Exercise-induced hypoxemia in athletes: Role of inadequate hyperventilation

Summary These experiments examined the exercise-induced changes in pulmonary gas exchange in elite endurance athletes and tested the hypothesis that an inadequate hyperventilatory response might explain the large intersubject variability in arterial partial pressure of oxygen (P _a0₂) during heavy exercise in this population. Twelve highly trained endurance cyclists [maximum oxygen consumption (VO_2max) range = 65-77 ml·kg^–1·min^–1] performed a normoxic graded exercise test on a cycle ergometer toVO_2max at sea level. During incremental exercise atVO_2max 5 of the 12 subjects had ideal alveolar to arterial P02 gradients (P _A-aO₂) of above 5 kPa (range 5-5.7) and a decline from restingP _aO₂ (P _aO₂) 2.4 kPa or above (range 2.4-2.7). In contrast, 4 subjects had a maximal exercise (P _A-aO₂) of 4.0-4.3 kPa with P _aO₂ of 0.4-1.3 kPa while the remaining 3 subjects hadP _A-aO₂ of 4.3-5 kPa with P _aO₂ between 1.7 and 2.0 kPa. The correlation between P_AO₂ andP _aO₂ atVO_2max was 0.17. Further, the correlation between the ratio of ventilation to oxygen consumption VSP _aO₂ and arterial partial pressure of carbon dioxide VSP _aO₂ atVO_2max was 0.17 and 0.34, respectively. These experiments demonstrate that heavy exercise results in significantly compromised pulmonary gas exchange in approximately 40% of the elite endurance athletes studied. These data do not support the hypothesis that the principal mechanism to explain this gas exchange failure is an inadequate hyperventilatory response.     

Is the balance between skeletal muscular metabolic capacity and oxygen supply capacity the same in endurance trained and untrained subjects?

We attempted to test whether the balance between muscular metabolic capacity and oxygen supply capacity in endurance-trained athletes (ET) differs from that in a control group of normal physically active subjects by using exercises with different muscle masses. We compared maximal exercise in nine ET subjects [Maximal oxygen uptake (VO₂max) 64 ml kg⁻¹ min⁻¹ ± SD 4] and eight controls (VO₂max 46 ± 4 ml kg⁻¹ min⁻¹) during one-legged knee extensions (1-KE), two-legged knee extensions (2-KE) and bicycling. Maximal values for power output (P), VO₂max, concentration of blood lactate ([La⁻]), ventilation (VE), heart rate (HR), and arterial oxygen saturation of haemoglobin (SpO₂) were registered. P was 43 (2), 89 (3) and 298 (7) W (mean ± SE); and VO₂max: 1,387 (80), 2,234 (113) and 4,115 (150) ml min⁻¹) for controls in 1-KE, 2-KE and bicycling, respectively. The ET subjects achieved 126, 121 and 126% of the P of controls (p < 0.05) and 127, 124, and 117% of their VO₂max (p < 0.05). HR and [La⁻] were similar for both groups during all modes of exercise, while VE in ET was 147 and 114% of controls during 1-KE and bicycling, respectively. For mass-specific VO₂max (VO₂max divided by the calculated active muscle mass) during the different exercises, ET achieved 148, 141, and 150% of the controls’ values, respectively (p < 0.05). During bicycling, both groups achieved 37% of their mass-specific VO₂ during 1-KE. Finally we conclude that ET subjects have the same utilization of the muscular metabolic capacity during whole body exercise as active control subjects.     

Quantitative continuous measurement of partial oxygen pressure on the skin of adults and new-born babies

Summary It is possible to perform continuous quantitativeP _{O 2} measurements on vasodilated skin by means of surface Pt electrodes according to Clark when the electrode is fixed to the skin with a synthetic plastic material and in situ calibration is performed. A new in situ calibration of theP _{O 2} electrode is described. At first the skinP _{O 2} increases with O₂ inspiration. After perfusion stop the skinP _{O 2} shows a linear decrease because of the skin respiration, down to aP _{O 2} at which hemoglobin liberates chemically bound O₂. As thisP _{O 2} value of hemoglobin is known it is possible to use it for calibrating the electrode. TheP _{O 2} of normal skin is about 0–7 Torr. After vasodilation obtained by rubbing with a nicotinic acid derivate (Finalgon^®, Anasco, Wiesbaden),P _{O 2} increases to a mean value of 38.1 (±8.1) Torr (n=77). Under these conditions, skinP _{O 2} reaches arterial values never in adults and rarely in new-born babies.Part of the results have been reported during the Workshop on Oxygen Transport in Tissue, 19–22 July, 1971, in Dortmund and at the 4. Deutsche Kongress für Perinatale Medizin, 4–6 Nov. 1971, in Berlin. The study was carried out with partial support from the German Research Council (DFG).     

Measurements of the criticalPO2 of renal mitochondria

Summary The criticalPO₂ of isolated mitochondria from the cortex and outer medullary region of the rat kidney was polarographically measured using the O₂-platinum-electrode. With succinate for substrate at 37°C and 25°C mean criticalPO₂-values of 1.54 Torr (SD±0.58) and 1.01 Torr (SD±0.46) were found resp. Using malate for substrate the corresponding mean values were 0.92 Torr (SD±0.28 and 0.65 Torr (SD±0.25). A positive linear relationship between O₂-uptake and criticalPO₂ was observed. The results are compared with data on the O₂-consumption of rat and dog renal cortex in situ and withPO₂-values measured in the same organs. On the basis of the results here presented with regard to the lowestPO₂-values found in the renal cortex of the dog an additional explanation of the flow limitation of the renal O₂-consumption is developed.This work was supported by the Deutsche Forschungsgemeinschaft, Bonn-Bad Godesberg.     

Exercise during hyperoxia and hyperbaric oxygenation

Physiological reactions during exercise were tested under hyperoxic and hyperbaric conditions. In 6 subjects walking and running at increasing speeds on a treadmill, maximum performance showed little change when the respired air was enriched with O₂. Maximum metabolism, measured by CO₂ production, increased by 3.2%. During exercise on a bicycle ergometer, maximum O₂ uptake increased by 3% in 5 subjects breathing pure O₂ at 1 ATA. During hyperoxia the maximum O₂ consumption measured at 2 and 3 ATA did not differ significantly from that measured at 1 ATA. Heart rate showed highly comparable maximum values under the various experimental conditions. During submaximal exercise, heart rate was consistently lower when the subjects breathed O₂. The O₂-linked difference became slighter with every increase in work load. Under hyperbaric and hyperoxic conditions, ventilation was invariably reduced during exercise.     

Effects of two successive maximal exercise tests on pulmonary gas exchange in athletes

Pulmonary extravascular water accumulation may be involved in exercise-induced hypoxaemia in highly aerobically trained athletes. We hypothesized that if such an alteration were present in elite athletes performing a maximal exercise test, the impairment of gas exchange would be worse during a second exercise test following the first one. Eight male athletes performed two incremental exercise tests separated by a 30-min recovery period. Pulmonary gas exchange and ventilatory data were measured during exercise tests performed in normoxia. Arterial blood samples were drawn each minute during rest, exercise, and recovery. Pulmonary diffusing capacity for CO (D _LCO) was measured at rest, after the first (T1) and the second (T2) test. All the subjects underwent a spirometric test at rest and after T2. Maximal and recovery data for 0₂ uptake and minute ventilation were not statistically different between T1 and T2. Partial pressure of arterial 0₂ (P _aO₂) decreased during both tests but was lower during T2 for rest, 60 W, and 120 W (P < 0.02). Alveolar-arterial difference in partial pressure of 0₂ (P _A-a0₂) increased during both the tests but was significantly larger during T2 for rest, 60 W, and 120 W (P < 0.01). The P _aO₂ and P _A-aO₂ data at maximal exercise were not significantly different between T1 and T2. Compared to rest, P _A-aO₂ remained significantly larger during recovery for both T1 and T2 (P < 0.0001). The P _A-aO₂ during T2 recovery was larger than T1 recovery (P < 0.008). Spirometric data did not change. The D _LCO measurements after T1 and T2 were not significantly different from rest. These results showed an alteration of P _aO₂ and P _A-aO₂ during T1, which tended to be worse during and after T2; however, these data do not allow us to make a definitive statement as to the cause of the hypoxaemia. Our study confirmed that exhausting exercise caused hypoxaemia. It also demonstrated that the disturbance in pulmonary gas exchange persisted for at least 30 min following the end of the exercise period and became worse during submaximal intensities of the following incremental exercise test.     

Physiological responses to intermittent and continuous exercise at the same relative intensity in older men

We investigated the physiological responses in older men to continuous (CEx) and intermittent (IEx) exercise. Nine men [70.4 (1.2) years, O_2peak: 2.21 (0.20) l min^–1; mean (SE)] completed eight exercise tests (two CEx and six IEx) on an electronically braked cycle ergometer in random order. CEx and IEx were performed at 50% and 70% O_2peak. IEx was performed using 60sE:60sR, 30sE:30sR and 15sE:15sR exercise to rest ratios. The duration of exercise was adjusted so that the total amount of work completed was the same for each exercise test. Oxygen uptake (O₂), minute ventilation (_E) and heart rate (HR) were measured at the mid-point of each exercise test. Arterialised blood samples were obtained at rest and during exercise and analysed for pH and PCO₂. At the same relative intensity (50% or 70% O_2peak), IEx resulted in a significantly lower (P<0.01) O₂, _E and HR than CEx. There were no significant differences (P>0.05) in O₂, _E and HR measured at the mid point of the three exercise to rest ratios at 50% and 70% O_2peak. pH and PCO₂ during CEx and IEx at 50% O_2peak were not significantly different from rest. CEx performed at 70% O_2peak resulted in significant decreases (P<0.05) in pH and PCO₂. There was a significant decrease (P<0.05) in pH only during the 60sE:60sR IEx at 70% O_2peak. Changes in arterialised PCO₂ during the 60sE:60sR, 30sE:30sR and 15sE:15sR at both 50% and 70% O_2peak exercise tests were not significant. When exercising at the same percentage of O_2peak and with the total amount of work fixed, IEx results in significantly lower physiological responses than CEx in older men. All results are given as mean (SE).     

Acute EPOC response in women to circuit training and treadmill exercise of matched oxygen consumption

The purpose of the study was to evaluate the effects of circuit training (CT) and treadmill exercise performed at matched rates of oxygen consumption and exercise duration on elevated post-exercise oxygen consumption (EPOC) in untrained women, while controlling for the menstrual cycle. Eight, untrained females (31.3±9.1 years; 2.04±0.26 l min^–1 estimated VO_2max; BMI=24.6±3.9 kg/m²) volunteered to participate in the study. Testing was performed during the early follicular phase for each subject to minimize hormonal variability between tests. Subjects performed two exercise sessions approximately 28 days apart. Resting, supine energy expenditure was measured for 30 min preceding exercise and for 1 h after completion of exercise. Respiratory gas exchange data were collected continuously during rest and exercise periods via indirect calorimetry. CT consisted of three sets of eight common resistance exercises. Pre-exercise and exercise oxygen consumption was not different between testing days (P>0.05). Thus, exercise conditions were appropriately matched. Analysis of EPOC data revealed that CT resulted in a significantly higher (p<0.05) oxygen uptake during the first 30 min of recovery (0.27±0.01 l min^–1 vs 0.23±0.01 l min^–1); though, at 60 min, treatment differences were not present. Mean VO₂ remained significantly higher (0.231±0.01 l min^–1) than pre-exercise measures (0.193±0.01 l min^–1) throughout the 60-min EPOC period (p<0.05). Heart rate, RPE, V_E and RER were all significantly greater during CT (p<0.05). When exercise VO₂ and exercise duration were matched, CT was associated with a greater metabolic disturbance and cost during the early phases of EPOC.     

The role of fitness on VO2 and VCO2 kinetics in response to proportional step increases in work rate

Summary The purpose of this study was to determine the effect of fitness and work level on the O₂ uptake and CO₂ output kinetics when the increase in work rate step is adjusted to the subject's maximum work capacity. Nine normal male subjects performed progressive incremental cycle ergometer exercise tests in 3-min steps to their maximum tolerance. The work rate step size was selected so that the symptom-limited maximum work rate would be reached in four steps at 12 min in all subjects. Oxygen consumption (VCO₂) and carbon dioxide production VCO₂ were calculated breath by breath. For the group, the time (mean, SEM) to reach 75% of the 3-min response (T _0.75) for VO₂ increased significantly (P<0.01) at progressively higher work rate steps, being 53.3 (5.5) s, 63.5 (4.6) s, 79.5 (5.0) s, and 94.5 (5.8) s, respectively. In contrast, T _0.75 for VCO₂ did not change significantly [74.9 (7.4) s,. 75.6 (5.0) s, 85.1 (5.3) s, and 89.4 (6.3) s, respectively]. VCO₂ kinetics were slower than VO₂ kinetics at the low fractions of the subjects' work capacities but were the same of faster at the high fractions because of the slowing of VO₂ kinetics. The first step showed the fastest rise in VO₂. While VO₂ kinetics slowed at each step, they were faster at each fraction of the work capacity in the fitter subjects. The step pattern in VO₂ disappeared at high work rates for the less fit subjects. The heart rate response paralleled that of VO₂. We conclude that VO₂ and VCO₂ kinetics are slower in the less fit subjects but only VO₂ kinetics are significantly attenuated in response to proportional step increases in work rate.     

Exercise stimulus increases ventilation from maximal to supramaximal intensity

This study investigated the influence of an exercise stimulus on pulmonary ventilation (V _E) during severe levels of exercise in a group of ten athletes. The altered ventilation was assessed in relation to its effect on blood gas status, in particular to the incidence and severity of exercise induced hypoxaemia. Direct measurements of arterial blood were made at rest and during the last 15 s of two intense periods of cycling; once at an intensity found to elicit maximal oxygen uptake (VO_2max; MAX) and once at an intensity established to require 115% ofVO_2max (SMAX). Oxygen uptake (VO₂) and ventilatory markers were continually recorded during the exercise and respiratory flow-volume loops were measured at rest and during the final 30 s of each minute for both exercise intensities. When compared to MAX exercise, the subjects had higher ventilation and partial pressure of arterial oxygen (P _aO₂) during the SMAX intensity. Regression analysis for both conditions indicated the levels ofP _aO₂ and oxygen saturation of arterial blood (S _aO₂) were positively correlated with relative levels of ventilation during exercise. It was apparent that mechanical constraints to ventilate further were not present during the MAX test since the subjects were able to elevateV _E during SMAX and attenuate the level of hypoxaemia. This was also confirmed by analysis of the flow volume recordings. These data support the conclusions firstly, that overwhelming mechanical constraints onV _E were not present during the MAX exercise, secondly, the subjects exhibiting the most severe hypoxaemia had no consistent relationship with any measure of expiratory flow limitation, and thirdly, ventilatory patterns during intense exercise are strong predictors of blood gas status.     

Respiratory muscle endurance training in humans increases cycling endurance without affecting blood gas concentrations

Isolated respiratory muscle endurance training (RMT) can prolong constant-intensity cycling performance. We tested whether RMT affects O₂ supply during exercise, i.e. whether the partial pressure of oxygen in arterial blood (P _aO₂) and/or its oxygen saturation (S _aO₂) are higher during exercise after RMT than before. A group of 28 sedentary subjects were randomly assigned to either an RMT (n=13) or a control group (n=15). The RMT consisted of 40×30 min sessions of normocapnic hyperpnoea. The control group did not perform any training. Breathing and cycling endurance time as well as P _aO₂ and S _aO₂ during cycling at a constant intensity of 70% maximum power output were measured before and after the RMT or the control period. Mean breathing endurance increased significantly after RMT compared to control [RMT 5.2 (SD 2.9) vs 38.1 (SD 6.8) min, control 6.5 (SD 5.7) vs 6.4 (SD 7.6) min; P<0.01], as did mean cycling endurance [RMT 35.6 (SD 11.9) vs 44.0 (SD 17.2) min, control 32.8 (SD 11.6) vs 31.4 (SD 14.4) min; P<0.05]. The RMT did not affect P _aO₂ which ranged from 11.6 to 12.3 kPa (87–92 mmHg), and S _aO₂ which ranged from 96% to 98% throughout all tests. In conclusion, RMT substantially increased breathing and cycling endurance in sedentary subjects. These changes, however, cannot be attributed to increased O₂ supply, as neither P _aO₂ nor S _aO₂ were increased during exercise after RMT. Electronic Publication     

The oxygen supply of the rat kidney: Measurements of intrarenalpO2

Summary Using a newly developed platinum-O₂-microeletrode [30] based on the design ofSilver [37] the construction and properties of which are described,pO₂-measurements in the parenchyma of the blood-perfused and the cell-free perfused rat kidney were carried out.By continuous recording of thepO₂ during slow (150 ×min^–1) insertion of the O₂-electrode into the respiring tissue two regions of distinctly different meanpO₂-values were found. In the outer region which extends from the renal surface to a depth of about 3–4 mm (corresponding anatomically with the renal cortex) largepO₂-differences exist close to each other. In the blood-perfused kidney the maximum corticalpO₂-values lie in the range of arterialpO₂ the lowest values at about 10 Torr. In the cortex of the cell-free perfused kidney the maximumpO₂-values lie considerably below the arterialpO₂.In both the blood perfused and in the cell-free perfused kidney at centripetal movement of the O₂-electrode the cortical region of high and fluctuatingpO₂ is followed by a narrow zone (200 radial extension) of a steep decrease of the meanpO₂. At further insertion in both preparations thepO₂ remains at lowpO₂-values of ca. 10 Torr. Anatomically, this latter region of low and constantpO₂ corresponds to renal medulla and pelvis.By recording the decrease of parenchymalpO₂ after sudden stop of the perfusion attempts were made at measuring the critical local O₂-supply pressure. In the cortex of the cell-free perfused kidney critical local O₂-supply pressures between 6 and 28 Torr with a maximum abundance at 8 Torr were found.The qualitative and quantitative implications of the presented data on the conditions of parenchymal O₂-supply are discussed. The results are interpreted as an indication for the arteriovenous shunt (bypass)-diffusion of considerable amounts of oxygen, especially under the conditions of the cell-free perfusion. Furthermore, it follows from the data presented that even at high venous O₂-pressures and high meanpO₂-values in the parenchyma regions of local anoxia may exist.     

Pulmonary gas exchange and breathing pattern during and after exercise in highly trained athletes

Summary Highly trained athletes (HT) have been found to show arterial hypoxaemia during strenuous exercise. A lack of compensatory hyperpnoea and/or a limitation of pulmonary diffusion by pulmonary interstitial oedema have been suggested as causes, but the exact role of each is not clear. It is known, however, that interstitial pulmonary oedema may result in rapid shallow breathing (RSB). The purpose of this study was therefore twofold: firstly, to determine the exact role of a lack of compensatory hyperpnoea versus a widened in ideal alveolar minus arterial oxygen partial pressure difference [P _A(i)-aO₂] in the decrease in partial pressure of oxygen in arterial blood (P _aO₂) and, secondly, to detect RSB during recovery in HT. Untrained subjects (UT) and HT performed exhausting incremental exercise. During rest, exercise testing, and recovery, breathing pattern, respiratory gas exchange, and arterial blood gases were measured. The P _A(i)-aO₂ and the difference in tidal volume (V _T) between exercise and recovery for the same level of ventilation, normalized to vital capacity of the subject [V _T(%VC)], were then calculated. A large positive V _T (%VC) was considered to be the sign of RSB. HT showed a marked hypoxaemia (F=11.6, P < 0.0001), higher partial pressure of carbon dioxide in arterial blood (F= 3.51, P < 0.05), and lower ideal partial pressure of oxygen in alveolar gas (P < 0.001). The relationship between P _A(i)-aO₂ and oxygen consumption was the same for the two groups. The widening P _A(i)-aO₂ persisted throughout recovery for both HT and UT. The RSB was observed in HT during recovery. These results would suggest that the lack of compensatory hyperpnoea in HT during submaximal exercise was the major factor in the decrease in P _aO₂. The RSB and the widening P _A(i)-aO₂ during recovery would suggest that interstitial pulmonary oedema was involved during the strenuous exercise in the case of HT. Lastly, the wide P _A(i)-aO₂ observed in UT during recovery would suggest that an increase in extravascular pulmonary water may also have been involved for these subjects, although to a lesser extent.     

Direct determination of local oxygen consumption of the brain cortex in vivo

Summary A method is described to determine local oxygen consumption quantitatively in the brain cortex under in vivo conditions. Local oxygen consumption is calculated from the slope of local tissue P_{O 2} decrease during a few seconds of total ischemia of the brain for each second after the stop of circulation. The decrease of tissue P_{O 2} is recorded simultaneously at several measuring sites. To be independent of oxygen chemically bound to hemoglobin, tissue P_{O 2} values are raised above 100 Torr. The calculation of local oxygen consumption for each second during the short period of ischemia showed that the O₂ consumption remains constant only for a few seconds ranging from 5 to maximally 15 s at different locations. Then O₂ consumption decreases continuously although the tissue P_{O 2} values are still above the full saturation of hemoglobin. The rate of local oxygen consumption varies considerably at different measuring sites of the superficial layers of the brain cortex (cat). The mean value amounts to 3±1.5 ml O₂/100 g tissue and minute.     

Oxygen transport in guinea pigs native to high altitude (Junin,Peru, 4,105 m)

In guinea pigs native to high altitude in the Andes (Peru) the arterial and mixed-venousP _{O 2},P _{CO 2}, pH, and O₂ content were measured at high altitude during breathing ambient air.Identical measurements were done in Nijmegen, The Netherlands, on sea-level natives and on guinea pigs exposed for 4–5 weeks to simulated altitude in a low pressure chamber, while breathing ambient air (normoxia) or an hypoxic mixture of O₂ in N₂ with aP _{I O 2} similar to that of the ambient air at high altitude. A standard blood O₂ dissociation curve (ODC) was estimated in vitro (at pH=7.4 and 37.5°C), and a standard in vivo ODC was derived from measuredP _{O 2},S _{O 2} and pH in all three groups.Both guinea pigs native to natural or simulated high altitude had a higher hematocrit and blood O₂ capacity than sea-level controls. These increased altitude values were, however, almost the same as the sea-level values of man or rat. No difference in the ideal alveolararterialP _{O 2} difference or lung diffusing capacity for O₂ was found between (natural or simulated) high altitude animals and their corresponding controls, when measured at hypoxia. Mixed-venousP _{O 2} was higher in guinea pigs from the natural high altitude (but not in those from the low pressure chamber) when compared with control sea-level natives studied at hypoxia. No difference among groups in cardiac output was found, while breathing the same inspiratory mixture. In the guinea pigs native to high altitude a higher P₅₀ and a lower Hill numbern for the in vitro ODC were found when compared with the controls or with the guinea pigs exposed to simulated high altitude. This was not observed when the ODC's were estimated in vivo.The rather modest polycythemic response to high altitude in guinea pigs coincides with a low value of P₅₀, when related to body weight. In this respect the guinea pig seems to be more closely related to the typical high altitude mammals like Andean camelids and rodents than to man or rat that respond to high altitude with a pronounced polycythemia and possess a rather high P₅₀ with respect to body weight.All data obtained in Peru are part of the scientific material acquired during the Italian Lake Mountain Scientific Expedition to Peru, march and April 1978, under the direction of Prof. Dr. P. G. Data from the University of Chieti, Italy.Part of the results were presented at the 12. Atmungsphysiologische Arbeitstagung, Göttingen, FRG, January 26–27, 1979     

Reduced arterial O2 saturation during supine exercise in highly trained cyclists

Performance of intense dynamic exercise in highly trained athletes is associated with a reduced arterial haemoglobin saturation for O₂ (SaO ₂) and lower arterial PO ₂ (PaO ₂). We hypothesized that compared with upright exercise, supine exercise would be accompanied by a smaller reduction in SaO ₂ because of a lower maximal O₂ uptake (VPO _2max) and/or a more even ventilation–perfusion distribution. Eight elite bicyclists completed progressive cycle ergometry to exhaustion in both positions with concomitant determinations of ventilatory data, arterial blood gases and pH. During upright cycling VPO _2max averaged 75±1.6 mL O₂ min^-1 kg^-1 (±SEM) and it was 10.6±1.7% lower during supine cycling (P<0.001). Also the maximal pulmonary and alveolar ventilation were lower during supine cycling (by 15±2% and 21±3%, respectively; P< 0.001) which related to a 0.8±0.1 L lower tidal volume (P<0.001). In all subjects and independent of work posture PaO ₂ and SaO ₂ decreased from rest to exhaustion (from 99±3 to 82±2 Torr and 98.1±0.2 to 95.2±0.4%, respectively; P<0.001); alveolar–arterial PO ₂ difference increased from 6±2 to 37±3 Torr in both body positions. At exhaustion arterial PCO ₂ was lower in upright than in supine (33.4±0.6 vs. 35.9±0.9 Torr; P<0.01), suggesting a greater relative hyperventilation in upright. Arterial pH was similar in upright and supine at rest (both 7.41±0.01) and at exhaustion (7.31±0.01 vs. 7.32±0.01, respectively). We conclude that despite a lower VPO _2max and supposedly an improved ventilation–perfusion distribution, altering body position from upright to supine does not influence arterial O₂ desaturation during intense exercise.     

The effect of acute hypoxia on left ventricular function during exercise

The effect of acute hypoxia on the human left ventricular function during exercise was evaluated by 2D and Doppler echocardiography on 11 healthy male college students. Each subject completed 6-min moderate intensity (100 W) supine cycling exercises in normoxia and hypoxia, respectively. The concentration of inspired O₂ was adjusted to keep arterial hemoglobin O₂ concentration (SpO₂) at 88–92% during hypoxia. Doppler indices obtained were compared between normoxia and hypoxia. The left ventricular myocardial diastolic function was increased during exercise in hypoxia compared with normoxia. The peak velocity of early filling wave increased at rest (P < 0.05) and during exercise (P < 0.05 at second minute, and P < 0.01 at sixth minute) in hypoxia. The heart rate (P < 0.01) and cardiac output (P < 0.001) were elevated markedly at rest during hypoxia. The left ventricular systolic function variables, such as stroke volume, ejection fraction, and end-systolic volume were relatively unaltered during hypoxia compared with normoxia. The results suggest that acute hypoxia increases the left ventricular myocardial diastolic function during moderate intensity supine cycling exercise without affecting the systolic function.     

The effect of prolonged submaximal exercise on gas exchange kinetics and ventilation during heavy exercise in humans

This study compared ventilation, gas exchange (oxygen uptake, V̇O₂) and the surface electromyogram (EMG) activity of four major lower limb muscles during heavy exercise before (Pre-Ex) and after (Post-Ex) a sustained 90-min cycling exercise at 60% V̇O_2peak. The 90-min exercise was incorporated under the hypothesis that sustained exercise would alter substrate availability in the second exercise bout causing differences in fibre recruitment patterns, gas exchange and ventilation. Nine trained male subjects [V̇O_2peak=60.2 (1.7) ml·kg⁻¹·min⁻¹] completed two identical 6-min bouts of cycling performed at high intensity [~90% V̇O_2peak; 307 (6) W, mean (SE)]. Ventilation and gas exchange were measured breath-by-breath and the EMG was recorded during the last 12 s of each minute of the two 6-min bouts. EMG signals were analysed to determine integrated EMG (iEMG) and mean power frequency (MPF). V̇O₂ at min 3 and min 6 in Post-Ex were significantly higher (i.e., +201 and 141 ml·min⁻¹, respectively, P<0.05) than in Pre-Ex but there was a ~25% decrease of the slow component, taken as the difference between min 6 and min 3 [187 (27) vs 249 (35) ml·min⁻¹, respectively, P<0.05]. The greater whole-body V̇O₂ after 3 min of exercise in Post-Ex was not accompanied by clear alterations in the iEMG and MPF of the examined leg muscles. Ventilation and heart rate were elevated (~12–16 l·min⁻¹ and ~10 beats·min⁻¹, respectively, P<0.05) as were the ratios V̇ _E/O₂ and V̇ _E/V̇CO₂ in the Post-Ex tests. It was concluded that the V̇O₂ and ventilation responses to high-intensity exercise can be altered following prolonged moderate intensity exercise in terms of increased amplitude without associated major changes in either iEMG or MPF values among conditions.     

Pituitary–adrenal responses to arm versus leg exercise in untrained man

The purpose of this study was to examine pituitary–adrenal (PA) hormone responses [beta-endorphin (β-END), adrenocorticotropic hormone (ACTH) and cortisol] to arm exercise (AE) and leg exercise (LE) at 60 and 80% of the muscle-group specific VO₂ peak. Eight healthy untrained men (AE VO₂ peak=32.4±3.0 ml kg⁻¹ min⁻¹, LE VO₂ peak=46.9±5.3 ml kg⁻¹ min⁻¹) performed two sub-maximal AE and LE tests in random order. Plasma β-END, ACTH and cortisol were not different (P>0.05) between AE and LE at either exercise intensity; the 60% testing elicited no changes from pre-exercise (PRE) values. For 80% testing, plasma β-END, ACTH and cortisol were consistently, but not significantly, greater during LE than AE. In general, plasma β-END and ACTH were higher (P<0.05) during 80% exercise, than PRE, for both AE and LE. Plasma cortisol was elevated (P<0.05) above PRE during 80% LE, and following 80% for both AE and LE. Plasma ACTH was higher (P<0.05) during 80% LE and AE versus 60% LE and AE, respectively. Plasma β-END and cortisol were significantly higher during and immediately after 80% LE than 60% LE. Thus, plasma β-END, ACTH and cortisol responses were similar for AE and LE at the two relative exercise intensities, with the intensity threshold occurring somewhere between 60 and 80% of VO₂ peak. It appears that the smaller muscle mass associated with AE was sufficient to stimulate these PA axis hormones in a manner similar to LE, despite the higher metabolic stress (i.e., plasma La^-) associated with LE.     

Exercise induced augmentation of myocardial oxygen extraction in spite of normal coronary dilatory capacity in dogs

Summary Myocardial O₂-extraction rate was studied during exercise induced augmentation of cardiac work in dogs.The O₂-extraction rate at rest was 75% of arterial content. Progressive levels of exercise increased the animals' O₂-consumption from 7 ml/min · kg up to 91 ml/min · kg. Cardiac output rose from 108 ml/min · kg at rest to 484 ml/min · kg at the highest exercise level. The increase in myocardial O₂-consumption from 9 ml/min·100 g at rest up to 57 ml/min·100 g at the highest exercise level was met by an increase in coronary flow from 59 to 256 ml/min·100 g and a rise of myocardial AVDO₂ from 15 to 22 Vol%. Thus the latter contributed 40% to the augmented myocardial O₂-requirements.Coronary venous O₂-saturation decreased to 9% saturation during highest levels of exercise. This low value was not the result of a limited coronary dilatory capacity, of inadequate state of exercise training, or of a relative underperfusion of the inner layers of the left ventricle.Thus, augmentation of myocardial O₂-extraction rate seems to be a mechanism of physiological relevance during exercise induced elevation of myocardial O₂-requirements in dogs and may be explained by capillary recruitment in the myocardium.Supported by Deutsche Forschungsgemeinschaft