Clinical Science and Molecular Medicine (1975) 48, 235-238.
SHORT COMMUNICATION
Maximal oxygen uptake, lung volume and ventilatory response
to carbon dioxide and hypoxia in a pair of identical twin athletes
A. G. LEITCH, L. CLANCY
AND
D. C. FLENLEY
Department of Medicine Royal Infirmary, and University of Edinburgh
(Received 16 December 1974)
Summary
1. Maximal oxygen uptake (Y0 2 max.), lung
volumes, and ventilatory responses to carbon dioxide and hypoxia have been measured in identical
twin athletes, who were trained to a similar high
degree.
.
2. The results confirm previous findings for V0 2
max. and lung volumes in identical twins, and are in
keeping with the suggestion that genetic factors play
a major part in determining the ventilatory response
to carbon dioxide and hypoxia.
Key words: athletes, hypoxia, identical twins,
ventilation.
Introduction
Studies of identical twins have shown a close correlation between twins in vital capacity (Arkinstall,
Nirmel Klissouras & Milic-Emili, 1974) and maximal o~ygen uptake (Klissouras, Pirnay & Petit,
1973). No such correlation was found for measurements of the ventilatory response to carbon dioxide
(Arkinstall et al., 1974) and the ventilatory response
to hypoxia has never been reported in identical twin
subjects.
The degree of physical activity is one environmental factor which is difficult to quantify in any
identical twin study. It is known that decreased
(Saltin, Blomquist, Mitchell, Johnson, Widdenthal
& Chapman, 1968) and increased (Astrand &
Rodahl, 1970) physical activity can produce marked
Correspondence: Dr A. G. Leitch, Department of
Medicine, Royal Infirmary, Edinburgh, U.K.
changes in maximal oxygen uptake. It has also
been shown that there may be a relation between the
ventilatory response to carbon dioxide and different
types of athletic activity (Rebuck & Read, 1970).
We have been able to eliminate variations in physical
activity from the environmental factors affecting
maximal oxygen uptake and chemical control of
breathing, by studying identical twin athletes who
were in training for the same athletic events.
Subjects and methods
The subjects, A and B, were two 16-year-old
Scottish female twins who were identical in physical
features and therefore almost certainly monozygotic
(Nichols, 1965). In addition, the HL-A phenotype
and all erythrocyte antigens tested (ABO, MNS., P,
Kk, Lea, Fya, Kpb, WI", CW and Rh) were identical.
Each was in training for the Scottish National Team
and each had represented their country at junior
level. Both participated in the 400 and 800 m track
events, but subject A was better at the 400 m distan~e
and subject B performed better over 800 m. Each IS
currently ranked in the top five for these events in
Scotland. Height and weight of the subjects are
shown in Table 1 with their best times for their
chosen events (1974).
Lung volumes were measured by helium dilution
and maximal oxygen uptake (Y0 2 max.) by a modification of the method ofTaylor, Buskirk & Henschel
(1955). After a 'warming-up' run at 11'25 km h- 1
(7 m.p.h.) on the level treadmill for 8 min, breathing
through an Otis-McKerrow valve, the subjects
ran at the same speed up a 5° gradient for 5 min,
expired air being collected for measurements of O 2
235
236
A. G. Leitch, L. Clancy and D. C. Flenley
TABLE
V0 2 max.
1. Height, weight and results obtained for identical twins A and B
= maximal oxygen
uptake; Se02 = slope of the line relating ventilation (I/min
BTPS) to end-tidal Pe02'
Height (ern)
Weight (kg)
Twin A
TwinB
161
51'0
161
49'5
13·1
Haemoglobin (g/IOO ml)
13'7
Time for 400 m (s)
Time for 800 m (s)
55'0
V0 2 max. (ml min " ! kg- 1 )
Ventilatory response to CO 2
(a) Se02 (I min " ! kPa- 1 )
(b) frequency (breaths/min)
at Pe02 8 kPa
Pe02 8'67 kPa
59
Normal range
12'0-16'0
129·3
60
8'4
5'0
16·6
18·8
18·3
18'7
Hypoxic index (%)
19
22
Lung volumes (litres)
Functional residual capacity
Vital capacity
Expiratory reserve volume
Residual volume (RV)
Total lung capacity (TLC)
RV/TLC(%)
Forced expiratory volume I s (FEV)
Forced vital capacity (FVC)
FEV/FVC(%)
2-91
3-65
1'55
1'36
5'09
28
3-45
3-80
91
2'91
3'50
1'55
1'36
5'16
26
3'70
3·90
95
and CO 2 concentration and minute ventilation
being measured during the last minute. After a
10 min rest the subjects then ran for 3 min up a 7
slope, measurements again being made in the last
minute of exercise. Neither subject could sustain this
exercise for 6 min, thus indicating that V0 2 max.
had been attained (Mitchell & Blomquist, 1971).
This was confirmed by measurements during the
last minute of a run for 2t min up an 8 slope.
Values for V0 2 obtained in this final run did not
differ by more than 30 ml/min from the preceding
ones, thereby confirming that V0 2 max. had been
attained. Inspiratory and expiratory resistance was
0'098 k Pa (1 em H 20) at 1·5 l/s.
The ventilatory response to CO 2 was measured
with a modification of Read's (1967) rebreathing
technique. The subject rebreathed from a 6 I bag
containing O 2 +C0 2 (93:7) via a valve and pneumotachograph (Fleisch no. 3). A Varian M3 mass
spectrometer probe monitored P0 2 and Pe02 in
the rebreathing system. Volume was calibrated
before and after each study, the gas mixture remaining in the bag at the end of rebreathing being used,
0
0
53-58
4,3-61,3
13-112
and the mass spectrometer was calibrated at this
time with gas mixtures analysed by the LloydHaldane apparatus. Off-line computer analysis from
magnetic tape recordings yielded values of frequency,
tidal volume, instantaneous minute ventilation,
P0 2 and Pe02 for each breath. The slope of the CO 2 response curve was calculated from the linear
regression of expired minute ventilation on Pe02,
after omitting the first 30 s of the record. Duplicate
measurements were performed in each subject, the
mean value being taken for each. P0 2 always
remained above 26·7 kPa (200 mmHg) in the rebreathing study.
The hypoxic drive to breathing was assessed by
the method of Flenley, Cooke, King, Leitch &
Brash (1973), which utilizes the known potentiation
of this drive by exercise (Asmussen & Neilsen,
1947). The subjects exercised on a level treadmill,
attaining a steady-state V0 2 of 950 ml/min when
breathing air, and were exposed at approximately
5 min intervals to a hypoxic stimulus in the form of
three breaths of 100% nitrogen. The method of
expressing the ventilatory response to this hypoxic
Ventilatory responses in twin athletes
stimulus as a hypoxic index, the apparatus used
and the normal range of response in healthy men
have been previously described (Flenley et al., 1973).
Venous blood was withdrawn from an antecubital
vein for estimation of haemoglobin before the study
began.
Results
The results are tabulated in Table 1. V0 2 max., lung
volumes and ventilatory responses to CO2 and
hypoxia are identical for each twin within the limitations of the methods employed. The normal range
for ventilatory response to CO 2 is taken from the
work of Rebuck & Read (1971) and our own studies
on athletes, for V0 2 max. from SaItin & Astrand's
(1967) studies on Swedish national athletes (400-800
m events for women), and for hypoxic index from
the studies of Flenley et al. (1973) on healthy males
and from studies on male and female Scottish
athletes (A. G. Leitch & L. Clancy, unpublished
work).
237
lished work) in both twins. There are reports of
depressed hypoxic drive in athletes (Byrne-Quinn,
Weil, Sodal, Filley & Grover, 1971) at rest, but this
depression did not persist when the subjects of the
studies exercised. We did not study the hypoxic
drive at rest in our subjects. The association of a low
ventilatory response to hypoxia with a low response
to inhaled CO 2 in our subjects accords with recent
suggestions that there is a correlation between
ventilatory responses to these two stimuli (Rebuck,
Kangalee, Pengelly & Campbell, 1973).
Although it is obviously impossible to draw firm
conclusions from a study of one identical twin pair,
we feel that our studies on these unique, highly
trained, identical twin athletes have shown that,
when the effect of a major environmental factor,
physical activity, is removed, genetic factors predominate in determining the maximal oxygen uptake
(Klissouras et al., 1973), the ventilatory response to
CO 2 (Beral & Read, 1971) and the ventilatory
response to hypoxia.
Acknowledgments
Discussion
The V0 2 max. results compared favourably with
values reported for Swedish national athletes (Saltin
& Astrand, 1967) and are consistent with the finding
by Klissouras et al. (1973) in twenty-three monozygotic twins of an insignificant mean intrapair
difference for V0 2 max. The full lung volumes
recorded in the subjects of this study are identical
within the limitations of the method and expand
the finding by Arkinstall et al. (1974) of identical
vital capacities in seventeen monozygotic twins.
Arkinstall et al, (1974) were unable to demonstrate
identity of ventilatory response to CO 2 in their
monozygotic twins, there being no difference in the
intrapair variance between their monozygous and
dizygous twins. They attribute this to difference
between twins in their frequency and tidal volume
response to inhaled C02, the frequency response
being determined by personality factors whereas
there is a strong genetic component to the tidal
volume response. The frequency responses in the
present study were similar for both twins (Table 1)
and this would explain the similarity of the ventilatory responses.
The hypoxic index was at the lower end of the
normal range for non-athletes and athletes (Flenley
et al., 1973; A. G. Leitch & L. Clancy, unpub-
We thank Professor K. W. Donald for laboratory
facilities, Dr Clarke of Glasgow for assistance,
Miss E. Paxton for technical help and Miss L.
Graham for typing the manuscript. We are
grateful to Mr C. Darg of the South Eastern
Regional Blood Transfusion Service for the bloodgrouping studies. A.G.L. received an Institute of
Sports Medicine Grant for equipment for these
experiments and L.C. held an S.H.H.D; Research
Fellowship.
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