From the Laboratory of Zoophysiolog5- (Professor A.

Krogh), the Laboratory

for the Theory of Gymnastics (Professor J . Lindhard), and the Institute for
Medical Physiology (Professor V. Henriqnes), Copenhagen University.

The lactate content of the blood during and after

muscular exercise in man.
By Ole Bang.
The work of E. Lundsgaard showing that muscles poisoned with
iodoacetic acid are able to contract without producing lactic acid is
most responsible for the revolution in muscle physiology which has
taken place in recent years.
We now know that muscular activity can go on experimentally at
the expense of oxidative processes without involving any lactic acid
production.
I am not entering here into a discussion of the chemistry of muscular
contraction; it will suffice to point out that the recovery energy
originates initially from a phosphagen breakdown and perhaps other
“a-lactacid” reactions and that subsequently the phosphagen is resyn-
thesised through energy derived from a) oxidative processes, andlor
from b ) glycogen breakdown into lactic acid (in its turn, the lactic
acid is restored to glycogen by oxidative energy).
In the living organism the muscles may be utilizing the mechanism
a when the oxygen supply is adequate, whereas only at times when
the oxygen supply is deficient, as at the start of exercise and during
very strenuous exertion, mechanism b sets to work.
According to what may be called the classical,view, a production of
lactic acid is constantly going on during exercise, whether aerobic or
anaerobic. It was assumed that an equilibrium must be attained at an
early stage of exercise between the processes of lactic acid production
and removal, and that for a given degree of exertion the lactate in
the blood (and “in all the watery tissues in direct contact with the
blood stream”) increases up to a level which it maintains throughout
the exercise. The lactate level was considered to be the “governor of
oxidation”, and it was assumed that the lactic acid forming in the
active muscles is continuously oxidised and rebuilt into glycogen kt
a rate capable of maintaining a “steady state” in lactate concentra-
tion.
 52
As it was a domiiiatiiig conception that no muscular activity might
occur without lactic acid production, a continuous oxidative resynthesis
had to be imagined, and was the more easily postulated as the existence
of such a mechanism is not readily disproved.
In marked contrast with the abundance of research dealing with the
recovery period is the scantiners of work considering the changes in
blood lactate actually during exercise. In fact the very few determina-
tions carried out (Hill and collaborators; Jervell) cannot give a clear
cut demonstration of the course of blood lactate concentration during
exercise and surely furnish 110 proof that a steady state is attained.
It is not difficult to see that the scantiness of the evidence gathered
must be due to the difficulties in obtaining blood samples under the
conditions in question. The quantity of blood required for lactic acid
determination in the usual way necessitates puncture of an arm vein.
and as stasis must be avoided and precautions taken against glycolysis,
frequent sampling presents great difficulties even in ergometer experi-
ments.
To reach a nearer approximation than that hitherto obtained it is
evidently desirable to investigate this and other related points by a
method capable of giving more detailed information. As pointed out
in a previous paper (1934), great advantage is derived from applying
to this study a method worked out by S. L . Orskou consisting in a
micro-titration of the ether-soluble acids of the blood.
The variations in the amount of ether-soluble acids due to niuscular
exertion account to a considerable extent for the variations in lactic
acid content, as may be seen from fig. 1, representing experiments
given in the paper quoted. This means that with a 10 per cent. limit
of error the rise and subsidence of blood lactate may be determined
through the Orskou micro-titration.
The determination of the ether-soluble acids of the blood according
to Orskou is based upon the rocking extraction principle of Widmark.
The blood is acidified by sulphuric acid and precipitated by a Na,SO,
solution. Ether extraction is carried out in special micro extraction
tubes containing in the receptacle a known amount of sodium hydroxide,
subsequently titrated (after addition of a known surplus of acid and
expulsion of carbon dioxide). The method is well suited for serial
determinations.
The advantages of a micro-method are evident: only 0.1 C.C. of blood
is needed for a single determination so that capillary blood from the
fiiiger tip (or ear lobe) will suffice. The process of sampling, apart
from being far less disagreable to the suhject than repeated punctures
of the veins, may be successfully carried out in ergometer experiments
 53
involving even the severest exercise. Furthermore, the capillary blood
may be regarded as representing the arterial blood (C. Lundsgaard &
E . Msller; Z'oster; Verzdr & collaborators; Goldschmidt & Light.) whereas
the venous blood has lost some lactate in passing through resting
muscles (Bttrr & Himwich).

zr.

.Arb
-$

Fig. 1.
Lactic acid ( 0 ) and total ether-soluble acid ( x ) o/
the blood before and after exercise.

It must be pointed out that an increasing amount of t?-hydroxybutyric

and acetoacetic acids, resulting in an increase in the amount of ether-
soluble acids, might simulate a rise in blood lactic acid as determined
by the Orskou method. According to Gemmill, however, we need not
fear that such an increase should occur in experiments as those
presented below, even if experiments be continued for a considerably
longer period than the experimeflts of fig. 1.
 54

EXPERIMENTAL CONDITIONS.
The experiments were performed on healthy young men aged 25 to
32 and weighing 75 to 80 kg. The subjects were well trained in these
and similar types of exercise, and this condition was maintained
throughout the period of investigation, excepting a few experiments
further elucidated below. The ergometer experiments were carried out
in the morning, the subject having fasted for about 15 hours and being
perfectly at rest for about an hour preceeding the experiment; as in
the recovery periods, he was resting on the ergometer cycle.
A Krogh electric brake cycle ergometer was employed. As a rule,
experiments were carried out at a rate of 60 pedal revoliitions per mi-
nute, a metronome being employed; additional control was provided
by a stop watuh. The subjects performed exercise in a bathing suit
and shoes, and were cooled by the air blast from one or two ventila-
tors; when at rest, they were covered by a bathing-gown.
For kctic acid determination, blood samples from the finger tip
were drawn at short intervals. In mast cases, the results given consti-
tute the mean of 3 determinations carried out on 3 samples drawn
'
within a 2 minute period. In all cases, the bleeding was lively and the
blood ,a bright red.

Hesults.
To facilitate a survey of the experiments a graphic representation
is given. As a rule, the resting value obtained before each experiment
is used for the zero line.
Blood lactate (as represented by the ether-soluble acids) is given
in millinormality.
Zntensity of exercise Is given in meterkilograms per minute.
Time is given in minutes, counted from start of exercise.
--- -period of exercise.
..
.. .. .. = - - recovery.
Start and stop are marked by vertical lines.
A =mean of 3 determinations.
L- - - 2 -
.,x = single determination.

I. BASAL VALUES.
At the conclusion of the resting period blood samples are taken and
the results, defined as the basal values, are given below.
 Table 1.
Subject .. .... . _13g. O.B. O.H. M.N. S.P. All.
Number of ohs. 9 8 8 10 4 39
Maximum , . . . . 2.58 2.69 2.49 1.80 2.48 2.69 miltinormal.
Minimum . . . . . . 1.17 1.61 1.90 1.17 2.02 1.17 -
Average . . . . . . . 1.84 2.19 2.19 1.52 2.25 1.94 --

11. BLOOD LACTATE DURING EXERCISE.

In this section are given the results obtained in exercise employing
moderately severe, conlstant exercise of long duration.

1 . The primary rise in blood lactate.

In fig. 2 is shown the course of blood lactate concentration during
constant, moderately severe exercise, which the subject is capable of
maintaining without fatigue for a considerable time.
It will be seen that shortly after the start of exercise a rather sharp
increase occurs in lactate concentration. This has been called the pri-
mary rise, as distinct from a secondary rise occasionally met with at
a later stage of the exercise.
After about 5 minutes' work the lactate concentration reaches a max-
imum. From this moment, the concentration is con'tinually decreasing
throughout the whole period of exercise, approaching and in sane
of the experiments even ,touching the basal level.
Such a course of the lactate concentration is incontestably at variance
with the classical conception of Hill and others, ac&rding to which
the blood lactate shortly after the beginning of exercise increases up
to a level which it then maintains throughout the exercise.
Not only the experiments collected in fig. 2 show the described type
of blood lactate curve; the same Is met with in a number of the fol-
lowing experiments and, SI) far as moderately severe exercise is con-
cerned, a r k e in lactate concentration during the first minutes of ex-
ercise, followd by a steady fall, undoubtedly must be said to repre-
sent the typical course of blood lactate concentration during constant
exercise.
In fig. 3 are given the results of a series of experiments in which the
same subject has been carrying out exercise (of the same intensity dur-
ing 10, 15, 39 and 65 minutes respectively. In these e x p e r i w t s the
maximum concentration is reached after approximately 5-10 minutes.
The steadily decreasing lactate concentration during the period of ex-
 3(i

ercise i \ encountered again, though in experiment 93 the sloping part

of the curve terminates in a plateau; in this experiment the subject
experienced some fatigue, and we probably find here the cause of
the irregular course, the plateau being the beginning of a “secondary
rise” (see helo\v).

276

277

140

Fig. 2.
Blood lactute during constant exercise.
Exp. 79 (20/10 32) Bg. 720 kgm/min.
- 205 ( 7/12 32) a n n
- 276*)( 7/9 33) M . N . 900 D
- 277 ( 9/9 33) n )) ))

- 140 (13/2 33) S. P . 800 n

An outstanding feature of these curves is the fact that the fall dur-
ing the period of exercise is continued almost uninterruptedly into the
period of recovery. I n fact we get almost the same curve whether ex-
ercise is maintlained o r discontinued. (At least, this can be said of
moderate exercise continued for not lass than 10 minutes). This re-
markable fact seems to be of fundamental significance. From the
*) Inspired air contains 45 ”/o oxygen.
Oxygen intake practically the same as in exp. 277.
 .57

Fig. 3 a .
Oxygen intake in expts. 85
and 89. (0. Hansen).

83

Fig. 3.
Blood lactate during and after exercise of varying duration.
Same subject in all experiments.
Bg. 900 kgm/min.
Exp. 197: 2/6 33
- 89: 1/11 32
- 83: 25/10 32 ,
85: 27/10 32
- 93: 5/11 32
 58
curves i n figs. 2 and I) we learn that the lactate concentration docs
not-as formerly assumed-attain a steady state coiiiparalde to the
steady state in oxygen intake (fig. 3 a ) . We oaiinot calculate, there-
fore, the lactate concentration during exercise from a determination
carried out at the beginning of recovery, and consequently results 01)-
tained through such a procedure have to be revised.
More emphasis, however, must be laid on the explanation of the
described course of blood lactate concentration. If we were to assume
that the blood lactate concentration during muscular exercise is the
result of a n equilibrium of lactate production with lactate disposal in
various tissues, then we must expect an altered course of the lactate
curve after the exercise is stopped. The lactate production is rapidly
decreasing here while on the other hand the disposal of lactate in rest-
ing tissues must be going on at an almost unaltered rate, and so, an ab-
rupt fall in blood lactate cencentration immediately after the exercise
wwuld be the course to expect-essentially similar to the course of the
oxygen intake curve at the commencement of recovery.
As such is not the case, there is evidently no analogy between the
blood lactate concentration and the oxygen intake.
We cannot assume that the lactate disposal in various tissues (rest-
ing muscles, liver, brain, heart, etc.) is diminishing a t the same rate
as the lactate production at the beginning of recovery (though in this
way we were able to explain the curves). Apart from the fact that
such a mechanism would not seem appropriate it is not easy to see
how it might come into action.
As the cessation of exercise does no1 influence the lactate curve,
the only reasonable explanation must be that the processes responsible
for the rise in blood lactate a r e confined to the first (less than ten)
minutes of exercise.*)
As a basis for discussion the following hypothesis is proposed: At
the start 'of and during the first minutes of exercise-and only during
this period-lactic acid production is leading to an accumulation of
lactate in the active muscles. This corresponds with the period of
deficient oxygen rsupply to the muscles. Part of the lactate accumu-

*) v. Noorden & Embden, Janssen & Jost, and other authors assume the
existence of a carbohydrate circuit as follows: The lactate produced in the
active muscles is carried by the blood stream into the liver where it is (to a
considerable extent) rebuilt into glycogen and subsequently, as glucose, re-
turned to the muscles where it was formed.
We have seen, however, that the blood lactate concentration may becomc
very low, even basal, during muscular exercise, and so the amount of lactate
carried by the blood and diffusing into the liver cells must, at this period of
exercise, be quite insignificant.
 59
lated is subsequently oxidised and restored to glycogen as the oxygen
supply becomes adequate. Another part of the lactate accumulated in
the muscles escapes through diffusion into the blood stream, causing
the observed changes in blood lactate concentration. As the blood
lactate is thus dependent on a dep6t of lactate formed in the muscles
during the initial stages of exercise, the blood lactate curve can be
influenced neither by continuation nor by discontinuation of exercise.
According to this hypothesis, no lactate is accumulated after the
first minutes of exercise. This may mean that the lactic acid which
is still*being produced is now immediately oxidised and rebuilt into
glycogen. It is more probable, however, that we reach the correct
explanation by assuming that at this period of exercise no lactic acid
at all is produced, the phosphagen resynthesis now being accomplished
by oxidative processes.

2. Effect of training.
In fig. 4 the effect of training is demonstrated. In the curve of
subject Bg. after two months’ training there is no conspicuous rise
(expt. 118) though a marked rise was seen before training (expt. 75).
The same relations are seen in the curves of subject F. G. C.: After

78

189
v
8 . /& ’ ’ ‘n6mn.

Fig. 4.
Biood lactate curves showing effect of training.
EXQ.75: 15/10 32. Subject Bg., not trained. Fatigued towards end of expt.
- 118: 10/12 32. Subject Bg., trained. No fatigue during expt.
- 78: 19/10 32. Subject F. G. C., not trained. Exhausted .by the expt.
- 189: 2415 33. Subject F. 0. C., trained. No conspicuous fatigue.

training (expt. 189) there occurs a rise far less pronounced than before
training (expt. 78). (The course of these two curves is not quite
typical, owing probably to the fact that the subject had never ridden
a bicycle and that in spite of training he had not grown quite familiar
 GO

with the iliachine and so was apt to change his driving technique
frequently (see section 3)).
It is not difficult to detect the cause of this effect of training. First,
a well-trained individual works economically and does not employ
any unnecessary muscles. Second, oxygen supply to the muscles is
considerably facilitated through training. The oxygen intake rises more
quickly and the steady state is gained sooner in a trained than in an
untrained subject. Furthermore, Vannotti & Magiday have shown in
rabbit experiments that after two months of training the number of
muscle capillaries is considerably augmented as compared to the muscle
capillaries of an untrained extremity.
These findings correspond with the theory of the lactate content
of the blood being dependent on the amount of anaerobic muscular
activity.

3. The secondary rise in blood lactafe.

In the discussion of the typical course of blood lactate curves, it has
been mentioned that in addition to the primary rise with consecutive
steady fall there occurs occasionally a secondary rise during exercise.
The experiments collected in fig. 5 lend themselves to the study of this
phenomenon. The first part of each curve presents the ordinary ascend-
ing and descending course. Then the course is interrupted by a new
rise, appearing after varying intervals of time in different experiments.
In expt. 135 this secondary rise presents itself just before cessation
of exercise, displacing the curve upward. In expt. 39 the secondary
rise appears after 20-25 minutes of exercise and is continued into a
plateau. In expt. 164, employing the same subject as the preceeding
one, the curve presents quite another aspect; the secondary rise begins
after 30-35 min. and reaches a maximum after about 40 min., where-
upon the curve slopes down, and a steady fall is continued almost
uninterrupted into the recovery period.
- Finally, a secondary rise conl-
pletes the curve in expt. 107.
In order to ascertain that the secondary rise is really originated
by a rise in lactic acid and not by other ether-soluble acids (com-
prised in the “x-acids” of Orskov), the last-mentioned experiment was
repeated (expt. 116) and large samples of capillary blood were drawn
for lactic acid determination (using the Orskou modification of
Lehnartz’s method.). From the agreement of experiments 107 and 116
we may conclude that the secondary rise is due to lactic acid and does
not in this respect differ from the primary rise.
Apparently the occurrence of the secondary rise varies capriciously.
It shows no regularity in the experiments of fig. 5 and it may, as we
 61
have seen, be absent altogether from experiiiienls carried out under
identical conditions.
The secondary rise, however, may be interpreted by analogy with the
m,lll"*,md.

Fig. 5 u.
Oxygen intake in exp. 105
(21/11 32) under same con-
ditions as exp. 107
(0.Hansen).

Fig. 5 .
Blood lactate curves presenting a primary and CI secondary rise
during the exercise period.
7

E x p . 135: 912 33 S . P . 890 kgm/min

- 39: 1016 32 M . N . 1080 x
- 164: 2113 33 3
- 107: 26/11 32 Bg. B 2

- 116: 8/12 32 D s 9

explanation of the primary rise. In other words, it can be referred

to a period in which muscles have been contracting without a suf-
ficient oxygen supply. The fact that the secondary rise may be fol-
lowed by a steady fall during the exercise indicates a transitory phe-
 62

nomenon and suggests the possibility that the subject for some reason
or other employs new muscle elements in the exercise. When em-
ployed, such hitherto resting muscle elements must behave exactly like
the muscles responsible for the primary rise, i.e., they must carry
out their work almost anaerobically until the (local) circulation grows
adequate. As a consequence, lactate is accumulating and the result, as
far as the blood is concerned, is a rise in lactate concentration.

* I I

Fig. 6.
Secondary rise in blood lactate produced at will.
Exp. 194: 3015 33. Bg. 720 kgm/min. After 15% min. of exer-
cise the arms are participating in the exercise for 1 min. through
a special transmission.
Expts. 191, 192, and 195: 0.B. 720 kgm/min.
Exp. 191: 26/5 33. Performing exercise with right arm and
left leg. i\fter 24 min. of exercise shift to left arm and right leg.
Exp. 192: 2715 33 and exp. 195: 30/5 33. Performing exercise
with right arm and left leg.

By changing his position and slightly modifying his tread (without

varying the intensity of work) the cyclist is able to utilize the muscles
in a new way and so bring into action fresh elements.
In the following experim'mts a group of resting muscles is purposely
put into action at some point during exercise. As was expected, this
procedure is followed by a "secondary rise" in blood lactate.
We see in expt. 194, fig. 6, the same phenomenon as was described
 0:s
in Part 1, viz., the rise and fall in blood lactate during exercise. At a
point of time when the fall is steadily proceeding the arms are sud-
denly put into action for one minute (a special transmission being
employed) whereupon the exercise is for some time carried on as usual.
A. noticeable rise in blood lactate occurs close upon this radical change
of technique. A maximum is attained after about 5 minutes, where-
upon the curve slopes down steadily.
Another procedure has been followed in experiments 191-192-195. The
subject is driving the cycle by his right arm and left leg (expt. 191).
At a point of time when the blood lactate shows a steady fall-this
has been ascertained in expts. 192 and 195-the active limbs are with-
drawn from exercise and rapidly replaced by the symmetrical groups
of muscles, the left arm and right leg. This change of technique results
i n a marked “secondary rise”.
In this experiment the primary rise attains a relatively higher value
than the secondary rise, though symmetrical muscles of equal size
are employed in the two phases of exercise, This is not surprising: The
muscles responsible for the secondary rise are favoured as regards their
oxygen supply; the oxygen intake and the general circulation have
attained the steady state a long time before these muscles are put into
action and so the local circulation only requires adjustment.
We may conclude from these results that a secondary rise in blood
lactate can be produced by fresh muscles entering into the exercise,
hut of course we are not able to tell whether such a mechanisni is
dominant in every “secondary rise” of any experiment.
In addition to the muscles actually employed in driving the ergo-
meter a number of muscles are active in preserving the body posture.
These muscles are partly contracting statically. During static con-
traction the blood supply to muscles is considerably hampered (Lind-
hard; Rein), and so lactate accumulates and escapes into the blood
stream as the muscles relax (Marschak; Jervell). Possibly this me-
chanism also leads to occasional rises in blood lactate during exercise.
It must be pointed out that the above discussed causes of the
secondary rise of course need not be confined to producing one single
rise. Probably a solitary secondary rise is a phenomenon rather seldom
met with, surely several rises mure frequently occur, eventually uniting,
forming a plateau, or completing the primary rise.

4. Blood lactate at varying intensities of exercise.

In the following, a comparison is given between the effect of moderate
exercise such as that discussed above and the effect of severe exercise.
 G4

The experiments in fig. 7 are carried out on the same subject, O.B.,
the intensities of work varying from 1080 to 1620 kgm./min.
In the curves we recognize the elements described above, which
may be submitted to a more detailed study.
The primary rise begins close upon the start of exercise. During
the first minute, however, no increase in blood lactate has ever appeared;
naturally the lactate needs time for traveling from the muscles where
it was produced to the finger capillaries where samples are drawn.

\ , ,
o *a ' zi &I io ' Z;, ' sb ' ?i ' i' ' 9o-A

Fig. 7.
Blood lactate at different infensifies of exercise. Same subject
i n all experiments.
Exp. 161 (15/3 39) O.B. 1620 kgm/min.
- 156 ( 8/3 33) m 1440 >
- 149 (2412 33) > 1260 >
- 20 (10/5 32) D 1080 B

At the intensities 1080 and 1260 kgm/min a maximum value is

attained after 5-10 minutes of exercise. At 1440 kgm/min the maximum
occurs between the 15th and 20th minute, and at 1620 kgm/min the
rise is continued throughout exercise. At the end of the last-mentioned
experiment the subject was absolutely exhausted.
The secondary rise does not appear during exercise at 1080 kgmlmin.
At 1260 kgm/min a slight rise i s encountered just as the exercise period
expires. At 1440 kgm/min the descending part of the curve runs into
a plateau: at the end of exercise a sharp rise is indicated by a single
determination.
Thus the secondary rise is seen more often in experiments involving
severe exercise.
The fall during the recovery period represents, i n expt. !20, a con-
tinuation of the fall during exercise and the same relations are seen
 63

i n expt. 149 though the secondary rise has displaced the curve a little
In the other experiinenls no fall in lactate concentration occurs during
exercise, on the contrary, the curve is continually rising and at the
end of exercise it breaks at :in angle into the descending curve typical
of the recovery period.
An account of a similar series of experiments carried out on subject
O.€I. is given i n fig. 8. The findings most closely correspond with
Iliose presented in the preceeding figure. (The extraordinary fact that

Fig. 8.
Blood luctate cit different intensities of exercise.
Same subject in all experiments.
Erp. 125 (19/12 32) 0.H . 1800 kgmjinin.
- 115 ( 7/12 32) )) 1620 2

- 109 (30jll 32) )) 1440 ))

- 70 (20,9 32) )) 1080 B

a secondary rise appears during exercise at 1620 kgm/min (expt. 115,

7/12 32) while at the same point of time the concentration is decreas-
ing during exercise at 1800 kgm/min (expt. 125, 19/12 32), may be due
to training during the interval). Such experiments may be carried
through only by a muscular and well-trained subject; indeed, 54,000
kgm in half an hour and 86,400 kgm in one hour must be said to be
an admirable performance.
Supplementing the preceding figures, the curves presented in fig. 9
show the results of experiments made upon various subjects at the
same intensity of exercise.
Noticeable in these experiments is the great difference between the
curves of subjects O.H. and Bg. While the curves of subjects O.B. and
M.N. are very much alike, they markedly differ from the two other
curves. These relations distinctly have a bearing upon the ability of
 66

the various subjects. The exercise is carried out easily by subject

O.H., whereas for subject Bg., who is not so well trained, the exercise
is rather straining. Arranging the subjects according to their strength,
i.e., their maximum performance, we get the same sequence as met
with in the figure, viz;, O.H. decidedly the best, then follows O.B. and
M.N. (of approximately equal ability), and Bg. lags far behind the
others.
It will be noticed thalt the blood lactate curves obtained in severe
exercilse do not always correspond to the account given of the typical
course during moderate exercise. Nor was this to be expected. The

Fig. 9.
Blood lactate curves of uarious subjects during exercise at the
same intensity, 1080 kgni fmin.
Exp. 107 (fig. 5 ) Bg.
-
- 164 ( 5) M . N .
-
- 20 ( 7 ) O . B .
- 70 ( -
8) O.H.

anaerobic muscular activity initiating any exercise is only incompletely

replaced by aerobic conditions during severe exercise, whereas in
moderate exercise m adequate oxygen supply to the muscles is already
effected a few minutes after the start. During most severe muscular
effort the oxygen intake does noit attain a steady state, i.e., it does
not meet the requirement, and so the muscles must to some extent con-
tract anaErobically, more land more as we approach the limit of the
subject'a powers. As a consequence, lactic acid production goes on
during the whole period of exercise, and in fact we have observed
the blood ladate curve breaking at an angle at the conclusion of exer-
cise, the production now decrealsing almost instantaneously.

5. Non-typical curves.
Sometimes the curves obtained are not quite easily recognized as
corresponding with the description given in the. preceding discussion.
 6'7
Such examples arc collected in fig. 10. These curves show a course
apparently in keeping with the view held by most authors, according
to which the blood lactate attains a constant level during exercise. In
~ i i yopinion, however. these, results merely empha'size the fact that :i
clear notion of the course cannot be acquired from few determina-

L!.
A d
A
I
-
A'
-.-
--A

dI I

Fig. 10.
Non-typical blood lactate curves.
Exp. 121 (14/12 32) 0. H. 1620 kgmlmin.
- 142 (151'2 33) O.B. 1080 P
- 182 (21/4 33) F . G . C . 1080

tions. Probably determinations carried out more frequently would

have exhibited, as in the foregoing experiments, a more complicated
course.
I am not prepared to deny the possibility of occasionally meeting with
a constant level of lactate concentration during exercise; referring, how-
ever, to the foregoing experiments, I feel justified in saying that such
a course is not the rule and that it can be interprded as a chance
combination of the elements pointed out and discussed above.
 111. BLOOD LiCTATE DURING RECOVERY.

PreI ious knowledge regarding the changes in lactate concentratiori

due to exercise is based mainly upon evidence gathered from deter-
minations carried out during recovery. I need not, therefore, go into
details describing the results obtained in the present investigation in
so far as they correspond with well established facts. In some points,
however, the results are somewhat at variance with the com~iionly
accepted view and so need further discussion.

1. Blood lactate after exercise o f long duration.

Provided the exercise had been extended for at least 10 minutes
(allowing the “equilibrium” to get established), it was formerly gen-
erally accepted that the intensity of exercise was the only factor gov-
erning blood lactate concentration.
We now see that the lactate concentration at the conclusion of ex-
ercise is dependent on three factors, viz., 1) the intensity of exercise,
2) the duration of exercise, and 3) the eventual occurrence of factors
leading to ‘a .secondary rise.
Emphasis must be laid on the occurrence of very low or even basal
values a,t the end of exercise of long duration. Such low concentra-
tions have been reported previously (Bock and collaborators (1928) ;
Hustings; Carlstriim; Vladimirov, Dmitriev & Urinson), and they are
conspicuous in several of my experiments. It is particularly interesting
that we are not dealing here with mild exercise, on the contrary, in
most cases the exercise must he characterized as moderately severe.
In Rock and collaborators’ experiment the exercise was even very
strenuous: The well-trained subject was exhausted by a 15 mile run.
In experiments where the blood lactate level is not basal at the end
of exercise the curve shows the well-known steady fall during re-
covery; this fall may constitute either the sequence to a fall already
begun during exercise, or the breaking off of a rise occurring during
the last part of exercise.

2 . Blood lactate after exercise of short durntion.

The laotate curve of the recovery period ordinarily presents a fall
corresponding, according to Margaria, Dill & Edwards, to a logarith-
mic equation.
I n some cases, however, the lactate concentraion rises during the
first 5 minutes or so of recovery; though this phenomenon is reported
several times (Hill &? collaborators; Egglefon & Evans; Schenk; Mar-
 199

mo

t-1--.

II..

Fig. 11.
Recovery f r o m exercise of short duration.
Subject M. N. at 1260 kgmlmin.
Exp. 199 (20,9 33). Exercise period 2 min.
- 200 (2219 33). n 1 n
- 201 (24,9 33). 9 n 3 n
- 202 (27,9 33). 9 2 P
- 203 (29,9 33). n 10 s
 50

guriu & colluborators) it is still unexplained in its irregular occurrence.

When appearing, the initial rising phase has been interpreted as signi-
fying that the “equilibrium” state has not been attained during exer-
cise. Margaria thus explains this lag in lactate concentration as caused
by delayed lactic acid production and the slowness of diffusion. The
explanation, however, does not cover the irregular occurrence of the
phenomenon, to which I shall return presently.
The effect of exercise of short duration is seen in fig. 11. The sanie

188
“1

Fig. 12.
Recovery froin short-time violent exertion.
Exp. 188 (18,’5 33) E . H . C . Standing running for 1 Inin.
- 113 ( 5112 33). S. P . 2495 kgml’min. for 1 % min.

subject, M.N., who has been practising exercise at 1260 kgm/min for
a week, carries out this exercise during 2, 1, 3, 2, and 10 minutes
on different days. The experiments are given in chronological order.
The likeness of the curves is noticeable. Though different maximum
values are attained, the differences are tsmdl and quite out of propor-
tion to the differences in duration of exercise. (Perhaps an effect of
increasing training is traceable through this series of experiments).
A comparison of experiments 199-202 with experiment 203 reveals
the fact that we get the same type of lactate curve whether the exer-
cise is of short or long duration, and these curves compared to those
given in fig. 2 p. 6 serve to emphasize the likeness further.
 71
Evidently all the curvcs mentioned (ire produced by the same me-
chanism, viz., initial, transitory, unaerobic muscular activity.
In fig. 12 are shown 2 experiments employing the subjects for 1
:tiid 11/2 minutes in violent exercise. Both curves show a marked
initial rise of 7-8 minutes’ duration, then follows the well-known
“~ogarithmic”fall.
In fig. 13 are shown 2 experiments, 225 and 245, where the exercise
period expires (accidentally) just as the rise is finished-no rise occurs
diiring recovery.

Fig. 13. ,
Recovery from severe exercise of short durafiori. Elrect of spurt.
Exp. 225 ( 9,’5 33) O.H. 1785 kgm,’min.
- 245 (22,6 33) B 1905
- 289 (19,’lO33) P 1700 Y for 5 min. and
2000 - 2.7 -

Evidently all lactate curves, whether obtained in exercise of long

of of short duration, present uniform pictures in that there is a rather
constant interval (averaging 7 minutes) between the start of exercise
and the attainment of maximum concentration. It is clear now that
an initial rising phase in the recovery lactate curve must aiways appear
when recovery begins during this interval, in other words, after exercise
lasting less than (about) 5 minutes. On the other hand, the initial
rising phase will not appear in recovery after an exercise outlasting
the “primary rise”, excepting cases where a “secondary rise” occurs
towards the end of exercise.
 Experiineut 289, fig. 13, s h o w an interesting curve. Instead of
constant exercise we have had the subject spurt driring the last few
minutes of exercise. Though the exercise period is longer than in
the preceding experiments (225 and 245), we find the curve rising
during the first part of recovery. The maximum value is not attained
until about 12 minutes from start of exercise. However, if we count
the spurt only, the maxiiiiuni is attained in about 7 minutes just as
in the other experiments, The spurt, of course, is a change of technique
bringing into action fresh muscle elements, and what we see is a
“secondary rise” continuing the “primary rise”.
No other function takes a parallel course. The oxygen intake, for
instance, is always rapidly decreasing during the first part of recovery.
and so we may conclude that the recovery processes are going on from
the very beginning of the recovery period. Why, then, can the blood
lactate lag so far behind, why is the maximum concentration delayed?-
I have touched upon the explanation before. The simplest way is to
assume that lactate is accumulating during the first minutes of exer-
cise, forniing a dep6t in the active muscles. This dep8t must be removed
1) by oxidative resynthesis as oxygen supply grows adequate and 2)
by diffusion into the blood and further afield. The last-mentioned
process, then, must be comparatively slow. (In fact, Eggleton, Eggleton
(e Hill have shown thaE lactate diffusion through live muscle is a rather
slow process). Further evidence is needed in support of this view
and I shall return to the discussion of this point presently.

1%’. RELATION BETWEEN INTENSITY OF EXERCISE AND

MAXIMUM CONCENTRATION OF BLOOD LACTATE.
The intensity of exercise, not the amount of work carried out, governs
the rise in blood lactate.
According to several authors (e.g., Owles; Margaria h collaborators)
the exercise must exceed a certain minimum limit before an increase
in lactate concentration is demonstrable; the minimum limit is variously
stated and is supposed to depend on the type of exercise as well as
on the subject’s ability.
The experiments which are the basis of these statements show a
shortcoming, however, in that the lactate concentration has been
determined at the conclusion of exercise, not during exercise. The
maximum value obtained in this way does not always represent the
real maximum, viz., the top of the primary rise, though this particular
 '73
quantity must be coilsidered to have by far the most important
dependence upon the intensity of exercise.
My experiments encompass various intensities of exercise as well
as various subjects, and as the course of blood lactate has been traced
in a manner allowing a fairly accurate estimate of the maximum
values attained, a study of the relation between the intensity of exercise
and the blood lactate rise might very well be based upon these results.
As, on the other hand, the lactate is determined by an indirect method,
and as the efrect of training must vary somewhat during the months
of experimenting (this can particularly be said of experiments employ-

u : . . . . .uu. . . .
I&. ' .-A&. . ' 'Ik *J-/w
Intensity of exercise ikgm/min.)
Fig..14.
The relation between maximum conrentration of
blood Iactafe and severity of exercise.

ing subject Bg.), the results obtained must be evaluated with a little
reservation.
In fig. 14 the highest values recorded in experiments employing the
four main subjects have been plotted against the intensity of exercise.
The curves represent lactate determinations carried out during
recovery as well as during exercise. The same mechanism is at work
producing the rise in either case; nevertheless an error possibly arises
from the fact that we do not know what length of time is occupied
by anaeobic conditions and so we cannot, in the experiments on exercise
of short duration, be sure that the rise would not have attained a
higher value had the exercise been continued (this probably influences
the results obtained in subject M.N.).
In spite of these objections we get valuable information from fig. 14.
We recognize the difference previously discussed between the subjects,
 74
an exercise at a given intensity resulting in different lactate concentra-
tions, and conversly we see that a rise of, say, 5 millinormal (45 mg%)
occurs in subject Bg. as a result of exercise at 900 kgm/min, in O.B.
(and h1.N.) at 1300 kgmlmin, and in O.H. not until exercise at 1600
kgm/min is undertaken. This very sequence was met with placing the
subjects according to their maximum performance.
Dealisnng with the curve of one subject at a time we find it in keep-
ing with the fact emphasized by Margariu that above a certain intensity
the llaotate increase accelerates rapidly.
Though the lower intensities of exercise are lacking in my material
I may draw attention to the fact that a basal level found at the con-
clusion of exercise does not exclude the possibility of a rise during
exeroise, and so the postulate of Margariu, viz., that slight exercise
does not involve many lactic acid production, cannot be accepted off-
hand (see expts. 205, 276, 277, fig. 2, and 70, fig. 8).

Discussion.
Before discussing the interpretation of the bood lactate *curves ob-
tained I wish to take up a point usually not given cadequate considera-
tion; viz., how far is it possible to reconstruct from the blood lactate
concentration the lactate concentrations of the active muscles and the
resting tissues?
In dealing with the blood lactate and the oxygen intake of recovery,
Hill, and several others, made the assumption that the lactate concen-
trations in blmood and muscle are equal on those occasions when they
are stationary or changing only slowly, or at a maximum value.
Admittedly it would facilitate the interpretation of the blood lactate
curves obbained if the relatims were that simple. In my opinion, how-
ever, it must be emphatically asserted that the existence of such an
equilibrium state ha6 never been demonstrated. On the contrary, evi-
dence has accumulated in favour of a different view. Thus Eggletoil
& Evans have carried out experiments on dogs showing that for a con-
siderable time after exercise there is a marked, though steadily di-
minishing difference in lactate concentmtions between the aotive
muscles and the blood, and also between the lactate concentrations of
the blood returning from an active extremilty and the arterial blood
(fig. 15). In a previous paper (1935) I have reported rabbit experi-
ments supporting the statements of Egglefon & Evans; even a.t a point
af time when blood lactate is decreasing there is a higher lactate con-
centration in the muscles. Though almost equal concentrations may
be reached towards end of recovery {when the values are nearly basal)
such a state is certainly not reached in 10 minutes.
 55
I have proposed the hypothesis that there is also between the arterial
blood and the tissues responsible for lactate disposal (resting muscles,
liver, etc.) a marked difference in 1,actate concentrations during a large
part of recovery. -4 priori, the speed of the chemical processes disposing
of the lactate may be thought to exceed the speed of lactate diffusion

c4
\
\
\
I
1
1
I
\

' a a +a 60

Fig. 15.
Diagram of recouery representing typical findings
of Eggleton & Evans.
The lactate concentrations of blood plasma from
0 vein of active muscle,
artery,
A vein of resting muscle.

into the cells, where a lactate concentration lower than that of the
blood may therefore be maintained. Indeed, recently Bott & Wilson
have shown that such is the case so far as the liver is concerned. These
authors find that the liver lactate concentration is lower than the
blood lactate concentration, particularly when blood lactate concen-
tration is high; in one case they found the blood lactate level decreas-
ing and at the same time a decreasing liver lactate level, the blood
lactate concentrafion constan4y exceeding the liver lactate concen-
 76
tration. The difference is so large that it cannot correspond to the
difference between *the watery phases (such an interpretation was
proposed by Eggleton & Evans).
Without any doubt we meet during a large part of recovery-and
during part of the exercise period as well-falling lactate concentra-
tions when passing from the active muscles via the blood to the liver
and the resting muscles, etc. (see fig. 16).

Lactate
concentrations

Blood

Resting muscle:
liver etc.

Oxygen I I:

-
intake I !..

Steady state
Fig. 16.
Diagram outlining probable course of lactate
concentrations.

A comparative slowness of lactate diffusion must be the came of

such relations. Results obtained by Orskov and Nielsen in perfusion
experiments carried out on hind limb preparations also seem to indi-
cate that slowness of lactate diffusion delays markedly the attainment
of an equilibrium.
We are now able to explain why the blood lactate shows a lag as
compared to the oxygen intake. The slowness of diffusion must lead
to. such a course, and a delayed lactic acid production need not be con-
sidered. .
The good agreement found bx Hill, and the relatively good agree-
nient found by Murgnriu, between the oxygen debt and the total anioiint
of lactate present in the organism at the conclusion of exercise, must
not be accepted as a proof that the lactate is evenly distributed in the
watery phalse of the organism.
In discussing in a previous paper (1934) the relations between blood
lactate and oxygen debt I have stated that an oxygen debt quite out
of proportion to the amount of lactate circulating may occur at con-
clusion of exercise of long duration (see point y, fig: 16). Evidently
other processes than lactate resynthesis are responsible for the excess
oxygen intake in such cases. On the other hand we may find-after
exercise of short duration-that blood lactate is still being removed
from the blood at a time when no measurable oxygen debt is being
repaid (see point x in fig. 16).
We nced not doubt that oxygen is required in lactate resynthesis.
Calculating, however, according to Hill and Margaria from the blood
lactate curve the oxygen required per minute-basing, as do these
ail thors, the calculations upon the assumption of an even distribution
of lactate through a large part of the body-we arrive at man amount
of excess oxygen intake of such magnitude as cannot possibly escapc
detection. (Possibly part of the material ordinarily oxidked in resting
metabolism is replaced by lactate so that an excess oxygen intake is
not necessary for the oxidative removal of the lactate).
3*
Consequently a parallelism between oxygen debt and lactate con-
centration at conclusion of exercise is no regular fi)nding. Neither the
studies of the relation between oxygen debt and Itactate concentra t’1011
nor the animal experiments mentioned, support the view that the lac-
tate is evenly distributed in the organism. We are justified in asserting
that we are un,able to estimlate at any moment the total amount of
lactate present in the body.
We cannot, therefore, accept the calculations of Margaria, Edwards
h Dill, dividing the oxygen debt into a “lactacid” and an “a-lactacid”
part-though in its principle the division is incontestable. (The authors
pertinently call the “lactacid” muscular activity a “mechanism of
emergency”).
If, however, an attempt be made at a rough estimate of the varia-
tions in lactate concentrations of the active muscles, blood, and resting
tissues, the diagram presented p. 26 must be looked upon as repre-
senting the most probable connection. (As in the following I am deal-
ing here by preference with the course of blood lactate concentration
during moderate exercise where the lactate curve shows a fall during
exercise).
Beyond any doubt the lactate concentration of the’ active miiscles
 78

exceeds by far the blood lactate concentration during the first minutes
of exercise where the blood lactate is rising rapidly.
Certainly we are right, too, in assuming that the lactate concen-
trations of muscles and blood are almost equal (or, rather. in equili-
brium) when they are approaching the bassal values.
It is very unlikely that a high lactate concentration is maintained
in the active muscles in spite of a low blood lactate level. Hill points
out the possibility of areas between the capillaries maintaining a high
lactate concentration. Experimental results, however, do not support
such a view. I may draw the attention to experiments on perfused
muscles reported by Embdeii & Jost and Okagawa showing that at
the end of exercise of long duration the perfusion fluid and the muscles
are very poor in lactate. The results obtained by Jokl, forcing rats
to run till exhaustion, show clearly that at the end of this exercise
of long duration the active muscles are practically free from lactate*).
As suggested in Part 1 the correct explanation of the blood lactate
curves may be reached best through abandoning the classical view
according to which there occurs a constant lactic acid production from
start to finish of the exercise.
This constant lactic acid production was supposed to .lead, in rela-
tively few minutes, to the attainment of a constant, increased lactate
level in the active muscles, subsequently maintained throughout the
“steady state”. The constant level was thought to be attained as the
rise in lactate concentration would induce a rise in the intensity of
oxidation, this again involving a rise in lactate resynthesis (Pasteur-
Meyerhof reaction) until an equilibrium was established between the
production and resynthesis at a level depending on the intensity of
lactic acid production, i.e., the intensity of exercise.
In this way only could an equilibrium between the processes of
lactic acid production and removal necessary for the attainment of a
constant level, be explained.

*) It must have escaped the author’s attention that the values obtained in
the control animals are far from basal (lactate averaging in muscle 145 mg%,
in blood 32 ma;”/.);the process of sampling has lead to a considerable gly-
colgsis.
This cause of error, on the other hand, i s considerably reduced where
muscles are sampled at conclusion of the exhausting exercise, as the amount
of glycogen liable to glycolysis is now (according to the determinations of
gIycogen reported) reduced to a minimum.
So the conclusion that muscular exercise leads to a fall in lacthe concen-
tration and recovery to a rise, i s quite erroneous.
The same author states that phosphagen cannot be the source of energy
since in the exhausted animals the muscles were rich in this substance. It
has not been ascertained (by direct stimulation) that the cause of exhaustion
is the muscles’ wearing out and does not lie elsewhere (Hypoglycemia?).
 59

The foundation stone of this view is the conception that Pastcur’%

reaction consists in a continuous resynthesis of anaerobic deconiposi-
tion products, a conception introduced by Meyerhof at a time when
lactic acid production was regarded as essential to the mechanism of
muscular contraction. The theory of Meyerhof could not then be dis-
missed, though, as a matter of course, it could not be based upon
experimental evidence.
As we can now regard the lactic acid production in active muscles
:IS an accessory process and not fundamental, the explanation of the
Pasfeur reaction is open to question.
It is very probal~lethat we are right i n intcrpreling the work of
Lipinuiiii in a way fatal to the Pasfeur-Meyerliof reaction in the clas-
sical sense. Though not finally proved, it appears that the enzymatic
syste’m necessary for glycolysis is inactive under aerobic conditions,
and so the disappearance of glycolysi5 under’ aerobic conditions is
not due to a resynthesis of the decomposition products, but is caused
by a real inhibition of the glycolytic process.
So far as I can see my experiments show that a dep6t of lactate
is formed in the active muscles during the first minutes of exercise.
This subsequently is removed, presumably, partly by resynthesis
into glycogen in the muscles where it was produced, and partly by
escape into the blood and further afield. This dep6t and the removal
thereof is independent of the continuation of exercise, granted the
, exercise has outlasted the time required in forming the dep6t.
If the classical view be maintained, we must assume that throughout
the “steady state” the lactic acid production is met, in the active muscles.
by a resynthesis to match. This resynthesis does not influence the
dep6t formed during the first minutes of exercise, and, furthermore
this very intense resynthesis ceases instantaneously the moment the
exercise is over.
What must seem particularly improbable and inconsistent with the
classical view is the fact that a consbant lactate removal of the magni-
tude in question should be accomplished at steadily decreasing and
even basal lactate concentrations.
Also, the uninterrupted course of the blood lactate curve after con-
clusion of exercise is incompatible with the classical view according
to which there occurs at this point of time a sudden change of the
intensity of lactic acid production.
The experimental results can be explained far more consisfently by
assuming that lactic acid is produced only (during the first minutes of
exercise, until oxygen intake becomes adequate, whereas no lactic acid
production, nor any lactic acid resynthesis in the cIassical sense,
occur during exercise under asrobic conditions.
 so
So to obtain an unbiased view we must discard the Pasteur-Meyer-
hof reaction as playing any part in aerobic muscular activity.
The muscles actually possess a mechanism suitable for cccrobic con-
ditions (Lundsgaard), and in all probability this mechrtnism is utilized
whenever possible, the organism as u whole striving t o furnish the
azrobic conditions required in lhis normal functioning.
The removal of the lactate produced during the initial anaerobic
muscular activity is going on during the steady state as an accessory
process (possibly some of the lactate is burned up in the oxidative
processes in the active muscles) until there is no more excess lactate
left. This accessory process runs the same course whether exercise is
or is not carried on, whether metabolism is increased or standard, pro-
bably dominated by the rate of diffusion of the lactate.

SUMMARY.
1. The changes in blood lactate concentration during and after exer-
cise have been studied in healthy young men, using the Krogh ergo-
meter.-A new method (Orskov) has been employed for lactate deter-
mination, and has proved to be well suited to this type of experiment.
2. Contrary to the d e w accepted by most authors, viz., that blood
lactate attains a constant level during moderate exercise, it is found
that an initial rise, followed by a steady fall-the lactate concentra-
tion approaching and somelimes even reaching the basal level-con-
stituZes the typical course of blood lactate concentration during con-
stant exercise of long duration.
3. As the same type of lactate curve is$obtained after exercise of
short duration it is concluded that the blood lactate rise is brought
about solely by the anaerobic muscular activity which obtains during
the initial staige of exercise.
The hypothesis is proposed that no latic acid production occurs in
the “steady state”, the phosphagen resynthesis being now accomplished
by oxidative processes.
4. Lactate curves showing disagreement with the “typical course”
may be explained without altering the hypothesis. A “secondary rise”
occasionally occurring at a later stage of exercise may thus be explained
as the result of fresh groups of muscles coming into use.
5. The lag found in blood lactate curves (as compared to the
oxygen intake) is explained as due to the comparative slowness of
lactate diffusion.
6. In discussing the results obtained, the theory is advanced that the
prodiiction of lactic acid in the muscles is confined to those occasions
 81

when muscles are contractiiig anaGrobically ; i.e., a t the start of excercise

and in the course of very strenuous exertion.
During a&rohic muscular activity the mechanism pointed out by
Lundsgctard, viz., the phosphagen breakdown and subsequent oxidative
resynthesis, is utilized solely.
The classical theory, assuming a continuous lactic acid production
and resynthesis during exercise, according to the Pasteur-Megerhof
reaction, must be rejected as being based on untenable assumptions.

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