not permitted.

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© 2016 EDIZIONI MINERVA MEDICA The Journal of Sports Medicine and Physical Fitness 2017 May;57(5):643-51
Online version at http://www.minervamedica.it DOI: 10.23736/S0022-4707.16.06159-4

ORIGINAL ARTICLE
EPIDEMIOLOGY AND CLINICAL MEDICINE

One night of partial sleep deprivation increased biomarkers of

muscle and cardiac injuries during acute intermittent exercise
Mohamed A. MEJRI 1, 2, Narimen YOUSFI 1, Omar HAMMOUDA 3 *, Amel TAYECH 4,
Mohamed C. BEN RAYANA 5, Tarak DRISS 3, Anis CHAOUACHI 1, Nizar SOUISSI 1, 6

1Research Laboratory “Sport Performance Optimization”, National Center of Medicine and Sciences in Sport (CNMSS), Tunis,
Tunisia; 2Faculty of Science, Carthage University, Bizerte, Tunisia; 3Research Laboratory CeRSM (EA 2931), Department of Physiology,
Biomechanic and Movement Imaging Group, UFR STAPS, Université Paris Nanterre, Nanterre, France; 4High Institute of Sport and
Physical Education, Ksar-Saïd, Manouba University, Manouba, Tunisia; 5Department of Clinical Biology, Research Laboratory SURVEN
(Nutritional Surveillance and Epidemiology in Tunisia), National Institute of Nutrition and Food Technology of Tunisia (INNTA), Tunis,
Tunisia; 6National Observatory of Sports, Tunis, Tunisia
*Corresponding author: Omar Hammouda, Laboratoire CeRSM (EA 2931), Equipe de Physiologie, Biomécanique et Imagerie du Mouvement, UFR STAPS,
Université Paris Nanterre, 200 avenue de la République, 92000 Nanterre, France. E-mail: hammouda.o@u-paris10.fr

A B S T RAC T
BACKGROUND: The aim of this study was to evaluate the effect of two types of partial sleep deprivation (PSD) on biomarkers of muscle and
cardiac injuries in response to acute intermittent exercise in professional athletes.
METHODS: In a counterbalanced order, ten healthy male Taekwondo athletes were asked to perform the Yo-Yo Intermittent Recovery Test
(YYIRT) in three conditions, allowing a 36 h recovery period in between: 1) following a full night of habitual sleep known as a reference sleep
night (RN); 2) following PSD in the beginning of the night (PSDBN); and 3) following PSD in the end of the night (PSDEN). Heart rate (HR)
and arterial oxygen saturation (SaO2) were measured during exercise. Blood samples were taken just before and 3 min after the YYIRT to meas-
ure biomarkers related to muscle and cardiac injuries (BRMCI).
RESULTS: No significant effect of PSD was observed for physiological parameters (i.e., HR and SaO2). However, a significant alteration of
resting ultra-sensitive C-reactive protein (us-CRP) (P<0.05) and myoglobin (MYO) (P<0.01) levels was detected after PSDEN. Furthermore,
all BRMCI were altered by exercise. Likewise, compared to RN, PSD affected creatine phosphokinase (CPK) and MYO levels in response to
exercise (P<0.05).
CONCLUSIONS: The present study indicates that PSDEN increase the resting us-CRP and MYO levels, and that the two types of PSD increase
the CPK and MYO levels in response to acute intermittent exercise, among Taekwondo athletes, in the evening of the following day. However,
no rise of the physiological responses has been observed after the two types of PSD, at rest and in response to the exercise.
(Cite this article as: Mejri MA, Yousfi N, Hammouda O, Tayech A, Ben Rayana MC, Driss T, et al. One night of partial sleep deprivation increased
biomarkers of muscle and cardiac injuries during acute intermittent exercise. J Sports Med Phys Fitness 2017;57:643-51. DOI: 10.23736/S0022-
4707.16.06159-4)
Key words: Sleep deprivation - Cardiovascular system - Risk - Myoglobin - Martial arts.

T here is ample scientific evidence to support the con-

clusion that adequate sleep is essential for general
healthy functioning, ameliorating recovery of body sys-
covery from competitions.2 The sleep-wake cycle, may
be disturbed by various factors and its disruption could
have adverse consequences on physical performances,2, 3
or other proprietary information of the Publisher.

tems, energy conservation, memory consolidation, brain and many physiological measures in athletes.4 Other-
development, and discharge of emotions.1 In athletes, it wise, previous epidemiological studies have shown that
has been evidenced that good sleep is generally associ- reduced sleep duration has been identified as a risk fac-
ated with better physical performances and adequate re- tor for cardiovascular morbidity and mortality.4, 5 The

Vol. 57 - No. 5 The Journal of Sports Medicine and Physical Fitness 643
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means which may allow access to the Article. The use of all or any part of the Article for any Commercial Use is not permitted. The creation of derivative works from the Article is not permitted. The production of reprints for personal or commercial use i
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MEJRI SLEEP DEPRIVATION INCREASED BIOMARKERS OF MUSCLE AND CARDIAC INJURIES
fundamental mechanisms linking between sleep restric-
tion and increased cardiovascular risks are unknown.4
Nevertheless, one potential pathway may be the activa-
tion of inflammatory processes 4, 5 and/or the disturbance
of endocrine and metabolic function during sleep loss.6
In this context, it has been shown that sleep restriction
results in a number of abnormal physiological changes
(i.e., heart rate [HR], arterial oxygen saturation [SaO2])
at rest 5, 7-9 and in response to physical exercise.7, 10, 11
However, scientific literatures have shown contrasting
results. Indeed, it has been evidenced that sleep depriva-
tion (SD) decreases,7 increases 5, 8, 9 or did not alter 9, 12, 13
resting HR and SaO2.13 To the best of the authors’ knowl-
edge, very few studies have examined the physiological
responses (HR, SaO2) to exercise after SD. It has been
reported that one night of total sleep deprivation (TSD)
did not affect heart rate peack (HRpeak) and SaO2 during
exhaustive aerobic exercise.13 However, Omiya et al.7
have shown that one night of partial sleep deprivation
(PSD) decreased HR at anaerobic threshold, but did not
affect the HRpeak following maximal exercise. However,
Mougin et al.10 noted that PSD in the middle of the night
significantly increased submaximal HR during a pro-
gressive incremental aerobic exercise.
Alternatively, several studies supported the associa-
tion between sleep, immune function and inflammation.
It has been shown that SD is associated with increased
inflammatory responses.5 In this light, several studies
have shown that aspartate aminotransferase (ASAT),
ultra-sensitive C-reactive protein (us-CRP), creatine
phosphokinase (CPK), lactate dehydrogenase (LDH)
and myoglobin (MYO), considered as biomarkers relat-
ed to cardiovascular risk and muscle damage,14-16 were
not previously analyzed for athletes who are most of-
ten faced to the sleep disorders. Analysis of the resting
measures of muscle and cardiac injuries changes after
SD has shown contrasting results. Indeed, in rats, ASAT
level was reported to increase after prolonged rapid
eye movement SD.17 Likewise, in human, it has been
documented that SD increases,5, 8, 18 decreases,19 or did
not affect 9, 18, 20, 21 resting measures of these biomark-
ers related to muscle and cardiac injuries (BRMCI) (i.e.,
ASAT, us-CRP, CPK, and LDH). Recently, in athletes, it
or other proprietary information of the Publisher.
has been found that one night PSD increases the morn-
ing levels of CPK and MYO.22 However, to the best of
the authors’ knowledge, no study has explored the effect
of SD on the BRMCI among athletes.
644 The Journal of Sports Medicine and Physical Fitness May 2017
Furthermore, muscle and cardiac biomarkers altera-
tion does not depend only on sleep. Indeed, it has been
well documented that both short-term maximal and
long-duration exercises induce systemic and tissue in-
flammations, and have adverse effects on immunologi-
cal function.3, 16, 23-25
To date, it seems that the effect of SD on BRMCI re-
sponses during exercise has not been investigated. Nev-
ertheless, few studies have examined the concomitant
effects of SD and exercise on inflammatory and immune
responses.3, 24, 25 It has recently been reported a distur-
bance in the immune function (i.e., white blood cells,
lymphocytes, monocytes, neutrophils) during maximal
exercise performed following one night PSD.25 More-
over, a significant alteration of IL-6 and TNF-α re-
sponses to high-intensity exercises, was reported after
one night PSD at the end of the night.3, 24
Recently, it has been documented that Yo-Yo Intermit-
tent Recovery Test (YYIRT), as a field acute intermittent
exercise, affect hematological responses in Taekwondo
athletes.25 Indeed, the YYIRT seems to be a suitable test
for Taekwondo athletes to evaluate their ability to per-
form high-intensity intermittent exercise.25 Furthermore,
the physiological responses during this test could inquire
us about the cardiac hemodynamic to different stressors
(i.e., sleep loss, strenuous exercise).22 In light of these
findings, the aim of the present study was to assess the
effects of PSD scheduled at the beginning and at the end
of the night on BRMCI, and physiological responses
during the YYIRT in Taekwondo athletes. In the current
study, we hypothesized that physiological and BRM-
CI measures at rest and in responses to acute exercise
would be affected after PSD, and that PSD at the end of
the night is more disturbing for athletes’ health than PSD
on the beginning of the night.
Materials and methods
Participants
Ten healthy male professional Taekwondo athletes
(age, 17.6±0.52 y; height, 175.8±6.21 cm; weight,
61.17±5.80 kg; % Body Fat, 9.88±1.77 %; mean±STD)
volunteered to participate in this study. They were
competitors at national standard with Black Belt and
6.60±1.26 (mean±STD) years of experience in Tae-
kwondo practices. They usually trained at least 3 d/week
for an average of 2 h daily evening training. They were
not permitted. It is not permitted to remove, cover, overlay, obscure, block, or change any copyright notices or terms of use which the Publisher may post on the Article. It is not permitted to frame or use framing techniques to enclose any trademark, log
means which may allow access to the Article. The use of all or any part of the Article for any Commercial Use is not permitted. The creation of derivative works from the Article is not permitted. The production of reprints for personal or commercial use i
This document is protected by international copyright laws. No additional reproduction is authorized. It is permitted for personal use to download and save only one file and print only one copy of this Article. It is not permitted to make additional copies
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©
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SLEEP DEPRIVATION INCREASED BIOMARKERS OF MUSCLE AND CARDIAC INJURIES MEJRI
given a through explanation of the protocol before sign-
ing an informed consent form. Participants were selected
based on their chronotype by means of a sleep question-
naire.26 Only those of intermediate (N.=7) or moderate
morning (N.=3) chronotypes participated to this study.
Participants reported no sleep disorder and they had
also regular sleeping schedules based on the Bastuji and
Jouvet calendar,27, 28 completed over one-month period
prior to the investigation; estimated sleep duration was
8.2±0.9 h (h±fraction). They were non-smokers, did not
consume alcoholic beverages, and none of them was
taking antioxidant compounds, including vitamins and
medications (e.g., anti-inflammatory agents). The study
protocol complied with the Helsinki declaration for hu-
man experimentation and was approved by the Clinical
Research committee of the National Centre of Medicine
and Sport Sciences of Tunis.
Experimental design
Before beginning the study, participants were fa-
miliarized with the experimental procedure. During
the first experimental adaptation day, they slept in the
laboratory between 10.30 pm and 6 am, in an individual
bedroom at controlled temperature (22-24 °C). Then,
they participated in three experimental sleep conditions,
in a counterbalanced order, allowing a recovery period
≥36 hours in-between them. The first condition was a
reference night (RN) during which the participants were
synchronized with a nocturnal sleep from 10.30 pm to 6
am. The second night is a condition of PSD in the begin-
ning of the night (PSDBN) during which they went to
bed at 3 am and were woken up at 6 am. They were not
allowed to sleep before 3 am; they were then allowed
to sleep until 6 am. The third night is a condition of
PSD in the end of the night (PSDEN) during which the
participants went to bed at 10.30 pm and were woken
up at 3 am. They were not allowed to sleep thereafter.
Participants were kept awake in the same constant envi-
ronment light (150-200 lux) by passive means such as
watching TV, playing computer and reading books. Fur-
thermore, they were not allowed to ingest food, caffeine
or other stimulant and they were observed continuously
or other proprietary information of the Publisher.
by a technician.
Upon arrival for their first test session, participants’
body mass (Tanita, Tokyo, Japan), height and percent-
age of body fat (skinfolds) were recorded. Throughout
Vol. 57 - No. 5 The Journal of Sports Medicine and Physical Fitness 645
the experimental period, the subjects were not allowed
to eat or drink any caffeinated substances and were re-
quested to maintain their habitual physical activity and
avoid strenuous activity during the 24 hours before the
test sessions. During each test session, subjects were
asked to perform the YYIRT in an indoor sports hall, in
the evening at 5 pm. Before each test session, partici-
pants took a standard isocaloric meal at 12 am, which
finished at least 4 h before the tests. After the meal, only
water ad libitum was allowed.
HR was measured continuously during the YYIRT
using a heart rate monitor (Polar Electro Oy, T61-coded,
Hungary). In addition, SaO2 was measured using a por-
table multiparameter monitor (Philips M4 M3046A) 5
min before and immediately after exercise. Blood sam-
ples were taken just before and 3 min after the YYIRT.
The level 1 YYIRT
As previously described,28 the test consisted of 20-m
shuttle runs performed at increasing speeds with 10 s of
active recovery in a distance of 5-m between runs until
exhaustion. Audio cues of the YYIRT were recorded on
a CD (www.teknosport.com, Ancona, Italy) and broad-
casted using a portable CD player (Philips, Az1030 CD
player, Eindhoven, Holland). The end of the test was
considered when the participant twice failed to reach
the front line in time (objective evaluation) or felt un-
able to complete another shuttle at the dictated speed
(subjective evaluation). The total distance covered dur-
ing the YYIRT was considered as the test score. Before
the test, all participants carried out a warm up period
consisting of the first four running bouts in the test.
Blood sampling and analysis
During each condition, blood samples were collected
by antecubital venipuncture after 5-min of seated rest
and 3-min following the exercise. All specimens were
put in a cooler and quickly transported to the laboratory
and processed within 60 minutes. A heparinized tube
was used to determine biochemical responses. Samples
were centrifuged immediately at 3000 × g and 4 °C for
5-min. Aliquots of the resulting plasma were stored at
-80 °C until analyzed. To eliminate inter-assay variance,
all samples were analyzed in the same assay run. All bio-
logical tests were performed in duplicate in the same lab-
not permitted. It is not permitted to remove, cover, overlay, obscure, block, or change any copyright notices or terms of use which the Publisher may post on the Article. It is not permitted to frame or use framing techniques to enclose any trademark, log
means which may allow access to the Article. The use of all or any part of the Article for any Commercial Use is not permitted. The creation of derivative works from the Article is not permitted. The production of reprints for personal or commercial use i
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(either sporadically or systematically, either printed or electronic) of the Article for any purpose. It is not permitted to distribute the electronic copy of the article through online internet and/or intranet file sharing systems, electronic mailing or any other
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MEJRI SLEEP DEPRIVATION INCREASED BIOMARKERS OF MUSCLE AND CARDIAC INJURIES
oratory with simultaneous use of a control serum from
Randox Laboratories (Crumlin, Northern Ireland, UK).
ASAT activity was determined with an enzymatic
rate method. The intra-assay coefficient of variation for
the ASAT kit was 6.8%. CPK activity was determined
spectrophotometrically by measuring nicotinamide
adenine dinucleotide phosphate (NADPH) formed by
hexokinase and the D-glucose-6-phosphate dehydroge-
nase coupled enzymatic system. The intra-assay coeffi-
cient of variation for the CPK kit was 4.5%. LDH activ-
ity was determined by measuring nicotinamide adenine
dinucleotide (NADH) consumption using a reagent kits.
The intra-assay coefficient of variation for the LDH kit
was 5.9%. Us-CRP concentration was determined us-
ing an immunoturbidimetric method. The intra-assay
coefficient of variation for us-CRP kit was 1.3%. Con-
centrations of us-CRP under the detection level of the
us-CRP assay (0.02 mg/dL) were assigned a value of
0.01 mg/dl.5 CRP below the detection level accounted
for 11 of the 60 points of this study. All these parameters
were measured with an automated analyser (Beckman
Coulter UniCel DxC 600 Synchron, Beckman Instru-
ments, Danville, CA, USA). MYO was measured us-
ing a chemiluminescent microparticle immunoassay
(Architect Stat Myoglobin, Abbott Laboratories). The
intra-assay coefficient of variation for the MYO kit was
5.4%. Blood samples were corrected for plasma volume
changes from before to after exercise, using the equa-
tion of Dill and Costill.29
Statistical analysis
All statistical tests were processed using the Statis-
tical Package for the Social Sciences (SPSS) for Win-
dows, version 19. All values within the text and ta-
bles are reported as the Mean and Standard Deviation
(mean±STD). The Shapiro-Wilk W-Test revealed that
data were normally distributed. Once the assumption
of normality was confirmed, parametric tests were per-
Table I.—Statistical results from analysis of variance of physiological parameters.
or other proprietary information of the Publisher.
Sleep condition
HR (bpm) F2, 18=1.22, P>0.05, ηp2=0.12
SaO2 (%) F2, 18=0.35, P>0.05, ηp2=0.04
HR: heart rate; SaO2: arterial oxygen saturation.
646 The Journal of Sports Medicine and Physical Fitness May 2017
formed. Data obtained during YYIRT following the two
conditions of SD (PSDBN, PSDEN) were compared to
those obtained after the RN. Data were analyzed using
a two-way analysis of variance (ANOVA) with repeat-
ed measures (3 [sleep condition] × 2 [before/after ex-
ercise]). When the ANOVA indicated significant sleep
condition or before/after exercise effects or a signifi-
cant interaction sleep condition × before/after exercise,
post-hoc multiple comparisons using the LSD Fischer
Test was conducted. Effect sizes (ES) were calculated
as partial eta-squared ηp2 to assess the practical signifi-
cance of our findings. ES was interpreted as follows:
~0.2=small, ~0.5=moderate and ~0.8=large. The level
of significance was set at P<0.05. When the SPSS out-
put demonstrated significance levels of P=0.000, these
were corrected to P<0.0005.
Results
Physiological parameters
There was no significant sleep condition effect and
no significant sleep condition × before/after exercise
interaction for HR and SaO2 (Table I). However, there
was a significant before/after exercise effect for these
physiological parameters (Table I).
The post-hoc Test revealed a significant increase of
HR (Figure 1A) and a significant decrease of SaO2 (Fig-
ure 1B) in response to the exercise after the three sleep
conditions (RN, PSDBN, PSDEN). However, no altera-
tion of these physiological parameters has been found
following these two types of PSD compared to RN, at
rest and after the exercise (Figure 1A, B).
BRMCI
There was a significant sleep condition effect for us-
CRP and MYO (P<0.05 and P<0.01, respectively) (Ta-
ble II). However, no sleep condition effect was detected
ANOVA
Before/after exercise Interaction
F1, 9=5114.74, P<0.0005, ηp2=0.99 F2, 18=0.65, P>0.05, ηp2=0.07
F1, 9 =69.02, P<0.0005, ηp2=0.89 F2, 18=0.83, P>0.05, ηp2=0.09
not permitted. It is not permitted to remove, cover, overlay, obscure, block, or change any copyright notices or terms of use which the Publisher may post on the Article. It is not permitted to frame or use framing techniques to enclose any trademark, log
means which may allow access to the Article. The use of all or any part of the Article for any Commercial Use is not permitted. The creation of derivative works from the Article is not permitted. The production of reprints for personal or commercial use i
This document is protected by international copyright laws. No additional reproduction is authorized. It is permitted for personal use to download and save only one file and print only one copy of this Article. It is not permitted to make additional copies
(either sporadically or systematically, either printed or electronic) of the Article for any purpose. It is not permitted to distribute the electronic copy of the article through online internet and/or intranet file sharing systems, electronic mailing or any other
©
COPYRIGHT 2017 EDIZIONI MINERVA MEDICA
SLEEP DEPRIVATION INCREASED BIOMARKERS OF MUSCLE AND CARDIAC INJURIES MEJRI

tion between sleep condition × before/after exercise was

**** **** **** significant for CPK and MYO only (P<0.05) (Table II).
This significant interaction indicates that the variation
in these biomarkers after exercise depended to sleep
condition. However, no interaction for ASAT, LDH and
us-CRP has been detected (Table II).
HR (bpm)

The post-hoc revealed a significant increase in the

resting plasma concentrations of the us-CRP (Figure
2D) and MYO (Figure 2E) following the PSDEN com-
pared to RN (P<0.05). However, no alteration has been
found for the resting values of ASAT (Figure 2A), CPK
(Figure 2B) and LDH (Figure 2C), following the two
types of PSD. Regarding the effect of exercise on the
A RN PSDBN PSDEN variation of these biomarkers, we found a significant
increase following the RN (ASAT [P<0.0005] [Fig-
ure 2-A], LDH [P<0.001] [Figure 2C], MYO [P<0.05]
[Figure 2E]), PSDBN (all biomarkers) (Figure 2) and
PSDEN (ASAT [P<0.001] [Figure 2-A], CPK [P<0.05]
[Figure 2-B], us-CRP [P<0.05] [Figure 2-D], MYO
[P<0.01] [Figure 2-E]). Moreover, in comparison with
SaO2 (%)

**** **** RN, the two SD conditions increased significantly the

****
RN PSDBN PSDEN
B to RN (Figure 2B), reflects thus the effect of interaction
Figure 1.—Means values of physiological parameters at rest (black bars)
and following the exercise (gray bars) after the three sleeping conditions
(RN, PSDBN, PSDEN).
HR: heart rate (A); SaO2: arterial oxygen saturation (B); RN: reference
night; PSDBN: partial sleep deprivation in the beginning of the night;
PSDEN: partial sleep deprivation in the end of the night.
****Significant difference from resting values (P<0.0005)
for the other biomarkers (ASAT, CPK, LDH) (Table II).
Moreover, there was a significant before/after exercise
effect for all biomarkers (Table II). However, interac-
MYO concentrations after exercise (Figure 2E), reflect-
ing the effect of interaction of sleep condition × before/
after exercise. However, the increase in us-CRP after
exercise following the PSDEN (Figure 2D), reflects
also the sleep condition effect; and the increase in CPK
after exercise following PSDBN and PSDEN compared
of sleep condition × before/after exercise.
Discussion
This study investigated the effects of two different
types of SD on the BRMCI before and after an acute
intermittent evening exercise in Taekwondo athletes. As
a result, we come up with no significant effect of SD on
the physiological parameters (HR and SaO2), and the

Table II.—Statistical results from analysis of variance of biomarkers related to muscle and cardiac injury.
ANOVA
Sleep condition Before/after exercise Interaction
ASAT (UI.L-1) F2, 18=3.53, P>0.05, ηp2=0.28 F1, 9=83.78, P<0.0005, ηp2=0.90 F2, 18=2.83, P>0.05, ηp2=0.24
CPK (UI.L-1) F2, 18=0.12, P>0.05, ηp2=0.01 F1, 9=8.55, P<0.05, ηp2=0.49 F2, 18=4.53, P<0.05, ηp2=0.34
or other proprietary information of the Publisher.

LDH (UI.L-1) F2, 18=0.95, P>0.05, ηp2=0.10 F1, 9=15.44, P<0.01, ηp2=0.63 F2, 18=0.51, P>0.05, ηp2=0.05
us-CRP (mg.dL-1) F2, 18=3.91, P<0.05, ηp2=0.30 F1, 9=47.04, P<0.0005, ηp2=0.84 F2, 18=1.19, P>0.05, ηp2=0.12
MYO (ηg.mL-1) F2, 18=6.74, P<0.01, ηp2=0.43 F1, 9=27.30, P<0.01, ηp2=0.75 F2, 18=4.83, P<0.05, ηp2=0.35
ASAT: aspartate aminotransferase; CPK: creatine phosphokinase; LDH: lactate dehydrogenase; us-CRP: ultra-sensitive C-reactive protein; MYO: myoglobin.

Vol. 57 - No. 5 The Journal of Sports Medicine and Physical Fitness 647
not permitted. It is not permitted to remove, cover, overlay, obscure, block, or change any copyright notices or terms of use which the Publisher may post on the Article. It is not permitted to frame or use framing techniques to enclose any trademark, log
means which may allow access to the Article. The use of all or any part of the Article for any Commercial Use is not permitted. The creation of derivative works from the Article is not permitted. The production of reprints for personal or commercial use i
This document is protected by international copyright laws. No additional reproduction is authorized. It is permitted for personal use to download and save only one file and print only one copy of this Article. It is not permitted to make additional copies
(either sporadically or systematically, either printed or electronic) of the Article for any purpose. It is not permitted to distribute the electronic copy of the article through online internet and/or intranet file sharing systems, electronic mailing or any other
©
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MEJRI SLEEP DEPRIVATION INCREASED BIOMARKERS OF MUSCLE AND CARDIAC INJURIES

ASAT and LDH concentrations at rest and in response

Before exercise to exercise. However, a significant alteration in the
After exercise
resting values of us-CRP and MYO was observed fol-
ASAT (UI.L-1)

lowing PSDEN. Likewise, CPK and MYO values have

A RN
been relatively affected due to the interaction between
SD and exercise. Furthermore, all the physiological pa-
rameters as well as the BRMCI have been altered by
exercise.
PSDBN PSDEN

Effects of sleep deprivation on physiological responses

CPK (UI.L-1)

to the YYIRT

According to previous reports, results of the present

B RN
LDH (UI.L-1)
study showed that SD did not affect resting 9, 12, 13, 22 or
exercise 7, 11, 13 measures of HR. Yet, the present findings
PSDBN PSDEN
are in disagreement with previous investigations which
demonstrated that SD decreased 7, 11 or increased 5, 8-10
resting and exercise HR. The present findings about

HR can be explained by previous reports denoting that

C RN
us-CRP (mg.dL-1)
SD did not alter plasma catecholamine levels.12 How-
ever, exceeding HR response after exercise, might be
a consequence of reduced parasympathetic tone and/or
PSDBN PSDEN increased sympathetic tone in the autonomic nervous
system,8 which could be also explained by the effect of

the increase of catecholamines synthesis and adrenergic

activity.10
On the other hand, the present finding showed that
one night PSD did not alter SaO2. These findings are in
agreement with those of previous investigations show-
RN PSDBN PSDEN ing that one night TSD,13 or PSD22 did not affect SaO2
D in athletes. This unaltered SaO2 can be justified by pre-
vious finding showing that SD did not alter spiromet-
MYO (ηg.mL-1)

ric variables.30 Moreover, the decrease of SaO2 at the

RN PSDBN PSDEN
E increase in cardiac output during exercise may have
Figure 2.—Means values of biomarkers related to muscle and cardiac
injury at rest and following the exercise after the three sleeping condi-
tions (RN, PSDBN, PSDEN).
ASAT: aspartate aminotransferase (A); CPK: creatine phosphoki-
nase (B); LDH: lactate dehydrogenases (C); us-CRP: ultra-sensitive
or other proprietary information of the Publisher.
end of exercise could be also attributed to the increase
of blood circulation of skeletal muscle and raised oxy-
gen consumption by the muscle metabolism.31 In this
context, Adami et al.32 suggested that the reduction in
pulmonary capillary transit time associated with the
evident effects on post-exercise SaO2 decrease. Conse-
quently, the SaO2 during exercise at any given inspired
O2 fraction diminishes with increased the workload
and remains low during recovery period. Overall, the

C-reactive protein (D); MYO: myoglobin (E); RN: reference night;

PSDBN: partial sleep deprivation in the beginning of the night; PSDEN:
partial sleep deprivation in the end of the night.
#, ##Significant difference compared to RN for the same period (P<0.05,
P<0.01, respectively). *, **, ***, ****Significant difference from resting val-
ues (P<0.05, P<0.01, P<0.001, P<0.0005, respectively).
controversy between results seems to be due to various
factors such as sex, body posture, physical activity, in-
tensity of illumination, food and beverage consumption,
and time of day of measurements that exert a significant

648 The Journal of Sports Medicine and Physical Fitness May 2017
not permitted. It is not permitted to remove, cover, overlay, obscure, block, or change any copyright notices or terms of use which the Publisher may post on the Article. It is not permitted to frame or use framing techniques to enclose any trademark, log
means which may allow access to the Article. The use of all or any part of the Article for any Commercial Use is not permitted. The creation of derivative works from the Article is not permitted. The production of reprints for personal or commercial use i
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SLEEP DEPRIVATION INCREASED BIOMARKERS OF MUSCLE AND CARDIAC INJURIES MEJRI
influence on the sympathetic nervous system were not
strictly controlled in previous studies.
Effects of sleep deprivation on biomarkers related to
muscle and cardiac injuries responses to the YYIRT
Effects of sleep deprivation
To the best of the authors’ knowledge, this is the first
work to describe the BRMCI responses to physical ex-
ercise in relation to sleep loss in professional athletes.
As previously reported,5, 8, 22 the present study results
showed that resting levels of us-CRP and MYO in-
creased after PSDEN. Indeed, Meier-Ewert et al.5 re-
ported that both acute total (one, two, or three nights
of TSD) and partial (4.2 h for 10 consecutive days) SD
resulted in elevated us-CRP concentrations in healthy
adults. Moreover, van Leeuwen et al.8 reported that
five nights PSD significantly increased serum levels of
CRP in healthy young men. However, the present find-
ings are divergent with previous investigations which
showed that TSD,9 or repetitive short-term SD, such as
four nights PSDEN (sleep from 11 pm to 3 am),20 three
nights PSD (sleep from 1 pm to 5 am),21 did not increase
serum levels of CRP. However, Frey et al.19 noted that
forty hours of TSD decreased significantly the levels of
this biomarker in healthy men and women. Concerning
MYO, the present data demonstrated that one night PSD
(PSDEN) increases resting circulating levels of MYO,
which is consistent with those of Mejri et al.,22 who
showed a significant rise of MYO concentrations, at the
morning, following one night of PSDEN. However, one
night PSD has no effect on the resting ASAT, CPK and
LDH responses. In disagreement with the present find-
ings, previous studies reported that prolonged TSD,18 or
one night PSD22 induced a significant rise in the resting
levels of these biomarkers among healthy males or ath-
letes, respectively. However, the present findings are in
agreement with Ilan’s study which has not found a sig-
nificant SD effect on the resting LDH levels.18 Several
methodological issues between the studies cited above
and the current study may contribute to the inconsistent
findings for the responses of these biomarkers.
or other proprietary information of the Publisher.
Effects of YYIRT
Current study results confirmed the findings of previ-
ous reports showing a significant increase in BRMCI
Vol. 57 - No. 5 The Journal of Sports Medicine and Physical Fitness 649
(i.e., ASAT, CPK, LDH, us-CRP, MYO) after acute
exercise.15, 16, 23, 33 In this context, it has been reported
that increased plasma ASAT, reflects disrupted perme-
ability of the cells, in which this enzyme can be found
(e.g., heart and skeletal muscle).34 On the other hand, it
has been established that CPK values were highly cor-
related with ASAT, LDH and MYO values, in response
to acute exercise.33 In fact, we speculate that, the dis-
ruption of the sarcomere and failure within the excita-
tion-contraction coupling system observed following
this type of exercise (i.e., YYIRT), are the primary fac-
tors initiating muscle injury.16 As a result, the efflux of
all these biomarkers (i.e., ASAT, CPK, LDH, us-CRP,
MYO) from muscle may occur because of increases in
the permeability of the myocellular membrane and/or
the intramuscular vasculature.35 As well as, the extent
of the response of these biomarkers has been related
mainly to the exercise intensity.15, 16
Concomitant effects of sleep deprivation and ex-
ercise
The results of the present study indicated that one
night PSD remarkably increase CPK and MYO re-
sponses to acute intermittent exercise, without alteration
in the others biomarkers (i.e., ASAT, LDH, us-CRP).
To the best of the authors’ knowledge, convincing as-
sociations between the biochemical evidence related to
muscle and cardiac injuries, and the combined effect of
SD and exercise have not been demonstrated. The sig-
nificant interaction between SD and exercise, causing
the increase of CPK levels in the present study, might be
justified by the theory of “inefficient isolated effects and
efficient combined effects” conceived from the study of
Coleman et al.36 Indeed, in the present work, isolated
effect of exercise did not increase CPK concentrations
following RN. Likewise, there is no significant isolated
effect of SD on resting CPK responses. However, after
PSDBN and PSDEN, CPK and MYO levels increased
significantly following exercise. This leads us to suggest
that the fatigue generated by the combined effects of SD
and evening exercise, is the principal cause of increased
levels of these biomarkers. Against this background, it
has been established that primary skeletal muscle dis-
order manifests with pain, fatigue, weakness, and se-
rum CPK elevation.15 Likewise, previous studies have
reported that post-exercise neutrophil counts correlated
not permitted. It is not permitted to remove, cover, overlay, obscure, block, or change any copyright notices or terms of use which the Publisher may post on the Article. It is not permitted to frame or use framing techniques to enclose any trademark, log
means which may allow access to the Article. The use of all or any part of the Article for any Commercial Use is not permitted. The creation of derivative works from the Article is not permitted. The production of reprints for personal or commercial use i
This document is protected by international copyright laws. No additional reproduction is authorized. It is permitted for personal use to download and save only one file and print only one copy of this Article. It is not permitted to make additional copies
(either sporadically or systematically, either printed or electronic) of the Article for any purpose. It is not permitted to distribute the electronic copy of the article through online internet and/or intranet file sharing systems, electronic mailing or any other
©
COPYRIGHT 2017 EDIZIONI MINERVA MEDICA
MEJRI SLEEP DEPRIVATION INCREASED BIOMARKERS OF MUSCLE AND CARDIAC INJURIES
with plasma MYO concentration and CPK activity. 23, 37
Therefore, it has been well reported that a host of bio-
chemical changes within the affected muscle areas such
as increased inflammatory cytokines and reactive oxy-
gen species may aggravate muscle injuries 38 and thus
increase the cardiac injury risk, mainly, following SD.
Based on these findings, concomitant effects of SD and
exercise on CPK and MYO concentrations found in the
present study, support the data found by the recent re-
ports.3, 24, 25 Indeed, it has been reported that one night
PSD (PSDBN, PSDEN) causes an immunosuppres-
sion in response to the YYIRT.25 Likewise, it has been
also established that one night PSD timed at the end of
the night induced a significant increase in IL-6 and/or
TNF-α response during acute exercises (i.e., repeated
high-intensity exercise, Wingate-test) performed in the
following day at 6 pm by athletes.3, 24 In summary, the
present study showed that concomitant effect of SD and
acute exercise may generate transient muscle and car-
diac injuries, above all in athletes. Several limitations
of the study include as the small sample size and the ab-
sence of the evaluation of a high-sensitive cardiac tropo-
nin T (hs-cTnT) which is considered as a very sensitive
marker of cardiac injury. Furthermore, this study warns
athletes interested to the acute intermittent exercise, as
well as coaches and researchers, to determine the role of
SD in the over-activation of BRMCI during acute exer-
cise. Further studies are needed to consider the potential
influence of hs-cTnT, cytokines, stress hormones and
oxidative stress when interpreting changes in biomark-
ers concentrations related to muscle and cardiac injury
in response to acute exercise, mainly after SD. These
findings may have direct applications in daily life of
the professional athletes. In fact, to prevent the adverse
effect of sleep loss on athletes’ health (e.g., cardiovas-
cular risk), mainly during the training and competition
sessions that will be held in the evening, precautions
should be taken by athletes and coaches. Indeed, a nor-
mal night of sleep (≈7 h of sleep /night) with appropriate
conditions (i.e., mainly no noise and light in bedroom)
prove to be very important on athletes’ health, to ensure
proper maintenance of bodily processes. On the other
hand, athlete must avoid circumstances that may trig-
or other proprietary information of the Publisher.
ger stress-related sleep loss (i.e., school requirements,
work pressures, relationship troubles), as well as fa-
tigue caused by training and competition during the late
night.39 In this context, recent data highlighted the po-
650 The Journal of Sports Medicine and Physical Fitness May 2017
tential role of sleep on professional athletes and how to
avoid factors that compromise an adequate sleep during
a season and after competition, as they have explained
as well the strategies that may help improve sleep in
professional athletes.39
Conclusions
The present study results indicate that PSDBN and
PSDEN did not affect physiological responses (i.e., HR,
SaO2) at rest and in response to the YYIRT, when per-
formed in the evening of the following day in Taekwon-
do athletes. In addition, results from this study suggest
that PSDEN increase the resting us-CRP and MYO lev-
els, and that the two types of PSD increase the CPK and
MYO levels in response to acute intermittent exercise.
However, from the present study findings, it seems that
transient rise of the BRMCI after YYIRT do not reach
clinical significance. Future studies will focus upon the
chronic effects of PSD on BRMCI.
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Funding.—This study was supported by The Research Laboratory ‘’Sports Performance Optimization’’ National Center of Medicine and Science in Sports
(CNMSS), and the Laboratory of Clinical Biochemistry, National Institute of Nutrition and Food Technology of Tunisia (INNTA).
Conflicts of interest.—The authors certify that there is no conflict of interest with any financial organization regarding the material discussed in the manuscript.
Acknowledgments.—The authors wish to express their sincere gratitude to all the participants for their maximal effort and cooperation and the staff of the
Laboratory of Clinical Biochemistry of INNTA. We especially thank Prof. Bechir Zouari for his assistance with statistics.
Article first published online: February 11, 2016. - Manuscript accepted: February 4, 2016. - Manuscript revised: January 19, 2016. - Manuscript received:
September 17, 2015.
or other proprietary information of the Publisher.

Vol. 57 - No. 5 The Journal of Sports Medicine and Physical Fitness 651