Physical exercise under hyperbaric oxygen pressure

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 . met by an Increase

The increased oxygen demand during muscle activity is 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-v 02 difference . A substantial

Increase of the arterial oxygen content Is possible by

oxygen breathing In a hyperbaric chamber . the total cardiac output as well

It has been shown that during rest

as, for example, the forearm and brain blood

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 .

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

9a9

930

EXERCIBE UFER PRE99URE

chamber .

vol . 8~, No . 17

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 : phere (ate),

I) during air breathing at 1 atmos-

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 :

~mex 6, for four minutes,

50 per cent of

t00 per cent of

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

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 Severinghaus 2 (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) .

931

EXERCISE UNDER PRESSURE

Vol. 8, No . 17

Results and Discussion The most important findings are summarized

In Table 1-II and Flg. I .

TABLE I Average values for performance time at the highest work Intensity, arterlovenous 02 difference and 02 saturation, C02 tension, pH, lactate and pyruvete concentration in the deep vein of the active forearm during a1r breathing at I ata and oxygen breathing at 3 ata. Blood was saeipled at rest and at the end of each work period (50, 100 and ISO ~ of Wax 6')' air I ata performance time, sec Sv 02

rest

so ~

loo

02 3 ata

x

1so ~

rest

50 ~

100

Z

110

ISO 1i 170

50 .1

34 .5

31 .1

27 .2

85 .9

56 .7

62 .4

59 .7

-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

Ca-v 02

TABLE II Difference between the values registered during oxygen breathing at 3 ate and air breathing at I ata . Mean value " standard error of the mean . x ~ probably significant (p <0 .05), xx ~ significant (p <0 .01), xxx ~ highly significant (p <0 .001) . 02 3 ata - eir I ata performance time, sec Sv ~ Ca-v O

2

Pv ~ 2 Lactatev

50 %

100 ~

ISO 60 " 31

22 .2~°°~ " 1 .7

31 .3~°°~ +1 .9

32 .5~°°~ +3 .3

19 .3~ "3.3

0 "3.7

-S .3 +4 .2

6.7 +3 .9

2.8 +4 .7

12 .7 "7 .6

-0 .78 +0 .33

-1 .47xx +0 .27

-1 .14 "0,68

Pyruvatev

-0 .029 +0 .015

-0 .014 "O.OIS

-0 .021 +0 .015

pHv

-0 .012 "O.ol4

0 .019 "0.013

-0 .003 "0.009

932

EXERCISE UNDER PRESSURE

Vol . 8, No .17

During air breathing no significant changes In P , P , pH or 02 C02 pyruwte concentration in the arterial blood were registered during work, whereas the arterial lactate concentration Increased slightly .

In the deep

ve n S O

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 differente 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 be 2 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 and hence a lower deep vein pH . A 15 per cent 2 difference in flow can nevertheless be calculated . This means that other lead to a higher deep win P~

factors must contribute to the flow regulation .

Of Interest is the lower

deep win pyruwte concentration during oxygen breathing ; shown to be wsodllatlng (10) .

pyruvate has been

The difference In concentration may not be

Vol .

8,

No .'17

EXERCISE UNDER PRESSURE

933

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 unchanged

(n three,

These findings make

and them was no significant difference in the, average time . It probable that the maximal oxygen uptake In the active

muscle Is not increased when the arterial oxygen content Is increased. the maximal oxygen uptake In an active muscle seems not to be

Thus

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 . the other hand It Is well

On

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 . FIG. 1 Dlfferoncs between oxygen breathing et 3 ata and air breathing at I ata In arterlo-wnous 02 difference, lactate concentrati and pH In the deep vein of the active forearm.

O= 7ata - air 1 ata

Vol. 8, No .17

EXERCISE UNDER PRESSURE

9S4

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 . example, brain tissue .

Muscle tissue is much less sensitive than, for

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 . References 1.

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

2.

A.D . BIRD and A .B .M . TELFER,

3.

1 . JACOBSON, A.M . tiARPER and D .G . MCDOYIALL,

4.

H . GROSSE -LOROENANN and E.A . t~fLLER,

S.

G. TÖRNVALL,

6.

H. IDBOFiRN and J . MAHREN,

7.

A. HOL.FGREN and B. PERNOYI,

8.

L. Ll1NDHOLM, E . MOFIhE-LUNDHOLM and N . VAMOS, 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) .

J . thorac .

Lancet I, 355 (1965) . Lancet 2, 549 (1963) .

Arbeitsphysiologie 9, 454 (1937) .

Acta physlol . stand. 58, Suppl . 201 (1963) . Acta physlol . stand . 61, 301 (1964) . Stand . J . clin . Lab. Invest . ll , 143 (1959) . Acta physlol . stand. _58,

10 .

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

II .

D.K . MYERS and E .C . SLATER,

Am . J . Physlol . _203,

Biochem. J. 67, 558 (1957) .