Starvation and respiratory rhythmic behavior in groups of light-dark synchronized Sprague-Dawley rats

Twenty adult male SPF Sprague-Dawley rats, grouped by 5 and synchronized by a light (L)-dark (D) 12:12 alternation, were deprived of food and water for 7 days; 20 other rats were taken as controls. Continuous measurement of emitted carbon dioxide (VCO2), which was taken as an index of respiratory and metabolic exchanges, shows that starvation significantly (p less than 0.001) decreases the amplitudes of the circadian VCO2 rhythms (by 42.5% during L and 35.6% during D) and also the L----D photic VCO2 responses (by 9.2%; p less than 0.05). Concerning ultradian rhythms of mean and great periods (40 min less than tau less than 24 hr), food and water suppression diminishes their amplitudes (by 58.4% in L and 32.4% in D) and changes their phases (by a 1.29 radian advance in L and a 0.68 radian delay in D). Rats recovered their prestarvation circadian and ultradian VCO2 rhythms 6-7 days after food and water had been given back to them.     

The energetic and metabolic effect of Ringerfundin (B. Braun) infusion and comparison with Plasma-Lyte (Baxter) in healthy volunteers

Measurement of parameters of energy requirement, respiratory quotient (RQ), rate of oxygen consumption (VO2) and rate of carbon dioxide production (VCO2) reveal Ringerfundin as an excellent and metabolically stable-acting balanced ionic solution, which does not increase the consumption of O2 or the total energy requirement. In conclusion, Ringerfundin was very well tolerated and in no case were observed undesirable effects.     

Metabolic control of pulmonary ventilation in the developing chick embryo

In birds, during the period from the breaking of the air cell by the beak (internal pipping) to hatching, pulmonary ventilation (VE) begins and gas exchange is jointly provided by the lungs and the chorioallantoic membrane (CAM). We asked to what extent, during this phase of two concurrent gas exchange organs, changes in the embryo's metabolic needs were accompanied by changes in VE. The carbon dioxide and oxygen exchange rates (VCO2, VO2) through lungs and CAM were separately, but simultaneously, measured in chicken embryos at 20-21 days of incubation, while VE was calculated from the measurements of pressure oscillations in the air cell during breathing. During the last 24 h of incubation, lung VO2 and VCO2 gradually progressed as the corresponding CAM values declined. An increase in egg temperature (T) from 33 to 39 degrees C increased the embryo's total metabolic rate, especially when the lungs were the predominant gas exchange route. Whether metabolism increased because of the embryo's development or because of the increase in T, VE was linearly proportional to lung VO2 and VCO2, and not to the embryo's total metabolic rate. Hence, in the developing chick embryo, VE control mechanisms sense the peripheral tissue requirements via the gaseous component of cellular metabolism.     

Ventilation and acid-base balance during graded activity in lizards

Arterial PCO2, hydrogen ion ([H+]a), and lactate ([L]a) concentrations, rates of metabolic CO2 production (VCO2) and O2 consumption (VO2), and effective alveolar ventilation (Veff) were determined in the lizards Varanus exanthematicus and Iguana iguana at rest and during steady-state treadmill exercise at 35 degrees C. In Varanus, VCO2 increased ninefold and VO2 sixfold without detectable rise in [L]a at running speeds below 1.0 to 1.5 km x h-1. In this range, Veff increased 12-fold resulting in decreased levels of PaCO2 and [H+]a. At higher speeds [L]a rose. Increments of 5 mM [L]a were accompanied by hyperventilation, reducing PaCO2 and thus maintaining [H+]a near its resting level. When [L]a increased further, [H+]a increased. Sustainable running speeds (0.3-0.5 km x h-1 and below) were often associated with increased VO2, VCO2, and [L]a in Iguana. Sixfold increases in VCO2 and 9-mM increments in [L]a were accompanied by sufficient increase in Veff (9-fold) to maintain [H+]a at or below its control level. When [L]a increased further, [H+]a increased. These results indicate that both lizard species maintain blood acid-base homeostasis rather effectively via ventilatory adjustments at moderate exercise intensities.     

The Effects of Caffeine on the Kinetics of O2Uptake, CO2Production and Expiratory Ventilation in Humans During the On-Transient of Moderate and Heavy Intensity Exercise

In order to test the hypothesis that glycogen sparing observed early during exercise following caffeine ingestion was a consequence of tighter metabolic control reflected in faster VO2 kinetics, we examined the effect of caffeine ingestion on oxygen uptake (VO2), carbon dioxide production (VCO2) and expiratory ventilation (VE) kinetics at the onset of both moderate (MOD) and heavy (HVY) intensity exercise. Male subjects (n = 10) were assigned to either a MOD (50% VO2,max, n = 5) or HVY (80% VO2,max, n = 5) exercise condition. Constant-load cycle ergometer exercise was performed as a step function from loadless cycling 1 h after ingestion of either dextrose (placebo, PLAC) or caffeine (CAFF; 6 mg (kg body mass)-1). Alveolar gas exchange was measured breath-by-breath. A 2- or 3-component exponential model, fitted through the entire exercise transient, was used to analyse gas exchange and ventilatory data for the determination of total lag time (TLT: the time taken to attain 63% of the total exponential increase). Caffeine had no effect on TLT for VO2 kinetics at either exercise intensity (MOD: 36 +/- 14 s (PLAC) and 41 +/- 10 s (CAFF); HVY: 99 +/- 30 s (PLAC) and 103 +/- 26 (CAFF) (mean +/- S.D.)). TLT for VE was increased with caffeine at both exercise intensities (MOD: 50 +/- 20 s (PLAC) and 59 +/- 21 s (CAFF); HVY: 168 +/- 35 s (PLAC) and 203 +/- 48 s (CAFF)) and for VCO2 during MOD only (MOD: 47 +/- 14 s (PLAC) and 53 +/- 17 s (CAFF); HVY: 65 +/- 13 s (PLAC) and 69 +/- 17 s (CAFF)). Contrary to our hypothesis, the metabolic effects of caffeine did not alter the on-transient VO2 kinetics in moderate or heavy exercise. VCO2 kinetics were slowed by a reduction in CO2 stores reflected in pre-exercise and exercise endtidal CO2 pressure (PET,CO2) and plasma PCO2 which, we propose, contributed to slowed VE kinetics.     

Gaseous metabolism of the chicken embryo and hatchling during post-hypoxic recovery

In neonatal mammals, the drop in oxygen consumption (VO2) during moderate degrees of hypoxia is a manifestation of metabolic depression, and occurs without anaerobic energy compensation. We examined the possibility that embryos also respond to hypoxia with a similar hypometabolic response, by measuring the extent of the O2 debt during post-hypoxic recovery. In chicken embryos at incubation days 11 (E11) and 16 (E16), and hatchlings on the day of hatching (H1), VO2 and carbon dioxide production (VCO2) were measured with an open flow system. The protocol consisted of 1h in air, followed by 40 min in hypoxia (either 17% or 11% O2) and additional 45 min of post-hypoxic recovery. VO2 dropped in hypoxia, more with 11% than 17% O2, and more the younger the animal. During post-hypoxic recovery VO2 returned to, but did not exceed, the pre-hypoxic level, indicating that no O2 debt was contracted during hypoxia. In H1, the changes of VCO2 during hypoxia and post-hypoxia matched those of VO2. Differently, in the embryos, the changes in VCO2 during hypoxia and post-hypoxic recovery were minimal. This phenomenon is explained by changes in the large CO2 stores of the eggs, which buffer the changes in CO2 output of aerobic origin. We conclude that in the chicken embryo and hatchling the energetic shortfall during the hypoxic decrease in VO2 is not compensated by anaerobic energy supply, and represents a phenomenon of metabolic depression.     

Change point in VCO2 during incremental exercise test: a new method for assessment of human exercise tolerance.

The main purpose of this study was to present a new method to determine the level of power output (PO) at which VCO2 during incremental exercise test (IT) begins to rise non-linearly in relation to power output (PO) - the change point in VCO2 (CP-VCO2). Twenty-two healthy non-smoking men (mean +/- SD: age 22.0 +/- 0.9 years; body mass 74.5 +/- 7.5 kg; height 181 +/- 7 cm; VO2max 3.753 +/- 0.335 l min-1) performed an IT on a cycloergometer. The IT started at a PO of 30 W, followed by gradual increases of 30 W every 3 min. Antecubital venous blood samples were taken at the end of each step and analysed for plasma lactate concentration [La]pl, blood PO2, PCO2 [HCO3-]b and [H+]b. In the detection of the change-point VCO2 (CP-VCO2), a two-phase model was assumed for the 'third-minute-data' of each step of the test. In the first phase, a linear relationship between VCO2 and PO was assumed, whereas in the second, an additional increase in VCO2 was allowed, above the values expected from the linear model. The PO at which the first phase ends is called the change point in VCO2. The identification of the model consists of two steps: testing for the existence of the change point, and estimating its location. Both procedures are based on suitably normalized recursive residuals (see Zoladz et al. 1998a. Eur J Appl Physiol 78, 369-377). In the case of each of our subjects it was possible to detect the CP-VCO2 and the CP-VO2 as described in our model. The PO at the CP-VCO2 amounted to 134 +/- 42 W. The CP- VO2 was detected at 136 +/- 32 W, whereas the PO at the LT amounted to 128 +/- 30 W and corresponded to 49 +/- 11, 49 +/- 8 and 47 +/- 8.6% VO2max, respectively, for the CP-VCO2, CP-VO2 and the LT. The [La]pl at the CP-VCO2 (2.65 +/- 0.76 mmol L-1), at the CP-VO2 (2.53 +/- 0. 56 mmol L-1) and at the LT (2.25 +/- 0.49 mmol L-1) were already significantly higher (P < 0.01, Students t-test) than the value reached at rest (1.86 +/- 0.43 mmol L-1). Our study illustrates that the CP-VCO2 and the CP-VO2 occur at a very similar power output as the LT. We therefore postulate that the CP-VCO2 and the CP-VO2 be applied as an additional criterion to assess human exercise tolerance.     

Effects of prenatal protein malnutrition on the electrical cerebral activity during development

Early protein restriction during the prenatal period has significant repercussions on the ontogeny and development of the central nervous system. The present study investigates whether early prenatal protein malnutrition could alter the electrical cerebral activity of the progeny. We used Sprague–Dawley female rats of 200 g randomly divided into three groups: a control group that received a diet with 25% of the protein content (lactalbumin), the experimental group, that received a diet with 6% of the protein content and the rehabilitated group that initially received a diet with 6% of the protein content, then switched to a diet with 25% of the protein content after the weaning period (P20D) up to 60 days of life (P60D). Reduction of the protein content from 25% to 6% of lactalbumin in the diet of pregnant rats produces impairment in the electrical cerebral activity in the progeny at P20D and at P60D. The power spectral analysis for each one of the electroencephalograms revealed that prenatal protein malnutrition in rats produced a significant reduction of the alpha (8–13 Hz) and the beta bands (13–30 Hz) and a significant increase of the theta (4–8 Hz), and delta bands (1–4 Hz), at two different stages of life (P20D and P60D). Similar results were obtained for the rehabilitated group. These results indicate that early malnutrition in life affects the ontogeny of the electrical cerebral activity. This insult probably disrupts the establishment of cortical neural circuits during the critical period of brain development. The rehabilitation period did not revert the impairment in the electrical cerebral activity produced by malnutrition. We used one-way ANOVA analysis, followed by Tukey test (*p < 0.001).     

The effect of treadmill incline on maximal oxygen uptake,gas exchange and the metabolic response to exercise in the horse

In healthy man, conditions that change muscle O2 delivery affect the achievable maximum rate of O2 uptake as well as the metabolic (e.g. lactate threshold, LT) and gas exchange (e.g. gas exchange threshold, Tge) responses to incremental exercise. Inclined (I) compared to level (L) running increases locomotory muscle EMG at a given speed in the horse, indicative of elevated metabolic demand. To our knowledge, the effect of treadmill incline on VO2,max, LT and Tge has not been addressed in the exercising quadruped. We used blood sampling and breath-by-breath expired gas analysis to test the hypothesis that I (10% gradient) would increase VO2,max and the rate of O2 uptake (VO2) at LT and Tge in six Thoroughbred horses during incremental running to volitional fatigue. VO2,max was significantly higher for I (I, 77.8 +/- 4.1; L, 65.5 +/- 5.3 1 min(-1); P < 0.05), but peak plasma lactate concentration was not (I, 28.0 +/- 3.7; L, 25.9 +/- 3.0 mM). Arterial Pco2 increased to 62.1 +/- 3.3 and 57.9 +/- 2.7 Torr (I vs. L; P < 0.05), yet despite this relative hypoventilation, a distinct Tge was present. This Tge occurred at a significantly different absolute (I, 49.6 +/- 3.2; L, 42.4 +/- 3.21 min(-1); P < 0.05), but nearly identical relative VO2 (I, 63.6 +/- 1.2; L, 63.9 +/- 1.6% VO2max) in I and L. Similarly, LT occurred at a significantly greater absolute VO2 (I, 37.3 +/- 2.8; L, 26.9 +/- 2.1 1 min(-1)), but a relative VO2 that was not different (I, 47.9 +/- 2.1; L, 43.9 +/- 4.5% VO2,max). In addition, Tge occurred at a significantly higher (P < or = 0.05) absolute and relative VO2 than LT for both I and L tests. In conclusion, VO2,max is higher during inclined than level running and both LT and Tge in the horse occur at a similar percentage of VO2,max irrespective of the absolute level of VO2,max. In contrast to humans, LT is a poor analogue of Tge in the horse.     

Ineffective ventilation during exercise in patients with chronic congestive heart failure.

The pathophysiologic mechanisms causing exertional breathlessness in patients with chronic congestive heart failure (CHF) are not fully understood. Therefore, we have studied whether the ventilation in such patients is ineffective during exercise. Thirteen patients with treated chronic CHF (New York Heart Association class II-IV) and eight healthy controls underwent a maximal bicycle ergometer test with continuous analysis of expired air and frequent arterial blood sampling for gas and lactate analysis. All subjects were non-smokers and none had any signs of a pulmonary disease. Peak O2 consumption of the patients was 14.9 +/- 5.3 ml min-1 kg-1 and that of controls 33.6 +/- 7.5 ml min-1 kg-1. In patients with CHF the ratio of pulmonary dead space to tidal volume was significantly elevated at peak exercise compared with that of the controls (0.36 +/- 0.08 vs. 0.20 +/- 0.07, P less than 0.05). The ventilatory equivalent for CO2 (VE:VCO2) was also significantly higher in patients than in controls during exercise (P less than 0.05). Furthermore, both the ventilatory equivalents for CO2 and O2 (VE:VO2) had a significant inverse correlation with peak O2 consumption (P less than 0.001 for VE:VCO2 and P less than 0.05 for VE:VO2), O2 consumption at anaerobic threshold (P less than 0.01) and O2-pulse (P less than 0.001) among the patients. During exercise the arterial PO2 and PCO2 remained normal in patients and controls. These data indicate that in patients with chronic CHF wasted ventilation is pathologically increased during exercise, and this is related to the severity of the disease. Chronic CHF is not associated with decreased ventilatory reserve, hypoxaemia or alveolar hyperventilation. The ineffectiveness of ventilation is probably an important cause of exertional breathlessness in patients with CHF.     

Validity, reliability and stability of the portable Cortex Metamax 3B gas analysis system

This study investigated the performance of the portable Cortex Metamax 3B (MM3B) automated gas analysis system during both simulated and human exercise using adolescents. Repeated measures using a Gas Exchange System Validator (GESV) across a range of simulated metabolic rates, showed the MM3B to be adequately reliable (both percentage errors, and percentage technical error of measurements <2%) for measuring expired ventilation (V (E)), oxygen consumption (VO(2)), and carbon dioxide production (VCO(2)). Over a 3 h period, the MM3B was shown to be acceptably stable in measuring gas fractions, as well as V (E), VO(2), and VCO(2) generated by the GESV, especially at moderate and high metabolic rates (drifts <2% and of minor physiological significance). Using eight healthy adolescents during rest, moderate, and vigorous cycle ergometry, the validity of the MM3B was tested against the primary criterion Douglas bag method (DBM) and a secondary criterion machine known to be accurate, the Jaeger Oxycon Pro system. No significant errors in V (E) were noted, yet the MM3B significantly overestimated both VO(2) and VCO(2) by approximately 10-17% at moderate and vigorous exercise as compared to the DBM and at all exercise levels compared to the Oxycon Pro. No significant differences were seen in any metabolic variable between the two criterion systems (DBM and Oxycon Pro). It is concluded the MM3B produces acceptably stable and reliable results, but is not adequately valid during moderate and vigorous exercise without some further correction of VO(2) and VCO(2).     

Time courses of pulmonary gas exchange and heart rate changes in supine exercise.

The time courses of ventilation (VE), O2 uptake (VO2), CO2 elimination (VCO2), respiratory exchange ratio (R), end-tidal PO2 and PCO2 and heart rate (HR) were studied in seven subjects performing light dynamic leg exercise in the supine position. Individual and group mean time courses in response to step changes in work load were computed and displayed graphically. A computer-based method was also used to fit mono- or bi-exponential mathematical functions to the recorded responses. The over-all rate of HR change in response to the transition from 0-load pedalling to exercise (on-response) was faster (mean response time, MRT = 31 s) than the corresponding VO2 response (MRT = 45 s) while VE responded considerably slower (MRT = 86 s). During the reverse transition (off-response), VO2 and VE changed with the same rate as in the on-response, while the HR-change was slower than during the on-response (MRT = 50 s). During the initial 15-sec period, VO2 changed only slightly, which contrasts to previous results in the sitting position, where 50% of the final change in VO2 has been reported to occur within the first 15-sec period, and where changes in blood distribution and stroke volume are known to be more pronounced than in the supine position. Our results emphasize the importance of central circulatory changes for the time course of VO2 at the start and end of exercise.     

Contribution of histamine type-1 receptor to metabolic and behavioral control of ventilation

Histaminergic neurons in the hypothalamus are well documented as being involved in the control of autonomic functions, such as the balance of energy metabolism and circadian rhythm. We tested the hypothesis that an activation of the histamine type-1 (H1) receptor is required for the control of ventilation during the course of a day in free-moving mice. Ventilation, aerobic metabolism, and electroencephalogram were measured by a whole-body-plethysmograph, a magnetic-type mass spectrometry system, and a telemetry system, respectively, in H1 receptor-knockout (H1RKO) and wild-type mice. Both genotypes showed daily oscillations in minute ventilation (V(E)) and oxygen consumption (VO(2)), with greater values during the dark period compared to the light period. In the latter, H1RKO mice showed increased V(E) and CO(2) excretion (VCO(2)) relative to wild-type mice, and V(E) was comparable to the VCO(2) increase. However, there was no change in VO(2) in H1RKO mice, suggesting that differences in VCO(2) between genotypes are responsible for differences in V(E) during the light period. During the dark period, VCO(2) was elevated in H1RKO mice compared with WT mice. Because there was no difference in V(E), the ratio of V(E) to VCO(2) was reduced in H1RKO mice. Electroencephalogram results suggested that this might be due to a depressed arousal state in H1RKO mice because the ratio of delta to theta band power spectrum densities was greater in H1RKO mice than in wild-type mice. We concluded that histamine modulates ventilation by affecting metabolism and arousal state via H1 receptors.     

Effects of (-)-hydroxycitrate on net fat synthesis as de novo lipogenesis

(-)-Hydroxycitrate (HCA) might promote weight maintenance by limiting the capacity for de novo lipogenesis (DNL). It was investigated whether HCA may reduce DNL in humans during a persistent excess of energy intake as carbohydrate. In a double-blind, placebo-controlled, randomized and cross-over design, 10 sedentary lean male subjects (mean+/-S.D., age: 24+/-5 years, BMI: 21.8+/-2.1 kg/m2) performed a glycogen depletion exercise test followed by a 3-day high-fat diet (F/CHO/P, 60/25/15% energy; 100% of energy expenditure (EE)) and a 7-day high-CHO diet (F/CHO/P, <5/>85/10% energy; 130-175% of EE; overfeeding). During overfeeding, they ingested 3 x 500 mg/day HCA or placebo (PLA). Each intervention ended with a 60-h stay in the respiration chamber (days 9 and 10). Body weight increased during overfeeding (mean+/-S.E., HCA: 2.9+/-0.2 kg, PLA: 2.8+/-0.2 kg). Respiratory quotient (RQ) was >1.00 in all subjects indicating that DNL was present. On day 9, 24-h EE was lower with HCA compared to PLA (P < 0.05). On day 10, resting metabolic rate and RQ during night were lower (P < 0.01 and P < 0.05, respectively). Non-protein RQ, fat balance and net fat synthesis as DNL tended to be lower (P < 0.1) with HCA compared to PLA indicating lower DNL; activity-induced EE was higher with HCA (P < 0.05) indicating the urge to eliminate the excess of energy ingested. We conclude that an experimental condition resulting in DNL in humans was created and that treatment with HCA during overfeeding with carbohydrates may reduce DNL.     

Age specific effect of MK-801 on hypoxic body temperature regulation in rats

Hypoxic exposure produces a consistent decrease of rectal temperature (Tb), which is recognized as a potent protective response. While some of the neural mechanisms underlying this response have recently been described, it remains poorly known how these mechanisms evolve during post-natal development. We recently reported that in rat pups NMDA glutamate receptor limits Tb drop upon hypoxic exposure, an effect that has not been reported by others in adult rats. Accordingly, we tested the hypothesis that the implication of NMDA receptors on temperature control during hypoxic exposure evolves during development. To this aim, we evaluated the hypoxic (30 min - 12% O(2)) responses of Tb, metabolic rate, and ventilation in rats after injection of vehicle, or the NMDA receptor antagonist MK-801, at different ages (post-natal days 4, 10, 20 and 2-3 month-old - P4, P10, P20 and P60). MK-801 amplified the magnitude of the hypoxic-induced Tb drop in P4, P10 and P20 rats, but this effect was not apparent in adults. In P20 rats MK-801 tripled the hypoxic induced Tb drop, which was 0.5 degrees C in control and 1.4 degrees C in treated rats (p<0.0001). This effect was specific to temperature regulation, and was not accompanied by similar changes of other recorded parameters. MK-801 induced a significant decrease of the hypoxic ventilatory response in adults only. We conclude that NMDA glutamate receptor acts as a counter-regulatory factor that limits the hypoxic-induced drop of rectal temperature during post-natal development in rats.     

Oxygen deficit is not affected by the rate of transition from rest to submaximal exercise

Five subjects cycled on an ergometer at power outputs corresponding to 20, 40, 60 and 80% of their maximal oxygen uptake (VO2 max). On one occasion the transition from rest to work was direct (D), while on the other occasion the power output was increased slowly (S) in a stepwise manner for 6-15 min prior to exercise at the predetermined intensity. Oxygen uptake (VO2) was measured, and O2 deficit and O2 debt were calculated. Oxygen deficit increased with the exercise intensities, the peak values being 2.1 +/- 0.2 and 1.9 +/- 0.1 litres (mean +/- SEM) at 80% of VO2 max after D and S respectively. No significant difference was observed in O2 deficit or O2 debt between D and S at any exercise intensity (P less than 0.05). The O2 debt was similar to the O2 deficit at 20, 40 and 60% of VO2 max but lower than the O2 deficit (P less than 0.05) at 80% of VO2 max. Femoral venous blood lactate remained unchanged at 20% of VO2 max but increased at the higher exercise intensities, reaching peak values of 7.6 +/- 0.6 and 7.4 +/- 1.1 mmol l-1 at 80% of VO2 max after D and S respectively. Blood lactate was not significantly different between D and S at any exercise intensity (P greater than 0.05). It is concluded that O2 deficit, O2 debt and blood lactate are not affected by the rate of transition from rest to submaximal exercise. The data contradict the hypothesis that O2 deficit is caused by an inadequate O2 transport at the onset of exercise.     

The differences in CO2 kinetics during incremental exercise among sprinters, middle, and long distance runners

The purpose of this study was to investigate the differences in kinetics of CO2 output (VCO2) during incremental exercise in sprinters (S), middle (MD), and long distance runners (LD). In the steady state exercise, the VCO2 was linearly related to the O2 uptake (VO2). In the incremental exercise below anaerobic threshold (AT), the VCO2 was also linearly related to the VO2. The difference between the VCO2 estimates from the regression lines obtained in steady state and incremental exercise was added from the start of exercise up to a given time. The added values were defined as CO2 stores. The CO2 stores per body weight were significantly related to mixed venous CO2 pressure (PVCO2) determined by the CO2 rebreathing method. The slopes of the regression lines between PVCO2 and CO2 stores per body weight were not different among three groups. If VCO2 above AT is estimated from the VO2 using the regression line obtained in incremental exercise below AT, the estimated VCO2 is lower than the measured VCO2. The sum of the differences in VCO2 up to a given time was defined as CO2 excess. The CO2 excess per body weight was significantly related to delta LA (the difference between blood lactates at 5 min after exercise and at rest). The ratios of CO2 excess per body weight to delta LA were 3.30 +/- 1.49, 4.16 +/- 2.33, and 5.55 +/- 2.05 for sprinters, middle, and long distance runners, respectively. This ratio obtained in sprinters was significantly lower than that in long distance runners (p less than 0.01).     

Respiratory gas exchange and physiological demands during a fire fighter evaluation circuit in men and women

We examined the oxygen uptake (VO2) and carbon dioxide output (VCO2) during completion of a circuit developed for testing fire fighters and related performance time to laboratory measures of fitness. Twenty-two healthy university students (ten women) were trained in the tasks then performed the circuit as quickly as possible. Breath-by-breath gas exchange and heart rate were continuously measured with a portable system. Median circuit time was 6:13 (min:s, 25-75% = 5:46-6:42) for men and 7:25 (25-75% = 6:49-10:21) for 8 women finishers (P = 0.023), and VO2 averaged 68 and 64% VO2max for the men and women during the circuit. Both men and women had high respiratory exchange ratios (>1.0) suggesting marked anaerobic energy contribution. Physiological variables associated with circuit time were assessed by backward stepwise regression yielding a significant model that included only peak work rate during arm cranking exercise as a function of circuit completion time across men and women combined (P < 0.001). For men, but especially for women, the time required for the simulated victim drag (68.2 kg mannequin) was positively correlated with total time to complete the other circuit elements (r = 0.51, r = 0.96 respectively). The simple correlation between circuit time and VO2max (mL/kg/min) revealed poor relationships for men (r = -0.37, P > 0.05) and women (r = 0.20, P > 0.05). These data demonstrated that upper body fitness as reflected by peak work rate during arm cranking correlated with total circuit time for the men and women in our population sample.