Association of VO2 and VCO2 rate variability with serum glucose, insulin, and glucose intolerance

Changes in the cellular metabolism assessed by the variability of oxygen consumption (VO(2) ) and carbon dioxide production (VCO(2) ) as well as the association of serum glucose and insulin to energy spectral density (ESD) of VO(2) and VCO(2) were evaluated. Ten nonglucose intolerant and 10 glucose intolerant subjects, aged 21-70 years, were included. Glucose and insulin concentrations and VO(2) and VCO(2) records were collected every 10 min during 3 h. ESD of VO(2) and VCO(2) was estimated and associated with glucose and insulin concentrations. Statistical significance in glucose levels, insulin, and ESD of VO(2) and VCO(2) among nonglucose intolerant subjects and glucose and insulin among glucose intolerance subjects at postload glucose (PLG) state compared with basal state was found. Moreover, glucose was significantly higher in glucose intolerance subjects than nonglucose intolerant subjects for basal and PLG states. These results show an increment in ESD of VO(2) and VCO(2) at PLG state among nonglucose intolerant subjects and suggest that their measurement may be a key indicator of the variability of cellular metabolic activity and contribute to confirm disturbances in glucose metabolism.     

Metabolic and cardioventilatory responses during a graded exercise test before and 24 h after a triathlon

Previous studies have reported respiratory, cardiac and muscle changes at rest in triathletes 24 h after completion of the event. To examine the effects of these changes on metabolic and cardioventilatory variables during exercise, eight male triathletes of mean age 21.1 (SD 2.5) years (range 17-26 years) performed an incremental cycle exercise test (IET) before (pre) and the day after (post) an official classic triathlon (1.5-km swimming, 40-km cycling and 10-km running). The IET was performed using an electromagnetic cycle ergometer. Ventilatory data were collected every minute using a breath-by-breath automated system and included minute ventilation (V(E)), oxygen uptake (VO2), carbon dioxide production (VCO2), respiratory exchange ratio, ventilatory equivalent for oxygen (V(E)/VO2) and for carbon dioxide (V(E)/VCO2), breathing frequency and tidal volume. Heart rate (HR) was monitored using an electrocardiogram. The oxygen pulse was calculated as VO2/HR. Arterialized blood was collected every 2 min throughout IET and the recovery period, and lactate concentration was measured using an enzymatic method. Maximal oxygen uptake (VO2max) was determined using conventional criteria. Ventilatory threshold (VT) was determined using the V-slope method formulated earlier. Cardioventilatory variables were studied during the test, at the point when the subject felt exhausted and during recovery. Results indicated no significant differences (P > 0.05) in VO2max [62.6 (SD 5.9) vs 64.6 (SD 4.8) ml x kg(-1) x min(-1)], VT [2368 (SD 258) vs 2477 (SD 352) ml x min(-1)] and time courses of VO2 between the pre- versus post-triathlon sessions. In contrast, the time courses of HR and blood lactate concentration reached significantly higher values (P < 0.05) in the pre-triathlon session. We concluded that these triathletes when tested 24 h after a classic triathlon displayed their pre-event aerobic exercise capacity, bud did not recover pretriathlon time courses in HR or blood lactate concentration.     

Kinetics of CO uptake and diffusing capacity in transition from rest to steady-state exercise.

In the transition from rest to steady-state exercise, O2 uptake from the lungs (VO2) depends on the product of pulmonary blood flow and pulmonary arteriovenous O2 content difference. The kinetics of pulmonary blood flow are believed to be somewhat faster than changes in pulmonary arteriovenous O2 content difference. We hypothesized that during CO breathing, the kinetics of CO uptake (VCO) and diffusing capacity for CO (DLCO) should be faster than VO2 because changes in pulmonary arteriovenous CO content difference should be relatively small. Six subjects went abruptly from rest to constant exercise (inspired CO fraction = 0.0005) at 40, 60, and 80% of their peak VO2, measured with an incremental test (VO2peak). At all exercise levels, DLCO and VCO rose faster than VO2 (P less than 0.001), and DLCO rose faster than VCO (P less than 0.001). For example, at 40% VO2peak, the time constant (tau) for DLCO in phase 2 was 19 +/- 5 (SD), 24 +/- 5 s for VCO, and 33 +/- 5 s for VO2. Both VCO and DLCO increased with exercise intensity but to a lesser degree than VO2 at all exercise intensities (P less than 0.001). In addition, no significant rise in DLCO was observed between 60 and 80% VO2peak. We conclude that the kinetics of VCO and DLCO are faster than VO2, suggesting that VCO and DLCO kinetics reflect, to a greater extent, changes in pulmonary blood flow and thus recruitment of alveolar-capillary surface area. However, other factors, such as the time course of ventilation, may also be involved.(ABSTRACT TRUNCATED AT 250 WORDS)     

Light-dark differences in the effects of ambient temperature on gaseous metabolism in newborn rats.

Body temperature (T(b)) of rat pups (7-9 days old) raised under a 12:12-h light-dark (L-D) regimen (L: 0700-1900, D: 1900-0700) was consistently higher in D than in L by approximately 1.1 degrees C. We tested the hypothesis that the L-D differences in T(b) were accompanied by differences in the set point of thermoregulation. Measurements were performed on rat pups at 7-9 days after birth. O(2) consumption (VO(2)) and CO(2) production (VCO(2)) were measured with an open-flow method during air breathing, as ambient temperature (T(a)) was decreased from 40 to 15 degrees C at the constant rate of 0.5 degrees C/min. At T(a) >/=33 degrees C, VO(2) was not significantly different between L and D, whereas VCO(2) was higher in L, suggesting a greater ventilation. Over the 33 to 15 degrees C range the VO(2) values in D exceeded those in L by approximately 30%. Specifically, the difference was contributed by differences in thermogenesis at T(a) = 30 to 20 degrees C. As T(a) was decreased, the critical temperature at which VO(2) began to rise was lower in L. We conclude that the higher T(b) of rat pups in D is accompanied by a higher set point for thermoregulation and a greater thermogenesis. These results are consistent with the idea that, in newborns, endogenous changes in the set point of thermoregulation contribute to the circadian oscillations of T(b).     

Effects of exercise and time elapsed after exercise on VO2, VCO2 and R responses to norepinephrine in rats

The effects of norepinephrine (NE) injection (300 microgram . kg-1 of body weight) on oxygen consumption (VO2), carbon dioxide production (VCO2) and respiratory exchange ratio (R) were investigated in female rats after 1 h of running on a treadmill (21.5 m . min-1) at 10% inclination. Six groups of animals were injected respectively at various times after the exercise (1, 3, 6, 9, 21, and 47 h), and were compared to six non-exercised groups injected at corresponding times. VO2 and VCO2 were monitored continuously during the 20 min preceding injection and for the 60 min following it. The increases in VO2 and VCO2, and the decrease in R were of similar magnitude in both exercised and non-exercised rats (about 30% and 20% for VO2 and VCO2, respectively, and -12% for R). Peak VO2 and R values attained after NE injection varied however with time of injection, specially in exercised animals 1 and 9 h after the run. Exercise significantly delayed time of response to NE for VO2 and VCO2 particularly 1 and 9 h after the running bout. It is concluded that time of day, exercise, and time elapsed after exercise are important factors to consider when studying metabolic responses to catecholamines. Furthermore, it is suggested that such experimental controls might be meaningful in human studies as well.     

Mechanistic basis for the gas exchange threshold in Thoroughbred horses.

The exercising Thoroughbred horse (TB) is capable of exceptional cardiopulmonary performance. However, because the ventilatory equivalent for O2 (VE/VO2) does not increase above the gas exchange threshold (Tge), hypercapnia and hypoxemia accompany intense exercise in the TB compared with humans, in whom VE/VO2 increases during supra-Tge work, which both removes the CO2 produced by the HCO buffering of lactic acid and prevents arterial partial pressure of CO2 (PaCO2) from rising. We used breath-by-breath techniques to analyze the relationship between CO2 output (VCO2) and VO2 [V-slope lactate threshold (LT) estimation] during an incremental test to fatigue (7 to approximately 15 m/s; 1 m x s(-1) x min(-1)) in six TB. Peak blood lactate increased to 29.2 +/- 1.9 mM/l. However, as neither VE/VO2 nor VE/VCO2 increased, PaCO2 increased to 56.6 +/- 2.3 Torr at peak VO2 (VO2 max). Despite the presence of a relative hypoventilation (i.e., no increase in VE/VO2 or VE/VCO2), a distinct Tge was evidenced at 62.6 +/- 2.7% VO2 max. Tge occurred at a significantly higher (P < 0.05) percentage of VO2 max than the lactate (45.1 +/- 5.0%) or pH (47.4 +/- 6.6%) but not the bicarbonate (65.3 +/- 6.6%) threshold. In addition, PaCO2 was elevated significantly only at a workload > Tge. Thus, in marked contrast to healthy humans, pronounced V-slope (increase VCO2/VO2) behavior occurs in TB concomitant with elevated PaCO2 and without evidence of a ventilatory threshold.     

Instrumentation simultaneously measuring VCO2 and VO2 in humans using titration methods

An instrument has been developed for the simultaneous measurement of carbon dioxide excretion (VCO2) and oxygen uptake (VO2). This instrument, the Nutrimeter, gives these breath-averaged measurements continuously without having to determine respiratory flow rate, perform timed spirometric gas collections, or determine absolute CO2 or O2 concentrations. It can be used on ventilated or nonventilated patients in long- and short-term studies. VO2 is determined via the replenishment technique. VCO2 is determined via a new technique, absorption-titration, described here. Bench test results of VCO2 measurements show a standard error of the estimate (SEE) +/- 0.591% of full scale (500 ml/min) and maximum single point error (MSPE) of +/- 3.54% over a 100--350 ml/min range. VO2 measurements show SEE +/- 0.518% of full scale (1,000 ml/min) and MSPE +/- 2.42% over a 100--450 ml/min range. In 31 human clinical trials the Nutrimeter was compared with the open-circuit spirometric collection and micro-Scholander analysis technique. VCO2 measurements show SEE +/- 2.208% and MSPE +/- 10.57% over 135--315 ml/min. VO2 measurements show SEE +/- 1.134% of full scale and MSPE +/- 9.54% over 170--360 ml/min. Response time is 60 s optimally for step changes in VO2 (0--90% of steady-state value), 90 s for VCO2.     

Unusual peaks of oxygen consumption under special alimentary conditions

Oxygen consumption (VO2), carbon dioxide production (VCO2), the resulting respiratory quotient (RQ), and motor activity were recorded simultaneously by an on-line computer every ten seconds during 16-20 hours in two decerebrate male rats. Being aphagic and adipsic the rats were fed twice daily by gastric intubation with a mixture of powdered milk plus sugar or plus sunflower oil (approx. 300 KJ daily) in 10-20 ml tap water. In all seven tests performed on these rats the recordings presented very steep reductions of RQ due every time to steep increases in VO2 without increases in VCO2. Mean number of VO2 peaks in all experiments was 12.4 +/- 1.8 (SE) with mean duration of 21.3 +/- 2.8 min. Two normal male rats were fed the same diet and on the same schedule: they presented similar VO2 peaks in 8 out of 12 experiments. Mean number was 8.7 +/- 1.0 with mean duration of 13.6 +/- 2.2 min. The VO2 peak periods never occurred in rats fed ad libitum. In the two normal rats oil ingestion produced more effect than sugar. It is suggested that the phenomenon could be due to a metabolic imbalance possibly of hepatic origin, more evident in decerebrate rats. VO2 peaks could be produced by enhanced ketogenesis, gluconeogenesis and/or extra-mitochondrial (peroxisomal, microsomal) oxidation.     

Frequency domain analysis of ventilation and gas exchange kinetics in hypoxic exercise.

The kinetics of O2 up-take (VO2), CO2 output (VCO2), ventilation (VE), and heart rate (HR) were studied during exercise in normoxia and hypoxia [inspired O2 fraction (FIO2) 0.14]. Eight male subjects each completed 6 on- and off-step transitions in work rate (WR) from low (25 W) to moderate (100-125 W) levels and a pseudorandom binary sequence (PRBS) exercise test in which WR was varied between the same WRs. Breath-by-breath data were linearly interpolated to yield 1-s values. After the first PRBS cycle had been omitted as a warm-up, five cycles were ensemble-averaged before frequency domain analysis by standard Fourier methods. The step data were fit by a two-component (three for HR) exponential model to estimate kinetic parameters. In the steady state of low and moderate WRs, each value of VO2, VCO2, VE, and HR was significantly greater during hypoxic than normoxic exercise (P less than 0.05) with the exception of VCO2 (low WR). Hypoxia slowed the kinetics of VO2 and HR in on- and off-step transitions and speeded up the kinetics of VCO2 and VE in the on-transition and of VE in the off-transition. Frequency domain analysis confined to the range of 0.003-0.019 Hz for the PRBS tests indicated reductions in amplitude and greater phase shifts in the hypoxic tests for VO2 and HR at specific frequencies, whereas amplitude tended to be greater with little change in phase shift for VCO2 and VE during hypoxic tests.(ABSTRACT TRUNCATED AT 250 WORDS)     

Response of respiratory exchange ratio (R) to sinusoidal work load in humans

An examination was made of the response of respiratory exchange ratio (R), carbon dioxide output (VCO2) and oxygen uptake (VO2) to sinusoidal work load with periods (T) of 1-16 min in six healthy men to determine whether R response is sinusoidal. The influence of the ratio of the amplitude of VCO2 to that of VO2 and the phase lag between them on R response was also studied by computer simulation. The results and conclusions obtained are as follows: 1) With decrease in the period, the amplitudes of VO2 and VCO2 dropped exponentially, becoming least at T of 1 min (T = 1 min). In contrast, the amplitude of R was largest at T = 4 min and subsequently decreased progressively. 2) The peak amplitude of R at T = 4 min can be explained by the larger phase lag and relatively low of amplitude of VCO2 to VO2. 3) The smallest amplitude of R at T = 1 min was due not to the ratio of amplitude or phase lag, but to remarkably smaller amplitudes of VO2 and VCO2. 4) The phase lag of VO2 to sinusoidal work load was smaller than that of VCO2. Phase lag of R was considerably larger than that of VO2 or VCO2. 5) The response curve of VO2 and VCO2 is a sinusoidal curve with the same period as exercise. However, the response of R is not a real sinusoidal but a deformed biphasic curve with a high crest and low trough. The deformity is determined by the phase lag between VO2 and VCO2 response and also the ratio of amplitude of VCO2 to that of VO2.     

Effect of inspiratory threshold loading on ventilatory kinetics during constant-load exercise

Humoral factors play an important role in the control of exercise hyperpnea. The role of neuromechanical ventilatory factors, however, is still being investigated. We tested the hypothesis that the afferents of the thoracopulmonary system, and consequently of the neuromechanical ventilatory loop, have an influence on the kinetics of oxygen consumption (VO2), carbon dioxide output (VCO2), and ventilation (VE) during moderate intensity exercise. We did this by comparing the ventilatory time constants (tau) of exercise with and without an inspiratory load. Fourteen healthy, trained men (age 22.6 +/- 3.2 yr) performed a continuous incremental cycle exercise test to determine maximal oxygen uptake (VO2max = 55.2 +/- 5.8 ml x min(-1) x kg(-1)). On another day, after unloaded warm-up they performed randomized constant-load tests at 40% of their VO2max for 8 min, one with and the other without an inspiratory threshold load of 15 cmH2O. Ventilatory variables were obtained breath by breath. Phase 2 ventilatory kinetics (VO2, VCO2, and VE) could be described in all cases by a monoexponential function. The bootstrap method revealed small coefficients of variation for the model parameters, indicating an accurate determination for all parameters. Paired Student's t-tests showed that the addition of the inspiratory resistance significantly increased the tau during phase 2 of VO2 (43.1 +/- 8.6 vs. 60.9 +/- 14.1 s; P < 0.001), VCO2 (60.3 +/- 17.6 vs. 84.5 +/- 18.1 s; P < 0.001) and VE (59.4 +/- 16.1 vs. 85.9 +/- 17.1 s; P < 0.001). The average rise in tau was 41.3% for VO2, 40.1% for VCO2, and 44.6% for VE. The tau changes indicated that neuromechanical ventilatory factors play a role in the ventilatory response to moderate exercise.     

Delayed kinetics of respiratory gas exchange in the transition from prior exercise

The kinetics of oxygen uptake (VO2), carbon dioxide output (VCO2), and expired ventilation (VE) in the transition from rest or from prior exercise were studied in response to step increases in power output (PO). The data were modeled with a single-component exponential function incorporating a time delay (TD). Each subject exercised on four occasions. Test 1 was an incremental test for determination of ventilatory anaerobic threshold (AT). Step increase tests were rest to 80% of PO at AT (test 2), rest-40% AT (3a), 40-80% AT (3b), rest-40% AT (4a), and 40-120% AT (4b). Respiratory gas exchange was monitored by open-circuit techniques. The VO2 kinetics showed the time constant (tau) to be longer in the transitions from prior exercise [tests 3b and 4b were 60.6 +/- 10.8 (SD) and 79.2 +/- 17.4 s] than from rest (tests 2, 3a, and 4a were 37.8 +/- 7.2, 30.0 +/- 7.8, and 39.6 +/- 17.4 s). The mean response time (MRT = tau + TD) was also longer for these tests. Kinetic analysis for VCO2 showed a tendency for tau to be shorter for the tests from prior exercise, but neither tau nor tau + TD were significantly different between tests. In contrast to VCO2, VE kinetics showed a significantly longer tau + TD for test 3b (P less than 0.05) and test 4b (P less than 0.01). This study has shown the VO2 kinetics to be delayed when a given increment in PO occurred from prior exercise, whether the final PO was below or above the AT. Further, the dissociation of VCO2 and VE kinetics does not support a direct link between these two variables as the sole control factor in exercise hyperpnea.     

Alterations in ventilation and gas exchange during exercise-induced carbohydrate depletion.

The relationship between ventilation (VE), oxygen consumption (VO2), and carbon dioxide production (VCO2) during work were studied in four trained males during exercise-induced carbohydrate depletion. Repeated bouts of heavy treadmill exercise (6 min at 95% VO2 max) were performed once per hour for 24 h in order to promote a shift in energy substrate from carbohydrate to fat. Measurements of VO2 and VCO2 recorded during each minute indicated that VO2 was unaffected by the number of runs, whereas VCO2 showed a progressive reduction which amounted to 24% during the final run. A corresponding decline of 19% was observed in the respiratory exchange ratio. No significant change in VE occurred between any of the runs. It is concluded that during heavy, repeated, muscular exercise, reductions in VO2, strongly suggestive of an increased fat oxidation, are not accompanied by a corresponding change in ventilation.     

A prototype gas exchange monitor for exercise stress testing aboard NASA Space Station

A monitor was developed to track weightlessness deconditioning aboard the National Aeronautics and Space Administration (NASA) Space Station by measuring the O2 uptake (VO2) and CO2 production (VCO2) and calculating maximum VO2 and anaerobic threshold during an exercise stress test. The system uses two flowmeters in series to achieve a completely automatic flow calibration, and it uses breath-by-breath compensation for sample line transport delay. The accuracy of the system was measured over the range of VO2 and VCO2 from 100 to 800 ml/min by means of simulation. Accuracy was 0.54% for VO2 and 2.9% for VCO2. The system was further evaluated using two laboratory methods, the first method being comparison with a breath-by-breath system. As volunteers performed a maximum effort on a cycle ergometer, the mean difference in readings between the two systems was 17 ml/min for VO2 and 8.0 ml/min for VCO2. The correlation coefficient squared was greater than 0.96 for both. The second laboratory test was to use the system for 2 mo in a Human Performance Laboratory. Readings of maximum VO2 (VO2max) and anaerobic threshold were repeatable and consistent with the individual's activity level. The accuracy and convenience of operation will make this a valuable instrument aboard the Space Station.     

Respiratory ultradian variations of mean and low frequencies (from 2-80 cycles per day) in premature human infants

Oxygen consumption (VO2) and carbon dioxide production (VCO2) were continuously measured in premature human (mean gestation age of 31 weeks at birth), nursed in incubators within a neutral thermal environment and submitted to a continuous lighting. At a mean postnatal age of 30 days, and for a mean body weight of 1.8 kg, spectral analysis shows VO2 and VCO2 ultradian variations of mean and low frequencies (2 less than f less than 80 c.day--1; i.e. periods 12 greater than t greater than 0.3 hr). It is hypothesized that these periodic variations can be compared to those previously evidenced in small laboratory vertebrates and in macaques.     

Ventilatory and gas exchange kinetics during exercise in chronic airways obstruction

The influence of chronic obstructive pulmonary disease (COPD) on exercise ventilatory and gas exchange kinetics was assessed in nine patients with stable airway obstruction (forced expired volume at 1 s = 1.1 +/- 0.33 liters) and compared with that in six normal men. Minute ventilation (VE), CO2 output (VCO2), and O2 uptake (VO2) were determined breath-by-breath at rest and after the onset of constant-load subanaerobic threshold exercise. The initial increase in VE, VCO2, and VO2 from rest (phase I), the subsequent slow exponential rise (phase II), and the steady-state (phase III) responses were analyzed. The COPD group had a significantly smaller phase I increase in VE (3.4 +/- 0.89 vs. 6.8 +/- 1.05 liters/min), VCO2 (0.10 +/- 0.03 vs. 0.22 +/- 0.03 liters/min), VO2 (0.10 +/- 0.03 vs. 0.24 +/- 0.04 liters/min), heart rate (HR) (6 +/- 0.9 vs. 16 +/- 1.4 beats/min), and O2 pulse (0.93 +/- 0.21 vs. 2.2 +/- 0.45 ml/beat) than the controls. Phase I increase in VE was significantly correlated with phase I increase in VO2 (r = 0.88) and HR (r = 0.78) in the COPD group. Most patients also had markedly slower phase II kinetics, i.e., longer time constants (tau) for VE (87 +/- 7 vs. 65 +/- 2 s), VCO2 (79 +/- 6 vs. 63 +/- 3 s), and VO2 (56 +/- 5 vs. 39 +/- 2 s) and longer half times for HR (68 +/- 9 vs. 32 +/- 2 s) and O2 pulse (42 +/- 3 vs. 31 +/- 2 s) compared with controls. However, tau VO2/tau VE and tau VCO2/tau VE were similar in both groups. The significant correlations of the phase I VE increase with HR and VO2 are consistent with the concept that the immediate exercise hyperpnea has a cardiodynamic basis. The slow ventilatory kinetics during phase II in the COPD group appeared to be more closely related to a slowed cardiovascular response rather than to any index of respiratory function. O2 breathing did not affect the phase I increase in VE but did slow phase II kinetics in most subjects. This confirms that the role attributed to the carotid bodies in ventilatory control during exercise in normal subjects also operates in patients with COPD.     

System of automated gas-exchange analysis for the investigation of metabolic processes.

Conventional gas-exchange instruments are confined to the measurement of O(2) consumption (VO(2)) and CO(2) production (VCO(2)) and are subject to a variety of errors. This handicaps the performance of these devices at inspired O(2) fraction (FI(O(2))) > 0.40 and limits their applicability to indirect calorimetry only. We describe a device based on the automation of the Douglas bag technique that is capable of making continuous gas-exchange measurements of multiple species over a broad range of experimental conditions. This system is validated by using a quantitative methanol-burning lung model modified to provide reproducible (13)CO(2) production. The average error for VO(2) and VCO(2) over the FI(O(2)) range of 0.21-0.8. is 2.4 and 0.8%, respectively. The instrument is capable of determining the differential atom% volume of known references of (13)CO(2) to within 3.4%. This device reduces the sources of error that thwart other instruments at FI(O(2)) > 0. 40 and demonstrates the capacity to explore other expressions of metabolic activity in exhaled gases related to the excretion of (13)CO(2).     

Energy expenditure during bicycling

This study was designed to measure the O2 uptake (VO2) of cyclists while they rode outdoors at speeds from 32 to 40 km/h. Regression analyses of data from 92 trials using the same wheels, tires, and tire pressure with the cyclists riding in their preferred gear and in an aerodynamic position indicated the best equation (r = 0.84) to estimate VO2 in liters per minute VO2 = -4.50 + 0.17 rider speed + 0.052 wind speed + 0.022 rider weight where rider and wind speed are expressed in kilometers per hour and rider weight in kilograms. Following another rider closely, i.e., drafting, at 32 km/h reduced VO2 by 18 +/- 11%; the benefit of drafting a single rider at 37 and 40 km/h was greater (27 +/- 8%) than that at 32 km/h. Drafting one, two, or four riders in a line at 40 km/h resulted in the same reduction in VO2 (27 +/- 7%). Riding at 40 km/h at the back of a group of eight riders reduced VO2 by significantly more (39 +/- 6%) than drafting one, two, or four riders in a line; drafting a vehicle at 40 km/h resulted in the greatest decrease in VO2 (62 +/- 6%). VO2 was also 7 +/- 4% lower when the cyclists were riding an aerodynamic bicycle. An aerodynamic set of wheels with a reduced number of spokes and one set of disk wheels were the only wheels to reduce VO2 significantly while the cyclists were riding a conventional racing bicycle at 40 km/h.(ABSTRACT TRUNCATED AT 250 WORDS)     

The relationship between the ventilation and lactate thresholds following normal, low and high carbohydrate diets

Five men performed an incremental exercise test following a normal, low and high carbohydrate dietary regimen over a 7-day period, to examine the influence of an altered carbohydrate energy intake on the relationship between the ventilation (VET) and lactate (LaT) thresholds. VET and LaT were determined from the ventilatory equivalents for O2 (VE.VO2(-1) and CO2 (VE.VCO2(-1) and the log-log transformation of the lactate (La) to power output relationship, respectively. The total duration of the incremental exercise test, carbon dioxide output (VCO2), respiratory exchange ratio, blood La values and arterialized venous partial pressure of CO2 (PCO2) were reduced, and VE.VCO2(-1), the slope of the VE-VCO2 relationship, blood beta-hydroxybutyrate and pH were increased during the low carbohydrate trial compared with the other conditions. Total plasma protein and Na+, K+, and Cl- were similar across conditions. LaT and VET were unaffected by the altered proportions of carbohydrate in the diets and occurred at a similar oxygen consumption (mean VO2 across trials was 1.98 L.min-1 for VET and 2.01 L.min-1 for LaT). A significant relationship (r = 0.86) was observed for the VO2 that represented individual VET and LaT values. The increased VE.VCO2(-1) and slope of the VE-VCO2 relationship could be accounted for by the lower PCO2. It is concluded that alterations in carbohydrate energy intake do not produce an uncoupling of VET and LaT as has been reported previously.     

Cardiogenic motion of right lung parenchyma in anesthetized intact dogs

Recent investigation suggests that both ventilation (VE) and the chemical sensitivity of the respiratory control system correlate closely with measures of metabolic rate [O2 consumption (VO2) and CO2 production (VCO2)]. However, these associations have not been carefully investigated during sleep, and what little information is available suggests a deterioration of the relationships. As a result we measured VE, ventilatory pattern, VO2, and VCO2 during sleep in 21 normal subjects (11 males and 10 females) between the ages of 21 and 77 yr. When compared with values for awake subjects, expired ventilation decreased 8.2 +/- 2.3% (SE) during sleep and was associated with a 8.5 +/- 1.6% decrement in VO2 and a 12.3 +/- 1.7% reduction in VCO2, all P less than 0.01. The decrease in ventilation was a product primarily of a significant decrease in tidal volume with little change in frequency. None of these findings were dependent on sleep stage with results in rapid-eye-movement (REM) and non-rapid-eye-movement sleep being similar. Through all sleep stages ventilation remained tightly correlated with VO2 and VCO2 both within a given individual and between subjects. Although respiratory rhythmicity was somewhat variable during REM sleep, minute ventilation continued to correlate with VO2 and VCO2. None of the parameters described above were influenced by age or gender, with male and female subjects demonstrating similar findings. Ten of the subjects demonstrated at least occasional apneas. These individuals, however, were not found to differ from those without apnea in any other measure of ventilation or metabolic rate.(ABSTRACT TRUNCATED AT 250 WORDS)