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These experiments were conducted to determine whether changes in skeletal muscle metabolism contribute to the previously reported increase in whole-body O2 uptake (VO2) during respiratory alkalosis. The hind-limb and gastrocnemius-plantaris preparations in anesthetized and paralyzed dogs were used. VO2 of the hindlimb and gastrocnemius muscle was calculated from measurements of venous blood flow and arterial and venous O2 concentrations (Van Slyke analysis). Whole-body VO2 was measured by the open-circuit method. Minute ventilation (hence blood gases and pH) was controlled by a mechanical respirator. Whole-body, hind-limb, and gastrocnemius muscle VO2 increased 14, 19, and 20%, respectively, during alkalosis (P less than 0.05). In all experiments, arterial lactate concentration increased significantly (P less than 0.05) during alkalosis. A positive venoarterial lactate difference across muscle during alkalosis indicated that skeletal muscle is a source of the elevated blood lactate. We concluded that VO2 of resting skeletal muscle is increased during states of respiratory alkalosis and that this increase can account for much of the increase in whole-body VO2.

The conventional Douglas bag calculation for estimating O2 uptake (VO2) during exercise in normoxia and hyperoxia, VO2 = VE . (FIO2 . FEN2/FIN2 - FEO2), was tested against two other valid calculations: the Fick equation, VO2 = VI . FIO2 - VE . FEO2, and the equation VO2 = VI - VE - VCO2 (VE and VI are expired and inspired ventilation, respectively; FEO2 and FIO2 are expired and inspired O2 contents, respectively; FEN2 and FIN2 are expired and inspired N2 contents, respectively; and VCO2 is CO2 production.). These calculations are based on different assumptions, in part, and are affected to a varying degree of errors in volume or gas fraction measurements. With the conventional Douglas bag technique, we found evidence of an overestimate of VO2 during hyperoxia. After the introduction of a mixing chamber for sampling expired air, the means of the three methods were not significantly different. The variability among the methods was least with the conventional calculation but increased with higher O2 fractions. The average VO2 for submaximal exercise in hyperoxia was not significantly different from that of normoxia. VO2 max was significantly higher in hyperoxia. The increased variability of the Douglas bag method in hyperoxia may lead to overestimates of VO2 max unless special precautions are taken.

These experiments were designed to study selected respiratory and metabolic responses to exercise in hyperoxia. Four subjects were examined during 30-min bicycle ergometer rides at both 40% and 80% of their aerobic maximum. The VO2 was significantly increased at both work levels breathing 60% O2 versus 21% O2, while VCO2 showed no significant change during the 40% exercise tests but was significantly decreased during the 80% intensity rides. The average increase in the volume of O2 taken up during 30 min of hyperoxic exercise, compared with normoxia, was 3.3 liters at the 40% exercise level and 5.6 liters at the 80% level. Neither the magnitude of the O2 nor the CO2 storage calculated for the exercise bouts could explain these increases. Steady-state criteria for the gas stores were established by the stable values of PETCO2, VO2, VCO2, and VI from minute 6 through 30 at both work levels. R values decreased during the hyperoxic tests suggesting the possibility of a shift toward increased fatty acid metabolism.

This study was undertaken to compare the efficiency of aerobic and anaerobic work. Nine subjects worked at approximately 100% VO2 max for 2 min while inspiring gas mixtures with O2 fractions ranging from 0.13 to 0.21. Exercise O2 uptake, recovery O2 uptake, and blood lactate concentration were measured. Steady level O2 uptake was measured in normoxia at submaximal loads of about 30, 50, and 70% of VO2 max. Fast recovery O2 uptake did not change as PIO2 was varied. Exercise O2 uptake and blood lactate concentrations were linearly related to PIO2. The ratio of the slopes of these lines provided an empirical expression of the O2 equivalent of blood lactate. This ratio was constant, suggesting that it is not less efficient to use ATP synthesized anaerobically. Energy input from lactate was calculated using this factor. Efficiency decreased as power output increased even at the submaximal work rates. This may result from either 1) a decrease in muscle efficiency, 2) an increase in metabolism that is not directly related to the external work, or 3) some combination of 1 and 2.

Six subjects rode a bicycle ergometer on three occasions breathing 17, 21, or 60% oxygen. In addition to rest and recovery periods, each subject worked for 10 min at 55% of maximal oxygen uptake (VO2 max) and then to exhaustion at approximately 90% VO2 max. Performance time, inspired and expired gas fractions, ventilation, and arterialized venous oxygen tension (PO2), carbon dioxide tension (PCO2), lactate, and pH were measured. VO2, carbon dioxide output, [H+]a, and [HCO3-]a were calculated. Performance times were longer in hyperoxia than in normoxia or hypoxia. However, VO2 was not different at exhaustion in normoxia compared with hypoxia or hyperoxia. During exercise, hypoxia was associated with increased lactate levels and decreased [H+]a, PCO2, and [HCO3-]a. The opposite trends were generally associated with hyperoxia. At exhaustion, [H+]a was not different under any inspired oxygen fraction. These results support the contention that oxygen is not limiting for exercise of this intensity and duration. The results also suggest that [H+] is a possible limiting factor and that the effect of oxygen on performance is perhaps related to control of [H+].

These experiments were conducted to determine whether changes in arterial O2 tension are related to changes in muscle metabolism during fatiguing contractions. Arterial and venous circulation to the gastrocnemius muscle (n = 8) was isolated, and the Achilles tendon was attached to a force transducer. Each muscle was electrically stimulated through the sciatic nerve for three 2-min periods of fatiguing contractions separated by 8 min of rest. The arterial O2 tensions were altered for each work period (mean PO2 = 44, 72, 391 Torr). Arterial and venous samples were drawn to measure lactate, O2 and CO2 concentrations (Van Slyke analysis), and [H+]. Muscle biopsies were taken to measure muscle [H+] (homogenate method) and lactate. Fatigue was evaluated as the decline in tension from peak initial tension. At the end of the contraction periods, values were significantly different (P less than 0.05) between the low arterial O2 tension and the high for flow [84 +/- 6 (mean +/- SE) vs. 70 +/- 8 ml X 100 g-1 X min-1], muscle lactate contraction (44 +/- 10 vs. 26 +/- 4 mmol/kg dry wt), and lactate release (122 +/- 12 vs. 57 +/- 14 mumol X 100 g-1 X min-1). O2 uptake and the rate of fatigue were not different among treatments during contractions. Muscle [H+] increased (work [H+] minus rest [H+]) to a significantly greater extent during low arterial O2 tensions compared with high (P less than 0.05). We conclude that alterations in arterial O2 tension during fatiguing contractions induce changes in blood and muscle acid-base status and in muscle metabolism that are independent of O2 uptake.

Six subjects exercised on the bicycle ergometer on three separate occasions. Each of the three tests that each subject performed consisted of a 5-min work period [95% maximal O2 uptake (VO2max)], followed by a 4-min rest period, and then a performance task to exhaustion (90% VO2max). Each test varied only in the inspired O2 fraction (FIO2) (16, 21, or 60% O2 in N2) that was breathed during the initial 5-min work period. The remainder of each test was carried out with 21% O2. Total power output was the same for each subject during the initial 5-min work bout. However, the varied FIO2 breathed during this initial work period resulted in significantly different mean blood lactate (and H+) concentrations at the start of the performance task (P less than 0.05). Mean performance time was significantly greater (P = 0.04) after the hyperoxic treatment (14.8 min) when compared with the hypoxic (9.1 min). Mean blood lactate and H+ levels at exhaustion were not significantly different. These data demonstrate that when various blood (or muscle) lactate and H+ levels were induced on different occasions by leg muscles, the subsequent performance of those muscles was significantly affected.

Six subjects pedaled a stationary cycle ergometer to exhaustion on three separate occasions while breathing gas mixtures of 17, 21, or 60% O2 in N2. Each subject rode for 3 min at work rates of 60, 90, 105 W, followed by 15-W increases every 3 min until exhaustion. Inspired and expired gas fractions, ventilation (V), heart rate, and blood lactate were measured. O2 uptake (VO2) and CO2 output (VCO2) were calculated for the last minute of each work rate; blood samples were drawn during the last 5 s. "Break points" for lactate, V, VCO2, V/VO2, and expired oxygen fraction (FEO2) were mathematically determined. VO2 was not significantly different at any work rate among the three different conditions. Nor did maximal VO2 differ significantly among the three treatments (P greater than 0.05). Lactate concentrations were significantly lower during hyperoxia and significantly higher during hypoxia compared with normoxia. Lactate values at exhaustion were not significantly different among the three treatments. Four subjects were able to work for a longer period of time during hyperoxic breathing. The variations in lactate accumulation as reported in this study cannot be explained on the basis of differences in VO2. The results of this research lend support to the hypothesis that differences in the performance of subjects breathing altered fractions of inspired oxygen may be caused by differences in lactate (or H+) accumulation.

These experiments were designed to investigate the effects of O2 breathing on limb blood flow and metabolism during exercise. Six subjects took part in the study. Four subjects breathed air or 100% O2 while pedaling a Krogh bicycle at 150 W (55-70% of maximal aerobic capacity). Two subjects breathed either 60% or 100% O2 while working at a power output at or slightly in excess of their maximal aerobic capacities. The major findings of the study were 1) leg blood flow is reduced during exercise when comparing hyperoxia with normoxia; 2) VO2 of the exercising limb is not different during hyperoxia; 3) O2 delivery to the leg (the product of blood flow and arteriovenous O2 difference) is not significantly different in the two conditions; and 4) blood pressure is not markedly affected in the experiments at 150 W. Since BP was not different during hyperoxia, at a time when flow was reduced by 11%, this suggests an increased resistance to flow in the exercising limb. In general, these findings are consistent with those reported for the in situ dog muscle but are at variance with results of experiments with humans, especially the reports indicating substantial increases in O2 uptake during hypertoxic conditions.

The use of inspired gas mixtures with an oxygen fraction in excess of 0.3 has been associated with a decrease in the gas exchange ratio (R) during prolonged work in humans. It had been hypothesized that the lower R was due to a lower plasma catecholamine concentration caused by the hyperoxia (Med. Sci. Sports 10: 167-170, 1978). We tested this hypothesis by measuring changes in plasma epinephrine and norepinephrine when the subjects were switched from breathing air to 60% O2 (and vice versa) during 40 min of cycle ergometer exercise at 67% maximal oxygen uptake (VO2max). The subject breathed one gas mixture for the first 30 min and was switched to the other in the last 10 min. The order was reversed in the second test. The switch in gas mixtures from air to 60% O2 resulted in a significant reduction in R, heart rate, minute ventilation, blood lactate concentration, and plasma epinephrine concentration (P less than 0.05). The plasma norepinephrine concentration (0.1 greater than P greater than 0.05) and the plasma free fatty acid concentration were not significantly changed. Although the direction of the epinephrine change was consistent with the change in R, the epinephrine change was quantitatively small (20 pg/ml) and of questionable physiological significance. This suggests a direct effect of PO2 on cellular metabolism as one cause of the change in R when the subjects were switched from air to 60% O2.