O2 Debt Research Articles

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.

Oxygen deficit at the onset of submaximal exercise is not due to a delayed oxygen transport.

Six subjects cycled on two occasions for 10 min at power output of 188 +/- 11 W (means +/- SEM), which corresponded to 70 +/- 2% of their maximal oxygen uptake (VO2 max). The exercise intensity was either increased gradually in a stepwise manner over about 15 min (slow transition-S), or increased directly (direct transition-D) to the predetermined power output. Muscle samples from the quadriceps femoris muscle were taken at rest and immediately after exercise in both trials. During exercise with both D and S muscle lactate increased approximately 10 times (P less than 0.01), phosphocreatine decreased about 50% (P less than 0.01) and ADP increased about 20% (P less than 0.05). There were no significant differences between S and D (P greater than 0.05). Furthermore, blood lactate, O2 deficit, O2 debt, and the calculated increase in muscle content of inorganic phosphate (Pi) were all similar between D and S (P greater than 0.05). It is concluded that the O2 deficit and the anaerobic energy utilization is not affected by the rate of transition from rest to exercise. Consequently, the O2 deficit at the onset of exercise is not due to a delay in O2 transport, but may be due to a limited peripheral O2 utilization as a result of metabolic adjustments at the cellular level. Increases in ADP and Pi are suggested to be primary metabolic regulators which activate both aerobic and anaerobic energy production resulting in the O2 deficit.

Maximum O2 uptake, O2 debt and deficit, and muscle metabolites in Thoroughbred horses.

This study determined maximal O2 uptake (VO2max), maximal O2 deficit, and O2 debt in the Thoroughbred racehorse exercising on an inclined treadmill. In eight horses the O2 uptake (VO2) vs. speed relationship was linear until 10 m/s and VO2max values ranged from 131 to 153 ml.kg-1.min-1. Six of these horses then exercised at 120% of their VO2max until exhaustion. VO2, CO2 production (VCO2), and plasma lactate (La) were measured before and during exercise and through 60 min of recovery. Muscle biopsies were collected before and at 0.25, 0.5, 1, 1.5, 2, 5, 10, 15, 20, 40, and 60 min after exercise. Muscle concentrations of adenosine 5'-triphosphate (ATP), phosphocreatine (PC), La, glucose 6-phosphate (G-6-P), and creatine were determined, and pH was measured. The O2 deficit was 128 +/- 32 (SD) ml/kg (64 +/- 13 liters). The O2 debt was 324 +/- 62 ml/kg (159 +/- 37 liters), approximately two to three times comparative values for human beings. Muscle [ATP] was unchanged, but [PC] was lower (P less than 0.01) than preexercise values at less than or equal to 10 min of recovery. [PC] and VO2 were negatively correlated during both the fast and slow phases of VO2 during recovery. Muscle [La] and [G-6-P] were elevated for 10 min postexercise. Mean muscle pH decreased from 7.05 (preexercise) to 6.75 at 1.5 min recovery, and the mean peak plasma La value was 34.5 mmol/l.(ABSTRACT TRUNCATED AT 250 WORDS)

Recovery O2 and blood lactic acid: longitudinal analysis in boys aged 11 to 15 years.

Nineteen boys were tested annually from age 11 to 15 years. Recovery O2 (or O2 debt in l and ml X kg-1) and blood lactate ([La], mmol X l-1) were measured following supramaximal treadmill tests (20% grade) designed to stress the anaerobic energy systems maximally. The purpose was to describe the rate of development of anaerobic capacity (AnC) from pre-puberty to adolescence. AnC improved from age 11 to 15 years, as indicated by a tripling of recovery O2 (l), 80% increase in recovery O2 per kg and 45% in [La]. Changes were similar from year to year with average yearly increments in recovery O2 of 0.8 l or 9 ml X kg-1 and in [La] of 0.9 mmol X l-1. Individual data also were plotted in relation to age of peak height velocity (PHV, 12.9 +/- 1.2 years). Changes in the measures of AnC were not significantly different when related to biological rather than chronological age. Development of AnC did not show a growth function curve and was not closely correlated with size, nor was the development of AnC enhanced immediately following maturation. Thus, in this longitudinal study, recovery O2 and [La] as measures of AnC showed large increases from age 11 to 15 years, but the gains were similar year to year rather than related to size growth, per se, or hormonal influences at maturation postulated to induce qualitative changes in glycolytic potential of muscle.

Oxygen debt in submaximal and supramaximal exercise in children at high and low altitude.

The effect of high altitude (HA) on O2 debt and blood lactate concentration [( L]) was examined in 10- to 13-yr-old children who exhibited the same level of physical fitness. Fifty-one children acclimatized to HA (3,700 m) were compared with 40 children living at low altitude (LA, 330 m) during submaximal (20-95% maximal aerobic power, MAP), maximal and supramaximal (115% MAP) bicycle exercise. Results showed that 1) maximal O2 uptake (VO2max) and maximal heart rate were significantly (P less than 0.001) lower at HA than at LA by 15% and 11 beats X min-1, respectively; 2) for a given absolute work load, O2 debt was higher at HA than at LA, and the slopes of the linear relationships between O2 debt and O2 uptake were significantly higher at HA; 3) when related to percent of VO2max, O2 debts in HA and LA were similar; for 115% MAP maximal O2 debt and [L] were not significantly different (maximal O2 debt, 45.7 +/- 2.7 and 45.9 +/- 3.8 ml X kg-1; [L], 6.0 +/- 0.3 and 6.7 +/- 0.5 mM); and 4) linear relationships between maximal O2 debt and [L] were the same at HA and LA. This suggests that HA did not modify the anaerobic capacity in children.

707 GASTROINTESTINAL (GI) BLOOD FLOW AND O2 UPTAKE IN PIGLETS: RECOVERY FROM HYPOXEMIA

The inability of the neonatal GI tract to restore circulatory homeostasis after acute hypoxemia may contribute to hypoxic tissue damage, and is relevant to the etiology of necrotizing enterocolitis. Measurements of cardiac output (CO) and GI blood flow (QGI; microspheres), arterio-venous O2 content gradient (ΔA-VO2), and O2 uptake (VO2GI) were made in 8 2-day old piglets before (baseline) and during hypoxemia, and then 5 and 60 minutes after restoration of nonnoxia (recovery). Hypoxemia (pO2 20 mmHg for 15”) was induced by lowering FiO2. Results: 5″ into recovery VO2GI increased above baseline; presumably, this effected repayment of the O2 debt incurred during hypoxemia. 60″ into recovery QGI fell while CO was unchanged, indicating an increase in GI vascular resistance. ΔA-VO2 also fell and VO2GI decreased well below baseline. Thus, the initial phase of recovery is appropriate, but the later phase involves a reduction in GI O2 transport and VO2GI. This response could contribute to GI tissue damage subsequent to hypoxemia.

After effects of chronic hypoxia on VO2 kinetics and on O2 deficit and debt.

Single breath O2 consumption (PB = 730, FI02 = 0.21) was measured at rest, during 10 min cycloergometric exercise at 125 W, and in the following recovery phase in seven subjects before, and 12 days after 6 weeks at 5,200 m or above. Peak blood lactate after exercise (Lâb) was measured. O2 deficits and debts and half times (t1/2) of the VO2 on- and off-kinetics were calculated. Before acclimatization, the VO2 on- and off-responses were close to a single exponential with t1/2 = 30 s. After return to sea level, the VO2 on-response curves were less steep in the initial phase, becoming closer to sigmoid. The t1/2, independent of the shape of the underlying function, was approximately 10 s longer. The VO2 off-responses during the initial 4 min of recovery were the same before and after acclimatization. Average O2 deficit was approximately 320 ml larger after acclimatization: the fast component of O2 debt was similar. Since steady state VO2 and Lâb were the same, the O2 deficit difference can be attributed to a greater utilization of O2 stores. Of these, about 1/3 is explained in terms of increased mixed venous blood O2 stores, due to increased [Hb] (16.6 vs 14.9 g X dl-1), while the remainder is ascribed essentially to increased Mb-bound O2. O2 stores utilization and replenishment is presumed to occur when muscle metabolism is low; as a consequence, while it is clearly detectable from the shape of the initial phase of the VO2 on-response, during recovery it is spread throughout, thus becoming more difficult to appreciate.

Metabolic bases of excess post-exercise oxygen consumption

The classical "oxygen debt" hypothesis formulated by Hill and associates in the 1920s was an attempt to link the metabolism of lactic acid with the O2 consumption in excess of resting that occurs after exercise. The O2 debt was hypothesized to represent the oxidation of a minor fraction (1/5) of the lactate formed during exercise, to provide the energy to reconvert the remainder (4/5) of the lactate to glycogen during recovery. In 1933 Margaria et al. modified this hypothesis by distinguishing between initial, fast ("alactacid"), and second, slow ("lactacid"), O2-debt curve components. They hypothesized that the fast phase of the post-exercise O2 consumption curve was due to the restoration of phosphagen (ATP + CP). It is now probable that the original lactic acid explanation of the O2 debt was too simplistic. Numerous studies on several species have provided evidence demonstrating a dissociation between the kinetics of lactate removal and the slow component of the post-exercise VO2. The metabolism of lactate, a readily oxidizable substrate, following exercise appears to be directed primarily toward energy production in mitochondria. The elevated concentration of lactate present at the end of exercise may be viewed as a "reservoir of carbon," which may serve as a source of oxidative ATP production or as a source of carbon skeletons for the synthesis of glucose, glycogen, amino acids, and TCA cycle intermediates. The metabolic basis of the elevated post-exercise VO2 may be understood in terms of those factors which directly or indirectly influence mitochondrial O2 consumption. Included among these factors are catecholamines, thyroxine, glucocorticoids, fatty acids, calcium ions, and temperature. Of these, elevated temperature is perhaps the most important. As no complete explanation of the post-exercise metabolism exists, it is recommended that the term "O2 debt" be used to describe a set of phenomena during recovery from exercise. The terms "alactacid debt" and "lactacid debt," which suggest a mechanism, are inappropriate. Use of alternative terms, e.g., "excess post-exercise oxygen consumption" (EPOC) and "recovery O2," will avoid implication of causality in describing the elevation in metabolic rate above resting levels after exercise.

Applied physiology of rowing.

Elite oarsmen and oarswomen possess large body dimensions and show outstanding aerobic and anaerobic qualities. Oarsmen have VO2max values of 6.1 +/- 0.6 L/min and have incurred O2 debts of between 10 and 20 litres. The caloric expenditure of rowing estimated from the O2 cost of a 6-minute rowing ergometer exercise was calculated at 36 kcal/min, one of the highest energy costs so far reported for any predominantly aerobic-type sport. Aerobic and anaerobic calculations show that 70 to 75% of the energy necessary to row the standard 2000m distance for men is derived from aerobiosis while the remaining 25 to 30% is anaerobic. Women achieve VO2max values of 4.1 +/- 0.4 L/min and slightly lower anaerobic values than men. The relative 60 to 65% energy contribution of aerobic metabolism and 35 to 40% for anaerobiosis is not surprising since women compete at 1000m. Rowers also exhibit excellent isokinetic leg strength and power when compared with other elite athletes and oarswomen produced higher relative leg strength values than men when lean body mass is considered. Muscle fibre type distributions in oarsmen resemble those of distance runners while women tend to have a slightly higher proportion of fast-twitch fibres. An average power output of 390 +/- 13.6W was produced by oarsmen for 6 minutes of simulated rowing while women were able to develop 300 +/- 18.4 for 3 minutes of the same activity. Mechanical efficiency for rowing was calculated at 20 +/- 0.9%. Oarsmen also achieve very high ventilation volumes being able to average above 200 L/min BTPS for 6 minutes of simulated rowing; women ventilate 170 L/min BTPS for 3 minutes of this exercise. Excellent VO2/VE and O2 pulse values demonstrate outstanding cardiorespiratory efficiency. Both oarsmen and oarswomen utilise a unique physiological pattern of race pacing; they begin exertion with a vigorous sprint which places excessive demands on anaerobic metabolism followed by a severely high aerobic steady-state and then an exhaustive sprint at the finish. Tolerance to excessive anaerobiosis is evident by very high lactates and O2 deficits measured during the first 2 minutes of exercise. Physiological profiles of successful international calibre rowing athletes have been established as a result of studies described in this review and the data have been used in a variety of ways to improve rowing performance.

Developmental changes in oxygenation and circulatory responses to hypoxemia in lambs.

We studied moderate [fractional inspired O2 (FIO2) 0.09] and severe (FIO2 0.06) hypoxemia in 21 lambs (group 1, 1 wk old; group 2, 3-4 wk old; group 3, 5-7 wk). With moderate hypoxemia, all groups increased heart rate, cardiac output, and pulmonary arterial pressure and decreased systemic and pulmonary vascular resistance; cardiac output and pulmonary arterial pressure increases were less in group 1, because of higher resting values. With severe hypoxemia, heart rate increased similarly, cardiac output was unchanged, and aortic pressure fell associated with severe metabolic acidosis or arrhythmias. Regional blood flow changed similarly in all groups; heart and brain flow increased, carcass flow was unchanged, and skin, GI tract, and kidney flow fell. O2 consumption (VO2) and mixed venous PO2 decreased, though O2 saturation was higher in group 1 due to the lower O2 half-saturation pressure of hemoglobin. With a given decreased VO2 there was more metabolic acidosis in older lambs and an increased VO2 after termination of hypoxemia, suggesting greater O2 debt. As in the fetus, young lambs are better able to tolerate a decreased VO2 than older lambs.

Oxygen deficit and stores at onset of muscular exercise in humans.

Single-breath O2 consumption (VO2) at the mouth and heart rate were determined in five healthy male subjects at rest, during 8 min of cycloergometric exercise (50, 100, 125, and 150 W), and in the recovery period following two experimental conditions: air breathing throughout (AA); hypoxic breathing (FIO2 = 0.11) for 6 min of preexercise rest followed by air breathing from the onset of exercise (HA). The O2 deficits and debts as well as the t 1/2 values of the VO2 on- and off-responses were determined and blood lactate concentrations measured at rest and in the recovery after 4 and 8 min of exercise. At all work loads: 1) O2 deficits were on the average 0.39 liter smaller in HA than in AA; 2) VO2 on-responses were faster in HA (t 1/2 approximately equal to 7 s) than in AA (t 1/2 = 20-30 s); and 3) O2 debts and VO2 off-responses were the same in the two conditions. Since the VO2 and heart rate levels at steady state as well as the blood lactate concentrations after 4 and 8 min of exercise were the same in AA and HA, the observed differences of O2 deficit cannot be attributed to changes of energy metabolism in the two conditions; they therefore depend on the reduction of body O2 stores at rest in HA. This, independently measured, was found to be 0.46 liters, not far from the observed O2 deficit difference (0.39 liters). Thus a decrease of O2 stores before exercise is accompanied by a reduction of the O2 deficit and faster VO2 kinetics at the onset of exercise.

Effects of hypoxia on blood gas and acid-base parameters of sea bass.

Continuous recordings have been made of pH, PO2, and PCO2 of arterial blood (pHa, PaO2, PaCO2) in an extracorporeal circulation during periods of hypoxia (inspired PO2 45-10 Torr) in sea bass, Morone labrax. During moderate hypoxia hyperventilation was accompanied by an increase in pHa. Continuation of moderate hypoxia for periods up to 24 h produces an increase in lactate and a consequent decrease in pHa. During deep hypoxia there is a very brief alkalosis as ventilation increases but a marked decrease in pHa as lactate levels rise. Recovery from hypoxia is associated with an increase in lactate concentration reaching values of more than 6 meq X l-1 following deep hypoxia, and pHa falls to 7.73. PaO2 recovers rapidly, but recovery of PaCO2 is not so rapid and together with the residual hyperventilation indicates that the fish is paying off an O2 debt.

Control and Co-Ordination of Ventilation and Circulation in Crustaceans: Responses to Hypoxia and Exercise

ABSTRACT The functional morphology, nervous and hormonal control and coordination of the cardiovascular and ventilatory systems in decapodan crustaceans is reviewed. Pacemaker function reflects the reliance of crustaceans on small numbers of large, multipolar neurones. Respiratory gas exchange and transport may be limited by the potential diffusion barrier presented by chitin on the gills and by the relatively low O2 capacity of the haemolymph, though this is compensated by the relatively high O2 affinity of haemocyanin and the large volume of the haemocoel. Haemolymph buffering capacity is attributable to haemocyanin and to bicarbonate, including an internal source of fixed base, possibly the exoskeleton. The typical hypoxic response includes a bradycardia and hyperventilation resulting in a respiratory alkalosis and resultant increase in O2 affinity of the haemocyanin. Diffusive conductance may increase. When 02 transport is limiting there is a switch to anaerobiosis with normoxic recovery including repayment of an O2 debt. Some species are facultative air-breathers and compensate for a respiratory and metabolic acidosis when in air by elevation of buffer base. Central and peripheral O2 receptors may be involved in determining respiratory and cardiovascular responses to hypoxia and airbreathers may respond to changes in haemolymph pH. Exercise induces a rapid increase in ventilation, diffusive conductance improves and O2 consumption is elevated. There is also a major anaerobic contribution causing a metabolic acidosis and recovery includes prolonged repayment of an O2 debt.

Respiratory gas exchange at lungs, gills and tissues: mechanisms and adjustments.

(1) A general model for external gas exchange organs of vertebrates is presented, in which the main parameters are the ventilatory, diffusive and perfusive conductances for O2 and CO2. The relevant properties of the external medium (air or water) and of the internal medium (blood) are analysed in terms of capacitance coefficients (effective solubilities) for O2 and CO2. The models for the main types of gas exchange organs (fish gills, amphibian skin, and avian and mammalian lungs) are compared in terms of their intrinsic gas exchange efficacy. The adjustments to increased metabolic rate or to hypoxia are achieved by increasing the conductances. (2) The gas exchange at tissue level is analysed using the Krogh cylinder and a simplified model containing a diffusive and a perfusive conductance. The adjustments to increased load (exercise, hypoxia) consist in both increased local blood flow and in improvement of diffusion conditions (enlargement and recruitment of capillaries). (3) Some particular features of respiration in transitional (unsteady) states, such as occurring at the beginning of exercise and of hypoxia, are examined. The additional physical variables are the O2 (and CO2) stores acting according to their capacitances and partial pressure changes. Delayed increase in O2 uptake at the beginning of exercise is due to the limited speed of physiological adjustments. The ensuing O2 debt is energetically covered by anoxidative energy releasing processes (hydrolysis of high-energy phosphates and anaerobic glycolysis). Finally, the reduction of metabolic rate as adjustment to hypoxia is discussed.

Haemolymph gas transport, acid‐base regulation, and anaerobic metabolism during exercise in the land crab (Cardisoma carnifex)

AbstractHaemolymph gases, acid‐base status, and metabolite levels were studied in Cardisoma carnifex at rest and after 10 minutes of mild (0.2 body lengths/second) or severe (exhausting, 0.5 BL/second) exercise. O2 transport is very similar to that in aquatic crabs. At rest, arterial haemocyanin saturation is ≃ 87%, venous saturation is ≃ 45%, and tissue utilization is ≃57%. During exercise, Ṁ rises 2–3‐fold. Ps fall so that O2 transport is shifted onto the steep part of the dissociation curve, venous saturation decreases markedly while arterial saturation remains high, and cardiac output rises. These adjustments raise the P gradient at the respiratory surface, tap the haemolymph O2 store, and maintain or increase the a–v O2 difference so that utilization reaches ≃82%. Postexercise acidosis augments these effects via the Bohr shift. Resting P's are low (≃15 torr) for an air‐breather, and Pa changes minimally despite 2.5–5‐fold evaluations in Ṁ. All haemolymph gas levels return to normal within 0.5–1.0 hours. Postexercise acidosis is largely metabolic, and smaller than in aquatic crabs. Lactate anions and protons enter the haemolymph in equivalent amounts and totally account for the metabolic acidosis. Elevated NH3 and pyruvic acid levels have negligible influence. During recovery, the metabolic acid load is reduced faster than the lactate load, resulting in alkalosis, possibly because of CaCO3 mobilization from the carapace. Exercise metabolism appears largely anaerobic, but changes in haemolymph lactate levels do not correlate with the O2 debt. However, the “excess lactate” concept which compensates for pyruvate elevation gives a good index of the debt. All changes are more marked after severe than after mild exercise, but the patterns are similar.

Oxygen and carbon dioxide exchange during exercise in the land crab (Cardisoma carnifex)

AbstractIn Cardisoma carnifex exercised on a treadmill, there is an inverse relationship between velocity and log fatigue time; crabs run indefinitely at 0.2 body lengths/second, for ≃5 minutes at 0.5 BL/second, and for only ≃30 seconds at burst speeds of 2.2 BL/second. Respiration was studied at rest and after 10 minutes of either mild (0.2 BL/second) or severe (exhausting, 0.5 BL/second) exercise. Gas exchange occurs in large branchial chambers that contain gills and are lined with a respiratory epithelium. The chambers are partially filled with water, and are ventilated with air by forward scaphognathite pumping. Motions of the flabellae, gills, and branchial chamber wall mix the air and water phases. CO2, but not O2, equilibrates between the phases, so the water represents a significant CO2 sink. At rest, the scaphognathites beat in short, often unilateral bursts, and air flow is intermittent. O2 utilization is > 11.4%, the ventilatory convection requirement is ≃1.3 L air/mMole O2, the gas exchange ratio (R) is ≃0.6, the O2 diffusing capacity is ≃0.4 μmole O2. kg−1 min−1. torr−1, or about 10% of the CO2 diffusing capacity, and Po2 and P gradients across the respiratory surface are comparable to those in air‐breathing ectothermic vertebrates. During exercise, scaphognathite activity becomes bilateral and continuous, ventilation rises, utilization falls, and gas tensions in the branchial chamber approach those in the inspired air. Heart rate rises slightly. Ṁ and Ṁ increase 2–5 ×, the latter to a greater extent, and a considerable O2 debt is incurred. R rises above 1.0 as metabolic acidosis converts bicarbonate stores to CO2. The increases in Ṁ and Ṁ reflect both elevations of the diffusion gradients and approximate doublings of the O2 and CO2 diffusing capacities. All changes are more marked during severe than during mild exercise, but the patterns are similar.

THE EFFECTS OF PHYSICAL VARIABLES AND ACCLIMATION ON SURVIVAL AND OXYGEN CONSUMPTION IN THE HIGH LITTORAL SALT-MARSH SNAIL,MELAMPUS BIDENTATUS SAY.

The physiological ecology of the salt-marsh pulmonate gastropod, Melampus bidentatus Say, was investigated in specimens from the Little Sippewisset saltmarsh, Cape Cod, Massachusetts. M. bidentatus is tolerant of submergence, surviving 2-3 days at 20° C and 14 days at 10° C in 25%-l00% seawater (SW). Snails acclimated at 10°C tolerated temperatures of 32.2°C-37.4°C, and snails acclimated at 20°C tolerated 35.2°C-40.7°C, when submerged in 0%-l00% SW. LD (T)50 in air was 44.5°C (10°C acclimated) and 44.7°C (20°C acclimated). Aerial weight-specific O2 consumption (vO2) was 3-5 times higher than aquatic rates. Aerial and aquatic VO2 was regulated (Q10, < 1.5) over the ambient temperature range in both acclimation groups. The VO2 of 10°C acclimated individuals was lower than 20°C acclimated specimens, a pattern of "reverse" acclimation associated with energy stores conservation. O2 debt occurred after 5 h anoxia. In addition, M. bidentatus compensates VO2 for hypoxia by increasing both uptake rates and the degree of O2 regulation of VO2 during decreasing O2 concentrations. M. bidentatus displays a ciradian rhythm associated with desiccation pressures, and thus VO2 is maximal during evening and minimal during daylight hours. Under the selection pressures associated with longterm aerial exposure in the high littoral salt-marsh environment, M. bidentatus has evolved the vast majority of physiological adaptations required for terrestrial life, except for its aquatic egg-masses and planktonic development.

End points of lactate and glucose metabolism after exhausting exercise.

To determine the extent of metabolite oxidation, rats were injected with [U-14C]lactate, -glucose, or -bicarbonate (n = 5, each) during rest or after continuous (CE) and intermittent (IE) exercises to exhaustion. Tissue analyses of resting rats, or rats killed following CE and IE and pulse injection with [14C]lactate or -glucose (n = 72, each), were used to determine the metabolic pathways of these two substrates. Oxygen consumption (VO2) declined rapidly for the first 15 min after exercise; thereafter, VO2 declined slowly and remained elevated above resting levels for 120 min. The slow phase of decline in VO2 during recovery did not coincide with lactate removal, which occurred within 15 min. Two-dimensional radiochromatograms produced from blood, kidney, liver, skeletal muscle, and heart indicated a rapid incorporation of 14C into several amino acid pools, including alanine, glutamine, glutamate, and aspartate. Four-hour postexercise recoveries (means of CE and IE) of injected [14C]lactate were lactate (0.75%), glucose (0.52%), protein (8.57%), glycogen (18.30%), CO2 (45.18%), and HCO3- (17.72%). Greater (P < 0.05) incorporation of 14C into protein and glycogen constituents after exercise, compared with rest, was demonstrated. Incorporation of [14C]lactate into glycogen represented a significant but only minor fraction of the metabolism of lactate after exhausting exercise. It is suggested that classical explanations of excess postexercise O2 consumption (i.e., "O2 debt") are too simplistic.

Alterations in aerobic-anaerobic proportions of metabolism during work in heat.

With a view to investigating the aerobic and anaerobic proportions of oxygen supply during different grades of muscular activity in varying thermal stress, studies have been conducted on six young healthy Indians naturally acclimatized to heat. The subjects were given submaximal exercises of 400, 500, and 600 kgm/min (equivalent to 65.40, 81.75, and 98.10 W) for 6 min on a bicycle ergometer in three different simulated conditions, i.e., comfortable, hot humid, and very hot humid. Their O2 consumption (VO2), pulmonary ventilation (VE) and heart rate (HR) were measured during rest and throughout the exercise period (6 min) and for 30 min post exercise. Blood lactate level (LA) was measured during rest and recovery. From these, the total O2 cost with aerobic and anaerobic proportions were calculated. Results indicated a significant increase in the total O2 cost for each exercise with increasing thermal stress, along with a significant increase in the anaerobic fraction and a decrease in the aerobic fraction. The increase in anaerobic contribution to the energy supply processes was further confirmed by a significant increase in relative O2 debt (l/kg) and in blood lactate level at each work load. Thus, a highly significant correlation (P < 0.001) was found between O2 debt contracted and increase in thermal stress. A significant fall in VO2 max was also observed in hot humid and very hot humid conditions as against comfortable temperature, with no change in HR max and VE max.

Faster adjustment to and recovery from submaximal exercise in the trained state.

This study was undertaken to evaluate the effects of endurance exercise training on O2 deficit and O2 debt, and on the time courses of the adjustment to, and recovery from, submaximal exercise of oxygen uptake (VO2) carbon dioxide production (VCO2), minute ventilation (VE), and heart rate (HR). Eight subjects participated in a 9-wk-long exercise program that increased their VO2max by 24%. It was found that O2 deficit and O2 debt were lower at the same absolute work rate and not significantly different at the same relative work rate after training. The increases in VO2, VCO2, VE, and HR at the onset of constant load submaximal work, and the decreases in VO2, VCO2, VE, and HR in recovery were more rapid at both the same absolute and the same relative work rates after training. These results show that the adaptations to endurance exercise training enable an individual to adjust to the energy requirement of constant load submaximal work more rapidly, resulting in a smaller O2 deficit. The rate of recovery is also more rapid after training, resulting in a smaller O2 debt.