The influence of PaO2, pH and SaO2 on maximal oxygen uptake

The in¯uence of PaO2, pH and SaO2 on maximal oxygen

uptake

H . B . N I E L S E N , P . M A D S E N , L . B . S V E N D S E N , R . C . R O A C H and N . H . S E C H E R

The Copenhagen Muscle Research Centre, Department of Anaesthesia, Rigshospitalet, University of Copenhagen, Blegdamsvej

Copenhagen é, Denmark

ABSTRACT

Influence of arterial oxygen pressure (PaO2) and pH on haemoglobin saturation (SaO2) and in turn on O2

uptake (VO2) was evaluated during ergometer rowing (156, 276 and 376 W; VO2max, 5.0 L min)1;

n � 11). During low intensity exercise, neither pH nor SaO2 were affected signi®cantly. In response to

the higher work intensities, ventilations (VE) of 129 � 10 and 155 � 8 L min)1 enhanced the end tidal

PO2 (PETO2) to the same extent (117 � 2 mmHg), but PaO2 became reduced (from 102 � 2 to 78 � 2

and 81 � 3 mmHg, respectively). As pH decreased during maximal exercise (7.14 � 0.02 vs.

7.30 � 0.02), SaO2 also became lower (92.9 � 0.7 vs. 95.1 � 0.1%) and arterial O2 content (CaO2) was

202 � 3 mL L)1. An inspired O2 fraction (FIO2) of 0.30 (n � 8) did not affect VE, but increased PETO2

and PaO2 to 175 � 4 and 164 � 5 mmHg and the PETO2±PaO2 difference was reduced (21 � 4 vs.

36 � 4 mmHg). pH did not change when compared with normoxia and SaO2 remained within 1% of

the level at rest in hyperoxia (99 � 0.1%). Thus, CaO2 and VO2max increased to 212 � 3 mL L)1 and

5.7 � 0.2 L min)1, respectively. The reduced PaO2 became of importance for SaO2 when a low pH

inhibited the af®nity of O2 to haemoglobin. An increased FIO2 reduced the gradient over the alveolar-

arterial membrane, maintained haemoglobin saturation despite the reduction in pH and resulted in

increases of the arterial oxygen content and uptake.

Keywords arterial oxygen pressure, arterial oxygen saturation, hyperoxia, lactate, pH, rowing.

Received 24 October 1997, accepted 24 March 1998

A pulmonary limitation to maximal O2 uptake (VO2max)

is indicated by a reduced arterial O2 pressure (PaO2

55 mmHg, Dempsey et al. 1984) and saturation (SaO2

85%; Rowell et al. 1964). The SaO2 is reduced especially

in the athlete (to 87 vs. 93% in control subjects; Williams

et al. 1986) indicating that a high cardiac output and in

turn a low pulmonary transit time is important. Those

subjects who demonstrate the lowest PaO2 tend to

hyperventilate less as indicated by the arterial carbon

dioxide pressure (PaCO2 > 35 mmHg) and a low alve-

olar O2 pressure (PAO2 < 110 mmHg, Dempsey et al.

1984). Equally, the acceptance of O2 by the erythrocytes

is of importance and during exercise, haemoconcentra-

tion facilitates the pulmonary O2 diffusion, while the

associated acidosis counteracts the binding of O2 to

haemoglobin (Rasmussen et al. 1991, Hanel et al. 1994).

Also, an uneven distribution of pulmonary ventilation

and perfusion may contribute (Hammond et al. 1986,

Hopkins et al. 1994), but the fact that SaO2 is reduced

similarly during supine and upright exercise is taken to

indicate that this mismatch is not critical (Pedersen et al.

1996). The alveolar-capillary membrane is subjected to

stress failure in the racing horse (West & Mathieu-

Costello 1995) and in humans (Hopkins et al. 1997). A

vulnerable membrane is indicated by the post-exercise

reduction in pulmonary diffusion capacity (Hanel et al.

1994) as only »50% of this reduction is related to a drop

in the pulmonary capillary blood volume (Hanel et al.

1997). Thus, the exercise PaO2 increases following a

polyunsaturated fatty acid supplemented diet (74±

81 mmHg, Aguilaniu et al. 1995) and the drop in PaO2

correlates to plasma histamine during maximal exercise

(Anselme et al. 1994).

An elevation of the inspired fraction of O2 (FIO2) to

only 0.26 overcomes the reduction in oximetry deter-

mined SaO2 and VO2max becomes elevated (Powers

et al. 1989) supporting that PAO2 is critical for O2

transport. With a larger elevation of FIO2 to 0.50, the

arterial O2 content (CaO2) and VO2max are elevated by 8

and 13%, respectively (Ekblom et al. 1975). However,

Correspondence: Henning Bay Nielsen M.D. Department of Anaesthesia 2041, Rigshospitalet, Blegdamsvej 9, DK-2100 Copenhagen é,

Denmark.

Acta Physiol Scand 1998, 164, 89±97

Ó 1998 Scandinavian Physiological Society 89

with a markedly elevated FIO2, the calculation of VO2

tends to be an overestimate (Welch & Pedersen 1981).

Equally, it may be that the oximetry determined SaO2 is

in¯uenced by vasoconstriction of the evaluated capil-

lary bed. Powers et al. (1984) found it equally reduced

during arm cranking and cycle ergometry, while the

invasively determined SaO2 immediately after exercise

correlates to pH and in turn to the muscle mass in-

volved in exercise (Rasmussen et al. 1991).

Thus, although several studies have investigated the

exercise-induced hypoxaemia, no study has integrated

arterial blood gas and acid±base analysis, ventilatory

variables and effects of hyperoxia during and after ex-

ercise. The aim of this study was to evaluate the in-

¯uence of PaO2 on SaO2 when it is challenged by a low

pH. Arterial blood samples were obtained both during

exercise and in the recovery with simultaneous deter-

mination of heart rate (HR) and ventilatory variables. A

pilot study indicated that an FIO2 of 0.30 secures SaO2

during maximal exercise and we hypothesised that

VO2max would increase in proportion to CaO2.

METHODS

Eleven competitive male oarsmen [age 26 (20±

29) years, body weight 80 (70±94) kg, and height 1.87

(1.79±2.00) m (median with range)] participated in the

study as approved by the Ethics Committee of Co-

penhagen (KF 01±349/96). No subject had any disease

or injury 3 weeks prior to the experiment, nor were

they taking any medication. They were not allowed to

drink or eat after midnight on the day of the experi-

ment, which began at 08 00 hours.

Rowing was performed on a Concept II ergometer

(Morrisville, VT, USA) connected to a computer

(Concept II) that displays the split-time for every

`500 m' and the average work capacity. The subjects

attended the laboratory on 3 days to establish the ex-

ercise intensity that provoked a reduction in SaO2. On

the ®rst day, rowing for 20 min aimed at a work in-

tensity ~50% VO2max (low intensity). After 5 min of

recovery, it was followed by `high intensity rowing' as

the subject was instructed to exert as high an intensity

as possible for 30 min with constant speed and stroke

rate. On the second day, they warmed up at an indi-

vidually determined pace for 10 min; recovered for

2 min and then rowed `all-out' for 6 min simulating a

2000-m competitive effort (maximal intensity). All

subjects were familiar with this type of exercise.

An FIO2 of 0.26 during exercise does not maintain

the oximetry determined SaO2 at the level of rest

(Powers et al. 1989). The pilot study showed that during

an all-out row, a FIO2 of 0.30 maintained PaO2 and

SaO2 at 153 mmHg and 98%, respectively, at an arterial

pH of 7.28. Also, that FIO2 was expected not to affect

the fraction of N2 to an extent that the calculation of

VO2 would become affected signi®cantly. Therefore,

eight oarsmen repeated the 6-min all-out row within

3 weeks while breathing 30% O2 in N2.

Respiratory values

Respiratory values were recorded breath by breath

(MedGraphics 2001, St. Paul, MN, USA). During

hyperoxia an extension of the pneumotach was pro-

vided with a T-valve (model 2700, Hans Rudolph,

Kansas City, MO, USA) to humidi®ed air in Douglas

bags. After 5 min to allow stabilization, ventilation

(VE), VO2, respiratory rate (RR), expired carbon diox-

ide (VCO2), end tidal partial pressures for O2 (PETO2)

and carbon dioxide (PETCO2) were averaged for 30 s;

or during maximal exercise for every 15 s. As the `dead

space' increases with tidal volume during exercise

(Asmussen & Nielsen 1956), the PETO2 and PETCO2

were taken to re¯ect PAO2 and PACO2. During all-out

rowing, the peak VO2 corresponds to VO2max as it is

similar to or slightly higher than that obtained during

cycling (Cunningham et al. 1975). The O2 debt (O2debt)

was the sum of VO2 in the ®rst 4 min of the recovery

and the O2 de®cit (O2def) was calculated assuming

linearity between metabolism and work rate (Medbù

et al. 1988). For VO2 determination on incremental

workloads, the subjects performed rowing at 100, 150,

200 and 250 W on a separate day. We assumed the

same linearity for VO2 and power during exercise in

ambient and hyperoxic air. HR was monitored every

15th second using a `Sport Tester' PE 3000 (Polar

Electro, Kempele, Finland).

Blood samples

Blood samples for arterial bicarbonate (BC), carbon

dioxide pressure (PaCO2), PaO2, pH, base excess (BE),

haemoglobin (Hgb), potassium and lactate were ob-

tained anaerobically (QS50, Radiometer, Copenhagen,

Denmark) from a catheter in the radial artery of the

non-dominant arm. Collections were made at rest, ev-

ery ®fth minute during the 20-min row, immediately

prior to the 30-min row followed by every second

minute. During all-out rowing, blood samples were

drawn every minute, 30 s before and after the termi-

nation of exercise, and one minute into the recovery.

Thereafter, they were collected every second minute.

All samples were placed immediately on ice until

measured at 37 °C (ABL4 apparatus; Radiometer) while

SaO2 and Hgb were determined on OSM3 apparatus

(Radiometer). Lactate in whole blood was determined

by a YSI 2300 (Yellow Springs Instruments Co., Inc.,

OH, USA). The CaO2 was the sum of bound (1.39 Hgb

SaO2) and dissolved O2 (0.003 PaO2).

O2 content and uptake � H B Nielsen et al. Acta Physiol Scand 1998, 164, 89±97

90 Ó 1998 Scandinavian Physiological Society

Statistical analysis

Variables are presented as mean with SEM. Changes

were evaluated by the Friedmann test across time and

exercise intensities and differences were located by the

Wilcoxon test by rank. A P-value <0.05 was considered

statistically signi®cant.

RESULTS

Ambient air

During low intensity rowing, the power was

156 � 15 W. In the ®rst few minutes of exercise, VE

and RR increased to a steady state of ~50 L min)1 and

~30 breath min)1 (Fig. 1, Table 1). PETCO2 became

elevated, whereas PaCO2, PETO2, PaO2 and the PETO2±

PaO2 difference did not change signi®cantly. However,

at the onset of exercise PaCO2 increased to

43 � 1 mmHg and PETO2 and PaO2 were reduced to

94 � 3 and 86 � 2 mmHg. Equally, pH and SaO2 were

below the resting level (7.39 � 0.02 and 96.8 � 0.2%,

respectively). Yet, all variables recovered during exer-

cise. BE and BC did not change signi®cantly, whereas

plasma potassium was elevated. CaO2 was enhanced

and HR and VO2 established a steady state.

During high intensity rowing, power was

276 � 12 W. The VE and RR increased without es-

tablishing a steady state (Fig. 1, Table 1). The PETCO2

and PaCO2 decreased, and PETO2 became elevated. Yet,

PaO2 was reduced and the PETO2±PaO2 difference

therefore increased. Lactate increased to

6.5 � 0.9 mmol L)1 and both pH and SaO2 were re-

duced to make CaO2 not different from that established

during low intensity rowing. HR increased throughout

exercise as did VO2.

After exercise, both VE and RR decreased imme-

diately but hyperventilation was indicated by a low

PETCO2 and PaCO2 (34 � 1 and 33 � 1 mmHg, res-

pectively) (Fig. 1). Thus, PETO2 (114 � 2 mmHg) and

PaO2 (105 � 2 mmHg) were elevated and although pH

was lower than during exercise (7.28 � 0.02), SaO2 in-

creased to 97.3 � 0.2%.

During maximal exercise, power was 376 � 22 W

re¯ected in both a large VE and RR (Fig. 2, Table 1).

PETCO2 and PaCO2 were similar to `high intensity' ex-

ercise, whereas VCO2 was higher. Yet, there was an

immediate drop in PETCO2 at the onset and although it

recovered, it decreased to the same level towards the

end of exercise. The PETO2 and PaO2 changed to the

same extent as during high intensity exercise, but the

PETO2±PaO2 difference became smaller. PETO2 in-

creased at the onset of exercise; then decreased and

thereafter, it became elevated to 119 � 1 mmHg.

Lactate reached 11.0 � 0.7 mmol L)1 with a lower

range of arterial pH at 7.06. Arterial desaturation was

pronounced and ®ve subjects demonstrated an SaO2

below 90% and in one subject it was 85%. Yet, with the

increase in Hgb, CaO2 was similar to that during a

lower work intensity. With a similar increase in HR as

during high intensity rowing, VO2max was

5.0 � 0.3 L min)1.

Immediately following exercise, VE and RR re-

mained at the exercise level, but after 30 s they de-

creased, while PETCO2 and PaCO2 remained low

(Fig. 2). Accordingly, PETO2 was high and PaO2 be-

came elevated to 43 � 5 mmHg above the resting level.

SaO2 increased although pH was lower than during

exercise.

Figure 1 Pulmonary ventilation (A), respiratory rate (B), end tidal

carbon dioxide pressure (C), and end tidal oxygen pressure (D) at rest

and in response to low and high intensity ergometer rowing. Values

are mean with SEM.


Acta Physiol Scand 1998, 164, 89±97 H B Nielsen et al. � O2 content and uptake

FIO2 of 0.30

Power (388 � 21 W) was not signi®cantly different

from that obtained in ambient air and VE and RR were

also at the level of the control exercise (Fig. 2, Table 1).

Yet, PETCO2, PaCO2, and VCO2 were higher. PETO2 and

PaO2 were elevated and not signi®cantly changed by

exercise, making the PETO2±PaO2 difference smaller.

The PETCO2±PaCO2 difference (4.4 � 0.7 vs.

2.9 � 0.4 mmHg, normoxia vs. hyperoxia) during ex-

ercise was marginally reduced by O2 supplementation

(P � 0.1). The SaO2 at rest was elevated and only a

minimal reduction occurred during exercise. Neither

Hgb nor CaO2 were affected at rest and Hgb increased

to a similar level as during exercise in ambient air. Thus,

the CaO2 became elevated by 8.5 � 0.1% (Fig. 3). Also,

HR was similar, but VO2max was enhanced by 11 � 3%

(5.7 � 0.2 L min)1). The concentration of lactate

reached 9.8 � 0.6 mmol L)1 and it was not signi®-

cantly changed by hyperoxia. Also, pH, BE, and BC

were not affected. Equally, the O2debt remained un-

changed by hyperoxia, whereas the O2def was reduced

from 10.4 � 5.0 to 8.3 � 5.5 L.

DISCUSSION

This study demonstrates that (i) the arterial oxygen

pressure and saturation of haemoglobin are reduced

only during intense exercise and (ii) an elevated inspired

oxygen fraction reduces the gradient over the alveolar-

arterial membrane and maintains haemoglobin satura-

tion despite a reduction in pH and (iii) the pulmonary

oxygen uptake increases in proportion to the arterial

oxygen content.

During exercise, the alveolar PO2 expressed as the

PETO2 was insuf®cient to maintain the PaO2 and with

marked acidosis, SaO2 became low. Conversely, after

exercise a low arterial pH was not critical for SaO2 as

the PaO2 increased. Equally, an elevation of the frac-

tion of inspired oxygen increased the PETO2 and in

turn the PaO2 to an extent where the SaO2 became

affected little by pH with subsequent increases in the

CaO2 and VO2. In other words, the relationship be-

tween PaO2, SaO2, and pH established at rest (Bohr

et al. 1904) also applied to exercise as SaO2 was within

0.5 � 0.3% of the calculated value (Severinghaus

1958). This was the case although no corrections of

arterial gases were made for changes in body temper-

ature. During maximal exercise, the central temperature

increases by »0.5 °C (Saltin et al. 1972, Bergh & Ek-

blom 1979) with only a small effect on PaO2 and SaO2

(Severinghaus 1979). It should be considered that the

subjects performed a warm-up before the all-out bout,

which would make an effect of the temperature from

rest to exercise small.

We con®rmed that SaO2 tends to be low in subjects

with a large aerobic capacity (Williams et al. 1986)

(r � 0.48, P � 0.05), but even in the subject with a

VO2max of only 3.7 L min)1, it was reduced to 93%

associated with a pH of 7.1. In those subjects with a

Table 1 Variables at rest and during rowing in ambient air and with an FIO2 of 0.30

Room air, W F1O2 0.30, W

Rest 156 276 376 Rest 388

VE (L min)1) 11 � 2 51 � 7* 129 � 10* 155 � 8* 12 � 1 150 � 8*

RR (breath min)1) 16 � 1 31 � 3* 53 � 3* 59 � 2* 12 � 1 59 � 3*

PETCO2 (mmHg) 41 � 1 45 � 1* 38 � 1* 36 � 1* 37 � 1 41 � 1* PaCO2 (mmHg) 39 � 1 41 � 1 33 � 1* 33 � 1* 41 � 1 37 � 1* VCO2 (L min)1) 0.3 � 0.0 1.8 � 0.2* 3.8 � 0.3* 4.6 � 0.3* 0.3 � 0.0 5.0 � 0.3* PETO2 (mmHg) 108 � 2 102 � 1 117 � 2* 117 � 1* 175 � 4 183 � 2 PaO2 (mmHg) 97 � 1 93 � 2* 78 � 2* 81 � 3* 164 � 5 165 � 5 P(ET-a)O2 (mmHg) 12 � 2 12 � 2 41 � 3* 36 � 3* 15 � 3 21 � 4 K+ (mmol L)1) 4.0 � 0.1 4.5 � 0.1* 5.2 � 0.1* 6.0 � 0.1* 4.1 � 0.1 5.9 � 0.1*

SBC (mmol L)1) 25 � 1 25 � 1 19 � 1* 15 � 1* 24 � 1 16 � 0*

pH 7.42 � 0.0 7.40 � 0.0 7.34 � 0.0* 7.23 � 0.0* 7.39 � 0.0 7.24 � 0.0*

SBE (mmol L)1) 0.8 � 0.7 1.0 � 0.5 )7.1 � 1.2* )12.3 � 1.0* )0.1 � 0.0 )10.2 � 0.6*

SaO2 (%) 97.9 � 0.1 97.3 � 0.1 95.1 � 0.5* 92.9 � 0.7* 99.1 � 0.1 98.3 � 0.2* Hgb (mmol L)1) 8.7 � 0.2 9.1 � 0.1* 9.3 � 0.1* 9.6 � 0.2* 8.5 � 0.2 9.4 � 0.1*

CaO2 (mL L)1) 193 � 4 202 � 3* 200 � 3* 202 � 3* 193 � 4 212 � 3* VO2 (L min)1) 0.3 � 0.0 2.2 � 0.3* 4.3 � 0.3* 4.5 � 0.3* 0.5 � 0.1 5.1 � 0.2* HR (beats min)1) 69 � 7 127 � 3* 178 � 4* 180 � 2* 59 � 2 176 � 2*

Values are the average and SEM of variables during exercise and in the last minute of rest. HR, heart rate; FIO2, inspired fraction of O2; K+,

potassium; PaO2 and PaCO2, partial pressure of oxygen and carbon dioxide in arterial blood; SaO2, oxygen saturation of arterial haemoglobin; SBC,

concentration of bicarbonate, SBC, base excess; VE, Pulmonary ventilation; VCO2, expired carbon dioxide; VO2, pulmonary O2 uptake; W, watt. *,

different value compared to rest; P < 0.05.



higher VO2 who did not demonstrate marked desatu-

ration, pH remained above 7.2 and the correlation was

improved when pH was taken into account (r � 0.76,

P < 0.01).

The effect(s) of a small increase in the FIO2 on the

arterial gases and/or SaO2 were shown by Dempsey

et al. (1984) and Powers et al. (1989). Dempsey et al.

investigated the effect of hyperoxia (FIO2, 0.24) only

during a submaximal exercise intensity although the

most marked reduction in PaO2 occurred at the maxi-

mum level of a graded treadmill test. Also, the SaO2

values were not presented during the exercise with

hyperoxia. Powers et al. (1989) used oximetry deter-

mined SaO2 with no evaluation of the role of pH. Only

Figure 2 Pulmonary ventilation (A), respiratory rate (B), end tidal carbon dioxide pressure (C), arterial carbon dioxide pressure (D), expired

carbon dioxide (E), end tidal oxygen pressure (G), PETO2±PaO2 difference (H), arterial bicarbonate (I), pH (J), oxygen saturation of arterial

haemoglobin (K), and oxygen uptake (L) at rest and in response to a 6-min ``all-out'' ergometer row in ambient air (s) and with an inspired

oxygen fraction of 0.30 (d). Values are mean with SEM.



the study by Peltonen et al. (1995) also investigates the

effect of hyperoxia (FIO2, 0.52) during an `all-out' er-

gometer row, but they did not evaluate arterial blood

gas variables.

Dempsey et al. (1984) considered that those subjects

who had a low PaO2 during maximal exercise also

tended to hyperventilate little, expressed as a relative

high PaCO2 and only a small increase in PAO2. Also,

decreased SaO2 during maximal exercise correlated with

PETO2 and the ventilatory equivalent for O2 (Miyachi &

Tabata 1992). In the present study, the subject that

desaturated the most (85%) showed both the lowest pH

(7.06) and PaO2 (67 mmHg) and although his PaCO2

was the highest (39 mmHg), a VE and PETO2 of

183 L min)1 and 123 mmHg, respectively, do not in-

dicate `hypoventilation'. Other subjects reached a

higher VE making PaCO2 lower and all subjects reached

a PETO2 above 120 mmHg. Thus, in contrast to rest

where an elevated PaCO2 increases VE, it appears that

during exercise, the correlation between VCO2 and VE

re¯ects CO2 elimination from bicarbonate. Also, in a

comparison of the different work rates, there was little

indication for PaCO2 control of VE. PETCO2 and to a

lesser extent PaCO2 were elevated during low intensity

exercise, whereas they became reduced during intense

exercise as VE increased implying that VE was more

linked to, e.g. pH than to PaCO2. In support, the ele-

vated FIO2 increased both PETCO2 and PaCO2 associ-

ated with similar deviations of VE and arterial pH.

An illustration of the role for a blood borne factor(s)

in control of breathing is that VE is reduced during

post-exercise muscle ischaemia with an increase fol-

lowing release of the cuff (Innes et al. 1989, Jùrgensen

et al. 1992). It is not established if this response relates

to, e.g. temperature, lactate, potassium, hormones or

even to venous return, and the results of this study

support an important role for pH. During light exercise,

RR and VE reached a steady state with no signi®cant

changes in pH. Conversely, at higher work rates, RR

and VE continued to increase (although PaCO2 re-

mained low) and pH continued to decrease. Also, im-

mediately following light exercise RR and VE

decreased, whereas they remained high for »30 s after

more intense exercise as arterial pH reached an even

lower level than during exercise.

A small central nervous in¯uence on VE is consid-

ered as VE and even more so, the ratio of VE to VO2, is

enhanced when exercise is made dif®cult during partial

neuromuscular blockade (Galbo et al. 1987). In this

study, such an in¯uence on VE may be re¯ected in the

temporary reduction in PETCO2 and increase in PETO2

at the onset of intense exercise. Conversely, at the onset

of low intensity exercise, the subjects tended to `hypo-

ventilate' as there was a temporary increase in PETCO2

and PaCO2 and a decrease in PETO2. CO2 retention

during light exercise is not speci®c to rowing but also

observed in response to light ergometer cycling, e.g. with

an increase in PaCO2 by 4 mmHg (Jùrgensen et al. 1992).

With hyperoxia, a high PaO2 is expected to reduce the

chemoreceptor sensitivity to CO2 (Asmussen & Nielsen

1946). Also, with increased CaO2 it could be that muscle

and splanchnic ischaemia is prevented, whereas prop-

rioceptive impulses remain unaffected by the O2 load.

During submaximal exercise VE is lower with hyperoxia

(Welch 1982) and we found VE to be slightly lower with

hyperoxia indicating only small hypoxic drive. Alterna-

tively, it may be that VE approaches a maximal level

during rowing where the respiratory muscles are used

not only for VE but also for stabilization of the upper

body. Thus, the ratio of VE to VO2 is reported to be

higher during cycling (Cunningham et al. 1975). During

rowing, oarsmen perform either one expiration during

the stroke and inspiration in the recovery or one com-

plete breath during each stroke and one complete breath

going up the slide (Steinacker et al. 1993). Also, stroke

frequency and RR increase in concert. It could be

speculated that ability to entrain breathing is of impor-

tance for suf®cient pulmonary gas exchange.

Of more relevance for the present study are the

deviations in the variables indicative of the role of the

alveolar-capillary membrane for O2 transport. The

PETO2±PaO2 difference increases during exercise

(Hesser & Matell 1965, Dempsey et al. 1984) and this

is taken to re¯ect ventilation±perfusion inequality, a

diffusion limitation and/or a pulmonary shunt (John-

son et al. 1996). During low intensity exercise, the

PETO2±PaO2 difference did not change, but it was

pronounced during intense exercise (Hopkins &

McKenzie 1989). Yet, it was smaller during maximal

exercise than during heavy exercise as PaO2 increased

Figure 3 Mean with SEM for arterial oxygen content (CaO2) at rest

and during a 6-min all-out ergometer row in ambient air (s) and with

an inspired oxygen fraction of 0.30 (d). Of note is the opposite

deviations in CaO2 and SaO2 [Fig. 2(K)] re¯ecting the increase in

haemoglobin during exercise.



at the same PETO2 of 117 mmHg when VE was ele-

vated from 129 to 155 L min)1. One explanation is

that the elevated VE raised PAO2 if the enhanced VE

compensated for the increase in dead space (Asmussen

& Nielsen 1956).

With hyperoxia, the PETO2±PaO2 difference was

lowered to about half indicating that PAO2 was elevated

to an extent where pulmonary O2 diffusion does not

limit O2 transport also indicating that a VA/Q mis-

match is not critical for pulmonary O2 transport during

maximal exercise. The reduction in the PETO2±PaO2

difference during exercise with hyperoxia is in contrast

with the ®ndings by Dempsey et al. (1984) where O2

supplementation was administered during submaximal

running associated with a lower VE than reached during

rowing. This is of importance as the exercise PETO2

with a FIO2 of only 0.24 is similar to that during rowing

in ambient air. Thus, in the study by Dempsey et al.

(1984) a PETO2 of 127 mmHg made PaO2 increase to

94 mmHg and arterial haemoglobin could not have

been fully saturated.

Turcotte et al. (1997) were not able to demonstrate a

relationship between desaturation and pulmonary dif-

fusion capacity during exercise. Yet, the time available

for O2 equilibration in the pulmonary-alveolar capillary

is of importance for O2 transport as evidenced when

FIO2 is elevated. If gas equilibration with haemoglobin

takes the full time for the passage of the erythrocyte

through the capillary, then little O2 will be dissolved in

plasma. Conversely, the high PaO2 (and SaO2) estab-

lished with hyperoxia suggests that haemoglobin was

saturated before the erythrocyte reached the `end' of

the capillary.

On the other hand, O2 breathing reduces VA/Q

inequality (Hammond et al. 1986) and this could relate

to hypoxic vasoconstriction (Kronenberg et al. 1971).

Although this is unlikely during exercise at sea level

(Hammond et al. 1986), an SaO2 of 85% could induce

some vasoconstriction in the pulmonary circulation.

Thus, it is possible that with O2 supplementation such

vasoconstriction is abolished.

Alternatively, although O2 is electrochemically de-

termined, the reduced PETO2±PaO2 difference may

relate to an underestimation of PETO2 in hyperoxic

conditions as with the error in CO2 determination with

an infrared gas analyser (Hornby et al. 1995). Hornby

et al. (1995) showed this with O2 concentrations from

86.2 to 95.9% and with O2 concentrations of 40 and

50%, the percentage error of CO2 analysis would be

expected to be reduced to 1% of the respective readings

and it may be that the error is even lower with a FIO2

of 0.30.

When the alveolar PO2 was calculated using the

ideal alveolar air equation (Wasserman et al. 1987), the

PAO2±PaO2 difference became reduced (34 � 2 vs.

13 � 5 mmHg). However, the PAO2 equation assumes

that there is true equilibrium between ideal mean al-

veolar PCO2 and PaCO2 but this has not been validated

during maximal exercise. Also, we assumed that FIO2

was 0.208 and 0.30 in normoxic and hyperoxic condi-

tions for all experiments, thus, small errors in FIO2

with O2 supplementation may be serious for the cal-

culation of PAO2.

With the unchanged PaO2 and SaO2 during hype-

roxia, CaO2 became elevated and equally so VO2max

indicating that VO2 was not overestimated (Welch &

Pedersen 1981). pH, lactate, BC, BE, and O2debt did not

change suggestive of a similar anaerobic metabolism

and yet, power was the same. Also, randomized O2

supplementation increases VO2max by 11%, whereas

performance is enhanced by only 2% (Peltonen et al.

1995). Both observations support that O2 delivery to

the working muscles is almost unchanged with hype-

roxia as their blood ¯ow decreases (Welch et al., 1977).

Also, hyperoxia reduces blood ¯ow and increases re-

sistance after forearm ischaemia (Crawford et al. 1997).

This is consistent with an increase in mean arterial

pressure during maximal exercise with hyperoxia

(Ekblom et al. 1975). Thus, the elevated VO2 with

hyperoxia may re¯ect enhanced metabolic rate in `non-

exercising' tissue. The splanchnic region is markedly

hypoperfused during intense rowing (Nielsen et al.

1995) and hyperoxia could increase its O2 extraction.

An increase in liver function during exercise with an

FIO2 of 0.30 could account for an elevated PaCO2 and

in turn VCO2.

In summary, exercise-induced hypoxaemia and

desaturation were reversed by an FIO2 of 0.30 and

VO2max increased in proportion to the arterial O2 con-

tent with no effect on work capacity and anaerobic

metabolism suggesting that the increase in VO2 re¯ects

metabolism in non-working tissues. Thus, the alveolar

O2 pressure is critical for O2 transport supporting the

importance of a large ventilation during intense exercise.

We are grateful to Heidi Hansen and Anette Uhlmann for expert

technical assistance. We thank Idrñttens ForskningsraÊd (1995-1-19)

and the `Team Denmark' foundation for economical support. The

study was also supported by the Danish National Research Founda-

tion grant no. 504-4. Per Madsen and Henning Bay Nielsen were

funded by the Danish Medical Research Council (9400846). Lars Bo

Svendsen was employed in the Danish Armed Forces.

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The influence of PaO2, pH and SaO2 on maximal oxygen uptake

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