rintédiâ~reat Britaiâl~8, Part I, pp . 929-934, 1989.

Pergamon Press

PFIYSICAL EXERCISE LIDER HYPERBARK OXYGEN PRESSlA2E

Lennart KaiJser

Department of Clinical Physiology

Karollnska sJukhuset, Stockholm, Sweden

(Received 27 May 1989; in final form 12 June 1989)Uhiscle activity for longer periods than about 2 minutes is dependent

on the availability in the muscle tissue of awlscular oxygen as the final

electrons acceptor . The increased oxygen demand during muscle activity is

met by an Increase In the blood flow and in the degree of oxygen extraction .

It is generally believed that the oxygen transport capacity of the circulatory

system limits the maximal oxygen uptake In an active muscle .

If this is true,

it should be possible to Increase the oxygen uptalfe by Increasing the oxygen

content in the arterial blood . The increase In oxygen uptake should then

mainly be caused by an increased

A substantial Increase of

oxygen breathing In a hyperbaric

the total cardiac output as well

flow are decreased during hyperbaric oxygen breathing (1,2,5) . No account has

been gl wn, however, of the extent to which the possibility of extrectirg

more oxygen per volume blood is utilized when the oxygen demand is increased

by heavy muscle activity . Nor is It known whether the situation a~skes possible

a larger maximal oxygen uptake in the active muscle, and hence a higher working

capacity .

a-v 02 difference .

the arterial oxygen content Is possible by

chamber .

It has been shown that during rest

as, for example, the forearm and brain blood

Material and Nsthods

Six healthy wale volunteers, aged 21-27. years, were studied during

rhythwic dynawlc forearw work on a spring-losded hand erpoweter In a A~erbrrte

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930

EXERCIBE UFER PRE99URE

vol. 8~, No . 17

chamber . Prior to the experiments their forearm working capacity was

msasuned by a procedure corresponding to the Tornvall test (4,5) . Thus,

the maximal work intensity they could perforn for 6 minutes was determined

two 6,) . The average value for the subjects studied was 14 kpm/min (range

10-18 kpm/min) .

Each volunteer was then studied :

I) during air breathing at 1 atmos-

phere (ate), 2) during aucygen breathing at 3 ate . Each experiment Included

measureawnts during rest and exercise, the intensity of which was the same

during air and oxygen breathing . The subjects exercised at three successive

work Intensities : 50 per cent of ~mex 6, for four minutes, t00 per cent of

>rmex 6, for four minutes, and 150 per cent of Amax 6, until exhaustion. The

first work intensity was presumed to be somewhat lower, the second somewhat

higher than the maximal aerobic capacity (own observation) . Arterial and

deep venous blood (almost exclusively draining the musculature)t6) from the

active for~ean~n was sampled through percutaneous catheters . Sampling was made

at rest and at the end of each period of exercise for assay of PO , P~ , pH,2 2

lactate and pyruvate concentrotlons .

P0 was measured with a polarographtc electrode (Instrumentation lab.,2

mod. 113~placed Inside the chamber .

The oxvaen saturation was considered 100 per cent when the oxygen

tension was more than 350 mm Hg . At lower blood PO^ the saturation was

measured spectrophotometrically (7) .

The oxygen content was calculated from the hemoglobin oxygen saturation,

hemoglobin conoentratton, and the P0 .2

P~ was measured with a glass electrode according to Severinghaus2

(lnstrumentatlon Lab., mod. 113) inside the chamber .

~ti wes measured with a mtcro-Astrup equipment .

Lactate and pyruvate concentrations were analyzed by an enzymatic

method (8,9) .

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EXERCISE UNDER PRESSURE

931

The most important findings are summarized In Table 1-II and Flg. I .

Results and Discussion

TABLE I

Average values for performance time at the highest work Intensity, arterlo-venous 02 difference and 02 saturation, C02 tension, pH, lactate and pyruveteconcentration in the deep vein of the active forearm during a1r breathing atI ata and oxygen breathing at 3 ata. Blood was saeipled at rest and at theend of each work period (50, 100 and ISO ~ of Wax 6')'

Difference between the values registered during oxygen breathing at 3 ate andair breathing at I ata . Mean value " standard error of the mean .x ~ probably significant (p <0.05), xx ~ significant (p <0 .01), xxx ~ highlysignificant (p <0.001) .

02 3 ata - eir I ata

rest

air I

so ~

ata

loo x 1so ~ rest

02 3

50 ~

ata

100 Z ISO 1iperformancetime, sec 110 170

Sv 02 50.1 34.5 31 .1 27.2 85.9 56 .7 62 .4 59 .7

Ca-v 02 -87.7 120 .9 129.1 140.4 82.9 140.2 129.1 133 .1

Pv C02 43.2 54,8 66 .0 63.5 45.5 61 .5 68.8 76 .2

Lactatev 0.85 1 .99 3 .92 4.76 0 .77 1 .22 2 .46 3.62

Pyruvatev 0.072 0.114 0.119 0.181 0.094 0.085 0.105 0.160

pHv 7.342 7 .258 7 .184 7.185 7.313 7.246 7.203 7,182

TABLE II

50 %performancetime, sec

Sv ~ 22.2~°°~" 1 .7

100 ~

31 .3~°°~+1 .9

ISO60

"31

32 .5~°°~+3 .3

Ca-v 19.3~O0 -S .3

2 "3.3 "3.7 +4.2

Pv ~ 6.7 2.8 12.72 +3.9 +4 .7 "7 .6

Lactatev -0 .78 -1 .47xx -1 .14+0 .33 +0.27 "0,68

Pyruvatev -0.029 -0.014 -0.021+0.015 "O.OIS +0 .015

pHv -0.012 0 .019 -0.003"O.ol4 "0.013 "0.009

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EXERCISE UNDER PRESSURE

Vol. 8, No.17

During air breathing no significant changes In P , P

, pH or02 C02pyruwte concentration in the arterial blood were registered during work,

whereas the arterial lactate concentration Increased slightly . In the deep

ve n SO was decreased at the first work Intensity compared to rest (p < 0.01),2

and It vas stil! loner at the highest work Intensity . Thus the a-v 02 differ-

ente vas higher at the lowest work Lntensity than during rest (p < 0.01> and

vas somewhat further increased at the time of exhaustion (p < 0.05) .

After four minutes" aocygsn breathing at 3 ata resting blood samples

wen drawn and immediately thereafter the exercise was started . The average

Pa~ at the first work intensity was 1877 mm Hg and it remained at the same

law 1 throughout the cork period .

In the arterial blood no other dhfferences

between oxygen and air breathing were noted, either at rest or during work .

From the Pa0 during oxygen breathing about 58 ml oxygen rnuld be2

calculated to .be physleally dissolved per Ilter blood .

At the lowest work

Intensity 19.3 ml per Ilter, that Is about 1/3 of the increase In arterial

oxygen content, was utilized In the forearm muscles . The lowest work intensity

was presumed to be less than the maximal aerobic capacity . Thus there ought

to De no difference In oxygen uptake between oxygen and air breathing at this

work intensity. Consequently the blood flow through the active muscle can be

calculated to be about 15 per cent lower during aotygen than air breathing .

TM deep vein pH at the lowest work Intensity was the same during

oxygen as air breathing . This seems to support the hypothesis that the local

H+ conantrotton is of Importance for the regulation of the local blood flow .

rihy the a-v OZ difference is Increased by only I/3 of the increase in arterial

ootygen content is then explained by the fact that a larger increase should

lead to a higher deep win P~ and hence a lower deep vein pH . A 15 per cent2

difference in flow can nevertheless be calculated . This means that other

factors must contribute to the flow regulation . Of Interest is the lower

deep win pyruwte concentration during oxygen breathing ; pyruvate has been

shown to be wsodllatlng (10) . The difference In concentration may not be

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EXERCISE UNDER PRESSURE

large enough, though, to explain the differonce In blood flow between air and

oxygen breathing.

Ylhen the work Intensity was Increased, no further Increase In the

a-v 02 difference was registered during oxygen broething. At exhaustion the

average a-v 02 difference was the same during oxygen as air breathing (Fig.l) .

The performance time to exhaustion was Increased in three subJects but un-

changed

(n three, and them was no significant difference in the, average time .

These findings make It probable that the maximal oxygen uptake In the active

muscle Is not increased when the arterial oxygen content Is increased. Thus

the maximal oxygen uptake In an active muscle seems not to be limited by the

blood flow to the muscle or the oxygen diffusion fran the blood to the Interior

of the muscle cell, but by the oxygen utilization system Inside the cell . On

the other hand It Is well known that a substantial decrease In arterial oxygen

content decreases the maximal oxygen uptake . Consequently in the nonmel

subJect the circulatory capacity seems to be adapted to the maximal metabolic

rots under the actual environmental conditions .

O= 7ata - air 1 ataFIG. 1

Dlfferoncs between oxygen breathinget 3 ata and air breathing at I ataIn arterlo-wnous 02 difference,lactate concentrati

and pH In thedeep vein of the active forearm.

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EXERCISE UNDER PRESSURE

The deep vein pH when the exercise was terminated by exhaustion was

the same during oxygen as air breathing. The Increasing local H` concentraFlon

may then be one of the factors limiting muscle performance of this kind . That

some of the processes necessary for muscle activity, for example for the

oxidative phosphorylatlon and the Interaction between ATP and the contractile

system are pH-dependent is shown in vitro (11) .

Prolonged tissue exposure at a high oxygen tension is known to decrease

the tissue respiration . Quite long exposure times are needed, though, before

sTgnlficant effects are seen. Muscle tissue is much less sensitive than, for

example, brain tissue. Furthermore, during work the oxygen consumption keeps

the tissue oxygen tension fairly low in the muscle . Consequently a toxic

effect of oxygen is not likely to be responsible for the tack of Increase in

muscle performance during hyperbaric oxygen breathing .

1 . P.B . FIAHNLOSER, E . DOMANIG, E. LIIMPHIER and W. SCHENK Jr, J . thorac .cardlovasc . Surg. ß2, 223 (1966) .

References

2 . A.D . BIRD and A .B.M . TELFER, Lancet I, 355 (1965) .

3 . 1 . JACOBSON, A.M . tiARPER and D .G . MCDOYIALL, Lancet 2, 549 (1963) .

4. H . GROSSE-LOROENANN and E.A . t~fLLER, Arbeitsphysiologie 9, 454 (1937) .

S. G. TÖRNVALL, Acta physlol . stand. 58, Suppl . 201 (1963) .

6. H. IDBOFiRN and J . MAHREN, Acta physlol . stand . 61, 301 (1964) .

7. A. HOL.FGREN and B. PERNOYI, Stand . J . clin . Lab. Invest. ll , 143 (1959) .

8.

L. Ll1NDHOLM, E . MOFIhE-LUNDHOLM and N . VAMOS, Acta physlol . stand. _58,243 (1963) .

9.

T. BUCHER, R. CZOK, W. LAFPRECHT and E . LATZKO,

Pyruvat. In H.V.Bergmeyer,Maioden der enzymatischen Analyse. Verlag Chemie, Neinheim (1962) .

10 . J .1 . MOLNAR, J . SCOTT, E .D . FRÖHLICH and F.J . HADDY, Am. J . Physlol . _203,125 (1963) .

II . D.K . MYERS and E .C . SLATER, Biochem. J. 67, 558 (1957) .

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