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Biomedical subjects

U Boutellier

Publications and source records attributed to U Boutellier.

At least 19 recordsLinked to original sources
PubMed1992

The respiratory system as an exercise limiting factor in normal sedentary subjects.

The present study was undertaken to investigate the respiratory system as an exercise limiting factor. Breathing and cycle endurance (i.e. the time until exhaustion at a given performance level) as well as physical working capacity 170 (i.e. the exercise intensity corresponding to a heart rate of 170 beats.min-1 on a cycle ergometer) were determined in four healthy sedentary subjects. Subsequently, the subjects trained their respiratory system for 4 weeks by breathing daily about 90 l.min-1 for 30 min. Otherwise they continued their sedentary lifestyle. Immediately after the respiratory training and 18 months later, all performance tests carried out at the beginning of the study were repeated. The respiratory training increased breathing endurance from 4.2 (SD 1.9) min to 15.3 (SD 3.8) min. Cycle endurance was improved from 26.8 (SD 5.9) min to 40.2 (SD 9.2) min whereas physical working capacity 170 remained essentially the same. During the endurance cycling test in the respiratory untrained state, the subjects continuously increased their ventilation up to hyperventilation [ventilation at exhaustion = 96.9 (SD 23.6) l.min-1] while after the respiratory training they reached a respiratory steady-state without hyperventilation [ventilation at exhaustion = 63.3 (SD 14.5) l.min-1]. The absence of this marked hyperventilation was the cause of the impressive increase of cycle endurance in normal sedentary subjects after respiratory training. The effects gained by the respiratory training were completely lost after 18 months. Our results indicated that the respiratory system was an exercise limiting factor during an endurance test in normal sedentary subjects.

Adult↗
PubMed1992

The respiratory system as an exercise limiting factor in normal trained subjects.

Recently, we have shown that an untrained respiratory system does limit the endurance of submaximal exercise (64% peak oxygen consumption) in normal sedentary subjects. These subjects were able to increase breathing endurance by almost 300% and cycle endurance by 50% after isolated respiratory training. The aim of the present study was to find out if normal, endurance trained subjects would also benefit from respiratory training. Breathing and cycle endurance as well as maximal oxygen consumption (VO2max) and anaerobic threshold were measured in eight subjects. Subsequently, the subjects trained their respiratory muscles for 4 weeks by breathing 85-160 l.min-1 for 30 min daily. Otherwise they continued their habitual endurance training. After respiratory training, the performance tests made at the beginning of the study were repeated. Respiratory training increased breathing endurance from 6.1 (SD 1.8) min to about 40 min. Cycle endurance at the anaerobic threshold [77 (SD 6) %VO2max] was improved from 22.8 (SD 8.3) min to 31.5 (SD 12.6) min while VO2max and the anaerobic threshold remained essentially the same. Therefore, the endurance of respiratory muscles can be improved remarkably even in trained subjects. Respiratory muscle fatigue induced hyperventilation which limited cycle performance at the anaerobic threshold. After respiratory training, minute ventilation for a given exercise intensity was reduced and cycle performance at the anaerobic threshold was prolonged. These results would indicate the respiratory system to be an exercise limiting factor in normal, endurance trained subjects.

Adolescent↗
PubMed1991

[Performance development in the Engadin ski marathon].

All competitions of the Engadin Ski marathon were analyzed in order to pursue the development of the participants' performances over time. Of special interest was the influence of the recently introduced free skating technique on the finish times. Statistical computations are based on quantiles (x0.1, x0.25, x0.5, x0.75, x0.9). Since the first competition in 1969, there is a continuous increase of performance. The introduction of the fast freestyle-technique didn't lead to a visible improvement of the performances. Probably, other variables like growing importance of leisure-time sport-leading to greater performance capability of the participants- and considerable progress in the development of the equipment contributed to the performance progress over time.

Female↗
PubMed1990

Oxygen transport system before and after exposure to chronic hypoxia.

Maximal VO2 on the treadmill (VO2max) and on the bicycle ergometer (VO2peak), maximal cardiac output (Qmax), by a CO2 rebreathing method, maximal heart rate (HRmax), blood hemoglobin concentration (Hb), and hematocrit (Hct) were measured on six subjects before (B) and 3 weeks after (A) prolonged exposure to chronic hypoxia. It was observed that after high-altitude exposure VO2max, VO2peak, and Qmax were lower (P less than 005) than before [A: 4.13 +/- 0.67; 3.28 +/- 0.41 and 16.89 +/- 2.49 (l/min +/- SD); B: 4.39 +/- 0.39; 3.53 +/- 0.34 and 21.81 +/- 1.27, respectively], whereas Hb and Hct were larger (A: 162 +/- 8 g/l and 0.46 +/- 0.02; B: 142 +/- 7 and 0.41 +/- 0.02) and HRmax was unchanged (178 +/- 7 vs 175 +/- 9 bts/min). Thus, the calculated stroke volume of the heart and the Hb flow at VO2 peak were lower in A than in B (95 +/- 15 vs 124 +/- 7 ml and 2,723 +/- 307 vs 3,129 +/- 196 g/min) (P less than 0.05, respectively), whereas the arteriovenous O2 difference was greater in A than in B (195 +/- 16 vs 162 +/- 19 ml O2/l; P less than 0.05). At any given submaximal work load, VO2 and HR were the same in B and in A, whereas Q was lower in A by approximately 2-3 l/min. However, because of the increased Hb, leading to a higher arterial O2 content, at any work load the O2 flow remained unchanged.

Acclimatization↗
PubMed1990

Aerobic performance at altitude: effects of acclimatization and hematocrit with reference to training.

The aim of the present investigation carried out on six members of the Swiss 1981 Mt. Lhotse Shar (8398 m) expedition was to assess the quantitative role of some of the determinants of VO2max at altitude. The loss of VO2max expected for the investigated altitude range was partially counterbalanced by the training undergone by the subjects during the approach to the base camp. delta VO2max was -18% instead of the expected 30%-35%. The VO2max value attained shortly after arrival at 5200 m was not significantly increased (38.4 +/- 4.4 SD vs 36.9 +/- 3.3 ml O2.kg-1.min-1) with a progressive rise of Hb from 16.4 +/- 0.8 to 18.2 +/- 1 g/100 ml of blood. Hemodilution, by oral administration of 2 liters of the isosmolar solution ISOSTAR, at 5200 m led to a 2.3% decrease of Hct and a 7.3% reduction of VO2max per kg of body weight. The product of heart rate times systolic arterial pressure ("double product") was somewhat (but not significantly) greater in hypoxia than in normoxia at all work loads. The maximum value for this product, however, was 10%-15% lower at 5200 than at 400 m. The increase of Hb from 15.1 +/- 0.7 to 17.1 +/- 1.6 g/100 ml of blood pre- to post-expedition was not accompanied by a significant increase of VO2max determined at 400 m either absolute or per kg of body weight.

Acclimatization↗
PubMed1989

[Physiological basis for the measurement of aerobic capacity].

Aerobic capacity should be determined from the anaerobic threshold and not from VO2max. The measurement of the anaerobic threshold via heart rate, introduced 1982 by Conconi et al. (3) and meanwhile improved, seems to be of practical value, although a number of fundamental questions remain open. A great advantage is its simple use when compared with the more complicated laboratory methods (respiratory or lactate curves). The determination of the anaerobic threshold based on the heart rate allows, in addition, to optimize the endurance training owing to the help of heart rate control.

Heart Rate↗
PubMed1989

Rate of erythropoietin formation in humans in response to acute hypobaric hypoxia.

This study was carried out to investigate the early changes in erythropoietin (EPO) formation in humans in response to hypoxia. Six volunteers were exposed to simulated altitudes of 3,000 and 4,000 m in a decompression chamber for 5.5 h. EPO was measured by radioimmunoassay in serum samples withdrawn every 30 min during altitude exposure and also in two subjects after termination of hypoxia (4,000 m). EPO levels during hypoxia were significantly elevated after 114 and 84 min (3,000 and 4,000 m), rising thereafter continuously for the period investigated. Mean values increased from 16.0 to 22.5 mU/ml (3,000 m) and from 16.7 to 28.0 mU/ml (4,000 m). This rise in EPO levels corresponds to 1.8-fold (3,000 m) and 3.0-fold (4,000 m) increases in the calculated production rate of the hormone. After termination of hypoxia, EPO levels continued to rise for approximately 1.5 h and after 3 h declined exponentially with an average half-life time of 5.2 h.

Adult↗
PubMed1988

Efficiency of work performance and contraction velocity in isotonic tetani of frog sartorius.

Mechanical work, ATP, ADP, PC, free creatine and lactate concentrations were determined on IAA poisoned frog sartorii tetanically stimulated in humidified N2 at 10 degrees C in isotonic conditions (0.25 or 0.45 Po). Tetanus duration was 0.35 s, number of tetani was varied from 0 (rest) to 25 (exhaustion). The mechanical work performed per mole ATP + PC split (W*P) amounted on the average to 16.7 kJ/mol. It was observed, however, that W*P increased from about 13 to about 24 kJ/mol with decreasing ATP concentration from about 2 (resting value) to about 1 mumol/g and that this decrease in ATP was associated with a decrease of the shortening (and relaxation) speed of the muscle to about 30% of the values observed on the first tetanus. It is concluded that the thermodynamic efficiency of muscle contraction, calculated from the ratio of WP* (measured) to the thermodynamic affinity (free energy change) of ATP hydrolysis (estimated) increases from about 0.3 to about 0.5 with decreasing ATP concentration and shortening speed.

Adenosine Triphosphate↗
PubMed1988

Effects of atropine and propranolol on the respiratory, circulatory, and ECG responses to high altitude in man.

In order to analyze the respiratory, cardiovascular, and ECG responses to acute hypoxic hypoxia, three experimental series were carried out in a randomized manner on 11 healthy, unacclimatized volunteers at rest during standardized stepwise exposure to 6000 m (PAO2 35.2 +/- 2.9 mmHg/4.7 +/- 0.4 kPa) in a low-pressure chamber a) without (control), b) with propranolol, and c) with atropine combined with propranolol. The results show that hypoxic hyperventilation and alveolar gases are not affected by activation of the sympatho-adrenal axis or by parasympathetic withdrawal. Sympathetic activity, however, increases heart rate, stroke volume (pulse pressure), estimated cardiac output and systolic blood pressure, whereas decreased parasympathetic activity increases heart rate and estimated cardiac output, but lowers stroke volume. The fall in peripheral resistance, observed during progressive hypoxia in all three groups, is thought to be due to hypoxia-induced depression of the vasomotor center. At altitude catecholamine secretion and vagal withdrawal synergistically account in the ECG for the R-R shortening, the relative Q-T lengthening, the elevation of the P wave and the ST-T flattening. Probable direct hypoxic effects on the heart are the increase in P-Q duration and the minor but still significant depression of the T wave. It is concluded that at altitude increased sympatho-adrenal and decreased parasympathetic activity is without effect on hypoxic hyperventilation, but accounts for most of the cardiovascular and ECG changes. Diminution of sympathetic activity and imminent vagotonia arising after acute ascent to 6000 m probably reflect hypoxia of the central nervous system.

Acclimatization↗
PubMed1988

The effect of gravity on the response of ventilation to abrupt change in FICO2.

Recently, Arieli and Farhi (1987) formulated a model for a previous suggestion made by their group that an increased ventilation as gravity increases is due to reduced perfusion of the respiratory center which causes an elevation of tissue PCO2. Extending the model to the dynamic response, we predict a slower ventilatory response to CO2 breathing as gravity increases. To test this prediction, ventilatory response to 5% CO2 was studied in 11 seated subjects at +1 and +2 Gz in a human centrifuge. Five of these subjects were studied at +3 Gz as well. In addition, ventilatory response to 5% CO2, using breath-by-breath analysis, was measured in three subjects in supine and upright postures. The ventilatory response (mainly through tidal volume) was faster as gravity increased from +1 to +2 and to +3 Gz, and from supine to the upright position. These findings disagree with the model prediction. Therefore, an alternative explanation is suggested based on the response of CO2 sensitive stretch receptors in the lung. Increased gravity causes increased ventilation, reduction of cardiac output and increased VA/Q mismatch; all enlarge the part of the lung with low CO2 where responsiveness of the CO2 sensitive stretch receptors is large.

Adult↗
PubMed1987

Respiratory phase detection and delay determination for breath-by-breath analysis.

The delay between air flow and gas concentration signals is generally assumed to be constant within a breath as well as from breath to breath, but it was not possible to examine the constancy of the delay with the delay determination techniques so far available. Thus we developed new methods for respiratory phase detection and delay determination. The presented algorithm for the detection of the start of inspiration and expiration (phase detection) replaces the generally used valve assembly with two pneumotachographs. Now, the pneumotachograph is used in a bidirectional mode, but with a volume criterion for phase detection replacing the less reliable threshold criterion. To measure the delay between flow and gas concentration signals, a test gas is periodically injected as a marker. This test gas contains less N2 than ambient air. Therefore, the delay is determined as time between the moment of injection and the drop of N2. These two methods rendered it possible to examine delay variations and their consequences. The investigation of various breathing patterns demonstrated that the usually assumed errors caused by delay uncertainty are underestimated. We suggest reliance on a breath-by-breath delay determination to account for delay variations.

Capillaries↗
PubMed1986

Influence of breathing frequency and tidal volume on cardiac output.

The aim of our experiment was to investigate the influence of increasing either breathing frequency or tidal volume on cardiac output (Q), in normocapnia. We measured Q with a CO2 rebreathing method in 6 men and 6 women in the sitting and the supine position, imposing different breathing patterns: in one set of experiments tidal volume was kept constant at 1 L while breathing frequency was randomly changed between 20, 30 and 40 breaths/min; in another breathing frequency was kept constant at 30 breaths/min while tidal volume was randomly altered between 1, 1.5 and 2 L. Switching from open circuit breathing to rebreathing (for measurement of Q) required no change in breathing pattern. From the beginning, CO2 was added to the inspired gas to maintain end-tidal FCO2 at 0.054, so as to obtain steady state conditions throughout the measurements. Q rose significantly when tidal volume was increased (938 ml/L rise in tidal volume when sitting, and 743 ml/L when supine). Breathing frequency had an insignificant effect (213 ml/10 breaths frequency increase when sitting and 142 ml/10 breaths when supine). The greater influence of ventilation on Q when sitting than when supine is best explained by the fact that in the latter position venous return is already high. There are no demonstrable differences in this effect between males and females.

Adult↗
PubMed1986

A fundamental problem in determining functional residual capacity or residual volume.

To measure a lung volume that is not directly accessible, one often follows dilution of a single-gas tracer, present initially only in the lung or in a rebreathing bag. The final volume available to the tracer is assumed to be the sum of the two initial components. Since O2 is taken up and CO2 is eliminated during the few breaths required for mixing, the total volume changes. The error in lung volume due to this volume change can exceed 10%. In this paper we 1) present theoretical and experimental data to demonstrate the effect of CO2 and O2 exchange, 2) introduce a general equation, based on N2 and Ar, which allows one to circumvent the problems created by these fluxes, and 3) show the pitfall of the back-extrapolation approach for a single tracer.

Biometry↗
PubMed1986

Effect of water immersion on cardiopulmonary physiology at high gravity (+Gz).

We compared the cardiopulmonary physiology of eight subjects exposed to 1, 2, and 3 Gz during immersion (35 degrees C) to the heart level with control dry rides. Immersion should almost cancel the effects of gravity on systemic circulation and should leave the lung alone to gravitational influence. During steady-state breathing we measured ventilation, O2 consumption (VO2), CO2 production, end-tidal PCO2 (PACO2), and heart frequency (fH). Using CO2 rebreathing techniques, we measured cardiac output, functional residual capacity, equivalent lung tissue volume, and mixed venous O2 content, and we calculated arterial PCO2 (PaCO2). As Gz increased, ventilation, fH, and VO2 rose markedly, and PACO2 and PaCO2 decreased greatly in dry ride, but during immersion these variables changed very little in the same direction. Functional residual capacity was lower during immersion and decreased in both the dry and immersed states as Gz increased, probably reflecting closure effects. Cardiac output decreased as Gz increased in dry rides and was elevated and unaffected by Gz during immersion. We conclude that most of the changes we observed during acceleration are due to the effect on the systemic circulation, rather than to the effect on the lung itself.

Adult↗
PubMed1985

Ventilation and CO2 response during +Gz acceleration.

During foot-to-head acceleration (+Gz) ventilation increases despite a drop in alveolar PCO2. In order to investigate the underlying mechanisms, we measured ventilation (VE), VO2, VCO2 and PACO2, cardiac output (Q) and mixed venous CO2 concentration (CVCO2) using non-invasive techniques in 5 subjects breathing either air or a gas mixture containing 5% CO2 at +1, +2 and +3 Gz in a human centrifuge. Arterial PCO2 was calculated from Fick's equation, using CVCO2, Q and VCO2. VE increased from 8.7 to 18.0 L/min during air breathing and from 19.6 to 36.9 L/min during CO2 breathing at +1 and +3 Gz, respectively. The corresponding values for PACO2 are 37.9 vs 26.9 Torr and 47.8 vs 46.4 Torr. Q dropped from 5.9 to 4.8 L/min during air breathing and remained the same during CO2 breathing (6.7 vs 6.5 L/min). As the decrease of PaCO2 almost paralleled that of PACO2, the arterio-alveolar CO2 difference increased only slightly. The CO2 response curve shifts gradually to the left with an increase in +Gz, a fact that does not support the hypothesis that foot-to-head acceleration increases CO2 sensitivity.

Acceleration↗
PubMed1984

After effects of chronic hypoxia on VO2 kinetics and on O2 deficit and debt.

Single breath O2 consumption (PB = 730, FI02 = 0.21) was measured at rest, during 10 min cycloergometric exercise at 125 W, and in the following recovery phase in seven subjects before, and 12 days after 6 weeks at 5,200 m or above. Peak blood lactate after exercise (Lâb) was measured. O2 deficits and debts and half times (t1/2) of the VO2 on- and off-kinetics were calculated. Before acclimatization, the VO2 on- and off-responses were close to a single exponential with t1/2 = 30 s. After return to sea level, the VO2 on-response curves were less steep in the initial phase, becoming closer to sigmoid. The t1/2, independent of the shape of the underlying function, was approximately 10 s longer. The VO2 off-responses during the initial 4 min of recovery were the same before and after acclimatization. Average O2 deficit was approximately 320 ml larger after acclimatization: the fast component of O2 debt was similar. Since steady state VO2 and Lâb were the same, the O2 deficit difference can be attributed to a greater utilization of O2 stores. Of these, about 1/3 is explained in terms of increased mixed venous blood O2 stores, due to increased [Hb] (16.6 vs 14.9 g X dl-1), while the remainder is ascribed essentially to increased Mb-bound O2. O2 stores utilization and replenishment is presumed to occur when muscle metabolism is low; as a consequence, while it is clearly detectable from the shape of the initial phase of the VO2 on-response, during recovery it is spread throughout, thus becoming more difficult to appreciate.

Acclimatization↗
PubMed1983

[Effect of catecholamines and propranolol on the acute acclimatization to high altitude in man].

The venous concentrations of epinephrine and norepinephrine and changes in ventilation, respiratory gases, circulation and ECG were determined in 20 young healthy male medical students during standardized stepwise ascent to 6000 m in a low pressure chamber, once without (control) and once with beta-receptor blockade (propranolol). The results show that the plasma concentration of norepinephrine increased significantly as a result of hypoxic hypoxia. The moderate increase in epinephrine was, besides the minor but significant hypoxic influence, mainly due to psychic tension. Since beta-receptor blockade does not prevent the respiratory and circulatory adjustment, beta-adrenergic stimulation is not thought to be necessary at altitude. Propranolol, on the contrary, lowers the hypoxia-induced increase in cardiac output and diminishes the ECG changes, in particular the S-T depression, significantly. By antagonizing the effects of epinephrine and by its central effects, propranolol improves subjective tolerance to altitude, and, on the other hand, by economizing the cardiac work load, the objective ability to withstand oxygen want.

Acclimatization↗