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CARDIOVASCULAR JOURNAL OF AFRICA • Volume 30, No 2, March/April 2019
108
AFRICA
Effects of acute hypoxic provocation on the autonomic
nervous system in ‘healthy’ young smokers, measured
by heart rate variability
Zdravko Z Taralov, Peter K Dimov, Kiril V Terziyski, Blagoi I Marinov, Mariyan K Topolov
,
Stefan S Kostianev
Abstract
Aim:
The aim of this study was to compare the activity of the
autonomic nervous system (ANS) using heart rate variability
(HRV) in ‘healthy’ young smokers and non-smokers before,
during and after exogenous hypoxic provocation.
Methods:
Twenty-one healthy non-smoking males aged 28.0
±
7.4 years (mean
±
SD) and 14 ‘healthy’ smoking males aged
28.1
±
4.3 years with 9.2
±
5.6 pack-years were subjected to
one-hour hypoxic exposure (F
i
O
2
=
12.3
±
1.5%) via a hypoxi-
cator. HRV data was derived via Kubios HRV, Finland soft-
ware by analysing the pre-hypoxic, hypoxic and post-hypoxic
periods.
Results:
Standard deviation of the intervals between normal
beats (SDNN) was higher in the non-smokers in the pre-
hypoxic period (62.0
±
32.1 vs 40.3
±
16.2 ms,
p
=
0.013) but
not in the hypoxic period (75.7
±
34.8 vs 57.9
±
18.3 ms,
p
=
0.167). When comparing intra-group HRV changes, shifting
from hypoxic to normoxic conditions, there was an increase
in the mean square root of successive R-R interval differences
(RMSSD) (65.9
±
40.2 vs 75.1
±
45.9 ms,
p
=
0.011), but these
changes were observed in only the group of non-smokers.
Conclusions:
Smoking probably impairs autonomic regulation
in healthy young males and may lead to decreased HRV, even
before subjective clinical signs and symptoms appear.
Keywords:
heart rate variability, smoking, hypoxia, autonomic
dysfunction
Submitted 6/8/18, accepted 17/1/19
Published online 14/2/19
Cardiovasc J Afr
2019;
30
: 108–112
www.cvja.co.zaDOI: 10.5830/CVJA-2019-007
Tobacco smoking is one of the most widespread bad habits
in the world, especially in eastern European countries. More
than half of the male Bulgarian population aged 20 to 44 are
smokers.
1
It is well known that tobacco smoke impairs the
respiratory and cardiovascular systems and is associated with
high-burden diseases, such as coronary artery disease (CAD),
stroke, sudden cardiac death and chronic obstructive pulmonary
disease (COPD). Some of these pathological conditions are
considered a result of the impaired autonomic regulation caused
by smoking.
2
It has been proven that nicotine increases the
activity of the sympathetic nervous system (SNS) and plasma
catecholamine levels. Therefore it can cause tachycardia and
vasoconstriction, which could contribute to cardiovascular
morbidity.
3
Heart rate variability (HRV) is a commonly used method
for assessment of autonomic dysfunction.
4-6
Manzano
et al
.
established that tobacco smoking leads to acute changes in
autonomic control associated with sympathetic over-activation
and diminished vagal activity. These changes in the autonomic
nervous system (ANS) continue for approximately 30 minutes
after a single cigarette is smoked.
7
Regular smoking also leads to
long-term effects such as permanent sympathetic predominance
[decreased overall variability and increased low-frequency/high-
frequency (LF/HF) index] in subjects without significant health
problems and on average 15 pack-years of smoking.
8,9
Smokers
also have decreased reactivity to vagal stimulation tests such as
the Valsalva manoeuvre. This could be associated with decreased
baroreflex sensitivity, which normally leads to parasympathetic
activation.
10,11
There is frequent speculation in alpine practice that smokers
are more resistant to hypoxia as a result of the daily hypoxic
‘training’ while smoking. This statement is disputable, since
nicotine does not increase the hypoxic ventilatory response
(HVR) and peripheral chemoreceptor sensitivity (PCS).
12
There
is no widely accepted consensus about the effects of smoking on
autonomic control during hypoxic exposure and more research is
needed. Furthermore, there are no data about the activity of the
ANS after removal of the hypoxic factor. The aim of our study
was to compare the activity of the ANS via HRV in ‘healthy’
young smokers and non-smokers before, during and after a
short-term exogenous hypoxic exposure.
Methods
Twenty-one healthy male non-smokers and 16 ‘healthy’ male
smokers with 9.2
±
5.6 (mean
±
SD) pack-years were included
in the study. All the subjects had regular physical activity and no
clinical symptoms or diagnosis. The age of the participants and
other antropometric data are shown in Table 1. Two of the tested
subjects in the smoking group were excluded from the analysis
due to more than 15% premature cardiac contractions. Therefore
14 smokers completed the study protocol.
Department of Pathophysiology, Faculty of Medicine,
Plovdiv Medical University, Plovdiv, Bulgaria
Zdravko Z Taralov, MD, PhD,
ztaralov@pathophysiology.infoPeter K Dimov, PhD
Kiril V Terziyski, MD, PhD
Blagoi I Marinov, MD, PhD
Stefan S Kostianev, MD, PhD
Department of Pharmacology and Drug Toxicology, Faculty
of Pharmacy, Plovdiv Medical University, Plovdiv, Bulgaria
Mariyan K Topolov, MD, PhD