oxygen uptake, acid-base status, and performance with

Oxygen uptake, acid-base status, and performance with varied inspired oxygen fractions

RICHARD P. ADAMS AND HUGH G. WELCH Departments of Zoology and Physical Education, University of Tennessee, Knoxville, Tennessee 37916

ADAMS,RICHARD P., AND HUGHG.WELCH. Oxygenuptake, acid-base status, andperformance with varied inspired oxygen fractions. J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 49(5): 863468, 1980.-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 (voz max) and then to exhaustion at approximately 90% Vo2 max. Performance time, inspired and expired gas fractions, ventilation, and arterialized venous oxygen tension (POT), carbon dioxide tension (Pco~), lactate, and pH were measured. v02, carbon dioxide output, [H+la, and [HCO& 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+la, Pco~, and [HCO& The opposite trends were generally associated with hyperoxia. At exhaustion, [H’la 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+].

bicarbonate; carbon dioxide output; hydrogen ion concentration; hyperoxia; hypoxia; lactate; limiting factors.

THERE HAVE BEENMANY STUDIES overthepast50years that have attempted to identify the factor or factors limiting physical performance. For exhausting exercise of moderate duration, the factors generally resolve into two possibilities. One of these is that oxygen availability at the muscle is limiting in that the cardiovascular system is not capable of delivering sufficient oxygen to the tissues (5, 8, 9, 15, 17). The other commonly mentioned possibility is that the oxygen supply to the muscle is normally adequate and the limiting factor is related to the inability to utilize that oxygen (4, 11, 13, N-20).

Most performance studies on human subjects show increased performance with increases in the inspired oxygen fraction (Fzo,) (1, 5, 10, 26). In addition, maximal oxygen uptake (voz max) in humans has been shown to increase or decrease as a function of F’IO, (1, 5, 16, 22, 23, 25). These results would seem to support oxygen availability as a limiting factor. However, recent studies with human subjects and with in situ dog gastrocnemius prep- arations have shown that, when hyperoxic gas mixtures were breathed, oxygen delivery to active muscle was not

increased (23, 24). An &lo% increase in arterial oxygen concentration (Cao,) produced by hyperoxic mixtures is accompanied by a roughly equivalent decrease in blood flow (Q) so that the oxygen delivery (Q x Cao,) is not significantly different from the normoxic control. In both human experiments and in animal experiments, To2 cal- culatedt from measurements of flow and blood gas concentrations was not different under hyperoxic and nor- moxie conditions (21-23, 24).

If oxygen delivery to working muscle is not increased during hyperoxia, and if vog is not different in the hyperoxic and normoxic conditions, then some explanation other than an alleviation of tissue hypoxia must be sought to account for the enhanced performance that is regularly observed with hyperoxia. There is evidence that performance can be affected by altering the acid-base balance of the body (12); an improvement in performance is associated with alkalosis and a deterioration with acidosis. Because there are reasons to expect acid-base variations in the blood with changes in blood 02 tension, we under- took to investigate the possibility that the relationship between FIO, and performance is the result of changes in the oxygen level leading to changes in the hydrogen ion concentration.

METHODS

Six males participated as subjects in this study (Table 1). All conducted personal running programs. None was specifically trained as a cyclist. All subjects gave written consent after having been informed of their rights, most of them after having seen someone else perform the test. The subjects were asked to keep their activities as con- stant as possible and to come to the test in a postabsorp- tive state. The tests were performed under uniform en- vironmental conditions (temperature 21.5-26.O”C; PB 736-745 Torr; relative humidity 48-63s).

After several rides to minimize the effects of training and after measurements of voz m8X on a bicycle ergometer (Monark), the subjects were tested three times, each subject waiting approximately 1 wk between successive tests. The tests were performed in an identical manner except that the FI 0, was changed each time (mean = 0.1682,0.2090,0.6003 in Nz). The six possible orderings of the three tests were assigned in a random fashion, and the subjects were unaware of what gas they were breathing.

0161-7567/SO/oooO-OffiOl.25 Copyright 0 1980 the American Physiological Society 863

864 R. P. ADAMS AND H. G. WELCH

TABLE 1. Subject personal data

-r---r Subj Test* Age, No. Order Yr

173 73.6 4.01 54.5 147 178 69.1 4.05 58.6 147 183 73.4 4.35 59.3 147 180 73.4 4.46 60.8 151 180 72.3 3.70 51.2 129 188 65.7 4.56 69.4 184

180 71.3 4.19 59.0 151

* 1, Hypoxia; 2, normoxia; 3, hyperoxia.

ml-kg-‘. min-’

Watts Percent

space and resistance. On three occasions during the test, the inspired gas was sampled for analysis by the Scho- lander technique.

Low

The test protocol called for the subject to report

High Low

258 55.5 258 52.0 294 52.1 302 51.5 202 57.8 248 59.6

260 54.8

The expired gas passed through a 3%cm length of 34-

quiet room 30 min before coming into the laboratory. An infusion needle (Deseret Minicath-PRN, 21 gauge, 0.75 in. with 3-in. extension length) was inserted into a super- ficial vein on the back of the hand and taped down to minimize movement. The hand was continuously warmed throughout the test with an electric heating pad to help ensure better arterialization of the blood. Upon entering the testing room, the subject sat quietly on the bicycle ergometer, breathing room air for 10 min. Next he put on the mouthpiece and noseclip and breathed that day’s gas mixture for an additional 15min rest equilibration period. A blood sample was drawn at the end of each of these periods. Ventilatory data collection began at min 12 of the equilibration period and continued throughout the test.

At the end of the equilibration period, the subject began pedaling the ergometer at a rate that was approximately 55% of Vo 2 max and continued for 10 min. Blood samples were taken at min 5 and 9 of this period. The work rate was then increased to a higher level (mean N 90% vo 2 max) at which the subject rode until exhaustion. Blood samples were taken every 4 min beginning at min 3 of this period. Upon exhaustion the subject continued to breathe the gas mixture while sitting at rest on the bicycle for an additional 20-min recovery period. Blood samples were taken every 4 min beginning at min 3 of this period also.

The ride to exhaustion was chosen as a measure of performance while the IO-min submaximal ride was chosen to ensure steady-state measurements. The low submaximal load was chosen to elicit a measurable increase in lactic acid concentration ([LA]) while still leaving room for another greater increase in the jump to the high work load. The higher work load was chosen to exhaust the subject in about 10 min so that adequate measurements could be made during the approach to the end point.

Inspired gas was provided from high-pressure cylin- ders. It was bubbled through heated water in a 2-liter aspirator bottle to ensure 100% saturation and then passed into a 120-liter Tissot gasometer, which acted as a reservoir. From there the gas passed through a Parkin- son-Cowan CD4 gas meter (with potentiometer coupled to a Physiograph) and then directly to the mouthpiece. The mouthpiece was a Daniels valve with minimal dead

High mm-ID tubing into a 5-liter mixing chamber. Expired gas fractions were monitored continuously from an Applied

93.9 87.8

Electrochemistry S-3A 02 analyzer and a Beckman LB-

97.6 2 CO2 analyzer and recorded by hand at 15-s intervals.

97.8 These analyzers sampled directly from the mixing cham- 90.8 ber by way of a 30-cm length of 6-mm-ID tubing. The 76.9 analyzers were frequently calibrated against known gases

90.8 during the test.

At predesignated intervals (usually 4 min), 50-ml samples were drawn from the mixing chamber into glass syringes and later analyzed by the Scholander method. The expired gas fractions obtained from the Scholander

to a and from the electronic analyzers were used to calculate separate values for Vo2 and Vco2. The accuracy of the measurement was demonstrated when it was found that the values for v02 and %k02 calculated from the two gas fractions were not significantly different (P > 0.20). The difference between the means for both VOW and VCO~ was less than 1 ml/min.

All variables measured from arterialized venous blood samples, with the exception of POT, have previously been shown to accurately reflect arterial values (6). The blood samples were drawn at designated intervals throughout the test into l-ml matched tuberculin syringes the dead space of which had been flushed with saline containing approximately 300 U/ml heparin. This blood was used for determinations of LA, pH, and carbon dioxide tension (Pcoz) and oxygen tension (POT). The Po2 values were used only as an index of relative oxygenation.

Approximately 0.3 ml of the blood sample was placed immediately into a spot-plate well that had previously been coated with 0.05 ml of a 4% NaF solution and then dried. The blood and NaF were mixed, two separate 50- ~1 samples were taken, and each was placed into 2 ml of 7% HClO4 and iced. Subsequent lactate analysis was performed according to a modification of the fluorometric enzymatic method of Gutmann and Wahlefeld (7).

From the remaining 0.7 ml of the blood sample, two separate determinations for pH, Pc02, and Po2 were made. The analyses were made at 37°C using a BMS MK2 Blood MicroSystem with PHM 73 pH/Blood Gas Monitor (Radiometer, Copenhagen) calibrated frequently with gases analyzed by the Scholander method and with Radiometer buffers. The analyses were performed within 10 min of sampling to overcome any problems with deterioration of the sample. Arterial hydrogen ion concentration [H’]a was calculated from the measured pH and [HCOT], from PCO~ and [H’]a using a pKof 6.1. We did not measure rectal temperatures during the experiments because of our observation that, under conditions similar to those described here (with the use of cooling fans), rectal temperature rarely exceeds 38.0°C, and there are no differences between hyperoxia and normoxia.

Repeated measure designs were used for the primary statistical analysis because each subject performed under all conditions. The Tukey HSD test was used for a posteriori analysis when overall significant differences

OXYGEN UPTAKE, ACID-BASE STATUS, AND PERFORMANCE 865

were indicated between treatments. A probability below 0.05 was considered significant, a value above 0.10 not significant, and 0.10 > P > 0.05 was considered margin- ally significant or approaching significance.

RESULTS

In Figs. 1-7, period I shows values for the subjects sitting at rest breathing room air. Period II is an additional 15-min rest period during which the subjects began breathing the specific gas mixture for that day. Period III indicates 10 min of exercise at approximately 55% ~oZ max, and period VI is the recovery period. Periods IV and Vshow the results for exercise at about 91% VOW max. Period IV gives the values for the first 7 min or relative to the onset of that work load. Period V on the other hand indicates values for the last 8 min or relative to exhaustion, which occurs at min 0 on the right-hand portion of the graph. The split in the heavy work period was necessary because this was a performance study and exhaustion occurred at different times in each test. Therefore, the division was made to see what happens both as the subjects begin work and as they approach exhaustion.

It should be noted that, due to the differences in performance time, there is some overlap between the data presented in periods IV and V. This is especially true for the hypoxic data where the performance times were shortest. The plotted points in the overlapping portion are not the same, however, because period IV shows the means of values obtained at a fixed time after the onset of work whereas period V shows the means of values, which were in some cases interpolated from the measurements actually taken. This interpolation was necessary in order to arrive at values reflective of conditions at a fixed time before the point of exhaustion, which was different for each subject.I was different for each subject.A

0 0 IO IO I5 15 20 20 25 30 35 40 25 30 35 40 I 1 I J

-5 0 5 IO I5

4.0

3.5

3.0

2.5

-

-E 2.0 \ - -

a5 0

l >

I .o

0.5

+.I 0 IO I5 20 25 30 35 40

TIME (min)

. ---HYPOXIA 1 -NORMOXlA

- l ***=* HYPEROXIA I I

- 1 I

.I I II I III

I I

FIG. 2. Mean values for carbon dioxide output (h02).

0 0 IO IO 15 15 20 20 25 25 30 30 35 35 40 40

TIME (mid TIME (mid

FIG. 3. Mean values for minute ventilation (VI).

Performance. Performance varied with no,. Mean performance during hyperoxia (15.8 min) was longer than during normoxia (12.5 min, P < 0.05), and even though performance during hypoxia (9.7 min) was less than during normoxia, the difference was not significant (0.15 > P > 0.1).

Oxygen uptake (Fig. 1). Analysis of v02 data showed that at no time during the test were the hyperoxic or hypoxic values significantly different from the control (all P > 0.05). At exhaustion the 2.8% lower value with hypoxia (3.68 vs. 3.78 l/min for normoxia) was not significantly different (P > 0.1); however, the 4.8% higher value with hyperoxia (3.96 l/min) was approaching significance (0.1 > P > 0.05). The difference between hypoxia and hyperoxia at this point was significant (P < 0.01).

TIME (min)

FIG. 1. Mean values for oxygen uptake (v02) at 02 fractions of 0.17, 0.21, and 0.60. In this and subsequent figures: period 1, rest prior to inspiration of actual mixture;period 11, rest while inspiring test mixture; period III, mild exercise (about 50% of voz max); andperiod VI, recovery. Periods IV and V both represent heavy exercise (mean - 90% of VO 2 ma,), IV h s owing that period relative to onset of heavy exercise, V showing data relative to point of voluntary exhaustion. See text for further details.

Carbon dioxide output (Fig. 2). The results for ho2

indicate that a significant difference from normoxic values exists only in the light work period where the hypoxic mixture is associated with a higher ho2 (P < 0.05).

VentiZation (Fig. 3). During rest inspiratory ventilation (VI) during hyperoxia was significantly higher than during hypoxia (P < 0.05)) with control ventilation inter- mediate and not sienificantlv different from either. Dur- ---_ ----- - - ---- -~ ~ d


55 I

* I II i 19

53 1

1111

I I I

hypoxia 9.8 mM, normoxia 7.2 mM, and hyperoxia 6.0 mM. Peak hypoxic value was 10.7 mM.

Carbon dioxide tension (Fig. 6). The only significant

- - \ r c -

r+ I u

IL 0 IO 15 20 25 30 35 40

TIME (mid

,A-- l ..A \

b /k=

differences from normoxia qre at the end of light work and during the first 7 min of heavy work. During light

.-•- /

4

I \ -0 \

/’ I *‘?a ‘,

and heavy work hypoxia produced lower Pcoz values, t ‘-0 8 and during heavy work hyperoxia produced higher values

I .

: f -k (all P < 0.05).

/ 1’

I l .

l . l .

Bicarbonate concentration (Fig. 7). Athough there

I \

I

a /

were significant differences between hypoxic and hy- i 1 HYPEROXIA peroxic conditions, at no time were values under those

HYPOXIA conditions different from normoxia.

I I DISCUSSION

I I I 1 -5 0 5 IO I5

The trends in this study are consistent with data published previously (e.g., 12, 18, 23). However, the small differences in To:! at exhaustion, which we observed, are

FIG. 4. Mean values for [H’]. considerably lower than in most previous reports (5, 8,

IO

I

I I II 9 I

0 I

- 0 IO 15 20 25 30 35 40

TIME (mid

7 17, 22). The differences found here are more consistent

I/ ‘\ with those obtained in studies that determined 'cj02 from =; ‘$I

/I measurements of blood flow and blood gas concentra-

\ I I \ tions. It may be that the higher values for pulmonary

HYPEROXIA =a. I -*A

I 36 -

34 -

32 - - I”

E 30 - 5

;28 - 0,

26 -

24 t 1 1 I I

\ \ I \ \ I

\ I (N 24)’

I

‘4: 91:

y l ,=--.

I

\ ‘./ l ’

,

u ’ ’ 1 ’ i 0 IO I5 20 25 30 35 40

TIME (min)

FIG. 6. Mean values for carbon dioxide tension (Pcoz).

FIG. 5. Mean values for blood lactate (LA) concentrations.

ing light work, VI during hypoxia was higher than under the other two conditions (P < O.Ol), which were not different from each other (P > 0.1). During heavy work and at exhaustion, all VI were different (P < 0.01) with hypoxia producing the highest and hyperoxia the lowest values.

Hydrogen ion concentration (Fig. 4). Though [H’la 19 - , I ofd \

l -.,, values in hyperoxia were generally higher than normoxic I

l .,

values during light and heavy work and lower during I*- I recovery, at no time were they significantly different (all :17- 1

I \ l \ 4

‘\ l .,

I I

‘, t . . P > 0.1). Hypoxic values were, however, lower during 7 light and heavy work and higher during early recovery - l6- I I

I \ ii

(all P < 0.05) than under either of the conditions. At 5, 5 - 1 I I z

\ ‘0

1 HYPEROXIA

exhaustion [H’] was the same under all conditions (mean $- I HYPOXIA-\

I I \

= 50.8 nM or 7.29 pH; P = 0.80). I4 - \

Blood lactate (Fig. 5). Again there was no significant I I I ! (N=4)

difference between normoxic and hyperoxic values throughout the test (all P > 0.1). However, hypoxic values, except during rest, were higher than control values for the entire test (all P < 0.05). Under no condition was the rate of increase in [LA] different from the nor- moxie rate (all P > 0.1). Mean values at exhaustion were

l3 _ I I I

12 - 1 I I ’ 1 -,I

0 IO I5 20 25 30 35 40

TIME (min]

FIG. 7. Mean values for [HCOT].

-5 0 5 IO I5

OXYGEN UPTAKE, ACID-BASE STATUS, AND PERFORMANCE 867

. . l .

. l .

. *

.

.

. .

. l t -1 t -1 .

. * *

.

( t )

.

:

. .

I - v l

-1 I’

H+ i,--,,,, --a-- 7 1 -- H+ a’ c I

t

(+I

,[ 1 La’ a

(+I

[ I HLa a PaC02 * \

Q GLY

. . . - . ( 1

PaO,

FIG. 8. Pathways for the effects of oxygen on [H+] during exercise. See text for explanation.

vo2 during hyperoxia, which appear in the literature, can be accounted for by the use of the Douglas bag method that, in our hands, gives values significantly higher than those obtained by the mixing chamber method.

The lack of a significant difference in TO:! at exhaustion between the normoxic and hyperoxic conditions raises the question of whether other factors affect performance under conditions similar to those in this study. One such possibility is apparent after finding that the arterial [H’] ([H+la) is the same at exhaustion under each of the conditions imposed here. This result is very likely not a coincidence because it has been obtained, though not commented upon, by several previous investigators. As- mussen & Nielsen (1) using hypoxia and normoxia obtained pH values of about 7.36 at exhaustion, as did Hughes et al. (10). Ekblom et al. (5) using a more intense work rate obtained values of 7.22 under hyperoxic, hypoxic, and normoxic conditions. Pirnay et al. (18) mea- suring venous blood found values of 7.08 with both hyperoxia and normoxia. In our protocol the pH values average 7.29 (50.8 nM) at exhaustion under all conditions. That is, at exhaustion under conditions where the acid- base status has not been directly changed, the [H+] is the same regardless of differences in performance time. This implies that some aspect of the acid-base state affects performance.

It cannot be said from these data whether [H’] directly limits performance under normal circumstances, or if it does whether that effect is intracellular or extracellular,

or in either case what the mechanism might be. However, in light of the fact that different values for [H+18 are reported at exhaustion both with protocols of different intensity and duration (5, 10, 18) and when the test is, or is not, preceded by other work (14), an extracellular effect does not seem likely. Furthermore, it is hard to argue that a pH, as high as 7.3 or 7.35 should be limiting. On the other hand, the similar arterial values at exhaustion within each protocol could be reflective of common but lower intracellular values. The fact that different protocols yield different [H’la values at exhaustion does not mean that the intracellular [H’] is different across those protocols. The low values obtained within the cell could certainly be limiting (19).

It is important to note here that there is a great deal of difference between considerations of acid-base levels produced indirectly by variations in Fro., and directly by administration of acidic or basic substances. The chang- ing of [H’], by means of FI 0, should have its effect first at the intracellular level; those conditions would then be reflected in the arterial measurements. Similar arterial measurements might then imply similar intracellular values. Bringing about changes in [H+la directly may be somewhat different. In this case intracellular [H’] may not quickly follow [H+],. Jones et al. (12) found that, by ingestion of acidic or basic substances, performance was reduced or enhanced, respectively. That finding supports the role of [H’] in the limitation of performance. How- ever, in that study the [H+la was not the same at exhaustion under the different conditions. This result is very likely a product of the fact that changes in acid-base status were affected directly by ingestion. It does not therefore eliminate the possibility that under more normal circumstances there is a critical [H’] beyond which performance is affected. If [H’] is limiting and if the effect is intracellular, then it is possible that levels in the blood that have been directly changed from the outside do not always reflect intracellular conditions. The intracellular [H’] might still be the same in all cases.

FIN, affects [H’]a in such a way that identical levels are encountered after performances of different lengths. There are both ventilatory and metabolic pathways as set forth in Fig. 8. Not all mechanisms are known (as denoted by the dotted lines) though there is evidence that such mechanisms should exist. All quantities en- closed in heavy boxes were measured in this study and all indications of an increase in one quantity leading to an increase (+) or decrease (-) in a subsequent quantity are supported here. The two pathways operate conjunc- tively but with opposite results. The net result of the pathway via ventilation is that hypoxia causes a decrease in [H+&. The net result of the pathway via glycolysis is just the opposite with hypoxia causing an increase in [H+],. That is, hypoxia, through its effect on chemore- ceptors, increases ventilation and lowers the arterial PCO~ (hyperventilation), as a result, the [H’la is lowered. On the other hand, hypoxia, through some unknown mechanism, increases the lactic acid produced by glycolysis with a resulting increase in [H+la. The two pathways share in the overall effect. During hyperoxia the same mechanisms may also come into play with the opposite


result for each pathway. The two pathways share in the overall effect.

is still operative, its capacity to lower the [H’la by means

However, during light work (period III), the ventilatory effect is seen to be predominant. Here VI is signifi-

of lowered Pcoz is gradually exceeded by the flux of [H+]

cantly higher in hypoxia (Fig. 3). As a result, more CO2 is blown off (Fig. 6) and the [H’] is lowered (Fig. 4). On the other h

into the blood from the production of lactic acid. In Fig.

.and, th

5, there seems to be a larger total amount of lactate with

.e hyperoxic and normoxic ventilations during this

hypoxia and less with hyperoxia. Although the rate of

period

increase of LA in the blood is the same under the three

are not different and therefore neither is Pcoz nor [H+],. During heavy work leading to exhaustion (periods IV and V), although the ventilatory effect

lactate u .nder that condition. ) In the long run, the between the two pathways allows a given [H’ reached and at that time, for whatever reason, exhaustion occurs. Performance and [H’lB seem to vary then as a result of the interplay between the two pathways.

balance Ia to be

extracellular. Measurement of arterial values alone cannot provide the answer. Measurement of intracellular

This study presents evidence to support the contention that oxygen availability is not a limiting factor for exercise performance but that acid-base levels might be. If

concentrations under these conditions has not been per-

[H’] limits performance, the results of this study cannot

formed and would be helpful in answering the question

be used to determine whether the effect is intra- or

of an acid-base role in the limitation of performance.

conditions with the onset of any work rate (Fig. 5), the The authors are grateful to a number of people without whose help

total amount produced causes differing levels of [H’] and this project could not have been completed. In particular, we acknowl-

subsequently [H+la. These differing levels of [H’& are edge the assistance of L. Sundahl, K. Riley, R. Cox, K. McNair, K.

then further changed by the different buffering encoun- Wessling, R. Ellis, S. Lemay, B. Seals, M. Sonnenfeldt, D. West, A. Woods . and K . Welch .

tered with different ventilations. This work was supported by a grant from the East Tennessee Heart

The supposition here is that glycolysis is slowed and Association and by National Science Foundation Grant 5507RR07088-

11* This work was done during R. P. Adams’ tenure as a Fellow of the

National Science Foundation. His present address is August Krogh Institute. Conenhagen. Denmark.

Address reprint yequests to H. G. Welch at University of Tennessee.

that less lactate is produced in hyperoxia (it is shown that less appears in the blood). The concurrent lowering of ventilation by the increased POT then buffers the lower [H+la (resulting from the lower lactate) to a lesser degree. (The higher ventilation of hypoxia acts to buffer the higher level of [H’] resulting from greater production of

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oxygen uptake, acid-base status, and performance with

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