]. Vopt was lower in women than in COPD men [72.6 (11.3) vs. 89.3 (13.8) rpm, P<0.05]. MHDEE was lower in COPD than in healthy subjects [8019 (1254) vs. 9093 (1660) kJ day-1]. In COPD, MHDEE was lower in women than in men (P<0.001). This study demonstrates that in COPD patients, the decrease in peak anaerobic power could play a role in their specific muscular dysfunction. Considerable differences were observed in peripheral muscle function, body composition and MHDEE between women and men. The skeletal muscle of women and men may therefore adapt to COPD in different ways.

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INTRODUCTION: The modifications of gas exchange on exercise reflect the consequences of the control and limits of adaptation of the respiratory apparatus to the mechanical loads imposed on the muscles and the oxygen requirements of the organism. In the majority of cases, even if the thoraco-pulmonary apparatus is perfectly adapted to the increase in these requirements, the balance between the metabolic demands of the tissues and the pulmonary supply appears difficult to satisfy beyond certain limits without hypoxaemia, particularly in those subjects with a low ventilatory response to exercise. Based on the populations reported in the literature the functional limits of the control of the thoraco-pulmonary system and the possible modifications of the structures of the lung are discussed for each of these mechanisms. STATE OF KNOWLEDGE: At certain levels of duration and intensity of exercise there is an increase in the alveolar-arterial oxygen gradient [P(A-a)O2] associated inconsistently with a fall in PaO2. It is mainly the use of inert gas techniques that has established over many years the respective roles of the different possible patho-physiological mechanisms: shunt, unequal distribution of VA/Q ratios, limitation of alveolar-capillary diffusion and its components. The inequalities of VA/Q increase at low levels of exercise but beyond certain levels of VO2 limitation of oxygen diffusion may develop. In effect, particularly in subjects capable of high levels of exercise, the interaction between diminished transit time of the red cells in the pulmonary capillaries and possible delay in equilibration of partial pressures between the blood and gas phases may create a limitation of diffusion. This added to the inequalities of distribution of VA/Q and reduction in PVO2 leads, in certain subjects, to a transitory exercise induced hypoxaemia. VIEWPOINTS AND CONCLUSIONS: New techniques of investigation seem to be necessary to clarify the sources of the observed changes and the development of modifications of pulmonary structure that establish the functional limits of the lungs on exercise. It remains to demonstrate the true impact of these anomalies on the limitation of human performance.

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BACKGROUND: The aim of the study was to investigate dynamic muscle function during all-out exercise in patients with chronic obstructive pulmonary disease (COPD) and to observe the relationship between body composition and skeletal muscle function. MATERIAL AND METHODS: Eight patients (FEV1: 53.0 +/- 9.3%) performed three tests i) three maximal sprints on a specialised cycle ergometer to assess individual Velocity-Power relationship, and measure of maximal anaerobic power (Pmax), optimal velocity (Vopt), ii) assessment of whole-body and subregional fat-free mass (FFM) by dual-energy X-ray absorptiometry, iii) determination of maximal oxygen consumption. RESULTS: Maximal anaerobic power and corresponding optimal velocity were 3.9 +/- 1.6 W x kg(-1) et 85.4 +/- 17.0 rpm, respectively. COPD showed a 30% decrease of Pmax, compared to healthy older subjects (5.6 +/- 1.1 W x kg(-1)). No such difference was observed with Vopt (85.4 +/- 13.0 rpm vs 86.8 +/- 9.5 rpm). Pmax and Vopt were highly significantly correlated with lower extremities FFM, but not with airflow obstruction parameters. CONCLUSION: Our results showed that skeletal muscle function parameters such as Pmax and Vopt could characterise peripheral muscle weakness of COPD.

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In this study, we examined the effect of creatine ingestion on muscle power output, muscle phosphocreatine resynthesis, inorganic phosphate and pH during repeated brief bouts of maximal exercise. Nine healthy males performed maximal plantar flexion before and after creatine ingestion (20 g x day(-1) for 6 days). The experimental protocol consisted of five 8 s bouts (bouts 1-5) interspersed with 30 s recovery, followed by bouts 6 (8 s) and 7 (16 s) separated by 1 and 2 min, respectively. Muscle phosphocreatine, inorganic phosphate and pH were estimated every 16 s by 31P magnetic resonance spectroscopy. After creatine ingestion, muscle power output increased by approximately 5% (P< 0.05) from bouts 3 to 7 and muscle phosphocreatine resynthesis increased (P< 0.05) during 10 min recovery. The higher phosphocreatine concentration observed after only 30 s of recovery was accompanied by lower inorganic phosphate accumulation and higher pH. Strong correlations were found between exercise power restoration and the corresponding pre-exercise phosphocreatine and inorganic phosphate concentrations and muscle pH after creatine ingestion. The better maintenance of muscle power output observed after creatine ingestion was attributed to a higher rate of phosphocreatine resynthesis, lower accumulation of inorganic phosphate and higher pH.

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The thioalkylation of unprotected 5-bromo-5-deoxy-D-ribono, D-arabinono, and D-xylono-1,4-lactone was performed with the alkylthiol-sodium hydride reagent. The corresponding 5-S-alkyl-5-thio-D-pentono-1,4-lactones were isolated in good yields (82-95%). Reduction with NaBH(4) of these derivatives gave the 1-S-alkyl-1-thio-L-ribitols, D-lyxitols and L-xylitols in 85-96% yields.

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Spontaneously hypertensive rats and Lewis rats differ in their anxiety levels and in their serotonergic and corticotropic responses to stress. Since the 5-HT transporter plays a key role in 5-HT neurotransmission, we have analyzed whether hippocampal and/or striatal [(3)H]5-HT reuptake kinetics are altered by stress in a strain-dependent manner. It was found that forced swimming, treadmill running, or restraint for 30 min affected neither hippocampal nor striatal [(3)H]5-HT reuptake K(m) and V(max) values in the two rat strains. This study, which is the first to examine the impact of acute stress on [(3)H]5-HT reuptake with respect to the nature of the stressor, the brain region analyzed, and the rat strain, could reinforce the hypothesis that extracellular 5-HT levels during stress are representative of 5-HT release.

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Cough is a reflex phenomenon occurring when sensitive receptors located in the larynx and upper airways are activated. These receptors generate information which reaches the central nervous system. The central organization of the cough reflex loop is poorly understood. The afferent pathways originate in receptors situated under and between airway epithelial cells. Most are rapidly adapting receptors (RAR) linked to myelinized fibers of the vagus nerve which can be directly stimulated by cough-inducing agents. Other receptors generate information carried by non-myelinized C fibers. When activated, these receptors release neuropeptides leading to neurogenic inflammation which can also activate RARs. The threshold of the cough reflex and its expression thus depends on a complex interaction between RARs and C fiber receptors with peripheral and central components. A better understanding of the mechanisms triggering cough and its control would be most useful for optimal management of patients with cough problems.

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The ability to cope with exercise training depends both on environmental and genetic background; however, whether the genetic status may affect (i) the hormonal status of trained subjects and, (ii) its responses to a heterotypic stressor is unknown. Herein, we have used Spontaneously Hypertensive Rats (SHR) and Lewis rats, that differ with regard to their psychoneuroendocrine profiles, to study the influences of an 8-week training programme and/or a 1-h immobilization stress on plasma adrenocorticotropin (ACTH) and corticosterone levels. In addition, brain serotonin metabolism was also measured as an index of neurochemical reactivity to stress. The amplitude of immobilization-elicited increases in ACTH levels which differed with the rat strain (Lewis > SHR), was amplified by prior training; besides, training decreased the strain difference in basal corticosterone (SHR > Lewis) and affected corticosterone response to immobilization in a strain-dependent manner. Thus, immobilization, which increased corticosterone levels in sedentary Lewis but not in SHRs, did not reveal interstrain differences in trained rats. Taken with the observation of a stimulatory effect of training on adrenal weights in SHRs, but not in Lewis, it is concluded that the effects of training on the corticotropic axis depend on the genetic profile of the individual. Lastly, training amplified the response of midbrain (but not striatum or hippocampus) serotonin metabolism to immobilization in a strain-independent manner although the levels of serotonin precursor, namely tryptophan, varied with training and immobilization in a strain-dependent manner. This study shows that some neuroendocrine and neurochemical effects of training undergo interindividual variability.

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OBJECTIVE: Leptin concentrations in humans are known to decrease in response to fasting. The aim of this work was to investigate whether leptin levels might also be modified by exercise-induced negative energy balance. SUBJECTS: Eight male runners reported in the morning from 0800 to 1200 h for (i) one resting session (sitting) and (ii) one exercise-and-rest session (2 h run and 2 h rest). MEASUREMENTS: Plasma leptin, free fatty acids (FFA), glycerol, cortisol and salivary cortisol were assayed in both sessions at 1200 h. RESULTS: After exercise-and-rest the leptin concentrations were lower than after rest (1.7 +/- 0.1 vs 2.5 +/- 0.2 micrograms/l, P < 0.05), i.e. a mean decrease of 30.3 +/- 4.5% (range 9.5-45.8). Plasma FFA, glycerol and cortisol concentrations increased: FFA 0.78 +/- 0.08 vs 0.18 +/- 0.04 mmol/l, glycerol 0.13 +/- 0.01 vs 0.04 +/- 0.01 mmol/l, and cortisol 428 +/- 36 vs 279 +/- 27 nmol/l. A negative correlation was found between plasma FFA and leptin levels (r = -0.5, P < 0.05) and between plasma glycerol and leptin levels (r = -0.05, P < 0.05). No correlation was found between leptin and cortisol levels. CONCLUSIONS: In normal subjects with low body fat, a strenuous exercise-and-rest lowers leptin levels by a mean of 30%. A role of lipolysis possibly via increased plasma free fatty acids and glycerol levels is suggested. Cortisol does not seem to be involved.

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The postexercise alteration in pulmonary gas exchange in high-aerobically trained subjects depends on both the intensity and the duration of exercise (G. Manier, J. Moinard, and H. Stoïcheff. J. Appl. Physiol. 75: 2580-2585, 1993; G. Manier, J. Moinard, P. Techoueyres, N. Varène, and H. Guénard. Respir. Physiol. 83: 143-154, 1991). In a recent study that used lung computerized tomography (CT), evidence was found for accumulation of water within the lungs after exercise (C. Caillaud, O. Serre-Cousine, F. Anselme, X. Capdevilla, and C. Prefaut. J. Appl. Physiol. 79: 1226-1232, 1995). On representative slices of the lungs, mean lung density increased by 0.040 +/- 0.007 g/cm(3) (19%, P < 0.001) in athletes after a triathlon. To verify and quantify the mechanism, we determined the change in pulmonary density and mass after strenuous and prolonged exercise using another exercise protocol and methodology for CT scanning. Nine trained runners (age 30-46 yr) volunteered to participate in the study. Each subject ran for 2 h on a treadmill at a rate corresponding to 75% of maximum O(2) consumption. CT measurements were made before and immediately after the exercise test with the subject supine and holding his breath at a point close to functional residual capacity. The lungs were scanned from the apex to the diaphragm and reconstructed in 8-mm-thick slices. Attenuation values of X-rays in each part of the lung were expressed in Hounsfield units (HU), which are related to density (D): D = 1 + HU/1,000. No significant alteration in pulmonary density (0.37 +/- 0.04 vs. 0.35 +/- 0.03, not significant) was observed after the 2-h run test. Although lung volume slightly increased (change of 166 +/- 205 ml, P < 0.05), lung mass remained stable because of a change in density distribution. We failed to detect any changes in postexercise lung mass, suggesting that other mechanisms need to be considered to explain the observed alterations in pulmonary gas exchange after prolonged strenuous exercise.

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OBJECTIVE: The aim of this study was to address the effect of endurance training on monocyte glucocorticoid sensitivity in vitro. METHODS: For this purpose, in vitro dexamethasone inhibition of lipopolysaccharide (LPS)-induced interleukin-6 (IL-6) secretion in cultures of peripheral monocytes was compared in 6 untrained subjects (UT) and in 6 endurance-trained (ET) men at 0800 h, 24 h after the end of the last session of exercise (ET men). Moreover, to test the plasticity of these monocytes glucocorticoid sensitivity in ET men, the effect of an acute bout of exercise was further studied 2 h after the end of a 2-h run at 65-75% VO2max (1200 h) and compared to the results of UT after 4 h of rest. RESULTS: At 0800 h, monocytes from ET were more sensitive to LPS: lower LPS concentration in ET compared to UT men (0.003 vs. 0.03 microg/ml) induced similar IL-6 concentrations in both ET and UT men (168.4 +/- 29.9 pg/ml with 0.003 microg/ml LPS vs. 160.1 +/- 34.4 pg/ml with 0. 03 microg/ml LPS, ET vs. UT, respectively, P > 0.05 for IL-6). No effect of sampling time was observed in UT subjects (0800 h vs. 1200 h). This was not the case for ET as at 1200 h, compared to pre-exercise values, the LPS-induced IL-6 production was not significantly different from that obtained in UT. Moreover, when sensitivity to dexamethasone (Dex) was studied and expressed as the percent inhibition of stimulated IL-6 production with 0.3 microg/ml LPS, at 0800 h the percent inhibition was lower in ET subjects compared to UT (P < 0.01 ET vs. UT men) for each Dex concentration used [10-11-10-8 M]. After exercise, the inhibitory effect of Dex on LPS-induced IL-6 production was restored in ET and was no longer significantly different from that obtained in UT. CONCLUSION: We demonstrate in vitro plasticity of monocyte glucocorticoid sensitivity of endurance trained men, with training-induced decreased glucocorticoid sensitivity and acute exercise-induced return to the levels of the control untrained men.

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beta-agonist bronchodilators are known to influence gas exchange and ventilation-perfusion relationships in asthmatic patients, where they induce hypoxaemia via hypoxic vasoconstriction. As this effect could have serious consequences in chronic obstructive pulmonary disease (COPD) patients with chronic hypoxaemia, alternative agents have been sought. It has been shown that inhaled anticholinergic drugs may be of value in this condition. In the present study, we compared the effects of salbutamol (Sb) and ipratropium bromide (IB) inhalation on gas exchange in 15 patients with stable COPD. All patients had a history of COPD (mean arterial oxygen tension (Pa,O2) = 8.2 +/- 1.0 kPa (61.8 +/- 7.3 mmHg) forced expiratory volume in one second (FEV1) = 39 +/- 12%; FEV1/vital capacity (VC) = 42 +/- 6%) and no evidence of acute respiratory failure. Haemodynamic and gas exchange data were recorded after right catheterization by the multiple inert gas elimination technique. Measurements were made under basal conditions, after two puffs of freon propellant (placebo) and after two puffs of either 200 micrograms Sb or 200 micrograms IB in a randomized design. Sb and IB reduced airway resistances to the same extent, but had no significant influence on the haemodynamic and ventilation parameters. There was a slight but significant decrease in arterial carbon dioxide tension (Pa,CO2) = 6.0 +/- 0.8 versus 6.4 +/- 0.8 kPa (45.4 +/- 5.9 versus 47.9 +/- 6.3 mmHg) p < 0.05 with an enhanced perfusion distribution heterogeneity and a slight improvement in ventilation homogeneity shown by a decrease of the decimal logarithm of SD of the ventilation distribution (LogSDV) after inhalation of IB relative to control. Since these alterations did not affect arterial oxygen tension we concluded that inhalation of these doses of salbutamol or ipratropium bromide do not affect gas exchange in patients with stable chronic obstructive pulmonary disease. The normal home treatment: inhalation of two puffs of these bronchodilating drugs thus appears to be safe. The choice of agent will depend on the extent of the bronchodilator effect in a given individual.

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OBJECTIVE: The present study was conducted in order to describe human hypothalamo-pituitary adrenal (HPA) axis adaptation in a model of repeated physical stress (endurance training) that causes a moderate increase in cortisol levels. SUBJECTS: We performed the same stimulation tests (adrenal stimulation with ACTH or pituitary stimulation with combined CRH/LVP) in a population of 8 endurance-trained athletes in two distinct situations: resting (baseline cortisol values) and 2 h after the end of strenuous exercise (increased cortisol values) to evaluate the HPA axis sensitivity to endogenous sustained increases in cortisol concentrations. MEASUREMENTS: During these tests, saliva and plasma cortisol (Fs and Fp, respectively) were assessed and compared. RESULT: Cortisol values in both plasma and saliva at the end of 2 h of exercise were significantly higher than in rested controls: Fs 11.5 +/- 1.3 vs 6.5 +/- 0.8 nmol.l-1 and Fp 428 +/- 36 vs 279 +/- 27 nmol.l-1 (post exercise vs post rest sessions, respectively, P < 0.001 for both). After either hormone test (CRH/LVP or ACTH), cortisol levels in plasma and saliva increased similarly when rest was compared to post exercise. Saliva variations (delta %) under exogenous hormone stimulation were dramatically greater than plasma variations. For example, under ACTH stimulation, the relative increments in cortisol were on control day: delta Fs 980 +/- 139 vs delta Fp 218 +/- 43% (saliva vs plasma, respectively, P < 0.05) and on exercise day: delta Fs 605 +/- 89 vs delta Fp 102 +/- 14% (saliva vs plasma, respectively, P < 0.05). CONCLUSIONS: In endurance-trained athletes, displaying a moderate but sustained endogenous cortisol increase: (1) ACTH responses following pituitary stimulation are not blunted, (2) cortisol responses following maximal adrenal stimulation are not blunted. Our results favour the hypothesis of a decreased pituitary sensitivity to cortisol negative feedback whereas the hypothesis of a major decreased adrenal sensitivity to ACTH was discarded. The greater ability of saliva assays to detect a cortisol increase strongly supports its use in the study of HPA physiology, whether under basal or dynamic conditions.

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The hypothalamo-pituitary-adrenal axis is involved throughout the exercise-recovery cycle. Nevertheless, differences in hormone responses during early recovery between sedentary and endurance trained subjects are not well known. The aim of this preliminary study was to monitor plasma cortisol and adrenocorticotropic hormone (ACTH) concentrations both during and after the end of running exercise performed by four endurance trained adults (marathon men) compared to four sedentary subjects. Two parameters, i.e. intensity and duration, were changed on 4 consecutive days. The 1st day (D0) was spent in the laboratory: all blood samples were obtained at rest to determine diurnal variations of each hormone. On the following days (D1-D4) the subjects exercised: D1 and D2 brief (20 min), light (50% maximal heart rate HRmax, D1) or strenuous (80% HRmax, D2), D3 and D4 prolonged (120 min), light (D3) or strenuous (D4). In both groups, neither brief (D1, D2) nor prolonged light exercise (D3) induced any significant variation in plasma ACTH or cortisol concentrations. Plasma ACTH and cortisol concentrations increased only if the exercise was intense and prolonged (D4). The training factor did not modify the intensity or duration thresholds for the activation of the pituitary-adrenocortical response to exercise in the conditions of our experiment. However, during immediate recovery from the four exercise regimens, the plasma ACTH concentrations of the marathon men were constantly above the values of the sedentary subjects, although plasma cortisol concentration remained similar in both groups. As an indirect means of evaluating the relationships between ACTH and cortisol we compared the areas under the cortisol and ACTH curves (AUC) from 0.5 to 3.5 h during recovery from D1 to D4 compared to D0 at the same time. Cortisol AUC were similar in the sedentary subjects and marathon men although the ACTH AUC were different in the sedentary subjects and marathon men, suggesting a change in the pituitary-adrenal relationship at some yet indeterminate level. During the immediate recovery from exercise whatever its intensity, the magnitude of the ACTH response was increased in the trained subjects but with a reduced effect upon its target, the adrenal glands. This phenomenon has not been described in the literature. Two non-exclusive phenomena may be involved, i.e. a decreased adrenal sensitivity to ACTH stimulation, and/or a decreased hypothalamo-pituitary axis sensitivity to cortisol negative feedback.

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In men, the hypothalamic-pituitary-testicular axis controls the secretion of testosterone which, in this sex, is a major anabolic hormone. Physical exercise modulates testosterone concentration, affecting the whole axis by poorly understood mechanisms. We have reported in this preliminary study the short and long-term effects of exercise on the function of the gonadotropic axis in trained compared to untrained subjects. Environmental factors known to interfere with pituitary function were minimized. Four marathon and four sedentary men, were studied during 5 days successively using different combinations of two factors: duration and intensity of running tests. Day 0 (D0) was a rest day, and the exercises were: D1 and D2 brief (20 min), light (50% maximal heart rate, HRmax, D1) or intense (80% HRmax, D2), D3 and D4 prolonged (120 min) and light (50% HRmax, D3) or intense (80% HRmax, D4). Testosterone (free and total) and luteinizing hormone (LH) concentrations were measured before, during and after exercise. The baseline concentrations of plasma testosterone were lower in the long distance runners than in the sedentary group [41.8 (SEM 5.5) vs 64.5 (SEM 7.9) pmol.l-1, respectively; P < 0.05]. This phenomenon was centrally mediated as LH concentration was apparently inappropriately low [3.4 (SEM 0.4) vs 4.3 (SEM 1.0) UI.l-1; P > 0.05]. Light to moderate exercise did not modify testosterone and LH concentrations. Conversely, intense and prolonged exercise increased testosterone concentration [73.2 (SEM 9.0) vs 92 (SEM 11.0) pmol.l-1 in the long distance runners and sedentary group, respectively; P < 0.05] and lowered LH concentrations [2.1 (SEM 0.3) vs 3.4 (SEM 0.3) UI.l-1 in the long distance runners and sedentary group, respectively; P < 0.05 compared to D0, at the same time]. In our conditions of exercise, negative feedback of testosterone upon LH persisted, as positive feedback of low testosterone concentrations was apparently lacking (inappropriately low LH concentration with regard to low basal testosterone concentration).

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Nitric oxide (NO) has been reported to be an endothelium-derived relaxing factor, and hypoxic pulmonary vasoconstriction seems to be enhanced by inhibitors of endothelially dependent vascular relaxation. We examined the circulatory effects of inhalation of 15 ppm NO in air in 14 hypoxic patients suffering from chronic obstructive pulmonary disease (COPD). Of these patients 4 breathed 100% O2 before NO. The effects of NO inhalation on pulmonary gas exchange were also studied in 12 of these patients using the multiple inert gas elimination technique, 3 of whom breathed air, 100% O2, and 15 ppm NO in air in succession. Under baseline conditions, both mean +/- SD pulmonary artery pressure and pulmonary vascular resistance were increased (Ppa = 24.3 +/- 10.4 mm Hg and PVR = 3.3 +/- 1.1 mm Hg/L/min, respectively). Although the pulmonary circulatory effects were not immediate, with no detectable changes after 1 min NO inhalation, Ppa and PVR fell significantly (-19.1 +/- 10.5%, p < 0.02 and -29.3 +/- 15.1%, p < 0.02, respectively) after 10 min NO inhalation. Moreover, the extent of the NO-induced reduction in Ppa was found to depend on the level of baseline pulmonary arterial hypertension. No systemic circulatory effects were observed. The mean VA/Q ratio and the dispersion of ventilation and blood flow distributions were not altered by NO inhalation, although there was a significantly higher percentage of ventilation (7.3 +/- 7.3%, p < 0.05) in poorly and unperfused areas (VA/Q > 10).(ABSTRACT TRUNCATED AT 250 WORDS)

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To determine the effect of maximal exercise on alveolocapillary membrane diffusing capacity (Dm), 12 professional handball players aged 23.4 +/- 3.3 (SD) yr were studied before and during early recovery from a progressive maximal exercise [immediately (t0), 15 min, and 30 min (t30) after exercise]. Lung capillary blood volume and Dm were determined in a one-step maneuver by simultaneous measurement of CO and NO lung transfer (DLCO and DLNO, respectively) with use of the single-breath breath-hold method. At t0, DLCO was elevated (13.1 +/- 12.0%; P < 0.01) but both DLNO and Dm for CO remained unchanged. Between t0 and t30, both DLCO and DLNO decreased significantly. At t30, DLCO was not different from the control resting value. DLNO (and consequently Dm for CO) was significantly lower than the control value at t30 (-8.9 +/- 8.1%; P < 0.01). Lung capillary blood volume was elevated at t0 (18.0 +/- 19.0%; P < 0.01) but progressively decreased to near control resting values at t30. Differences in the postexercise kinetics of both DLCO and DLNO point to a role of the transient increase in pulmonary vascular recruitment during the recovery period. We concluded that Dm was somewhat decreased in the 30 min after maximal exercise of short duration, but the exact pulmonary mechanisms involved remain to be elucidated.

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We investigated interactions between cardiac output, VA/Q distribution pattern, pulmonary gas exchange, O2 transport, and tissue oxygenation in 16 patients during the acute phase of pulmonary embolism (PE). The effects of breathing room air, O2 therapy (FIO2 = 0.40) (11 patients), and dobutamine (four patients) were studied after right catheterization using the multiple inert gas elimination technique. The pattern of VA/Q ratio distributions was found to depend essentially on cardiac output level. The individual blood flow perfusing ventilated areas was found to be inversely related to the mean VA/Q ratio of blood flow distribution. PVO2 was directly related to cardiac index (p less than 0.02), and negatively related to the mean VA/Q of blood flow distribution. In view of the influence of low VA/Q ratios and PVO2 on arterial hypoxemia, our results showed that the heart's response to PE conditioned the strategy of pulmonary gas exchange and O2 transport. Oxygen breathing led to a slight but consistent fall in cardiac output (-0.6 +/- 0.5 L/min, p less than 0.01). However, although PaO2 remained normal and PVO2 was slightly improved, we found no evidence for a role of hypoxic pulmonary vasoconstriction in the pulmonary hypertension observed during the acute phase of PE. Administration of dobutamine improved O2 transport and tissue oxygenation, although PaO2 remained constant or even fell in some cases because of increased VA/Q mismatch.

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To determine the effect of strenuous prolonged exercise on systolic and diastolic left ventricular function, 11 non-elite marathon runners aged 37 +/- 7 years (mean +/- SD) were studied before and during early recovery from a marathon race. Cavity dimensions, wall thickness, and fractional shortening were computed from two-dimensionally guided M-mode echocardiograms. Doppler left ventricular inflow tract recordings were analysed for peak early and late velocities and their ratio. In seven subjects, heart frequency was recorded throughout the race. These subjects ran the marathon at 87 +/- 4% of their maximal heart rate. Left ventricular diastolic dimension was slightly reduced at the end of the race (49.4 +/- 4.2 mm to 47.3 +/- 5.1 mm; P less than 0.05). Fractional shortening remained unchanged, although blood pressure (P less than 0.001) and systolic wall stress (P less than 0.01) were decreased. The left ventricular filling pattern was unchanged, and the ratio of early to late velocities remained constant. These results suggest that the fractional shortening was a result of the opposing effects of changes in preload and afterload. However, the absence of a change in the end systolic dimension, despite a marked reduction in afterload and the occurrence of septal akinesia in one subject after the race could only suggest that strenuous prolonged exercise may alter myocardial performance.

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