Decreasing diffusion limitation on exercise in lower-graded interstitial lung disease

 In this study we investigated the contribution of diffusion limitation to the exercise-induced hypoxaemia in interstitial lung disease (ILD). We applied isotopic analysis to the composition of the stable isotopic oxygen molecules ¹⁶O₂ and ¹⁶O¹⁸O in expiratory gas mixtures obtained from six ILD patients and six healthy subjects at rest and during ergometer work (60 W). The changes in the ¹⁶O¹⁸O/¹⁶O₂ ratios were interpreted by using the overall fractionation factor of respiration (α _O) which would be increased towards 1.03 on increasing diffusion limitation. In addition, the O₂ partial pressures of alveolar gas and arterial blood (P _AO₂, P _aO₂) were determined. In the patients, α _O was significantly reduced from 1.0066 ± 0.0004 (mean ± SD) at rest to 1.0035 ± 0.0004 during exercise and in the healthy subjects from 1.0072 ± 0.0008 to 1.0044 ± 0.0004. Furthermore, the exercise-induced reduction of P _aO₂ (from 77 to 69 mmHg) was due to a drop of alveolar PO₂ found in each patient, whereas in each healthy subject P _aO₂ was increased on exercise. On the basis of a resistance model we conclude that the patients’ data were inconsistent with increasing diffusion limitation but showed an increasing impairment of O₂ transport by ventilation. Received: 18 September 1997 / Received after revision: 20 November 1997 / Accepted: 26 November 1997     

Aggravated hypoxia during breath-holds after prolonged exercise

Hyperventilation prior to breath-hold diving increases the risk of syncope as a result of hypoxia. Recently, a number of cases of near-drownings in which the swimmers did not hyperventilate before breath-hold diving have come to our attention. These individuals had engaged in prolonged exercise prior to breath-hold diving and it is known that such exercise enhances lipid metabolism relative to carbohydrate metabolism, resulting in a lower production of CO₂ per amount of O₂ consumed. Therefore, our hypothesis was that an exercise-induced increase in lipid metabolism and the associated reduction in the amount of CO₂ produced would cause the urge to breathe to develop at a lower P O₂, thereby increasing the risk of syncope due to hypoxia. Eight experienced breath-hold divers performed 5 or 6 breath-holds at rest in the supine position and then 5 or 6 additional breath-holds during intermittent light ergometer exercise with simultaneous apnoea (dynamic apnoea, DA) on two different days: control (C) and post prolonged sub-maximal exercise (PPE), when the breath-holds were performed 30 min after 2 h of sub-maximal exercise. After C and before the prolonged submaximal exercise subjects were put on a carbohydrate-free diet for 18 h to start the depletion of glycogen. The respiratory exchange ratio ( RER) and end-tidal P CO₂, P O₂, and SaO₂ values were determined and the data were presented as means (SD). The RER prior to breath-holding under control conditions was 0.83 (0.09), whereas the corresponding value after exercise was 0.70 (0.05) ( P <0.01). When the three apnoeas of the longest duration for each subject were analysed, the average duration of the dynamic apnoeas was 96 (14) s under control conditions and 96 (17) s following exercise. Both P O₂ and P CO₂ were higher during the control dynamic apnoeas than after PPE [PO₂ 6.9 (1.0) kPa vs 6.2 (1.2) kPa, P <0.01; P CO₂ 7.8 (0.5) kPa vs 6.7 (0.4) kPa, P <0.001; ANOVA testing]. A similar pattern was observed after breath-holding under resting conditions, i.e., a lower end-tidal P O₂ and P CO₂ after exercise (PPE) compared to control conditions. Our findings demonstrate that under the conditions of a relatively low RER following prolonged exercise, breath-holding is terminated at a lower P O₂ and a lower P CO₂ than under normal conditions. This suggests that elevated lipid metabolism may constitute a risk factor in connection with breath-holding during swimming and diving.     

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.     

Prediction of Extravascular Burden of Carbon Monoxide (CO) in the Human Heart

Clinically significant myocardial abnormalities (e.g., arrhythmias, S-T elevation) occur in patients with mild-to-severe carbon monoxide (CO) poisoning. We enhanced our previous whole body model [Bruce, E. N., M. C. Bruce, and K. Erupaka. Prediction of the rate of uptake of carbon monoxide from blood by extravascular tissues. Respir. Physiol. Neurobiol. 161(2):142–159, 2008] by adding a cardiac compartment (containing three vascular and two tissue subcompartments differing in capillary density) to predict myocardial carboxymyoglobin (MbCO) and oxygen tensions (P_cO₂) for several CO exposure regimens at rest and during exercise. Model predictions were validated with experimental data in normoxia, hypoxia, and hyperoxia. We simulated exposure at rest to 6462 ppm CO (10 min) and to 265 ppm CO (480 min), and during three levels of exercise at 20% HbCO. We compared responses of carboxyhemoglobin (HbCO), MbCO and P_cO₂ to estimate the potential for myocardial injury due to CO hypoxia. Simulation results predict that during CO exposures and subsequent therapies, cardiac tissue has higher MbCO levels and lower P_cO₂’s than skeletal muscle. CO exposure during exercise further decreases P_cO₂ from resting levels. We conclude that in rest and moderate exercise, the myocardium is at greater risk for hypoxic injury than skeletal muscle during the course of CO exposure and washout. Because the model can predict CO uptake and distribution in human myocardium, it could be a tool to estimate the potential for hypoxic myocardial injury and facilitate therapeutic intervention.     

Enhanced cerebral CO2 reactivity during strenuous exercise in man

Light and moderate exercise elevates the regional cerebral blood flow by ~20% as determined by ultrasound Doppler sonography (middle cerebral artery mean flow velocity; MCA V _mean). However, strenuous exercise, especially in the heat, appears to reduce MCA V _mean more than can be accounted for by the reduction in the arterial CO₂ tension (P _aCO₂). This study evaluated whether the apparently large reduction in MCA V _mean at the end of exhaustive exercise relates to an enhanced cerebrovascular CO₂ reactivity. The CO₂ reactivity was evaluated in six young healthy male subjects by the administration of CO₂ as well as by voluntary hypo- and hyperventilation at rest and during exercise with and without hyperthermia. At rest, P _aCO₂ was 5.1±0.2 kPa (mean ± SEM) and MCA V _mean 50.7±3.8 cm s⁻¹ and the relationship between MCA V _mean and P _aCO₂ was linear (double-log slope 1.1±0.1). However, the relationship became curvilinear during exercise (slope 1.8±0.1; P<0.01 vs. rest) and during exercise with hyperthermia (slope 2.3±0.3; P<0.05 vs. control exercise). Accordingly, the cerebral CO₂ reactivity increased from 30.5±2.7% kPa⁻¹ at rest to 61.4±10.1% kPa⁻¹ during exercise with hyperthermia (P<0.05). At exhaustion P _aCO₂ decreased 1.1±0.2 kPa during exercise with hyperthermia, which, with the determined cerebral CO₂ reactivity, accounted for the 28±10% decrease in MCA V _mean. The results suggest that during exercise changes in cerebral blood flow are dominated by the arterial carbon dioxide tension.     

Analysis of end-tidal and arterial PCO2 gradients using a breathing model

The aim of this paper was to analyse the difference between end-tidal carbon dioxide tension (P _ETCO₂) and arterial carbon dioxide tension (P _aCO₂) at rest and during exercise using a homogeneous lung model that simulates the cyclic feature of breathing. The model was a catenary two-compartment model that generated five non-linear first-order differential equations and two equations for gas exchange. The implemented mathematical modelling described variations in CO₂ and O₂ compartmental fractions and alveolar volume. The model also included pulmonary capillary gas exchange. Ventilatory experimental data were obtained from measurements performed on a subject at rest and during four 5-min bouts of exercise on a cycle ergometer at 50, 100, 150 and 200 W, respectively. Analysis of the P _ETCO₂-P _aCO₂ difference between experimental and sinusoidally adjusted ventilatory flow profiles at rest and during exercise showed that the model produced similar values in P _ETCO₂-P _aCO₂ for different respiratory flow dynamics (P ≅ 0.75). The model simulations allowed us to study the effects of metabolic, circulatory and respiratory parameters on P _ETCO₂-P _aCO₂ at rest and during exercise. During exercise, metabolic CO₂ production, O₂ uptake and cardiac output affected significantly the P _ETCO₂-P _aCO₂ difference from the 150-W workload (P < 0.001). The pattern of breathing had a significant effect on the P _ETCO₂-P _aCO₂ difference. The mean (SD) P _ETCO₂-P _aCO₂ differences simulated using experimental profiles were 0.80 (0.95), 1.65 (0.40), 2.40 (0.20), 3.30 (0.30) and 4.90 (0.20) mmHg, at rest and during exercise at 50, 100, 150 and 200 W, respectively. The relationship between P _ETCO₂-P _aCO₂ and tidal volume was similar to data published by Jones et al. (J Appl Physiol 47: 954–960, 1979). Accepted: 30 May 2000     

Transcutaneous,noninvasiveP O 2 monitoring in adults during exercise and hypoxemia

A new, commercially available, transcutaneous (tc)P _{O 2} monitor was tested in adult females and in laboratory animals to assess its applicability in measuring arterial oxygen tension during physiological stress. Observed values on dogs correlated well with direct measurements of arterialP _{O 2} and with previous data obtained from measurements of arterial blood during exercise and hypoxemia. In our female subjects the unit responded rapidly to changes in inspired ambient oxygen and electrical stability was excellent during maximal exercise tests. TranscutaneousP _{O 2} decreased to an average of 87.8 Torr during maximum exercise breathing 20.9% O₂, and to 32 Torr while breathing 12.6% O₂ at maximum work. Two distinct patterns of response in tcP _{O 2} were observed during hypoxic and normoxic exercise. The technique appears to have substantial future application both in clinical and physiological investigation involving adult subjects.     

Effect of O2 availability on neuroendocrine variables at rest and during exercise: O2 breathing increases plasma prolactin

Neuroendrocrine and substrate responses were investigated in eight male athletes during inhalation of either 100% O₂ (HE), 14% O₂ (HO) or normoxic gas (NO) before, during and after 60 min of cycle ergometry at the same absolute work rate. Concentrations of prolactin (PRL), growth hormone (GH), testosterone (T), adrenocorticotropic hormone (ACTH), cortisol (COR), adrenalin (A), noradrenalin (NA), insulin (INS), ammonia (NH₃), free fatty acids, serotonin (5-HT), total protein, branched-chain amino acids (BCAA) and free tryptophan (free TRP) were determined in venous blood and lactate concentration [LA⁻], partial pressure of oxygen (PO₂), oxygen saturation (SO₂), partial pressure of carbon dioxide and pH in capillary blood. ThePO₂ andSO₂ were augmented in HE and decreased in HO (P ≤ 0.01). In HO and NO no significant changes were found for any other parameter during 30 min of rest prior to exercise. In HE, PRL increased by about 400% during this time, while NA declined (P ≤ 0.01). Heart rate (HR) and [LA⁻] were higher during exercise in HO (P ≤ 0.01). In all trials, NH₃, NA, A, T, GH and ACTH increased during exercise (P ≤ 0.01), while BCAA and INS declined. In comparison to NO and HE, increases of NA, A, GH, COR and ACTH were higher in HO (P < 0.01). The PRL in NO and COR in NO and HE did not change significantly. In HE, after the initial increase at rest, PRL declined during exercise but remained higher than in HO. Higher values for NA, A, GH, COR and ACTH in HO were likely to have reflected an augmented relative exercise intensity. Our results showed that PRL but no other hormone increased during acute exposure to hyperoxia. This PRL release was independent of exercise stress and greater than PRL augmentation during hypoxia, which was related to a higher relative exercise intensity as indicated by [LA⁻] and HR. Responses of plasma NH₃, BCAA, free TRP and 5-HT could not explain PRL augmentation induced by the increment in bloodSO₂ during hyperoxia. Deceased     

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.     

Relationship between muscle T2 * relaxation properties and metabolic state: a combined localized 31P-spectroscopy and 1H-imaging study

A multi-volume ³¹P-magnetic resonance spectroscopy localization procedure was implemented to compare directly muscle metabolism and proton T₂ ^* relaxation properties in the human plantar flexor muscles during exercise. Localized ³¹P-spectra were collected simultaneously from the medial gastrocnemius, lateral gastrocnemius and soleus muscles during exercise using β ₁-insensitive Hadamard Spectroscopic Imaging (HSI). ¹H T₂ ^*-weighted gradient-echo images were acquired at rest and immediately following high-intensity plantar flexion exercise. T₂ ^* mapping of the individual calf muscles showed that plantar flexion with the knee extended produces significant increases (P < 0.0001) in the mean (SEM) T₂ ^* of the medial [35.6 (1.2) ms vs 28.5 (0.5) ms at rest] and lateral gastrocnemius [35.6 (0.9) ms vs 26.2 (0.9) ms at rest], but not in the soleus [26.7 (0.6) ms vs 27.3 (0.8) ms at rest]. In accordance with the changes in T₂ ^*, the ratio of inorganic phosphate to phosphocreatine (P_i:PCr) and the intracellular muscle pH shifted significantly in the gastrocnemii, while the soleus showed no change in muscle pH and only a moderate increase in P_i-to-Ph. Comparison of spectroscopic and relaxation parameters in both gastrocnemius muscles revealed a significant relationship between post-exercise T₂ ^* and intracellular pH (r=0.72–0.76) and P_i-to-Ph ratios (r=0.81–0.88) during exercise. Using an improved method of localization, this study confirms the existence of a strong relationship between transverse relaxation properties and the metabolic state in skeletal muscles engaged in heavy exercise. Accepted: 28 December 1999     

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.     

Oxygen transport and utilization in chronic nonpulsatile blood flow

Oxygen transport and utilization during rest and progressive exercise in chronic nonpulsatile blood flow was reviewed. In a chronic nonpulsatile animal model, (1) basal oxygen consumption of a 4-month old calf was 6.3±0.3 ml/kg/min; (2)PvO₂ decreased when the pump flow rate was reduced (29.6±1.0, 28.3±1.2, and 23.8±0.9 mmHg at 120, 100, and 90 ml/kg/min of pump flow, respectively); (3) serum lactate concentration increased significantly at 90 ml/kg/min of pump flow compared with other rates of pump flow. These results suggest that a critical flow level to maintain oxidative metabolism in the calf with chronic nonpulsatile flow exists between 90 and 100 ml/kg/min, andPvO₂ at the critical flow rate was between 24 and 28 mm Hg. Exercise data showed a significant correlation between O₂ delivery and the maximal O₂ consumption at each nominal flow rate, and suggested that a maximum of 78% of the oxygen delivered can be extracted and utilized during maximal exercise in animals with chronic nonpulsatile blood flow. These data suggest that chronic nonpulsatile blood flow is not a limiting factor for oxygen transport during rest and progressive exercise. However, further studies are needed to directly compare oxygen transport properties in pulsatile and nonpulsatile blood flow models.     

Effects of improvement in aerobic power on resting insulin and glucose concentrations in children

In this study we determined the influence of improving aerobic power (V˙O_2max) on basal plasma levels of insulin and glucose of 11- to 14-year-old children, while accounting for body fat, gender, pubertal status, and leisure-time physical activity (LTPA) levels. Blood samples were obtained from 349 children after an overnight fast and analyzed for plasma insulin and glucose. Height, mass, body mass index (BMI), and sum of skinfolds (Σ triceps + subscapular sites) were measured. LTPA levels and pubertal status were estimated from questionnaires, and V˙O_2max was predicted from a cycle ergometry test. Regardless of gender, insulin levels were significantly correlated (P = 0.0001) to BMI, skinfolds, pubertal stage, and predicted V˙O_2max, but were not related to LTPA levels. Fasting glucose levels were not correlated to measures of adiposity or exercise (LTPA score, V˙O_2max) for females; however, BMI and skinfolds were correlated for males (P < 0.006). The children then took part in an 8-week aerobic exercise program. The 60 children whose V˙O_2max improved (≥3 ml · kg⁻¹ · min⁻¹) had a greater reduction in circulating insulin than the 204 children whose V˙O_2max did not increase −16 (41) vs −1 (63) pmol · l⁻¹; P = 0.028. The greatest change occurred in those children with the highest initial resting insulin levels. Plasma glucose levels were slightly reduced only in those children with the highest insulin levels whose V˙O_2max improved (P < 0.0506). The results of this study indicate that in children, adiposity has the most significant influence on fasting insulin levels; however, increasing V˙O_2max via exercise can lower insulin levels in those children with initially high levels of the hormone. In addition, LTPA does not appear to be associated with fasting insulin status, unless it is sufficient to increase V˙O_2max. Accepted: 2 June 1999     

Estimation of %V˙O2 reserve from heart rate during arm exercise and running

The purpose of the present investigation was to examine the relationship between the percent heart rate reserve (%HRR) in arm exercise and the corresponding percent oxygen uptake (V˙O₂) reserve, and to compare this relationship to that occurring in running. Fourteen male physical education students took part in the study. Each subject performed a maximal running exercise test and a maximal arm cycling test. The subjects also performed three submaximal exercise bouts (in both exercise modes) at 30%, 60% and 80% of their HRR. The subjects were monitored for their heart rate (HR) at rest, maximal HR (HR_max), HR at submaximal work loads, maximal V˙O₂ (V˙O_2max), V˙O₂ at rest and V˙O₂ at submaximal loads. For each subject, load and exercise mode, %HRR and %V˙O₂ reserve were calculated (from HR_max and V˙O_2max as measured during running and arm cycling) and the relationship between the two was evaluated. The main finding of the present investigation is that the prediction of %V˙O₂ reserve in arm cycling from %HRR is grossly overestimated when calculated from HR_max and V˙O_2max measured during running. The prediction is better but still overestimated when calculated from HR_max and V˙O_2max measured during arm cycling. The findings indicate a better prediction of %V˙O₂ reserve from %HRR for running than for arm exercise. These findings should be taken into consideration when prescribing the target HR for arm training. Accepted: 24 July 2000     

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.     

Relationship of middle cerebral artery blood flow velocity to intensity during dynamic exercise in normal subjects

Summary Cerebral blood flow has been reported to increase during dynamic exercise, but whether this occurs in proportion to the intensity remains unsettled. We measured middle cerebral artery blood flow velocity (m) by transcranial Doppler ultrasound in 14 healthy young adults, at rest and during dynamic exercise performed on a cycle ergometer at a intensity progressively increasing, by 50 W every 4 min until exhaustion. Arterial blood pressure, heart rate, end-tidal, partial pressure of carbon dioxide (P _ETCO₂), oxygen uptake ( O₂) and carbon dioxide output were determined at exercise intensity. Mean vM increased from 53 (SEM 2) cm · s^–1 at rest to a maximum of 75 (SEM 4) cm · s^–1 at 57% of the maximal attained O₂( O_2max), and thereafter progressively decreased to 59 (SEM 4) cm · s^–1 at O_2max. The respiratory exchange ratio (R) was 0.97 (SEM 0.01) at 57% of O_2maxand 1.10 (SEM 0.01) at O_2max. The P _ETCO₂ increased from 5.9 (SEM 0.2) kPa at rest to 7.4 (SEM 0.2) kPa at 57% of O_2maxand thereafter decreased to 5.9 (SEM 0.2) kPa at O_2max. Mean arterial pressure increased from 98 (SEM 1) mmHg (13.1 kPa) at rest to 116 (SEM 1) mmHg (15.5 kPa) at 90% of O_2max, and decreased slightly to 108 (SEM 1) mmHg (14.4 kPa) at O_2max. In all the subjects, the maximal value of v _m was recorded at the highest attained exercise intensity below the anaerobic threshold (defined by R greater than 1). We concluded that cerebral blood flow as evaluated by middle cerebral artery flow velocity increased during dynamic exercise as a function of exercise intensity below the anaerobic threshold. At higher intensities, cerebral blood flow decreased, without however a complete return to baseline values, and it is suggested that this may have been at least in part explained by concomitant changes in arterial PCO₂.     

In humans the oxygen uptake slow component is reduced by prior exercise of high as well as low intensity

The aim of the study was to examine to what extent prior high- or low-intensity cycling, yielding the same amount of external work, influenced the oxygen uptake (V˙O₂) slow component of subsequent high-intensity cycling. The 12 subjects cycled in two protocols consisting of an initial 3 min period of unloaded cycling followed by two periods of constant-load exercise separated by 3 min of rest and 3 min of unloaded cycling. In protocol 1 both periods of exercise consisted of 6 min cycling at a work rate corresponding to 90% peak oxygen uptake (V˙O_2peak). Protocol 2 differed from protocol 1 in that the first period of exercise consisted of a mean of 12.1 (SD 0.8) min cycling at a work rate corresponding to 50% V˙O_2peak. The difference between the 3rd min V˙O₂ and the end V˙O₂ (ΔV˙O₂₍₆₋₃₎) was used as an index of the V˙O₂ slow component. Prior high-intensity exercise significantly reduced ΔV˙O₂₍₆₋₃₎. The ΔV˙O₂₍₆₋₃₎ was also reduced by prior low-intensity exercise despite an unchanged plasma lactate concentration at the start of the second period of exercise. The reduction was more pronounced after prior high- than after prior low-intensity exercise (59% and 28%, respectively). The results of this study show that prior exercise of high as well as low intensity reduces the V˙O₂ slow component and indicate that a metabolic acidosis is not a necessary condition to elicit a reduction in ΔV˙O₂₍₆₋₃₎. Accepted: 8 July 2000     

Thermal responses of men and women during cold-water immersion: influence of exercise intensity

Summary The influence of exercise intensity on thermoregulation was studied in 8 men and 8 women volunteers during three levels of arm-leg exercise (level I: 700 ml oxygen (O₂) · min^–1; level II: 1250 ml O₂ · min^–1; level III: 1700 ml O₂ · min^–1 for 1 h in water at 20 and 28°C (T _w). For the men inT _w 28°C the rectal temperature (T _re) fell 0.79°C (P<0.05) during immersion in both rest and level-I exercise. With level-II exercise a drop inT _re of 0.54° C (P < 0.05) was noted, while at level-III exerciseT _re did not change from the pre-immersion value. AtT _w of 20°C,T _re fell throughout immersion with no significant difference in finalT _re observed between rest and any exercise level. For the women at rest atT _w 28°C,T _re fell 0.80°C (P<0.05) below the pre-immersion value. With the two more intense levels of exercise,T _re did not decrease during immersion. InT _w 20°C, the women maintained higherT _re (P<0.05) during level-II and level-III exercise compared to rest and exercise at level I. The_{T re} responses were related to changes in tissue insulation (I _t) between rest and exercise with the largest reductions inI _t noted between rest and level-I exercise acrossT _w and gender. For men and women of similar percentage body fat, decreases inT _re were greater for the women at rest and level-I exercise inT _w 20°C (P< 0.05). With more intense exercise, the women maintained a higherT _re than the men, especially in the colder water. These findings indicate that exercise is not always effective in offsetting the decrease inI _t and facilitated heat loss in cool or cold water compared to rest. The factors of exercise intensity,T _W, body fat, and gender influence the thermoregulatory responses.     

31P nuclear magnetic resonance study on changes in phosphocreatine and the intracellular pH in rat skeletal muscle during exercise at various inspired oxygen contents

We measured ATP, phosphocreatine (PCr), inorganic phosphate (P_i), and the intracellular pH in rat hindlimb muscles during submaximal isometric exercise with various O₂ deliveries using³¹P nuclear magnetic resonance spectroscopy (³¹P NMR) to evaluate changes in energy metabolism in relation to O₂ availability. Delivery of O₂ to muscles was altered by controlling the fractional concentration of inspired oxygen (F _IO₂) at 0.50, 0.28, 0.21, 0.11 and 0.08 with monitoring partial pressure of oxygen and carbon dioxide, and bicarbonate at the femoral artery. The steady-state ratio of PCr : (PCr + P_i) during exercise decreased as a function ofF _IO₂ even at 0.21. Significant acidification of the intracellular pH during exercise occurred at 0.08F _IO₂. Change in the PCr : (PCr + P_i) ratio demonstrated that the oxidative capacity, i.e. the maximal rate of the oxidative phosphorylation reaction, in muscle was not limited by O₂ delivery at 0.50F _IO₂, but was significantly limited at 0.21F _IO₂ or below. Change in the intracellular pH at 0.08F _IO₂ could be interpreted as an increase in lactate, suggesting activation of glycolysis. Correlation between the PCr : (PCr + P_i) ratio and the intracellular pH revealed the existence of a critical PCr : (PCr + P_i) ratio and pH for glycolysis activation at around 0.4 and 6.7, respectively.     

Systemic oxygen extraction during incremental exercise in patients with severe chronic obstructive pulmonary disease

To determine if decreased systemic oxygen (O₂) extraction contributes to the exercise limit in severe chronic obstructive pulmonary disease (COPD), 40 consecutive incremental cycle ergometer exercise tests performed by such patients, from which a “log-log” lactate threshold (LT) was identified, were compared to those of 8 patients with left ventricular failure (LVF) and 10 normal controls. Pulmonary gas exchange and minute ventilation were measured continuously and arterial blood gas tensions, pH, and lactate concentrations were sampled each minute. Cardiac output (Q˙ _c) was measured by first-pass radionuclide ventriculography. The systemic O₂ extraction ratio (O₂ER) was calculated as arterial − mixed venous O₂ content difference (C _aO₂ − C _vO₂)/C _aO₂. Peak exercise O₂ uptake (V˙O_2peak) was markedly reduced in both COPD and LVF [41 (3) and 42 (3)% predicted, respectively], compared to controls [89 (2)% predicted, P < 0.0001 for each]. Similarly, the LT occurred at a low percentage of predicted maximal oxygen consumption in both COPD and LVF [25 (2) and 27 (3)%] compared to normals [46 (3)%, P < 0.0001 for each]. The systemic O₂ER at peak exercise was severely reduced in COPD [0.36 (0.02)] compared to the other groups [P < 0.0001 for each], for whom it was nearly identical [0.58 (0.03) vs 0.63 (0.04), LVF vs control, P > 0.05]. In the COPD group, an early LT correlated with reduced systemic O₂ER at peak exercise (r = 0.64, P < 0.0001), but not with any index of systemic O₂ delivery. These data suggest that lactic acidemia during exercise in patients with severe COPD is better related to abnormal systemic O₂ extraction than to its delivery and contributes to the exercise limit. Accepted: 10 March 1998