Submaximal exercise in emphysema and malnutrition at two levels of carbohydrate and fat intake

Eight malnourished patients with emphysema (EMPH) and eight malnourished patients without evidence of lung disease (MLAN) received an infusion of 5% dextrose plus electrolytes (D5W) for 48 h and were then randomly assigned to a hypercaloric diet with either 53% of the calories as carbohydrate (CB) or with 55% as fat (FB) for the 1st wk, maintaining a constant protein intake. The alternate diet was given the following week. Ventilation and gas exchange were measured during supine cycle ergometry at 0, 12, and 25 W during the D5W, CB, and FB diet periods. At each exercise intensity, the EMPH group demonstrated a 12–15% greater O2 consumption, a lower respiratory quotient, and an O2 debt larger than that of the MALN group. Resting ventilation was higher during the CB than FB regimen in both groups of patients, but during the CB diet the EMPH group had a more exaggerated ventilatory response than the MALN group. The results demonstrate that EMPH patients have an unusual metabolic pattern during hypercaloric feeding and exercise. Furthermore in EMPH patients a FB regimen does not appear to create the additional stress on the respiratory system during exercise that is generated with a CB regimen.

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)

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.

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.

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.

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

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 O2 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.

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.