Prediction of maximum oxygen uptake during physical exercise on bicycle ergometer

Possibilities to predict maximum oxygen uptake (VO2max) during exercising on bicycle ergometer using the Russian Rating Perceived Exertion (RPE) was studied. Results of examination of 13 athletes demonstrate the possibility of predicting individual and group average VO2max on the basis of data from submaximum testing and the empirical formulas from the value of VO2max registered at RPE numbers 13 and 15. These VO2max values can serve as markers for assessing the dynamics of physical performance.     

Maximal oxygen uptake during exercise with various combinations of arm and leg work

Oxygen uptake (VO2) was determined in 10 males during the following types of maximal exercise (work time: about 5 min): uphill running, bicycling, arm work (cranking), and combined arm work and bicycling (A + L). The A + L exercise was performed in four different ways, the arms doing 10%, 20%, 30%, or 40% of the same total rate of work; and also with the maximal bicycle work load plus either maximal or submaximal arm work. VO2 was the same in running as in all types of A + L exercise, except when the arm work load was 10% and 40% of the total rate of work, where VO2 was 2.5% (P less than 0.05) and 9.4% (P less than 0.001) lower, respectively. Bicycle VO2 was lower than VO2 in running but equal to A + L VO2 when arm work intensity was 40% of the total rate of work. It is concluded that VO2 during maximal exercise a) to a certain extent depends on the exercising muscle mass, b) is lower than the oxygen-consuming potential of the muscles involved in A + L exercise, and c) in A + L exercise is influenced by the ratio of arm work to total rate of work and the subject's fitness for arm work and bicycling.     

Determinants of oxygen uptake. Implications for exercise testing

For exercise modalities such as cycling which recruit a substantial muscle mass, muscle oxygen uptake (VO2) is the primary determinant of pulmonary VO2. Indeed, the kinetic complexities of pulmonary VO2 associated with exercise onset and the non-steady state of heavy (> lactate threshold) and severe [> asymptote of power-time relationship for high intensity exercise (W)] exercise reproduce with close temporal and quantitative fidelity those occurring across the exercising muscles. For moderate (< lactate threshold) exercise and also rapidly incremental work tests, pulmonary (and muscle) VO2 increases as a linear function of work rate (approximately equal to 9 to 11 ml O2/W/min) in accordance with theoretical determinations of muscle efficiency (approximately equal to 30%). In contrast, for constant load exercise performed in the heavy and severe domains, a slow component of the VO2 response is manifest and pulmonary and muscle VO2 increase as a function of time as well as work rate beyond the initial transient associated with exercise onset. In these instances, muscle efficiency is reduced as the VO2 cost per unit of work becomes elevated, and in the severe domain, this VO2 slow component drives VO2 to its maximum and fatigue ensues rapidly. At pulmonary maximum oxygen uptake (VO2max) during cycling, the maximal cardiac output places a low limiting ceiling on peak muscle blood flow, O2 delivery and thus muscle VO2. However, when the exercise is designed to recruit a smaller muscle mass (e.g. leg extensors, 2 to 3kg), mass-specific muscle blood flow and VO2 at maximal exercise are 2 to 3 times higher than during conventional cycling. consequently, for any exercise which recruits more than approximately equal to 5 to 6kg of muscle at pulmonary VO2max, there exists a mitochondrial or VO2 reserve capacity within the exercising muscles which cannot be accessed due to oxygen delivery limitations. The implications of these latter findings relate to the design of exercise tests. Specifically, if the purpose of exercise testing is to evaluate the oxidative capacity of a small muscle mass (< 5 to 6kg), the testing procedure should be designed to restrict the exercise to those muscles so that a central (cardiac output, muscle O2 delivery) limitation is not invoked. It must be appreciated that exercise which recruits a greater muscle mass will not stress the maximum mass-specific muscle blood flow and VO2 but rather the integration of central (cardiorespiratory) and peripheral (muscle O2 diffusing capacity) limitations.     

The reliability of lactate measurements during exercise

The study of the epidemiology of dementia, specifically Alzheimer's disease, in developing countries requires specialized instruments and personnel. Cultural and sub-cultural differences among populations are highly relevant to the design of such instruments. Over and above the cultural issues, it is widely recognized that low education and illiteracy pose considerable challenges to reliable and valid cognitive screening. The overall objectives of the Indo-US Cross-National Dementia Epidemiology Study were: a) to determine the prevalence and incidence of, and risk factors for, Alzheimer's and other dementias in a defined Indian community; and b) to compare these results with those found in a defined American community. To achieve these epidemiological objectives, our first task was to develop, systematically and empirically, suitable cognitive and activities assessment screening instruments for use in India, which would 1) be culturally fair, psychometrically sound, and valid for a population with little or no education; 2) be optimally sensitive and specific for dementia; and 3) allow not only the identification but also the more detailed characterization of dementia, and of normal and abnormal cognitive aging. In this paper we address the practical issues involved in the development and administration of the modified cognitive screening battery in our rural Indian context.     

Correlates of maximal oxygen consumption during treadmill exercise

According to the Balke treadmill protocol, 39 healthy male USAF volunteers were subjected to maximal exercise. The subjects as a group passed the anaerobic threshold by the end of exercise since average venous lactate concentrations increased from 11.2 +/- 1.6 mg% (95% confidence limits) to 93.0 +/- 8.5 mg% (95% confidence limits), and the average gas exchange ratio (R) at the end of the exercise was greater than unity (p less than 0.0005). Tests for correlations showed weak but statistically significant (p less than 0.05) relationships between change in venous lactic acid concentrations and R (r = 0.44) and maximal heart rate (r = 0.34). Maximal oxygen consumption was correlated with time of exercise (r = 0.70) and subject weight (r = 0.33). Subject age and initial plasma lactate concentrations were not significantly correlated with any other variables. Multiple linear regression yielded an equation for prediction of maximal oxygen consumption which included terms for time of exercise and subject weight. Although the multiple correlation coefficent (r = 0.75) was statistically significant (p less than 0.05), it was considered insufficient for accurate prediction of maximal oxygen consumption.     

Kinetics of oxygen uptake at the onset of exercise in boys and men

The objective of this study was to compare the O2 uptake (VO2) kinetics at the onset of heavy exercise in boys and men. Nine boys, aged 9-12 yr, and 8 men, aged 19-27 yr, performed a continuous incremental cycling task to determine peak VO2 (VO2 peak). On 2 other days, subjects performed each day four cycling tasks at 80 rpm, each consisting of 2 min of unloaded cycling followed twice by cycling at 50% VO2 peak for 3.5 min, once by cycling at 100% VO2 peak for 2 min, and once by cycling at 130% VO2 peak for 75 s. O2 deficit was not significantly different between boys and men (respectively, 50% VO2 peak task: 6.6 +/- 11.1 vs. 5.5 +/- 7.3 ml . min-1 . kg-1; 100% VO2 peak task: 28.5 +/- 8.1 vs. 31.8 +/- 6.3 ml . min-1 . kg-1; and 130% VO2 peak task: 30.1 +/- 5.7 vs. 35.8 +/- 5.3 ml . min-1 . kg-1). To assess the kinetics, phase I was excluded from analysis. Phase II VO2 kinetics could be described in all cases by a monoexponential function. ANOVA revealed no differences in time constants between boys and men (respectively, 50% VO2 peak task: 22. 8 +/- 5.1 vs. 26.4 +/- 4.1 s; 100% VO2 peak task: 28.0 +/- 6.0 vs. 28.1 +/- 4.4 s; and 130% VO2 peak task: 19.8 +/- 4.1 vs. 20.7 +/- 5. 7 s). In conclusion, O2 deficit and fast-component VO2 on-transients are similar in boys and men, even at high exercise intensities, which is in contrast to the findings of other studies employing simpler methods of analysis. The previous interpretation that children rely less on nonoxidative energy pathways at the onset of heavy exercise is not supported by our findings.     

VO2 kinetics in the horse during moderate and heavy exercise

The horse is a superb athlete, achieving a maximal O2 uptake (approximately 160 ml . min-1 . kg-1) approaching twice that of the fittest humans. Although equine O2 uptake (VO2) kinetics are reportedly fast, they have not been precisely characterized, nor has their exercise intensity dependence been elucidated. To address these issues, adult male horses underwent incremental treadmill testing to determine their lactate threshold (Tlac) and peak VO2 (VO2 peak), and kinetic features of their VO2 response to "square-wave" work forcings were resolved using exercise transitions from 3 m/s to a below-Tlac speed of 7 m/s or an above-Tlac speed of 12.3 +/- 0.7 m/s (i.e., between Tlac and VO2 peak) sustained for 6 min. VO2 and CO2 output were measured using an open-flow system: pulmonary artery temperature was monitored, and mixed venous blood was sampled for plasma lactate. VO2 kinetics at work levels below Tlac were well fit by a two-phase exponential model, with a phase 2 time constant (tau1 = 10.0 +/- 0.9 s) that followed a time delay (TD1 = 18.9 +/- 1.9 s). TD1 was similar to that found in humans performing leg cycling exercise, but the time constant was substantially faster. For speeds above Tlac, TD1 was unchanged (20.3 +/- 1.2 s); however, the phase 2 time constant was significantly slower (tau1 = 20.7 +/- 3.4 s, P < 0.05) than for exercise below Tlac. Furthermore, in four of five horses, a secondary, delayed increase in VO2 became evident 135.7 +/- 28.5 s after the exercise transition. This "slow component" accounted for approximately 12% (5.8 +/- 2.7 l/min) of the net increase in exercise VO2. We conclude that, at exercise intensities below and above Tlac, qualitative features of VO2 kinetics in the horse are similar to those in humans. However, at speeds below Tlac the fast component of the response is more rapid than that reported for humans, likely reflecting different energetics of O2 utilization within equine muscle fibers.     

The effect of sedation on oxygen uptake during spontaneous breathing

Sedation may be used in intensive care and emergency medicine to improve the oxygen demand/delivery ratio. The influence of sedation has most frequently been investigated in a dose-related manner. The aim of the present study was to determine the effect-related influence of different sedatives on oxygen uptake (VO2) in relation to defined resting conditions. METHODS. Forty ASA I patients who had to undergo a minor surgical procedure were investigated 1.5 h before surgery at basal energy-expenditure measurement conditions. One of the following substances was given with a preset bolus rate in a double-blind, randomised order until a defined level of sleep or side effects was encountered: propofol (n = 8), midazolam (n = 8), thiopentone (n = 8), sodium chloride (n = 8), and fentanyl (n = 8). The sleep level was defined as sluggish response to a loud voice or tapping on the forearm. The variables VO2, carbon dioxide elimination (VCO2), end tidal CO2 (p(et)CO2), oxygen saturation (SaO2), heart rate, systemic blood pressure, skin temperature, and skin resistance on the sole of the foot were documented on-line on a computer. All variables were compared using differences of averages from 10-min periods before and after sedation during which the VO2 was minimal. RESULTS. The mean VO2 before sedation was 264 +/- 60 ml/min, and the measured energy expenditure did differ by -0.2% (+/- 14%) from mean predicted values using the Harris-Benedict equation. The VO2 was reduced by 15 +/- 2% with propofol, by 12 +/- 8% with midazolam, and by 10 +/- 5% with thiopentone. This was statistically significant compared to placebo treatment, as was the difference between propofol and thiopentone effects. All patients in these groups reached the defined sleep level, which was not achieved by the placebo and fentanyl groups. Placebo treatment changed the VO2 by 0.1% (+/- 2%). Fentanyl increased the VO2 by 5% (+/- 8%), which did not reach significance. In the fentanyl group the bolus application had to be stopped at a p(et)CO2 of 50 mm Hg in all patients. In the propofol, midazolam, and thiopentone groups the phasic changes of skin resistance were reduced to zero and the skin temperature increased from 27 +/- 2 degrees C to 32 +/- 2 degrees C. The fentanyl group showed an increase in changes of skin resistance without changes in temperature. CONCLUSIONS. Sleep induced by propofol, midazolam, or thiopentone to a clinically maximal desirable level in spontaneously breathing patients reduced VO2 by 10% to 15%. This level of sedation did not induce a relevant change in P(et)CO2 or SaO2. The effect of propofol appeared to be the most pronounced and least variable. This may be attributable to a more pronounced reduction in single-organ VO2 or to an undetected difference in level of sedation. Fentanyl did, in contrast to most publications on opioid effects, seem to increase VO2. Underlying mechanisms may be sought in an increased rate-pressure product and sympathetic activity on the basis of hypercapnia and changes in muscle tension.     

Improved oxygen utilization during mild exercise in heart failure

In heart failure with low cardiac output, exercise tolerance is reduced despite modulated regional blood distribution and oxygen extraction. However, low cardiac output does not necessarily lead to reduced exercise tolerance especially during mild exercise. In the present study, in order to understand the mechanisms regulating exercise tolerance in heart failure, we measured oxygen consumption (VO2) and cardiac output (CO) during both mild and intense exercise. Patients with heart failure were divided into 2 groups; group L (n = 8) consists of patients with low anaerobic threshold (AT) < 13 ml/min per kg and group H (n = 7) consisting of patients with AT > 13 ml/min per kg. At rest, VO2 was similar between groups L and H, whereas CO was lower in group L than in group H (3.5 + 0.3 vs 4.8 + 1.4 ml/min, p < 0.01). Increase in VO2 during warm-up exercise was not significant between the 2 groups (7.4 +/- 0.5 (group L) vs 6.2 +/- 0.3 ml/min per kg (group H), ns), but increase in CO was lower in group L than in group H (2.5 +/- 0.6 vs 3.4 +/- 0.4 ml/min, p < 0.01). After warm-up to the AT point, however, the increase in not only VO2 but also CO was markedly reduced in group L than in group H (VO2: 0.5 +/- 0.4 vs 3.7 +/- 0.8 ml/min per kg, p < 0.01, CO: 0.2 +/- 0.3 vs 1.1 +/- 0.3 L/min, p < 0.01). Based on these measurements, we calculated the arteriovenous oxygen difference (c(A-V)O2 difference) during exercise in individual patients using Fick's equation. The c(A-V)O2 difference was markedly increased in severe heart failure during the warm-up stage, but between the end of warm-up and the AT point, it remained at the same level as that of group H. These results suggest the presence of a unique mechanism regulating the c(A-V)O2 difference in severe heart failure patients, activation of which may, at least during mild exercise, contribute to efficient oxygen delivery to the peripheral tissues thus compensating for the jeopardized exercise tolerance in those patients.     

Unaltered oxygen uptake kinetics at exercise onset with lower-body positive pressure in humans

The purpose of this study was to determine the influence of a reduced skeletal muscle blood flow on oxygen uptake (VO2) kinetics at the onset of cycle ergometer exercise. Seven healthy subjects performed rest-to-exercise transitions with a lower-body positive pressure (LBPP) of 45 Torr. Two work rates were selected for each subject: a moderate intensity (VO2, approximately 1.9 l min-1; delta[lactate], approximately 1 mequiv l-1) below the estimated lactate threshold and a heavy intensity (VO2, approximately 2.6 l min-1; delta[lactate], approximately 3 mequiv l-1) above this threshold. Pulmonary gas exchange variables and ventilatory (VE) responses were computed breath-by-breath from mass spectrometer and turbine volume meter signals, respectively, and mean response times (MRT) calculated. Samples of 'arterialized' venous blood were used for the determination of [lactate], pH and [K+]. While the application of 45 Torr LBPP had no effects on VO2 kinetics during moderate exercise (MRT: 33.5 +/- 1.2 s at 45 Torr vs. 32.8 +/- 1.3 s at 0 Torr; P > 0.05) or on [lactate], pH or [K+], breathing frequency (f) was increased (P < 0.05) and tidal volume (VT) reduced (P < 0.05). The addition of LBPP during heavy exercise did not alter VO2 kinetics (MRT: 35.2 +/- 1.5 s at 45 Torr vs. 34.8 +/- 1.5 s at 0 Torr; P > 0.05), or [lactate], pH or [K+]. Although both the VE (via an increased f) and CO2 output (VCO2) were significantly greater with LBPP by approximately 30 l min-1 and approximately 500 ml min-1, respectively, end-tidal CO2 partial pressure was decreasing, suggesting an additional ventilatory stimulus. These data can be interpreted to suggest that oxygen delivery is not critically dependent upon blood flow to the working muscle at exercise onset, while LBPP-induced increases in VE during suprathreshold exercise may be related to an accumulation of metabolites at the working muscle or the effects of pressure per se.     

Effect of voluntary exercise on maximal oxygen uptake in young female Fischer 344 rats

The effect of voluntary exercise on maximal oxygen uptake (VO2 max) was studied in young female Fischer 344 rats. After 10 weeks of wheel-running training, the absolute VO2 max and VO2 max relative to body mass increased without a decline in body mass. The running speed eliciting VO2 max, heart and soleus muscle mass, and succinate dehydrogenase (SDH) activity in the soleus muscle also increased. These results suggest that voluntary exercise is an effective means of increasing the aerobic exercise capacity of young female Fischer 344 rats.     

Influence of chronic undernutrition on oxygen consumption of rats during exercise

The current study was undertaken to examine the effects of dithiothreitol (DDT), a sulfhydryl-reducing agent and heavy metal chelator, on the course of heavy metal-induced acute renal failure in the rat. Groups of rats in metabolic cages received uranyl nitrate (UN) alone, UN plus DTT, mercuric chloride (HgCl2) alone, and HgCl2 plus DTT. UN injected alone produced azotemia, decreased creatinine clearance, and rising fractional sodium excretion over the 48 hr of study. These effects of UN on renal function were not observed when DTT was administered 30 min after UN injection. Qualitatively similar results were obtained with HgCl2-induced acute renal failure. Groups of rats were killed at 6 hr after UN plus DTT, HgCl2 alone, or HgCl2 plus DTT; and determinations of plasma renin activity (PRA) and renin activities of the superficial and deep juxtaglomerular apparatus (JGA) were performed. PRA's and JGA renins were increased in animals receiving either UN or HgCl2 alone, but not in the rats receiving both DTT and UN or HgCl2. The effect of DTT on distribution of 203Hg was also examined. Treatment with DTT did not alter the renal accumulation of 203Hg, suggesting that this agent does not act by limiting renal exposure to the heavy metals. Thus, DTT ameliorates the course of heavy metal-induced ARF, and this effect is associated with prevention of heavy metal-induced alterations in sodium excretion and renin-angiotensin system activity.     

O2 uptake kinetics after acetazolamide administration during moderate- and heavy-intensity exercise

Inhibition of carbonic anhydrase (CA) is associated with a lower plasma lactate concentration ([La-]pl) during fatiguing exercise. We hypothesized that a lower [La-]pl may be associated with faster O2 uptake (V(O2)) kinetics during constant-load exercise. Seven men performed cycle ergometer exercise during control (Con) and acute CA inhibition with acetazolamide (Acz, 10 mg/kg body wt iv). On 6 separate days, each subject performed 6-min step transitions in work rate from 0 to 100 W (below ventilatory threshold, VE(T). Gas exchange was measured breath by breath. Trials were interpolated at 1-s intervals and ensemble averaged to yield a single response. The mean response time (MRT, i.e., time to 63% of total exponential increase) for on- and off-transients was determined using a two- (VE(T)). Arterialized venous blood was sampled from a dorsal hand vein and analyzed for [La-]pl. MRT was similar during Con (31.2 +/- 2.6 and 32.7 +/- 1.2 s for on and off, respectively) and Acz (30.9 +/- 3.0 and 31.4 +/- 1.5 s for on and off, respectively) for work rates VE(T), MRT was similar between Con (69.1 +/- 6.1 and 50.4 +/- 3.5 s for on and off, respectively) and Acz (69.7 +/- 5.9 and 53.8 +/- 3.8 s for on and off, respectively). On- and off-MRTs were slower for >VE(T) than for VE(T) exercise but was lower at the end of the transition during Acz (1.4 +/- 0.2 and 7.1 +/- 0.5 mmol/l for VE(T) respectively) than during Con (2.0 +/- 0.2 and 9.8 +/- 0.9 mmol/l for VE(T), respectively). CA inhibition does not affect O2 utilization at the onset of VE(T) exercise, suggesting that the contribution of oxidative phosphorylation to the energy demand is not affected by acute CA inhibition with Acz.     

Glucose infusion partially attenuates glucose production and increases uptake during intense exercise

Glucose infusion can prevent the increase in glucose production (Ra) and increase glucose uptake (Rd) during exercise of moderate intensity. We postulated that 1) because in postabsorptive intense exercise (>80% maximal O2 uptake) the eightfold increase in Ra may be mediated by catecholamines rather than by glucagon and insulin, exogenous glucose infusion would not prevent the Ra increment, and 2) such infusion would cause greater Rd. Fit young men were exercised at >85% maximal O2 uptake for 14 min in the postabsorptive state [controls (Con), n = 12] or at minute 210 of a 285-min glucose infusion. In seven subjects, the infusion was constant (CI; 4 mg . kg-1 . min-1), and in seven subjects it was varied (VI) to mimic the exercise Ra response in Con. Although glucose suppressed Ra to zero (with glycemia approximately 6 mM and insulin approximately 150 pM), an endogenous Ra response to exercise occurred, to peak increments two-thirds those in Con, in both CI and VI. Glucagon was unchanged, and very small increases in the glucagon-to-insulin ratio occurred in all three groups. Catecholamine responses were similar in all three groups, and correlation coefficients of Ra with plasma norepinephrine and epinephrine were significant in all. In all CI and VI, Rd at rest was 2x Con, increased earlier in exercise, and was higher for the 1 h of recovery with glucose infusion. Thus the Ra response was only partly attenuated, and the catecholamines are likely to be the regulators. This suggests that an acute endogenous Ra rise is possible even in the postprandial state. Furthermore, the fact that more circulating glucose is used by muscle during exercise and early recovery suggests that muscle glycogen is spared.     

Augmented upper body contribution to oxygen uptake during upper body exercise with concurrent leg functional electrical stimulation in persons with spinal cord injury

The purpose of this pilot study was to compare the contribution of upper body musculature to VO2 with and without concurrent leg FES (LFES). Eight subjects with spinal cord injury, lesion levels range C6-T12, performed upper body exercise (UBE) during no LFES (NOS), LFES at 40 mA (LOS), and 80 mA (HIS), at rest, 60% and 80% of VO2peak. Resting VO2 values were obtained during NOS, LOS and HIS conditions and were then subtracted from their respective whole body VO2 values to give an estimate of upper body VO2. Small and non significant increases were found in the HIS vs NOS condition at 60% VO2peak. Larger differences of 7.8% were found in the HIS vs NOS condition at 80% VO2peak (11.35+/-3.8 ml kg(-1) min(-1) to 12.24+/-4.0 ml kg(-1) min(-1)), although this too was not significant, perhaps due to the small number of subjects in this study and the consequently low statistical power to detect a significant difference. We discuss the implications for these preliminary results in the context of the existing literature on this topic.     

A catecholamine-mediated increase in cerebral oxygen uptake during immobilisation stress in rats

Anxiety and grave apprehension have been supposed to increase cerebral metabolism, and it has earlier been suggested that intravenous infusion of adrenaline may increase cerebral blood flow (CBF) and cerebral oxygen consumption (CMR02). In an experimental model on rats, it could be shown that immobilisation stress increased CBF and CMR02 after 5 min (about 150% of control values) and 30 min (about 190% of control values). By previous adrenalectomy or by administration of a beta-receptor blocker (propranolol, 1.4 mg/kg) the changes in CBF and CMR02 could be prevented. It is concluded that the excessive increase in CBF and CMR02 was mediated via release of catecholamines from the adrenal glands.     

Mechanisms facilitating oxygen delivery during exercise in patients with chronic heart failure

The aim of the study was to estimate the relative importance of the Bohr effect and redistribution of blood from the non-exercising tissues on the arterial-venous oxygen content differences across the exercising extremities and the central circulation in patients with chronic heart failure; the relationship among femoral vein, systemic and pulmonary artery oxygen partial pressure and hemoglobin saturation was determined. It has been reported that the maximal reduction in femoral vein pO2 precedes peak oxygen consumption and lactic acidosis threshold in patients with chronic heart failure and normal subjects during exercise. The increase in oxygen consumption at work rates above lactic acidosis threshold, therefore, must be accounted for by increase in blood flow in the exercising muscles and right-ward shift on the oxyhemoglobin dissociation curve. Since the total cardiac output increase is blunted in patients with chronic heart failure, diversion of blood flow from non-exercising to exercising tissues may account for some of the increase in muscle blood flow. Ten patients with chronic heart failure performed a progressively increasing leg cycle ergometer exercise test up to maximal effort while measuring ventilation and gas concentration for computation of oxygen uptake and carbon dioxide production, breath-by-breath. Blood samples were obtained, simultaneously, from systemic and pulmonary arteries and femoral vein at rest and every minute during exercise to peak oxygen consumption. At comparable levels of exercise, femoral vein pO2, hemoglobin saturation and oxygen content were lower than in the pulmonary artery. PCO2 and lactate concentration increased steeply in femoral vein and pulmonary artery blood above lactic acidosis threshold (due to lactic acid build-up and buffering), but more steeply in femoral vein blood. These increases allowed femoral vein oxyhemoglobin to dissociate without a further decrease in femoral vein pO2 (Bohr effect). The lowest femoral vein pO2 (16.6 +/- 3.9 mmHg) was measured at 66 +/- 22% of peak VO2 and before the lowest oxyhemoglobin saturation was reached. Artero-venous oxygen content difference was higher in the femoral vein than in the pulmonary artery; this difference became progressively smaller as oxygen consumption increased. "Ideal" oxygen consumption for a given cardiac output (oxygen consumption expected if all body tissues had maximized oxygen extraction) was always higher than the measured oxygen consumption; however the difference between the two was lost at peak exercise. This difference positively correlated with peak oxygen consumption and cardiac output increments at submaximal but not at maximal exercise. In conclusion, femoral vein pO2 reached its lowest value at a level of exercise at or below the lactic acidosis threshold. Further extraction of oxygen above the lactic acidosis threshold was accounted for by a right shift of the oxyhemoglobin dissociation curve. The positive correlation between increments of cardiac output vs "ideal" and measured oxygen consumption suggests a redistribution of blood flow from non-exercising to exercising regions of the body. Furthermore the positive correlation between exercise capacity and the difference between "ideal" and measured oxygen consumption suggests that patients with the poorer function have the greater capability to optimize blood flow redistribution during exercise.     

Oxygen uptake kinetics during low level exercise in patients with heart failure: relation to neurohormones, peak oxygen consumption, and clinical findings

OBJECTIVE: To investigate whether oxygen uptake (VO2) kinetics during low intensity exercise are related to clinical signs, symptoms, and neurohumoral activation independently of peak oxygen consumption in chronic heart failure. DESIGN: Comparison of VO2 kinetics with peak VO2, neurohormones, and clinical signs of chronic heart failure. SETTING: Tertiary care centre. PATIENTS: 48 patients with mild to moderate chronic heart failure. INTERVENTIONS: Treadmill exercise testing with "breath by breath" gas exchange monitoring. Measurement of atrial natriuretic factor (ANF), brain natriuretic peptide (BNP), and noradrenaline. Assessment of clinical findings by questionnaire. MAIN OUTCOME MEASURES: O2 kinetics were defined as O2 deficit (time [rest to steady state] x DeltaVO2 -sigmaVO2 [rest to steady state]; normalised to body weight) and mean response time of oxygen consumption (MRT; O2 deficit/DeltaVO2). RESULTS: VO2 kinetics were weakly to moderately correlated to the peak VO2 (O2 deficit, r = -0.37, p < 0.05; MRT, r = -0.49, p < 0.001). Natriuretic peptides were more closely correlated with MRT (ANF, r = 0.58; BNP, r = 0.53, p < 0.001) than with O2 deficit (ANF, r = 0.48, p = 0.001; BNP, r = 0.37, p < 0.01) or peak VO2 (ANF, r = -0.40; BNP, r = -0.31, p < 0.05). Noradrenaline was correlated with MRT (r = 0. 33, p < 0.05) and O2 deficit (r = 0.39, p < 0.01) but not with peak VO2 (r = -0.20, NS). Symptoms of chronic heart failure were correlated with all indices of oxygen consumption (MRT, r = 0.47, p < 0.01; O2 deficit, r = 0.39, p < 0.01; peak VO2, r = -0.48, p < 0. 01). Multivariate analysis showed that the correlation of VO2 kinetics with neurohormones and symptoms of chronic heart failure was independent of peak VO2 and other variables. CONCLUSIONS: Oxygen kinetics during low intensity exercise may provide additional information over peak VO2 in patients with chronic heart failure, given the better correlation with neurohormones which represent an index of homeostasis of the cardiovascular system.     

Alveolar oxygen uptake and femoral artery blood flow dynamics in upright and supine leg exercise in humans

We tested the hypothesis that the slower increase in alveolar oxygen uptake (VO2) at the onset of supine, compared with upright, exercise would be accompanied by a slower rate of increase in leg blood flow (LBF). Seven healthy subjects performed transitions from rest to 40-W knee extension exercise in the upright and supine positions. LBF was measured continuously with pulsed and echo Doppler methods, and VO2 was measured breath by breath at the mouth. At rest, a smaller diameter of the femoral artery in the supine position (P < 0. 05) was compensated by a greater mean blood flow velocity (MBV) (P < 0.05) so that LBF was not different in the two positions. At the end of 6 min of exercise, femoral artery diameter was larger in the upright position and there were no differences in VO2, MBV, or LBF between upright and supine positions. The rates of increase of VO2 and LBF in the transition between rest and 40 W exercise, as evaluated by the mean response time (time to 63% of the increase), were slower in the supine [VO2 = 39.7 +/- 3.8 (SE) s, LBF = 27.6 +/- 3.9 s] than in the upright positions (VO2 = 29.3 +/- 3.0 s, LBF = 17.3 +/- 4.0 s; P < 0.05). These data support our hypothesis that slower increases in alveolar VO2 at the onset of exercise in the supine position are accompanied by a slower increase in LBF.     

Transcranial Doppler sonographic measurements of middle cerebral artery flow velocity during hyperbaric oxygen exposures

In the present study, experimental exposures to hyperbaric oxygen (HBO2) were performed (30-min exposure to 2.8 bar (280 kPa) pure oxygen). During all phases of the experiment, blood flow velocity in the right middle cerebral artery was monitored with transcranial Doppler (TCD) sonography. Time courses of heart rate, blood pressure, respiratory rate, end-tidal CO2, and TCD mean velocity (Vmean) are described for a group of 23 subjects during uncomplicated exposure to HBO2 and for three subjects who showed signs of central nervous system (CNS) O2 toxicity, including one subject with a HBO2-induced generalized tonic-clonic seizure. Hyperbaric oxygen decreased Vmean an effect that could not completely be explained by changes in end-tidal CO2. The findings of the present study are in agreement with the concept that an increase in partial oxygen pressure is the primary factor underlying CNS O2 toxicity. Of the variables analyzed, the TCD Vmean is the most valuable variable for monitoring a HBO2 exposure. The Vmean showed the most pronounced change during HBO2 application, and in one subject a sudden increase in Vmean during HBO2 exposure heralded toxicity before clinical signs. It should be realized, however, that the small series of subjects with toxicity in this study does not allow us to draw definite conclusions.