Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: HUMANGGP:003739 (CO2)
 48,959 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An experiment to validate predictions concerning submersible survivability was performed in December, 1975, by members of the Canadian Forces in the CF Submersible Lockout Vehicle SDL-1 in Halifax Harbour in water of 4 degrees C temperature at a depth of 40 ft. Data was collected relevant to the life support equipment to determine if it would operate for a simulated 6-h mission followed by a 24-h immobility period, at the end of which rescue was presumed to have occurred. Physiological data was collected from the submersible occupants in order to assess the degree of thermal stress experienced in this exercise. The experiment was terminated after a duration of approximately 25 h at 1 atm internal pressure due to exhaustion of two of the three on-board power supplies, causing the CO2 scrubbers to be inoperative and the CO2 content in the breathing gas to increase to toxic levels. Only two of the three submersible occupants experienced cold stress, one in the forward sphere and one in the aft sphere. At the end of 24 h, the core temperatures of both individuals had decreased by 0.5 degrees C and, during this time, skin temperatures, particularly of the extremities, had steadily and slowly decreased. Neither individual was hypothermic, but it was considered likely that after a 3-d exposure, at least two of the crew members would have had core temperatures of 35 degrees C or lower, assuming that CO2 poisoning had not occurred earlier.
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PMID:Survival test of submersible life support systems. 1 83

Eight subjects exercised on an ergometer until exhaustion. Femoral venous blood was analyzed for lactate, pyruvate, protein, electrolytes, and acid-base parameters. Muscle samples taken during the recovery period from m. quadriceps femoris were analyzed for water, electrolytes, lactate, and acid-labile CO2. Water content in the muscle biopsy sample was increased after exercise to 78.7 +/- 0.5% compared with the normal 76.7 +/- 0.8% at rest. The distribution of water between the extra- and intracellular space was calculated by the chloride method. In spite of elevated PCO2 in femoral venous blood the content of acid-labile CO2 was decreased in muscle after exercise. One minute after termination of exercise muscle CO2 was about half of the normal content at rest. During the recovery period muscle CO2 increased but was 20 min after termination of exercise still significantly below the value at rest. Intracellular pH (pHi) and bicarbonate concentration ([HCO3-]i) in muscle have been calculated. The validity of the assumptions underlying the calculations are thoroughly discussed. pHi decreased from the normal value at rest, 7.00 +/- 0.06 (mean +/- SD), to about 6.4 after exercise. [HCO3-] decreased from 10.2 +/- 1.2 mmol/l at rest to about 3 mmol/l after exercise. The changes are the greatest so far reported for an in vivo situation. After 20 min recovery pHi was almost the same as at rest, whereas bicarbonate was still well below.
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PMID:Intracellular pH and bicarbonate concentration in human muscle during recovery from exercise. 2 68

In progressive exercise increased tidal volume (VT) accompanies increased ventilation (VE) until a VT plateau is reached. We observed in 13 subjects a correspondence between the arrival of the VT plateau and the anaerobic threshold (AT). To examine this association between a mechanical event (the VT plateau) and a metabolic event (the AT), we changed those variables that change at the AT and looked for changes in VT. We found in 13 subjects that CO2 addition to prevent alveolar hypocapnia during cycle ergometer exercise progressing to exhaustion in 12-15 min significantly elevated the VT plateau (mean increase 4.4%; P less than 0.01) as compared with a spontaneous test that induced a mean end-tidal carbon dioxide tension fall of 5.5 Torr. This VT increase was mediated by a significant increase in inspiratory time (TI; P less than 0.02); both the ratio of TI to the total breath duration (TI/Ttot) and the mean rate of inspired airflow (VT/TI) were unchanged at matched VE. Changing other variables known to change at the AT--blood lactate ion concentration and alveolar oxygen tension--left ventilatory pattern unchanged. These results suggest that hypocapnia in severe exercise measurably lowers the VT plateau in normal man.
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PMID:CO2 and exercise tidal volume. 42 48

Twenty-four oxygen exposures lasting 80 to 271 min were performed by six immersed exercising subjects at 25 fsw (1.76 ATA) in both warm and cold water. Two types of exercise were performed, moderate work (50 watts) for long periods of time, and graded exercise (25-150 watts) lasting 85 min. In 21 degrees C water, moderate exercise lasted 228 +/- 39 min, with a mean VO2 of 1.72 +/- 0.11 liter/min. In 4 degree C water, the duration was 163 +/- 22 min, with a mean VO2 of 1.83 +/- 0.16 liter/min. The differences in duration of oxygen exposure in warm and cold water reflect termination at an inspired PCO2 of 7.6 mmHg, a level reached earlier in cold water because of CO2 absorbent exhaustion. In 21 degrees C water, the VO2 for graded exercise ranged from 1.51 to 3.00 liter/min and in 4 degrees C water, from 2.00 to 3.16 liter/min. Central nervous system oxygen toxicity was not observed during these exposures, although two divers had clinical and spirometric evidence of early pulmonary oxygen toxicity. The absence of CNS oxygen toxicity is attributed to low resistance and minimization of dead space, which caused a low inspired PCO2, although the divers' experience with oxygen diving and their excellent physical condition may have contributed as well.
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PMID:Prolonged oxygen exposures in immersed exercising divers at 25 fsw (1.76 ATA). 53 63

This study examined whether the ventilatory (V) compensation for metabolic acidosis with increasing O2 uptake (VO2) and CO2 output (VCO2) might be more in accord with the theoretical expectation of a progressive acceleration of proton production from carbohydrate oxidation rather than a sudden onset of blood lactate (BLa) accumulation. The interrelationships between V, VO2, VCO2 and BLa concentration, [BLa], were investigated in 10 endurance-trained male cyclists during incremental (120 +/- 15 W min-1) exercise tests to exhaustion. Regression analyses on the V, VCO2 and [BLa] vs VO2 data revealed that all were better fitted by continuous Y = A.exp.[B.VO2] + C rate laws than by threshold linear rate equations (P < 0.0001). Plots of V vs VCO2 and [BLa] were also non-linear. Ventilation increased as an exponential V = 27 +/- 4.exp.[0.37 +/- 0.03.VCO2] function of VCO2 and as a hyperbolic function of [BLa]. In opposition to the 'anaerobic (lactate) threshold' hypothesis, we suggest these data are more readily explained by a continuous development of acidosis, rather than a sudden onset of BLa accumulation, during progressive exercise.
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PMID:Ventilation and blood lactate increase exponentially during incremental exercise. 830 3

Juvenile rainbow trout (approximately 6 g) were exercised to exhaustion in two 5 min bouts given 6 h apart. Resting levels of whole-body lactate and glycogen were restored prior to the second bout. The rate of O2 consumption increased about threefold 5 min after each bout of exercise, while recovery time decreased from 4 h after the first bout to 2-3 h after the second. The excess post-exercise oxygen consumption, i.e. 'oxygen debt', was significantly reduced by 40% after the second exercise bout, despite almost identical rates of lactate clearance and glycogen resynthesis. The rates of CO2 and ammonia excretion increased sixfold and threefold, and recovery times decreased from 4-6 h to 3 h and from 3 h to 1.5 h, respectively. After the first bout, whole-body lactate levels peaked at 5 min post-exercise at about 8.5 times pre-exercise levels. After the second bout, lactate levels peaked at 0 min post-exercise and fell more rapidly during recovery. Whole-body glycogen levels decreased by 70% and 80% and ATP levels decreased by 75% and 65% after the first and second bouts, respectively, while glucose levels increased about 1.5-fold immediately after both bouts. Creatine phosphate levels decreased by 70% and 80% after the first and second bouts, respectively. After 6 h of recovery, creatine phosphate levels were higher after the second bout than after the first. These findings suggest that exhaustive exercise may cause a 'non-specific' increase in metabolic rate not directly related to the processing of metabolites, which is reduced upon a subsequent exercise bout. This is in contrast with the classical 'oxygen debt hypothesis', which states that the oxygen debt and lactate clearance are linked. Furthermore, it appears that two sequential exercise bouts are sufficient to induce a 'training effect', i.e. improved rates of metabolic recovery.
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PMID:Gas exchange, metabolite status and excess post-exercise oxygen consumption after repetitive bouts of exhaustive exercise in juvenile rainbow trout. 163 61

Oxygen uptake (VO2) kinetics are generally agreed to be first-order for moderate work rates with a time constant (tau VO2) that is thought to reflect the kinetics of intramuscular creatine phosphate depletion. However, when there is a concomitant lactic acidosis, tau VO2 is appreciably longer, reflecting an additional, delayed and slowed component that leads to VO2S greater than the aerobic equivalent of that work rate and which therefore invalidates current techniques for O2 deficit estimation. This "excess" VO2 is no more than approximately 250-300 ml/min at work rates for which [lactate] and [H+]a can be stabilized. At higher work rates which demand sustained and progressive increases in [lactate] and [H+]a, however, VO2 also continues to increase progressively, yielding excess VO2S greater than 11/min at exhaustion. The trajectory of excess VO2 therefore is to the maximum VO2: the resulting exercise limitation becomes progressively more pronounced the higher the work rate, which accounts for the hyperbolic character of the power-duration curve. Factors which speed VO2 kinetics in this domain reduce the excess VO2 mechanism and lead to improved exercise performance. We have demonstrated that, in addition to appropriately-designed training regimens, induction of a metabolic acidosis prior to exercise speeds VO2 kinetics at high work rates, reducing the increase in both [lactate] and [H+]a and reducing the CO2 load to ventilation during the transient phase of the work. The optimum procedure for inducing these improved pulmonary gas-exchange kinetics, however, remains to be determined.
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PMID:Pulmonary gas exchange dynamics and the tolerance to muscular exercise: effects of fitness and training. 164 16

We analyzed the changes in water content and electrolyte concentrations in the vascular space during graded exercise of short duration. Six male volunteers exercised on a cycle ergometer at 20 degrees C (relative humidity = 30%) as exercise intensity was increased stepwise until voluntary exhaustion. Blood samples were collected at exercise intensities of 29, 56, 70, and 95% of maximum aerobic power (VO2max). A curvilinear relationship between exercise intensity and Na+ concentration in plasma ([Na+]p) was observed. [Na+]p significantly increased at 70% VO2max and at 95% VO2max was approximately 8 meq/kgH2O higher than control. The change in lactate concentration in plasma ([Lac-]p) was closely correlated with the change in [Na+]p (delta[Na+]p = 0.687 delta[Lac-]p + 1.79, r = 0.99). The change in [Lac-]p was also inversely correlated with the change in HCO3- concentration in plasma (delta[HCO3-]p = -0.761 delta[Lac-]p + 0.22, r = -1.00). At an exercise intensity of 95% VO2max, 60% of the increase in plasma osmolality (Posmol) was accounted for by an increase in [Na+]p. These results suggest that lactic acid released into the vascular space from active skeletal muscles reacts with [HCO3-]p to produce CO2 gas and Lac-. The data raise the intriguing notion that increase in [Na+]p during exercise may be caused by elevated Lac-.
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PMID:Water and electrolyte balance in the vascular space during graded exercise in humans. 188 73

The effects of 30-h sleep deprivation on cardiorespiratory function either at rest or in exercise were studied in 15 young healthy male volunteers. All subjects performed 1-min incremental exercise tests on a bicycle ergometer until exhaustion and endurance exercise tests at 3/4 of their maximal work rates. Arterialized venous blood samples were withdrawn at rest and during exercise tests to investigate the influence of sleep loss on blood gases. In addition, resting plasma catecholamine levels were also measured in ten subjects. The results showed that 1) resting heart rate, plasma catecholamine levels, and blood pH were decreased while minute ventilation (VI) and CO2 production (VCO2) were increased after 30 h of sleep loss (P less than 0.05), and 2) the maximal exercise performance was reduced by sleeplessness, as indicated by the decreases in the maximal heart rate, peak VI, peak VCO2, peak O2 consumption, and time to exhaustion (P less than 0.05). However, no significant changes in exercise endurance, arterialized venous pH, and PCO2 were found in exercise after sleep deprivation either. We therefore conclude that 30-h sleep loss alters cardiorespiratory function at rest and the ability to perform maximal exercise but not exercise endurance.
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PMID:Effects of 30-h sleep loss on cardiorespiratory functions at rest and in exercise. 190 33

The mechanisms leading to rapid changes in arterial blood gas values soon after exercise ends have not been well established. To further study these phenomena, we exercised seven normal male volunteers to exhaustion on a cycle ergometer with a 25-W/min ramped protocol measuring arterial blood gas values, and breath-by-breath gas exchange from rest to exercise and through 15 minutes of recovery. Arterial PO2 (PaO2) increased from 108 mm Hg at peak exercise to 125 mm Hg at 2 minutes of recovery. There was a smaller rise in calculated alveolar PO2 (PAO2) from 121 to 128 mm Hg over the same period. Arterial PCO2 (PaCO2) fell from 35.0 mm Hg to 31.9 mm Hg. The gas exchange ratio R rose from 1.21 to 1.52, after having peaked at 1.68 at 1 minute. The alveolar-arterial O2 gradient (P[A-a]O2) fell from 12.3 mm Hg at peak exercise to 3.2 mm Hg at 2 minutes. Following exercise, the rise in R is related to a more rapid fall in O2 uptake than in CO2 output, and the fall in P(A-a)O2 is probably related to improved V/Q relationships and to a rise in mixed venous PO2. We conclude that the rise in PaO2 in the recovery period after progressive nonsteady state exercise is due to several factors, including a fall in P(A-a)O2 and a rise in PAO2 due primarily to an elevation of R and also to a fall in PaCO2.
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PMID:Transition from exercise to rest. Ventilatory and arterial blood gas responses. 190 60


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