Respiratory Physiology & Neurobiology 186 (2013) 206–213
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Respiratory Physiology & Neurobiology
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Cardiac output, O
2
delivery and
˙
V
O
2
kinetics during step exercise in acute
normobaric hypoxia
Frédéric Lador
a,b
, Enrico Tam
c
, Alessandra Adami
a
, Marcel Azabji Kenfack
a
, Aurélien Bringard
a
,
Michela Cautero
c
, Christian Moia
a
, Denis R. Morel
d
, Carlo Capelli
c,∗
, Guido Ferretti
a,e
a
Département des Neurosciences Fondamentales, Centre Médical Universitaire, Genève, 1 rue Michel Servet, 1211 Geneva 4, Switzerland
b
Service de Pneumologie, Département des Spécialités de Médecine, Hôpital Cantonal Universitaire, Rue Gabrielle-Perret-Gentil 4, 1211 Genéve 14, Switzerland
c
Dipartimento di Scienze Neurologiche, Neuropsicologiche, Morfologiche e Motorie, School of Exercise and Sport Sciences, Università di Verona, Verona, Italy
d
Département d’Anesthésiologie, Pharmacologie et Soins Intensifs, Hôpital Cantonal Universitaire, Rue Gabrielle-Perret-Gentil 4, 1211 Genéve 14, Switzerland
e
Sezione di Fisiologia Umana, Dipartimento di Scienze Biomediche e Biotecnologie, Università di Brescia, Viale Europa 11, 25123 Brescia, Italy
a r t i c l e i n f o
Article history:
Accepted 30 January 2013
Keywords:
Cardiovascular response
Oxygen flow
Oxygen uptake
Oxygen deficit
Blood lactate accumulation
a b s t r a c t
We hypothesised that phase II time constant (
2
) of alveolar O
2
uptake (
˙
V
O
2A
) is longer in hypoxia than
in normoxia as a consequence of a parallel deceleration of the kinetics of O
2
delivery (
˙
Q
aO
2
). To test
this hypothesis, breath-by-breath
˙
V
O
2A
and beat-by-beat
˙
Q
aO
2
were measured in eight male subjects
(25.4 ± 3.4 yy, 1.81 ± 0.05 m, 78.8 ± 5.7 kg) at the onset of cycling exercise (100 W) in normoxia and acute
hypoxia (FI
O
2
= 11%). Blood lactate ([La]
b
) accumulation during the exercise transient was also measured.
The
2
for
˙
Q
aO
2
was shorter than that for
˙
V
O
2A
in normoxia (8.3 ± 6.8 s versus 17.8 ± 3.1 s), but not in
hypoxia (31.5 ± 21.7 s versus 28.4 5.4 ± 5.4 s). [La]
b
was increased in the exercise transient in hypoxia
(3.0 ± 0.5 mM at exercise versus 1.7 ± 0.2 mM at rest), but not in normoxia. We conclude that the slowing
down of the
˙
Q
aO
2
kinetics generated the longer
2
for
˙
V
O
2A
in hypoxia, with consequent contribution of
anaerobic lactic metabolism to the energy balance in exercise transient, witnessed by the increase in
[La]
b
.
© 2013 Elsevier B.V. All rights reserved.
1. Introduction
The kinetics of alveolar O
2
uptake (
˙
V
O
2A
) upon step exercise
onset is usually described by a double exponential model (Barstow
and Molé, 1987; Grassi et al., 1996). The first exponential, with a
time constant of the order of a few seconds, characterises the rapid
phase (phase I) of the
˙
V
O
2A
kinetics (Lador et al., 2006; Whipp and
Ward, 1990) elicited by a rapid increase in cardiac output (
˙
Q ) at
exercise start (Loeppke et al., 1981; Wasserman et al., 1974; Lador
et al., 2006; Yoshida et al., 1993). The second exponential (phase II)
is classically attributed to the kinetics of metabolic adjustment in
contracting skeletal muscles (Barstow and Molé, 1987; Grassi et al.,
1996, 1998; Whipp and Ward, 1990) and it is not dictated by the
dynamic response of systemic O
2
delivery (
˙
Q
aO
2
), at least in adult,
healthy subjects (Poole et al., 2008).
∗
Corresponding author at: Dipartimento di Scienze Neurologiche, Neuropsico-
logiche, Morfologiche e Motorie – Sezione di Scienze Motorie, Via Felice Casorati,
43, I-37131 Verona, Italy. Tel.: +39 045 8425140; fax: +39 045 8425131.
E-mail addresses: frederic.lador@hcuge.ch (F. Lador), enrico.tam@univr.it
(E. Tam), alessandra.adami@unige.ch (A. Adami), azabji@gmail.com
(M.A. Kenfack), aurelien.bringard@unige.ch (A. Bringard), michela.cautero@libero.it
(M. Cautero), christian.moia@unige.ch (C. Moia), denis.morel@unige.ch (D.R. Morel),
carlo.capelli@univr.it, carlo.capelli@mac.com (C. Capelli), guido.ferretti@unige.ch
(G. Ferretti).
In acute normobaric hypoxia, with respect to normoxia, the
phase II time constant (
2
) of the
˙
V
O
2A
kinetics was found either
slower (Engelen et al., 1996; Hughson and Kowalchuk, 1995;
Springer et al., 1991; Xing et al., 1991) or unchanged (MacDonald
et al., 1999), depending on exercise intensity.
In phase II, the
˙
V
O
2A
kinetics would reflect the muscle
˙
V
O
2
adjust-
ments only if it was tightly matched to the kinetics of systemic O
2
delivery (
˙
Q
aO
2
). Thus, it appears logical to hypothesise that a slower
phase II kinetics of
˙
V
O
2A
in hypoxia would be the consequence of
a parallel deceleration of
˙
Q
aO
2
kinetics. Testing of this hypothesis
would require a detailed beat-by-beat description of the
˙
Q
aO
2
kinet-
ics at the onset of exercise in normoxia and hypoxia. To the best
of our knowledge, this was not carried out so far in hypoxia dur-
ing cycling exercise of moderate intensity. Thus, we performed the
present study, in which we determined simultaneously the kinetics
of
˙
V
O
2A
on a breath-by-breath basis, and of
˙
Q and
˙
Q
aO
2
on a beat-by-
beat basis, at the onset of square-wave exercise in both normoxia
and acute normobaric hypoxia.
2. Methods
2.1. Subjects
Eight healthy non-smoking young male subjects took part in
the experiments. They were 25.4 ± 1.8 years old, 1.81 ± 0.05 m tall,
1569-9048/$ – see front matter © 2013 Elsevier B.V. All rights reserved.
http://dx.doi.org/10.1016/j.resp.2013.01.017