ArticlePDF Available

One night of partial sleep deprivation impairs recovery from a single exercise training session

Authors:

Abstract and Figures

Purpose The effects of sleep deprivation on physical performance are well documented, but data on the consequence of sleep deprivation on recovery from exercise are limited. The aim was to compare cyclists’ recovery from a single bout of high-intensity interval training (HIIT) after which they were given either a normal night of sleep (CON, 7.56 ± 0.63 h) or half of their usual time in bed (DEP, 3.83 ± 0.33 h). Methods In this randomized cross-over intervention study, 16 trained male cyclists (age 32 ± 7 years), relative peak power output (PPO 4.6 ± 0.7 W kg−1) performed a HIIT session at ±18:00 followed by either the CON or DEP sleep condition. Recovery from the HIIT session was assessed the following day by comparing pre-HIIT variables to those measured 12 and 24 h after the session. Following a 2-week washout, cyclists repeated the trial, but under the alternate sleep condition. Results PPO was reduced more 24 h after the HIIT session in the DEP (ΔPPO −0.22 ± 0.22 W kg−1; range −0.75 to 0.1 W kg−1) compared to the CON condition (ΔPPO −0.05 ± 0.09 W kg−1, range −0.19 to 0.17 W kg−1, p = 0.008, d = −2.16). Cyclists were sleepier (12 h: p = 0.002, d = 1.90; 24 h: p = 0.001, d = 1.41) and felt less motivated to train (12 h, p = 0.012, d = −0.89) during the 24 h recovery phase when the HIIT session was followed by the DEP condition. The exercise-induced 24 h reduction in systolic blood pressure observed in the CON condition was absent in the DEP condition (p = 0.039, d = 0.75). Conclusions One night of partial sleep deprivation impairs recovery from a single HIIT session in cyclists. Further research is needed to understand the mechanisms behind this observation.
This content is subject to copyright. Terms and conditions apply.
1 23
European Journal of Applied
Physiology
ISSN 1439-6319
Volume 117
Number 4
Eur J Appl Physiol (2017) 117:699-712
DOI 10.1007/s00421-017-3565-5
One night of partial sleep deprivation
impairs recovery from a single exercise
training session
Dale E.Rae, Tayla Chin, Kagiso
Dikgomo, Lee Hill, Andrew J.McKune,
Tertius A.Kohn & Laura C.Roden
1 23
Your article is protected by copyright and
all rights are held exclusively by Springer-
Verlag Berlin Heidelberg. This e-offprint is
for personal use only and shall not be self-
archived in electronic repositories. If you wish
to self-archive your article, please use the
accepted manuscript version for posting on
your own website. You may further deposit
the accepted manuscript version in any
repository, provided it is only made publicly
available 12 months after official publication
or later and provided acknowledgement is
given to the original source of publication
and a link is inserted to the published article
on Springer's website. The link must be
accompanied by the following text: "The final
publication is available at link.springer.com”.
Vol.:(0123456789)
1 3
Eur J Appl Physiol (2017) 117:699–712
DOI 10.1007/s00421-017-3565-5
ORIGINAL ARTICLE
One night ofpartial sleep deprivation impairs recovery
fromasingle exercise training session
DaleE.Rae1· TaylaChin1· KagisoDikgomo1· LeeHill1· AndrewJ.McKune3,4·
TertiusA.Kohn1· LauraC.Roden2
Received: 11 October 2016 / Accepted: 6 February 2017 / Published online: 28 February 2017
© Springer-Verlag Berlin Heidelberg 2017
variables to those measured 12 and 24h after the session.
Following a 2-week washout, cyclists repeated the trial, but
under the alternate sleep condition.
Results PPO was reduced more 24h after the HIIT ses-
sion in the DEP (ΔPPO 0.22 ± 0.22Wkg1; range
0.75 to 0.1Wkg1) compared to the CON condition
(ΔPPO 0.05 ± 0.09Wkg1, range 0.19 to 0.17Wkg1,
p = 0.008, d = 2.16). Cyclists were sleepier (12h:
p = 0.002, d = 1.90; 24h: p = 0.001, d = 1.41) and felt less
motivated to train (12h, p = 0.012, d = 0.89) during the
24h recovery phase when the HIIT session was followed
by the DEP condition. The exercise-induced 24h reduction
in systolic blood pressure observed in the CON condition
was absent in the DEP condition (p = 0.039, d = 0.75).
Conclusions One night of partial sleep deprivation
impairs recovery from a single HIIT session in cyclists.
Further research is needed to understand the mechanisms
behind this observation.
Keywords Sleep deprivation· Recovery strategies·
Maximal performance· High-intensity interval training·
Cyclists
Abbreviations
BP Blood pressure
CK Creatine kinase
CON Control condition: normal night of sleep
DBP Diastolic blood pressure
DEP Partial sleep deprivation condition: 50% of nor-
mal sleep
HIIT High-intensity interval training
HR Heart rate
HRmax Maximum heart rate
IgA Immunogammaglobulin A
PPO Peak power output
Abstract
Purpose The eects of sleep deprivation on physical
performance are well documented, but data on the conse-
quence of sleep deprivation on recovery from exercise are
limited. The aim was to compare cyclists’ recovery from
a single bout of high-intensity interval training (HIIT)
after which they were given either a normal night of sleep
(CON, 7.56 ± 0.63h) or half of their usual time in bed
(DEP, 3.83 ± 0.33h).
Methods In this randomized cross-over intervention
study, 16 trained male cyclists (age 32 ± 7years), rela-
tive peak power output (PPO 4.6 ± 0.7Wkg1) performed
a HIIT session at ±18:00 followed by either the CON or
DEP sleep condition. Recovery from the HIIT session
was assessed the following day by comparing pre-HIIT
Communicated by Nicolas Place.
Electronic supplementary material The online version of this
article (doi:10.1007/s00421-017-3565-5) contains supplementary
material, which is available to authorized users.
* Dale E. Rae
Dale.Rae@uct.ac.za
1 Division ofExercise Science andSports Medicine,
Department ofHuman Biology, Faculty ofHealth Sciences,
University ofCape Town, PO Box115, Newlands,
CapeTown7725, SouthAfrica
2 Department ofMolecular andCell Biology, Faculty
ofScience, University ofCape Town, CapeTown,
SouthAfrica
3 Research Institute forSport andExercise, University
ofCanberra, Canberra, Australia
4 Discipline ofBiokinetics, Exercise andLeisure Sciences,
School ofHealth, University ofKwaZulu-Natal, Durban,
SouthAfrica
Author's personal copy
700 Eur J Appl Physiol (2017) 117:699–712
1 3
RER Respiratory exchange ratio
RPE Rating of perceived exertion
SBP Systolic blood pressure
sIgA Salivary immunogammaglobulin A
VO2max Maximum volume of oxygen uptake
Introduction
In the context of sport and exercise, sleep is recognized as
being critical for an athlete’s well-being and performance.
Much of sleep’s value may lie in its role in recovery, from
both training and competition, an important factor deter-
mining performance. In a recent survey of 890 team sport
athletes, sleep was identified as one of the most impor-
tant recovery strategies (Venter 2014). When elite foot-
ball players had night matches, their sleep duration was
typically reduced on the night of the match and the fol-
lowing day they reported feeling less recovered compared
to day matches (Fullagar etal. 2016). Kölling etal. (2016)
observed 55 junior, national-level rowers during a 4-week
training camp. Following just one night of shortened sleep
at the end of the first week of the camp, the rowers reported
feeling less recovered and in a worsened emotional state
compared to the previous day, which had been preceded by
a normal night of sleep (Kölling etal. 2016). Furthermore,
the fact that more rowers napped on training days compared
to rest days suggests a higher sleep need on training days.
These studies provide some evidence that athletes intui-
tively value sleep in the context of recovery.
Despite this, sleep complaints are prevalent in athletes
(Swinbourne etal. 2015; Gupta etal. 2016). Not only does
competition and travel interfere with their sleep (Fullagar
etal. 2016; Gupta etal. 2016), but also training itself may
reduce sleep quality and quantity. Training periods in which
intensity is increased or early morning sessions are sched-
uled have both been shown to reduce sleep duration in ath-
letes (Sargent etal. 2013; Schaal etal. 2015; Kölling etal.
2016). Thus athletes and coaches are challenged to balance
training programmes, travel and competition schedules,
and sleep routines to facilitate optimal performance. Perti-
nently, a recent consensus statement from the International
Olympic Committee called on coaches to ensure sucient
rest and recovery periods in training programmes for youth
athletes to “encourage positive adaptations and progressive
athletic development” (Bergeron etal. 2015).
A single bout of exercise perturbs the homeostasis of
the skeletal muscle, cardiovascular, nervous, endocrine,
metabolic and immune systems (Reilly and Ekblom
2007; Heinonen etal. 2014; Walsh and Oliver 2016) and
the ensuing recovery of these systems can be viewed as
an adaptation to the specific training stimulus in anticipa-
tion of future exposures. One of the functions of sleep is
to provide an opportunity for both neurological and phys-
iological systems to recover and repair (Akerstedt and
Nilsson 2003). Both complete and partial sleep depriva-
tion are understood to compromise various physiologi-
cal systems (Zhong 2005; Van Cauter etal. 2008; Ruiz
etal. 2012) and reduce physical performance the next
day (Souissi etal. 2003; Oliver etal. 2009; Temesi etal.
2013). Reducing sleep only partially (4h for 6days) has
been shown to decrease glucose tolerance, increase even-
ing cortisol levels, elevate sympathovagal balance, and
disrupt the normal pattern of growth hormone at night
(Akerstedt and Nilsson 2003). Reduced sleep may inter-
fere with muscle recovery due to increased signalling to
initiate proteolysis, essentially creating a more catabolic
state (Dattilo etal. 2011). The fact that resting systolic
blood pressure increases after partial sleep deprivation
(±3.5h), potentially indicates that sympathetic nervous
system activity is altered by reduced sleep (Tochikubo
etal. 1996). Sleep deprivation is also understood to dis-
rupt the immune system (Faraut etal. 2012), with eects
similar to those of intense exercise on both the innate
and acquired immune systems (Walsh and Oliver 2016).
Sleep loss also reduces mood and motivation (Reilly and
Piercy 1994; Scott etal. 2006), both of which may impact
eort produced during a subsequent training session.
Collectively, these data suggest that recovery from exer-
cise may be impaired by sleep deprivation through the
compromised function of any number of systems.
While numerous recovery enhancing modalities such
as nutrition (Beelen etal. 2010), ice (Poppendieck etal.
2013) and compression (MacRae etal. 2011) having been
investigated, studies measuring the eect of sleep depriva-
tion on recovery from exercise are scant (Skein etal. 2013).
As early as 1984 recovery from a 20min training session
was assessed in five males, under both normal sleep and
complete sleep deprivation conditions. While submaximal
performance was not compromised with sleep deprivation,
recovery was hampered, as indicated by altered profiles
of blood glucose, lactate, minute ventilation and oxygen
uptake during submaximal exercise (McMurray and Brown
1984). More recently, recovery of lower limb power in
rugby players who underwent complete sleep deprivation
the night after a match was shown to be impaired compared
to a normal night of sleep (Skein etal. 2013).
Both of these previous studies (McMurray and Brown
1984; Skein etal. 2013) made use of complete sleep depri-
vation models. While they are useful designs to understand
the extreme eects of sleep restriction, athletes may be
more likely to experience poor sleep or reduced sleep dura-
tion following competition or during training phases (Sar-
gent etal. 2013; Schaal etal. 2015; Kölling etal. 2016; Ful-
lagar etal. 2016). Therefore, investigation of the eects of
partial sleep deprivation on recovery from exercise would
Author's personal copy
701Eur J Appl Physiol (2017) 117:699–712
1 3
expand previous research in this area by providing informa-
tion on a sleep scenario many athletes may face.
The aim of this study was to determine whether par-
tial sleep deprivation impairs recovery from training. The
objective was to compare cyclists’ recovery from a single
bout of high-intensity interval training (HIIT) after which
they were given either a normal night of sleep or were par-
tially sleep deprived. Recovery was assessed by monitoring
motivation to train; muscle soreness and tiredness; sleepi-
ness; resting heart rate and blood pressure; maximal power,
heart rate and oxygen uptake; creatine kinase activity; leu-
kocyte cell counts and salivary IgA secretion rate during
the 24h after the HIIT session. The hypothesis was that a
full, normal night of sleep after a HIIT session would be
necessary to facilitate recovery, assessed by the ability to
perform at close to maximum in a peak power output test
24h after the HIIT. Specifically, it was hypothesised that
even one night of partial sleep deprivation would be suf-
ficient to impair recovery.
Methods
Participants
Sixteen trained male cyclists participated in this study. To
be included they needed to be 20–50years old, usually
sleep >6h per night, train at least three times per week
(past 6months) and have ridden the Cape Town Cycle
Tour, an annual 110km road race in South Africa, within
the last year in a time of <3h 45min. Exclusion criteria
were diagnosed chronic cardiovascular or metabolic dis-
ease, psychiatric condition, sleep disorder, or any other
condition known to aect sleep; current or recent use of
sleep medication (past 2months); recent trans-meridian
travel exceeding three time zones (past 2months); and shift
work. The Human Research Ethics Committee of the Fac-
ulty of Health Sciences, University of Cape Town approved
this study (HREC No: 272/2014) and all participants pro-
vided written informed consent. Descriptive characteristics
of the participants are presented in Table1.
Study overview
An overview of the design of this randomized crossover
intervention study is depicted in Fig.1. Briefly, in session 1
(17:30) participants completed a questionnaire to document
medical and cycling histories, assess chronotype using the
Horne–Östberg morningness–eveningness personality ques-
tionnaire (Horne and Östberg 1976) and measure sleep qual-
ity using the Pittsburgh Sleep Quality Index (Buysse etal.
1989). They also practiced the peak power output (PPO)
test. For the next seven consecutive days participants wore a
wrist actigraph (Actiwatch AW2, Philips Respironics, Bend,
OR, USA) to establish their usual sleep habits. Sleep timing
was verified using a diary. They were asked to refrain from
training 48h before and to avoid caeine and alcohol 24h
before session 2. A dietary log completed in the 24h period
prior to sessions 2 and 5 was used to verify this. There was
94% compliance to the 24h alcohol restriction for both the
CON and DEP conditions, and 100 and 88% compliance to
the caeine restriction prior to the CON and DEP sessions,
respectively. Participants also used the dietary log to match
their food intake times, content and quantity before session 5
to that of session 2.
Participants fasted for 3h before session 2 (17:30) at
which baseline measures (Pre) were taken. These included
weight, sleepiness, motivation to train, muscle soreness and
tiredness scores, resting heart rate and blood pressure, saliva
and blood samples, and a PPO test. This was followed imme-
diately by the HIIT session at 18:00. Participants then slept
in the laboratory under either control sleep (CON) or par-
tial sleep deprivation (DEP) conditions. Follow-up sessions
3 (06:30–07:00) and 4 (18:30) took place 12 and 24h after
session 2, respectively, during which all baselines measures
were repeated, with the exception of the PPO test, which was
only performed at session 4. After a 2-week washout, cyclists
repeated the trial (sessions 5–7) under the alternate sleep con-
dition. The order in which participants underwent the inter-
vention was randomized. While it was not possible to blind
participants to the condition (CON or DEP), they were only
told their condition after the first HIIT session.
Detailed testing procedures
Subjective, heart rate (HR) andblood pressure (BP)
measurements
The Epworth Sleepiness Scale was used to measure sleepi-
ness (Johns 1991). Participants rated their “motivation to
Table 1 Participant characteristics (n = 16)
BMI body mass index, VO2max maximum oxygen uptake volume
a 11 of the cyclists were morning-types (69%), 5 were neither-types
(31%), and there were no evening-types
Mean ± SD Range
Age (years) 32.3 ± 7.1 22–47
Height (m) 1.80 ± 0.08 1.62–1.94
Weight (kg) 76.9 ± 9.5 60.6–95.7
BMI (kgm2) 23.8 ± 1.6 21.2–27.4
Chronotype score 63 ± 9 44–76a
Sleep quality 4 ± 1 2–7
VO2max (mlmin1kg1) 57.6 ± 8.3 45.1–79.3
Peak power output (Wkg1) 4.61 ± 0.70 3.69–6.37
Author's personal copy
702 Eur J Appl Physiol (2017) 117:699–712
1 3
train” on a 10-point scale (1: “not into it” through to 10:
“extremely motivated”). Leg muscle soreness and tiredness
were assessed when standing, during a quadriceps stretch
and immediately after climbing two flights of stairs (2 steps
per second), since each scenario may elicit soreness or
tiredness to dierent extents in dierent individuals. These
ratings made use of an 11-point scale (0: “no soreness or
tiredness” through to 10: “extreme soreness or tiredness”),
and the global leg muscle soreness and tiredness scores
summed all three measurements. Only the global values are
presented in the results. Resting HR and BP measurements
represent the average of three values taken after 10min of
seated rest using an automated monitor (Omron HEM-907,
Omron Health Care, Kyoto, Japan).
Immune function andmuscle damage
Saliva samples were collected from participants during ses-
sions 2–7 by unstimulated passive drool to assess immune
function. Salivary immunoglobulin A (sIgA) secretion
rate (µgmin1) was determined using an indirect enzyme
immunoassay kit (Salimetrics, State College, USA). Details
of this procedure have been published previously (McKune
etal. 2006). Venous blood samples were obtained from
participants to measure indices of muscle damage (cre-
atine kinase (CK) activity) and immune function (white
blood cell count, WBC, and dierential). Samples for CK
activity were collected into lithium heparin vacutainer
tubes, placed on ice, centrifuged at 3000×g for 10min at
4 °C, after which the plasma was removed and stored in
microfuge tubes at 80 °C. CK activity was determined
using a commercial enzymatic assay kit (CK-NAC-acti-
vated, Boehringer Mannheim, Meylan, France) and a spec-
trophotometer (Beckman Instruments DU-530, Fullerton,
CA, USA). Samples for WBC analyses were collected into
EDTA vacutainers and immediately sent to a medical diag-
nostic laboratory (Metropolis, Cape Town) that performed
the leukocyte counts.
Peak power output (PPO) test
The cyclists performed PPO tests during sessions 1, 2, 4, 5
and 7. The PPO test in session 1 was for familiarisation and
to establish maximum heart rate. Those performed in ses-
sions 2 and 5 provided baseline values for maximal aerobic
performance and those in sessions 4 and 7 were to assess
24h recovery in maximal performance following the HIIT
under the CON and DEP conditions. Participants used their
own bicycles mounted on a cycle ergometer (Computrainer
Pro 3D, RacerMate, Seattle, USA) and set-up was the
same for each session. To warm up, cyclists completed the
Lamberts and Lambert Submaximal Cycling Test (Lam-
berts etal. 2011). This 15min test comprises three stages:
6min at 60% of maximum heart rate max (HRmax), 6min
at 80% HRmax and 3min at 90% HRmax. Following this, the
ramp format PPO test began at 2.5Wkg1 body weight
Fig. 1 Study overview
Author's personal copy
703Eur J Appl Physiol (2017) 117:699–712
1 3
for 1min. Power then increased by 20Wmin1 until par-
ticipants were unable to maintain a minimum cadence of
70rpm or reached volitional exhaustion. During the test,
HR (bpm), power (W), oxygen uptake and carbon dioxide
production (mlkg1min1) were measured continuously
and rating of perceived exertion (RPE) at the end of every
minute. HR was monitored using a Suunto t6d heart rate
monitor (v2.1.0.3, Suunto, Oy, Vantaa, Finland), RPE using
the 20-point Borg scale (Borg 1998), and respiratory vari-
ables using an online breath-by-breath gas analyser and
pneumotach (Oxycon, Viasis, Hoechberg, Germany).
HIIT session
This 54min session took place 5min after the baseline
PPO test in sessions 2 and 5, and simulated a hard train-
ing bout from which recovery was measured. Cyclists com-
pleted 18 × 1min intervals at PPO, with 2min of active
recovery (50W) between each interval. During the session
they had adlibitum access to water and a 7% carbohydrate
drink (CarboFuel, Cadence Nutrition, Cape Town, South
Africa). The volume of carbohydrate drink consumed
during the HIIT was similar between conditions (CON
360 ± 231ml, DEP 358 ± 187ml, p = 0.983). The same was
true for the volume of water drunk (CON 272 ± 257ml,
DEP 222 ± 165ml, p = 0.523).
Meals
Participants ingested a recovery drink (200ml low fat choc-
olate-flavoured milk; 482kJ, 6g protein, 18g carbohydrate
and 4g fat per serving) within 30min of the HIIT session,
and ate dinner (beef lasagne) within 90min. Portion sizes
were standardised so that each cyclist consumed 0.42g car-
bohydrate, 0.62g protein and 0.35g fat per kg body mass.
A standardised breakfast consisting of oats, milk, fruit and
caeine-free tea was provided.
Usual sleep habits andsleep intervention
Participants wore a wrist-worn actigraph (Actiwatch AW2,
Philips Respironics, Bend, OR, USA) and kept a sleep
diary for seven consecutive days between sessions 1 and 2
to establish their usual sleep habits. Data for all 7days were
Table 2 Usual (n = 16), CON
(n = 16) and DEP (n = 16) sleep
characteristics
Data are presented as mean ± SD or median (interquartile range)
CON control sleep condition, DEP partial sleep deprivation condition, USUAL habitual sleep characteris-
tics, WASO wake after sleep onset time
Significance was determined using either a paired t test or Wilcoxon signed-rank test. p1: USUAL vs.
CON; p2: USUAL vs. DEP; p3: CON vs. DEP
Usual CON DEP p1p2p3
Bed time (h:min) 22:50 ± 0:45 22:42 ± 0:40 00:33 ± 0:19 0.368 <0.001 <0.001
Wake-up time (h:min) 06:24 ± 0:37 6:16 ± 0:25 4:23 ± 0:22 0.109 <0.001 <0.001
Time-in-bed (h) 7.58 ± 0.69 7.56 ± 0.63 3.83 ± 0.33 0.919 <0.001 <0.001
Sleep length (h) 6.81 ± 0.50 6.50 ± 0.56 3.38 ± 0.41 0.126 <0.001 <0.001
Eciency (%) 90.2 ± 3.5 86.4 ± 8.0 88.3 ± 8.1 0.059 0.386 0.246
Latency (min) 6.0 (3.4) 7.5 (0.6) 1.4 (0.4) 0.309 0.522 0.032
WASO (min) 26.9 ± 11.2 32.4 ± 17.7 11.9 ± 7.5 0.156 <0.001 0.002
No. of awakenings 46 ± 14 45 ± 17 20 ± 12 0.609 <0.001 0.002
Table 3 Twelve-hour responses
to the HIIT session under the
CON and DEP conditions
Changes in actual values are presented as mean ± SD or median (IQR), with the range in parentheses
CON control sleep condition, DEP partial sleep deprivation condition, HIIT high-intensity interval training
session, HR heart rate, SBP systolic blood pressure, DBP diastolic blood pressure
The p value indicates significance determined using either a paired t test or Wilcoxon signed-rank test.
Cohen’s d indicates eect size
nCON DEP d p value
ΔSleepiness 16 1 (3) (9 to 1) 4 (6) (3 to 14) 1.88 0.001
ΔMotivation to train 15 0 ± 1 (2 to 2) 1 ± 1 (4 to 0) 0.97 0.018
ΔMuscle soreness 16 3 ± 3 (5 to 8) 3 ± 3 (2 to 8) 0.03 0.882
ΔMuscle tiredness 16 4 ± 4 (4 to 11) 4 ± 3 (0 to 12) 0.02 0.834
ΔResting HR (bpm) 16 1 ± 6 (10 to 12) 1 ± 8 (12 to 12) 0.10 0.734
ΔResting SBP (mmHg) 16 10 ± 6 (19 to 1) 4 ± 8 (19 to 10) 0.96 0.012
ΔResting DPB (mmHg) 16 2 ± 8 (14 to 18) 3 ± 6 (14 to 7) 0.05 0.845
Author's personal copy
704 Eur J Appl Physiol (2017) 117:699–712
1 3
averaged and the following outcome variables obtained:
bed time, wake-up time, time-in-bed (TIB, h), total sleep
time (TST, h), sleep onset latency (SOL, min), sleep
eciency (SE, %), wake-after sleep onset time (WASO,
min) and number of awakenings (count). These data
(USUAL) are presented in Table2.
Participants slept in a sound- and light-proof sleep lab-
oratory following the HIIT sessions. Between the end of
the HIIT session and bed time in both the DEP and CON
conditions, participants showered, ate dinner (±20:00) and
were then allowed to either read, watch TV or make use of
their laptops in the sleep laboratory lounge. They were not
permitted to recline or rest in their beds, and were in the
company of the investigator at all times to ensure they did
not fall asleep. Participants undertook these same activities
in the period between wake-up time and the start of ses-
sions 3 or 6 in the DEP condition.
Bed time and wake-up time during the control night
(CON) replicated their USUAL sleep habits. Participants
wore the wrist actigraph during the CON and DEP nights
to confirm sleep timing and length. There were no dier-
ences in any of the sleep variables between the USUAL and
CON nights (Table2).
For the partial sleep deprivation (DEP) night participants
were allowed only half of their usual time-in-bed. Thus
mean required TIB during the DEP night was calculated to
be 3.77 ± 0.35h and mean TST 3.38 ± 0.23h. The precise
bed time and wake-up time for each participant was deter-
mined individually based on his USUAL TIB, and mid-
point of sleep during the DEP night was matched to that of
USUAL sleep by delaying bed time and advancing wake-
up time. The actigraphy data for the DEP night (Table2)
indicate that actual TIB (p = 0.602) and TST (p = 0.623)
were not dierent to the required times. Furthermore, SE
(p = 0.386) and SOL (p = 0.522) were also similar between
the USUAL and DEP nights, while the cyclists had reduced
WASO time (p < 0.001) and fewer awakenings (p < 0.001)
on the DEP night. Together these data suggest that the par-
ticipants obtained the required sleep durations on the CON
and DEP nights and that the quality was similar to their
usual sleep.
Data andstatistical analyses
Data are expressed as mean ± standard deviation or median
with interquartile range. Time data are represented as
h:min. Normality was confirmed using the Shapiro–Wilks
test and homogeneity of variance using Levene’s test.
Paired t tests or Wilcoxon signed-rank tests were used to
compare single variables between the DEP and CON condi-
tions. A two-way analysis of variance with repeated meas-
ures was used to compare dierences between conditions
in variables measured before and 24h after the HIIT ses-
sion. Eect sizes were calculated using Cohen’s d, where
d < 0.2 was considered trivial, 0.20–0.39 small, 0.40–0.79
moderate and >0.80 large. 12 and 24h measurements
Fig. 2 Individual changes in sleepiness (a), motivation to train (b)
and resting systolic blood pressure (c) from Pre to 12h after the
HIIT session under the CON and DEP conditions. Each data point
represents an individual’s response to the HIIT session (12h minus
Pre), expressed as percentage change. Open and closed circles rep-
resent the normal sleep (CON) and partial sleep deprivation (DEP)
conditions, respectively. The dotted line at y = 0 represents no change
in the variable measured before and 12h after the HIIT session (i.e.
0% change). The slope of the connecting line indicates the extent to
which the change in a variable after HIIT was dierent in the DEP
compared to the CON condition, in one individual. SBP systolic
blood pressure, Pre prior to the HIIT session, 12h 12h after the HIIT
session. Significance was determined using a paired t test. Cohen’s d
indicates eect size
Author's personal copy
705Eur J Appl Physiol (2017) 117:699–712
1 3
were analysed separately to minimise misinterpretation
of data due to circadian variation in physiology. Measure-
ments taken 12h after the HIIT session were obtained in
the morning (±06:30) and therefore were not directly com-
parable to those measured immediately before the HIIT
session (±17:30). Therefore, 12h data are expressed as
changes from baseline (pre HIIT), and these changes are
compared between conditions. Since the pre HIIT and 24h
variables were taken at the same time-of-day (±17:30),
they were compared directly. Correlations were performed
using Pearson’s product moment test and Spearman’s rank
correlation tests. Taking into account that (1) the typi-
cal error of measurement of the PPO test is 1% (Lamberts
2009), (2) the expected relative PPO in trained athletes is
5Wkg1 (Capostagno etal. 2014), and (3) sleep depriva-
tion may reduce aerobic performance by 3% (Oliver etal.
2009), sample size was estimated based on an expected dif-
ference in change of peak power output between the two
conditions of 4% (0.2 ± 0.1Wkg1). For an α level of 0.05
and a power of 95%, 15 participants were required. Data
were analysed using Stata (v12, StataCorp, TX, USA). Sig-
nificance was accepted when p 0.05.
Results
Ecacy oftheHIIT session
Participants reported similar amounts of sleep (CON
7.59 ± 1.10h, DEP 7.88 ± 0.98h, p = 0.244) and had
similar weights (CON 77.4 ± 9.5kg, DEP 78.3 ± 9.4kg,
p = 0.369) prior to the HIIT sessions. Twenty-four-hours
after the HIIT session under the CON condition, cyclists
felt less motivated to train (p < 0.034, d = 2.07), reported
more muscle soreness (p = 0.014, d = 3.07) and tiredness
(p < 0.001, d = 5.09) and had lower resting SBP (p = 0.011,
d = 0.85), absolute PPO (p = 0.012, d = 0.44), and HRmax
(p < 0.001, d = 2.00) values. Collectively these data suggest
that the HIIT session disturbed the cyclists’ physiology,
producing a stimulus from which they needed to recover.
Eects ofpartial sleep deprivation onrecovery
fromexercise
Twelve hours after the HIIT session, participants were
sleepier (p = 0.001), felt less motivated to train (p = 0.018)
and demonstrated a blunted reduction in SBP (p = 0.012)
under the DEP condition compared to the CON condition
(Table3). Figure2 shows the individual 12h responses,
where data are expressed as percentage change (i.e. 12h
value minus Pre value) for the CON (open circles) and DEP
(closed circles) conditions. Compared to before the HIIT
session, all but two participants reported feeling sleepier
12h after the HIIT session in the DEP condition compared
to the CON condition (Fig.2a). Ten participants felt less
motivated to train after the HIIT under the DEP condi-
tion compared to the CON condition; for two cyclists the
change in motivation to train after the HIIT was the same
between conditions; and another two felt more motivated to
train 12h after the HIIT in the DEP condition compared
to the CON condition (Fig.2b). Twelve participants expe-
rienced a smaller reduction or even increase in SBP 12h
after the HIIT under the DEP condition, while four showed
larger reductions in SBP under the DEP condition (Fig.2c).
Twenty-four hour responses to the HIIT session are pre-
sented in Table4 and Figs.3 and 4. Dierences between
the conditions in sleepiness (p = 0.004) and SBP (p = 0.043)
persisted 24h after the HIIT session, accompanied by
Table 4 Twenty-four-hour responses to the HIIT session under the CON and DEP conditions
Data are presented as mean ± SD, (range)
CON control sleep condition, DEP partial sleep deprivation condition, HIIT high-intensity interval training, Pre prior to the HIIT session, 24h
24h after the HIIT session, HR heart rate, SBP systolic blood pressure, DBP diastolic blood pressure, PPO peak power output
The p value represents the time-by-condition interaction eect as determined using a two-way ANOVA with repeated measures. Cohen’s d indi-
cates eect size
nCON DEP d p value
Pre 24h Pre 24h
Sleepiness 16 5 ± 4 (0–14) 7 ± 3 (2–12) 6 ± 3 (2–13) 12 ± 6 (2–23) 1.41 0.004
Motivation to train 15 7 ± 2 (3–10) 6 ± 2 (2–10) 7 ± 1 (6–10) 5 ± 2 (2–8) 0.74 0.128
Muscle soreness 16 4 ± 3 (0–11) 7 ± 5 (0–19) 4 ± 3 (0–11) 7 ± 5 (0–15) 0.15 0.873
Muscle tiredness 16 5 ± 4 (1–13) 10 ± 5 (3–21) 5 ± 4 (0–14) 11 ± 5 (3–21) 0.29 0.344
Resting HR (bpm) 16 59 ± 6 (46–70) 58 ± 8 (46–78) 59 ± 7 (51–70) 60 ± 7 (50–74) 0.27 0.395
Resting SBP (mmHg) 16 128 ± 8 (106–138) 121 ± 8 (112–141) 127 ± 11 (100–146) 127 ± 9 (113–145) 0.75 0.043
Resting DBP (mmHg) 16 72 ± 9 (54–87) 70 ± 8 (59–88) 73 ± 7 (59–83) 71 ± 8 (58–83) 0.04 0.906
Absolute PPO (W) 16 352 ± 44 (291–424) 347 ± 40 (285–413) 355 ± 38 (295–423) 337 ± 36 (280–411) 1.98 0.004
Author's personal copy
706 Eur J Appl Physiol (2017) 117:699–712
1 3
Author's personal copy
707Eur J Appl Physiol (2017) 117:699–712
1 3
a time-by-condition interaction eect for absolute PPO
(p = 0.004, d = 1.98, Table4). Individual responses for
relative PPO, sleepiness, motivation to train and SBP are
plotted in Fig.3. The left hand panel shows the absolute
data for the Pre, 12h and 24h time points, and the right
hand panel shows the 24h percentage change in the vari-
able (i.e. 24h value minus Pre value) for the CON (open
circles) and DEP (closed circles) conditions.
Relative PPO was lower 24h after the HIIT session
under the DEP condition compared to the CON condition
(p = 0.005, d = 1.89, Fig.3a). Relative PPO was lower
24h after the HIIT session under the DEP condition com-
pared to the CON condition (p = 0.005, d = 1.89, Fig.3a).
As indicated by the slope of the connecting line in Fig.3b,
12 cyclists had greater reductions in relative PPO 24h
after the HIIT session under the DEP condition compared
to the CON condition, three had greater reductions under
the CON compared to the DEP condition and for one the
reduction in PPO was not dierent between the conditions
(Fig.3b). As indicated by the slope of the connecting line
in Fig.3d, 15 cyclists were sleepier 24h after the HIIT ses-
sion under the DEP compared to the CON condition, while
one was less sleepy 24h after the DEP compared to the
CON condition (Fig.3d). All but three cyclists had smaller
reductions or even increases in SBP 24h after the HIIT ses-
sion under the DEP condition compared to the CON con-
dition (Fig.3h). Motivation to train was no longer dier-
ent between the groups (d = 0.74, Table4). Sleep duration
was correlated with change in relative PPO, but was not
significant for either condition (CON: r = 0.21, p = 0.457,
n = 16; DEP: r = 0.42, p = 0.119, n = 16).
Individual responses for HRmax, VO2max and RERmax
reached during the PPO are plotted in Fig.4. As for Fig.3,
the left hand panel shows the absolute data and the right
hand panel shows the 24h percentage change in the
variable. The extent to which HRmax was reduced at 24h
was not dierent between conditions (Fig.4a), (d = 0.81).
For all but three of the cyclists HRmax was lower during
the PPO completed 24h after the HIIT compared to before
(Pre) under the DEP condition compared to the CON con-
dition (Fig.4b). Neither VO2max nor RERmax changed
dierently in the DEP compared to the CON condition
(Fig.4c, e, respectively), and the individual responses were
varied (Fig.4d, f, respectively).
The cyclists had similar changes in CK activity, sIgA
secretion rate and leukocyte cell counts at 12 and 24h
after the HIIT session under both sleep conditions (Online
Resource 1, FiguresS1 and S2, Tables S1 and S2, respec-
tively). Time eects indicated that WBC (p = 0.020) and
neutrophil (p < 0.001) counts were lower and basophil
counts (p < 0.001) higher 24h after the HIIT session.
Discussion
Athletes have identified sleep as an important recovery
strategy (Venter 2014; Kölling etal. 2016; Fullagar etal.
2016). This study provides some support for this concept.
The main finding was that peak power output was reduced
to a larger extent 24h after the HIIT session when cyclists
were partially sleep deprived compared to having had a
normal night of sleep. In addition, the cyclists reported
higher levels of sleepiness and less motivation to train,
and the HIIT-induced reduction in resting systolic blood
pressure the following day was blunted in the partial sleep
deprivation condition. Collectively these data suggest that
recovery from a HIIT session is compromised when fol-
lowed by a single night of partial sleep deprivation, and
that a night of normal sleep facilitates near full recovery in
maximal performance capacity.
The extent to which relative peak power was decreased
following the HIIT session in the DEP condition was 5%,
compared to a reduction of only 1% in the CON condition.
Alternatively, a normal night of sleep following HIIT may
facilitate up to 99% of recovery from the training stimu-
lus, while one night of partial sleep deprivation may limit
this recovery to approximately 95%. Laboratory measure-
ment of peak power output is routinely used to assess per-
formance in cycling since it is well correlated with time-
trial performance (Hawley and Noakes 1992). In terms of
performance amongst elite cyclists, where a 1% alteration
in performance is considered to be important (Currell and
Jeukendrup 2008), the observed 5% reduction appears to be
meaningful.
The variation in the extent to which peak power was
aected in the recovery phase of the HIIT session under the
partial sleep deprivation condition demonstrates individual
sensitivity of physical performance to sleep loss. Twelve of
Fig. 3 Individual peak power output (a, b), sleepiness (c, d), motiva-
tion to train (e, f) and resting systolic blood pressure (g, h) responses
to the HIIT session under the CON and DEP conditions. In the left
panel (a, c, e, g), individual raw data are plotted for the pre HIIT,
12 and 24h time points. The 12h data are for visual purposes, and
are not included in the statistical analysis. The right panel (b, d, f,
h) compares individual responses to each condition, where each data
point represents an individual’s response to the HIIT session (24h
minus Pre), expressed as percentage change. Open and closed circles
represent the normal sleep (CON) and partial sleep deprivation (DEP)
conditions, respectively. The dotted line at y = 0 (right panel) repre-
sents no change in the variable measured before and 24h after the
HIIT session (i.e. 0% change). The slope of the connecting line indi-
cates the extent to which the change in a variable after HIIT was dif-
ferent in the DEP compared to the CON condition, in one individual.
PPO peak power output, DBP systolic blood pressure, Pre prior to
the HIIT session, 12h 12h after the HIIT session, 24h 24h after the
HIIT session. Significance was determined using a two-way ANOVA
with repeated measures (left panel) and a dependent t test (right
panel). Cohen’s d indicates eect size
Author's personal copy
708 Eur J Appl Physiol (2017) 117:699–712
1 3
the 16 cyclists had greater reductions in peak power when
partially sleep deprived, one experienced similar levels
of power reduction between the two conditions, and one
showed a smaller power decrement after partial sleep dep-
rivation and two actually showed improvements in power
after the sleep deprivation intervention.
Possible explanations for dierences in susceptibility
to sleep deprivation and the ensuing influence on maxi-
mal performance may relate to chronotype or habitual bed
times or sleep lengths (Taillard etal. 2003). For example,
evening-types may cope better with sleep deprivation com-
pared to morning-types (Taillard etal. 2011; Barclay and
Myachykov 2016). Individuals with a large sleep debt may
appear to be less susceptible to the eects of one night of
partial sleep deprivation, as their baseline performance
may be impaired by their sleep debt. Change in relative
peak power under the CON and DEP conditions were cor-
related against chronotype score, usual bed time and total
sleep duration, however, no significant relationships were
observed (data not shown). One explanation for this may
be that these cyclists were more morning-oriented than the
general South African population (Kunorozva etal. 2012;
Henst etal. 2015) and lacked any evening-types. Thus the
potentially moderating role of chronotype on sleep depriva-
tion and the ensuing recovery could not be assessed. Future
work would need to be done in this area to test this concept.
The 24h reduction in peak power observed in both con-
ditions occurred in the absence of any change in VO2max.
This suggests a dissociation between VO2max and peak
power, and potentially a lower gross eciency (Noordhof
etal. 2010) 24h after the HIIT session; an eect which
was not altered by recovery sleep length. Neither did sleep
length appear to moderate the reduction in maximum RER
observed 24h after the HIIT session. Together these data
suggest that any perturbances to the metabolic system
induced by the HIIT were able to recover similarly regard-
less of sleep length.
An acute, exhausting bout of exercise, such as HIIT, is
understood to both increase blood volume (Convertino
1991) and alter the sympathovagal balance in favour of
the parasympathetic system (Bellenger etal. 2016). Thus
when physically tired or unrecovered individuals exercise
maximally, they typical reach lower maximum heart rates
(Le Meur etal. 2013), indicative of reduced sympathetic
drive. The reductions of resting SBP and maximum heart
observed in the HIIT recovery phase following normal
sleep in the present study are understood to reflect these
changes, and have been shown previously (Tochikubo etal.
1996).
In the partial sleep deprivation condition, however, the
HIIT-induced reduction in resting SBP did not occur. In
contrast to a fatiguing bout of exercise, acute sleep dep-
rivation is thought to increase sympathetic and decrease
parasympathetic contributions to cardiovascular modula-
tion (Zhong 2005). One of the ways in which this could
manifest is via an increase in resting SBP the day after sleep
deprivation (Lusardi etal. 1996). Therefore, one might
hypothesise that the smaller post-HIIT session reduction
in resting SBP pressure observed in this study under the
DEP condition suggests that any exercise-induced increase
in parasympathetic activity may have been marginalised
by the sleep deprivation-induced increase in sympathetic
activity. Future research investigating the potential role of
the autonomic nervous system on physical recovery in the
sleep deprived state is warranted.
Both intense exercise in athletes and sleep deprivation
are understood to decrease innate and acquired immunity
(Faraut etal. 2012; Walsh and Oliver 2016). Although this
study observed some blood leukocyte changes 24h after the
HIIT, likely representative of tracking (Dhabhar 2002),
the extent to which this occurred was not dierent between
the conditions. Therefore perturbation of the immune sys-
tem does not appear to have a role in recovery from a single
bout of HIIT under a condition of partial sleep deprivation.
Although not measured in this study, the longer term
consequences of repeated nights of partial sleep depriva-
tion on recovery should be considered. Not only could
adaptation to training be compromised, but repeated train-
ing sessions with insucient sleep in the recovery phase
may increase the risk for non-functional overreaching and
ultimately overtraining (Lehmann etal. 1997). To improve
performance, athletes finely balance training stimulus with
recovery; since increasing training load elicits a greater
adaptation (functional overreaching), while insucient
recovery results in a maladaptive response (non-functional
overreaching) (Meeusen etal. 2013). Longer term non-
functional overreaching is understood to eventually lead
to a state of overtraining, in which accumulated train-
ing stresses result in long term performance decrements
and fatigue, recovery from which may take several weeks
(Meeusen etal. 2013). The data from this study suggest
that inadequate sleep following a single high load training
session increases the time needed to recover. Therefore,
one might speculate that regular short sleep patterns dur-
ing high load training periods may result in non-functional
overreaching. In contrast, athletes with sucient sleep
during such periods may be more likely to remain in the
functional overreaching zone, maximising adaptation to
training.
A limitation to this study is that neither heart rate vari-
ability nor catecholamine levels were measured to assess
alterations in autonomic nervous system function. Fur-
thermore, given the relatively small sample size, and fairly
large variation in ability of these cyclists, the results need to
be interpreted with caution. Another limitation is that two
of the participants consumed one caeine beverage each in
Author's personal copy
709Eur J Appl Physiol (2017) 117:699–712
1 3
Fig. 4 Individual maximum heart rate (a, b), oxygen uptake (c, d)
and respiratory exchange ratio (e, f) responses to the HIIT session
under the CON and DEP conditions. In the left panel (a, c, e), indi-
vidual raw data are plotted for the pre HIIT and 24h time points.
The right panel (b, d, f) compares individual responses to each con-
dition, where each data point represents an individual’s response to
the HIIT session (24h minus Pre), expressed as percentage change.
Open and closed circles represent the normal sleep (CON) and par-
tial sleep deprivation (DEP) conditions, respectively. The dotted line
at y = 0 (right panel) represents no change in the variable measured
before and 24h after the HIIT session (i.e. 0% change). The slope
of the connecting line indicates the extent to which the change in a
variable after HIIT was dierent in the DEP compared to the CON
condition, in one individual. HRmax maximum heart rate, VO2max max-
imum oxygen uptake volume, RERmax maximum respiratory exchange
ratio, Pre prior to the HIIT session, 24h 24h after the HIIT session.
Significance was determined using a two-way ANOVA with repeated
measures (left panel) and a dependent t-test (right panel). Cohen’s d
indicates eect size
Author's personal copy
710 Eur J Appl Physiol (2017) 117:699–712
1 3
the 24h period prior to their Baseline session, following
which they were partially sleep deprived. Ingested caeine
may enhance physical performance, although the eects are
varied and depend on factors such as dose, form, individual
tolerance to caeine and type of exercise performed (Rog-
ers and Dinges 2005; Spriet 2014). Therefore the baseline
performance of these two athletes may have been artifi-
cially raised. The performance analysis for this study was
repeated excluding these two individuals, but the results
for peak and absolute power remained the same (data not
shown). Although individuals with diagnosed sleep disor-
ders were excluded from this study, the WASO and num-
ber of awakenings measured using the Actiwatch during the
participant’s usual sleep are higher than expected. While
these data cannot be used diagnostically, it is possible that
some of these individuals may have had an undiagnosed
sleep disorder. Alternatively, these variables measured with
the Actiwatch are not directly comparable to those obtained
using polysomnography.
Conclusions
While there is a significant body of work describing the
eects of sleep deprivation on physical performance, few
studies have investigated the consequences of limited sleep
on recovery from exercise. This study confirms a role for
sleep in recovery from training and contributes to our
understanding of the physiological eects of partial sleep
deprivation on recovery. It diers from and is complemen-
tary to previous similar studies (McMurray and Brown
1984; Skein etal. 2013) in that it used a model of partial
sleep deprivation for only one night and tested endurance
sports athletes recovering from a single training session.
From the perspective of athletes and coaches, these
data suggest that recovery of the systems needed to pro-
duce maximal eorts is incomplete when an athlete does
not obtain a full night of sleep following a HIIT session.
The consequence of this may be that if a training session is
scheduled for the following day, the athlete may not be able
to work at a high intensity. In part, this may be reinforced
by the athlete’s lower level of motivation to train follow-
ing sleep restriction. In periods of training where intensity
is more important than duration, an inability to train at the
prescribed intensity may mean that a lower training stimu-
lus is applied, and as a consequence, the level of adaptation
induced might be lower.
• Future research in this area could investigate individual
sensitivity to sleep deprivation on recovery, paying par-
ticular attention to the role of chronotype. Given that
there is some evidence to suggest that a number of ath-
letes suer from poor quality sleep, the eect of frag-
mented sleep on recovery deserves attention. Finally, it
remains to be determined whether or not chronic insu-
cient sleep in the recovery phase of training predisposes
an athlete to worsened performance or non-functional
overreaching.
Acknowledgements Thanks to the cyclists for volunteering; Hendr-
iena Victor, David Leith and Chris Webster for help with data collec-
tion; and Mike Lambert for input into the study design. This study
was funded through a Research Development Grant from the Univer-
sity of Cape Town (DER), South African National Research Founda-
tion Incentive Funding for Rated Researchers (AJM and TAK), and
TAK is a recipient of the Tim and Marilyn Noakes Sports Science
Postdoctoral Fellowship.
Compliance with ethical standards
Conflict of interest The authors have no conflicts of interest to de-
clare.
References
Akerstedt T, Nilsson PM (2003) Sleep as restitution: an introduction.
J Int Med 254:6–12
Barclay NL, Myachykov A (2016) Sustained wakefulness and
visual attention: moderation by chronotype. Exp Brain Res.
doi:10.1007/s00221-016-4772-8
Beelen M, Burke LM, Gibala MJ, van Loon L JC (2010) Nutritional
strategies to promote postexercise recovery. Int J Sport Nutr
Exerc Metab 20:515–532
Bellenger CR, Fuller JT, Thomson RL, etal (2016) Monitoring ath-
letic training status through autonomic heart rate regulation: a
systematic review and meta-analysis. Sports Med 46:1461–1486.
doi:10.1007/s40279-016-0484-2
Bergeron MF, Mountjoy M, Armstrong N etal (2015) Interna-
tional Olympic Committee consensus statement on youth ath-
letic development. Br J Sports Med 49:843–851. doi:10.1136/
bjsports-2015-094962
Borg G (1998) Borg’s perceived exertion and pain scales. Human
Kinetics, Champaign
Buysse DJ, Reynolds CF, Monk TH etal (1989) The Pittsburgh Sleep
Quality Index: a new instrument for psychiatric practice and
research. Psychiatry Res 28:193–213
Capostagno B, Lambert MI, Lamberts RP (2014) Standardized ver-
sus customized high-intensity training: eects on cycling per-
formance. Int J Sports Physiol Perform 9:292–301. doi:10.1123/
IJSPP.2012-0389
Convertino VA (1991) Blood volume: its adaptation to endurance
training. Med Sci Sport Exerc 23:1338–1348.
Currell K, Jeukendrup AE (2008) Validity, reliability and sensitivity
of measures of sporting performance. Sports Med 38:297–316
Dattilo M, Antunes HKM, Medeiros A etal (2011) Medical
hypotheses. Med Hypotheses 77:220–222. doi:10.1016/j.
mehy.2011.04.017
Dhabhar FS (2002) Stress-induced augmentation of immune func-
tion–the role of stress hormones, leukocyte tracking, and
cytokines. Brain Behav Immun 16:785–798
Faraut B, Boudjeltia KZ, Vanhamme L, Kerkhofs M (2012)
Immune, inflammatory and cardiovascular consequences of
Author's personal copy
711Eur J Appl Physiol (2017) 117:699–712
1 3
sleep restriction and recovery. Sleep Med Rev 16:137–149.
doi:10.1016/j.smrv.2011.05.001
Fullagar HHK, Skorski S, Dueld R etal (2016) Impaired sleep and
recovery after night matches in elite football players. J Sport Sci
34:1333–1339. doi:10.1080/02640414.2015.1135249
Gupta L, Morgan K, Gilchrist S (2016) Does elite sport degrade
sleep quality? A systematic review. Sports Med. doi:10.1007/
s40279-016-0650-6
Hawley JA, Noakes TD (1992) Peak power output predicts maximal
oxygen uptake and performance time in trained cyclists. Eur J
Appl Physiol Occup Physiol 65:79–83.
Heinonen I, Kalliokoski KK, Hannukainen JC etal (2014) Organ-spe-
cific physiological responses to acute physical exercise and long-
term training in humans. Physiology 29:421–436. doi:10.1152/
physiol.00067.2013
Henst RHP, Jaspers RT, Roden LC, Rae DE (2015) A chronotype
comparison of South African and Dutch marathon runners: The
role of scheduled race start times and eects on performance.
Chronobiol Int 32:858–868. doi:10.3109/07420528.2015.10488
70
Horne JA, Östberg O (1976) A self-assessment questionnaire to deter-
mine morningness-eveningness in human circadian rhythms. Int
J Chronobiol 4:97–110
Johns MW (1991) A new method for measuring daytime sleepiness:
the Epworth sleepiness scale. Sleep 14:540–545
Kölling S, Steinacker JM, Endler S etal (2016) The longer the bet-
ter: sleep–wake patterns during preparation of the World Rowing
Junior Championships. Chronobiol Int 33:73–84. doi:10.3109/07
420528.2015.1118384
Kunorozva L, Stephenson KJ, Rae DE, Roden LC (2012) Chronotype
and PERIOD3 variable number tandem repeat polymorphism in
individual sports athletes. Chronobiol Int 29:1004–1010. doi:10.
3109/07420528.2012.719966
Lamberts R (2009) Measurement error associated with performance
testing in well-trained cyclists: application to the precision of
monitoring changes in training status. Int Sport Med J 10:33–44.
Lamberts RP, Swart J, Noakes TD, Lambert MI (2011) A novel
submaximal cycle test to monitor fatigue and predict cycling
performance. Br J Sports Med 45:797–804. doi:10.1136/
bjsm.2009.061325
Le Meur Y, Hausswirth C, Natta F etal (2013) A multidisci-
plinary approach to overreaching detection in endurance
trained athletes. J Appl Physiol 114:411–420. doi:10.1152/
japplphysiol.01254.2012
Lehmann MJ, Lormes W, Opitz-Gress A etal (1997) Training and
overtraining: an overview and experimental results in endurance
sports. J Sports Med Phys Fitness 37:7–17
Lusardi P, Mugellini A, Preti P etal (1996) Eects of a restricted
sleep regimen on ambulatory blood pressure monitoring in nor-
motensive subjects. Am J Hypertens 9:503–505
MacRae BA, Cotter JD, Laing RM (2011) Compression gar-
ments and exercise: garment considerations, physi-
ology and performance. Sports Med 41:815–843.
doi:10.2165/11591420-000000000-00000
McKune AJ, Smith LL, Semple SJ etal (2006) Changes in mucosal
and humoral atopic-related markers and immunoglobulins in
elite cyclists participating in the Vuelta a España. Int J Sports
Med 27:560–566. doi:10.1055/s-2005-865858
McMurray RG, Brown CF (1984) The eect of sleep loss on high
intensity exercise and recovery. Aviat Space Environ Med
55:1031–1035
Meeusen R, Duclos M, Foster C, etal (2013) Prevention, diagnosis,
and treatment of the overtraining syndrome: joint consensus
statement of the European College of Sport Science and the
American College of Sports Medicine. Med Sci Sport Exerc
45:186–205. doi:10.1249/MSS.0b013e318279a10a
Noordhof DA, de Koning JJ, van Erp T etal (2010) The between
and within day variation in gross eciency. Eur J Appl Physiol
109:1209–1218. doi:10.1007/s00421-010-1497-4
Oliver SJ, Costa RJS, Laing SJ etal (2009) One night of sleep dep-
rivation decreases treadmill endurance performance. Eur J
Appl Physiol 107:155–161. doi:10.1007/s00421-009-1103-9
Poppendieck W, Faude O, Wegmann M, Meyer T (2013) Cooling
and performance recovery of trained athletes: a meta-analyti-
cal review. Int J Sports Physiol Perform 8:227–242
Reilly T, Ekblom B (2007) The use of recovery methods post-exer-
cise. J Sport Sci 23:619–627. doi:10.1080/02640410400021302
Reilly T, Piercy M (1994) The eect of partial sleep deprivation
on weight-lifting performance. Ergonomics 37:107–115.
doi:10.1080/00140139408963628
Rogers NL, Dinges DF (2005) Caeine: implications for alert-
ness in athletes. Clin Sports Med 24:e1–e13. doi:10.1016/j.
csm.2004.12.012
Ruiz FS, Andersen ML, Martins RCS etal (2012) Immune altera-
tions after selective rapid eye movement or total sleep depri-
vation in healthy male volunteers. Innate Immun 18:44–54.
doi:10.1177/1753425910385962
Sargent C, Halson S, Roach GD (2013) Sleep or swim? Early-morn-
ing training severelyrestricts the amount of sleep obtained by
elite swimmers. Eur J Sport Sci 14:S310–S315. doi:10.1080/1
7461391.2012.696711
Schaal K, Le Meur Y, Louis J, etal (2015) Whole-body cry-
ostimulation limits overreaching in elite synchronized swim-
mers. Med Sci Sport Exerc 47:1416–1425. doi:10.1249/
MSS.0000000000000546
Scott JPR, McNaughton LR, Polman RCJ (2006) Eects of
sleep deprivation and exercise on cognitive, motor perfor-
mance and mood. Physiol Behav 87:396–408. doi:10.1016/j.
physbeh.2005.11.009
Skein M, Dueld R, Minett GM etal (2013) The eect of over-
night sleep deprivation after competitive rugby league matches
on postmatch physiological and perceptual recovery. Int J
Sports Physiol Perform 8:556–564
Souissi N, Sesboüé B, Gauthier A etal (2003) Eects of one
night’s sleep deprivation on anaerobic performance the fol-
lowing day. Eur J Appl Physiol 89:359–366. doi:10.1007/
s00421-003-0793-7
Spriet LL (2014) Exercise and sport performance with low
doses of caeine. Sports Med 44:175–184. doi:10.1007/
s40279-014-0257-8
Swinbourne R, Gill N, Vaile J, Smart D (2015) Prevalence of poor
sleep quality, sleepiness and obstructive sleep apnoea risk factors
in athletes. Eur J Sport Sci 1–9. doi:10.1080/17461391.2015.11
20781
Taillard J, Philip P, Coste O etal (2003) The circadian and homeo-
static modulation of sleep pressure during wakefulness dif-
fers between morning and evening chronotypes. J Sleep Res
12:275–282
Taillard J, Philip P, Claustrat B etal (2011) Time course of neurobe-
havioral alertness during extended wakefulness in morning- and
evening-type healthy sleepers. Chronobiol Int 28:520–527. doi:1
0.3109/07420528.2011.590623
Temesi J, Arnal PJ, Davranche K etal (2013) Does central
fatigue explain reduced cycling after complete sleep depri-
vation? Med Sci Sport Exerc 45:2243–2253. doi:10.1249/
MSS.0b013e31829ce379
Tochikubo O, Ikeda A, Miyajima E, Ishii M (1996) Eects of insu-
cient sleep on blood pressure monitored by a new multibiomedi-
cal recorder. Hypertension 27:1318–1324
Van Cauter E, Spiegel K, Tasali E, Leproult R (2008) Metabolic con-
sequences of sleep and sleep loss. Sleep Med 9(Suppl 1):S23–
S28. doi:10.1016/S1389-9457(08)70013-3
Author's personal copy
712 Eur J Appl Physiol (2017) 117:699–712
1 3
Venter RE (2014) Perceptions of team athletes on the importance of
recovery modalities. Eur J Sport Sci 14(Suppl 1):S69–S76. doi:1
0.1080/17461391.2011.643924
Walsh NP, Oliver SJ (2016) Exercise, immune function and respira-
tory infection: An update on the influence of training and envi-
ronmental stress. Immunol Cell Biol 94:132–139. doi:10.1038/
icb.2015.99
Zhong X (2005) Increased sympathetic and decreased parasympa-
thetic cardiovascular modulation in normal humans with acute
sleep deprivation. J Appl Physiol 98:2024–2032. doi:10.1152/
japplphysiol.00620.2004
Author's personal copy
... 14 Laboratory studies have shown that acute total sleep deprivation (i.e., no sleep for a whole night) or severe sleep restriction impairs muscle recovery as a result of sleep debt's effects on catabolic and anabolic hormones. 5,6,15 In addition, sleep deficit may increase circulating markers of inflammation. 5 Besides health, it is well documented that either acute sleep deprivation or acute severe sleep restriction can significantly compromise human performance the subsequent day in exercise tasks requiring skill, anaerobic power, strength, and endurance. ...
... It is known, for instance, that a single night of sleep deprivation increases resting blood interleukin-6 concentration the following day. 15 Accordingly, acute or sustained sleep deprivation has been shown to impair exercise performance and muscle recovery, 15 and to modify inflammatory and hormonal markers following training. Notably, however, in most of these studies, the subjects employed were not athletes, making implementation of the results in sport settings challenging. ...
... It is known, for instance, that a single night of sleep deprivation increases resting blood interleukin-6 concentration the following day. 15 Accordingly, acute or sustained sleep deprivation has been shown to impair exercise performance and muscle recovery, 15 and to modify inflammatory and hormonal markers following training. Notably, however, in most of these studies, the subjects employed were not athletes, making implementation of the results in sport settings challenging. ...
... Indeed, important physical (endurance performance, anaerobic capacity and strength) and cognitive aspects of performance have been shown to decrease following sleep loss (Abedelmalek et al., 2013;Hurdiel et al., 2014;Souissi et al., 2013). (Rae et al., 2017), has been observed in athletes following a night of partial sleep deprivation. Third, sleep loss may affect both the next-day well-being and sensation of effort (Cullen et al., 2020). ...
Article
Full-text available
Participation in many important sport events (e.g., World championships, Olympics) requires athletes to fly >4 h and to cross several time zones. This transmeridian travel results in a transient desynchronization of the body's circadian rhythms due to a disconnect between the timing of the endogenous circadian oscillator and the external stimuli, manifested as ‘jet lag’. While recent reviews highlight the importance of managing jet lag, the time required for resynchronization of the internal clock and dissipation of jet lag symptoms has not yet been summarized. Further, although the literature reports that rapid transmeridian travel is detrimental for athletes’ performance, empirical evidence from studies involving athletes is equivocal. Herein, we summarize the evidence that the variability in responses to transmeridian travel can be attributed to differences in (i) travel (real vs. simulated, westbound vs. eastbound, time zones crossed, during normal waking hours vs. normal sleep time), (ii) testing (assessment of performance vs. factors related to performance), and (iii) timing of the testing (destination time vs. ‘body time’), and we offer the possibility that differences in (iv) teams, (v) traits, and (vi) tournaments may also be implicated. We focus on (i) aerobic power/endurance, (ii) anaerobic power and capacity, (iii) strength, and (iv) mood state, sleep quantity and quality, and jet lag symptoms in this literature review, which is limited to athletes or physically active participants, travelling west or east crossing four or more time zones.
... Sleep loss, whether total sleep deprivation (TSD, >24-h awake) or the more common partial sleep deprivation (PSD, total sleep time per day reduced to only a few hours), negatively impacts exercise training quality, competition preparation, exercise performance, and exercise-induced recovery processes (e.g., impaired muscle damage and repair and/ or an increased exercise-induced inflammatory response) (Abedelmalek et al. 2013;Fullagar et al. 2016;Nédélec et al. 2015;Rae et al. 2017). PSD, which can occur due to a delayed onset of sleep or an earlier wake-up time, is particularly prevalent among athletes, often experienced before competition due to pre-game anxiety or travel schedules (Fullagar et al. 2015;Halson 2014). ...
Article
Full-text available
Introduction Whether acute caffeine supplementation can offset the negative effects of one-night of partial sleep deprivation (PSD) on endurance exercise performance is currently unknown. Methods Ten healthy recreational male runners (age: 27 ± 6 years; V˙O2max{\dot{\text{V}}\text{O}}_{2\,\max }: 61 ± 9 mL/kg/min) completed 4 trials in a balanced Latin square design, which were PSD + caffeine (PSD-Caf), PSD + placebo (PSD-Pla), normal sleep (NS) + caffeine (NS-Caf) and NS + placebo (NS-Pla). 3 and 8 h sleep windows were scheduled in PSD and NS, respectively. 10-km treadmill time trial (TT) performance was assessed 45 min after caffeine (6 mg/kg/body mass)/placebo supplementation in the morning following PSD/NS. Blood glucose, lactate, free fatty acid and glycerol were measured at pre-supplementation, pre-exercise and after exercise. Results PSD resulted in compromised TT performance compared to NS in the placebo conditions by 5% (51.9 ± 7.7 vs. 49.4 ± 6.9 min, p = 0.001). Caffeine improved TT performance compared to placebo following both PSD by 7.7% (PSD-Caf: 47.9 ± 7.3 min vs. PSD-Pla: 51.9 ± 7.7 min, p = 0.007) and NS by 2.8% (NS-Caf: 48.0 ± 6.4 min vs. NS-Pla: 49.4 ± 6.9 min, p = 0.049). TT performance following PSD-Caf was not different from either NS-Pla or NS-Caf (p = 0.185 and p = 0.891, respectively). Blood glucose, lactate, and glycerol concentrations at post-exercise, as well as heart rate and the speed/RPE ratio during TT, were higher in caffeine trials compared to placebo. Conclusions Caffeine supplementation offsets the negative effects of one-night PSD on 10-km running performance.
... Despite limited experimental research on the topic, the available evidence consistently supports the importance of sleep for recovery from training. Multiple studies have found that performance markers (e.g., peak power output, countermovement jump distance) that are assessed following an intense training bout or match are impaired when the recovery period occurred under sleep restriction or deprivation, indicating incomplete recovery from the training bout (Chase et al., 2017;Rae et al., 2017;Skein et al., 2013). However, in most of these studies, maximal strength has not been impaired (Chase et al., 2017;Dáttilo et al., 2020;Skein et al., 2013). ...
Article
Full-text available
Background Sleep deprivation can significantly affect sports performance and the perception of fatigue. However, the impact of sleep deprivation on sports performance remains a subject of ongoing debate across different populations. Objectives This study aimed to investigate the effects of sleep deprivation on sports performance and ratings of perceived exertion (RPE) in different groups, as well as how different types of sleep deprivation affect these aspects. Methods This systematic review followed the PRISMA guidelines (PROSPERO CRD42023492792). Randomized controlled trials (RCTs) and randomized crossover studies published in any language or up to any date were eligible based on the P.I.C.O.S. criteria. The systematic search included databases such as PubMed, Cochrane, Embase, Web of Science, and EBSCO, covering studies up to September 2024. The Cochrane RoB 2 tool was used to assess the risk of bias. Meta-analysis was conducted using either a fixed-effect model or a random-effects model. This study conducted subgroup analyses based on different populations, types of sleep deprivation, and testing times. Results This review includes 45 studies, comprising 16 on aerobic endurance (AE) performance, 8 on anaerobic endurance (AnE) performance, 23 on explosive power (EP), 10 on maximum force (MF), 4 on speed, 4 on skill control, and 12 on rating of perceived exertion (RPE). The results indicate that sleep deprivation significantly impaired AE in athletes [SMD = −0.66; 95% CI (−1.28, −0.04); P = 0.04], as well as EP [SMD = −0.63; 95% CI (−0.94, −0.33); P < 0.00001], MF [SMD = −0.35; 95% CI (−0.56, −0.14); P = 0.001], speed [SMD = −0.52, 95% CI (−0.83, −0.22); P = 0.0008], skill control [SMD = −0.87; 95% CI (−1.7, −0.04); P = 0.04], and RPE [SMD = 0.39; 95% CI (0.11, 0.66); P = 0.006]. Additionally, AE was also reduced in healthy non-athletes [SMD = −1.02; 95% CI (−1.84, −0.21); P = 0.01]. During the sleep deprivation process, early sleep deprivation (PSDE) significantly reduced EP [SMD = −1.04; 95% CI (−1.58, −0.5); P = 0.0002], MF [SMD = −0.57; 95% CI (−0.94, −0.19); P = 0.003], speed [SMD = −0.78; 95% CI (−1.35, −0.2); P = 0.008], and RPE [SMD = 0.6; 95% CI (0.17, 1.02); P = 0.006]. Late sleep deprivation (PSDB) impacted speed [SMD = −0.57; 95% CI (−1.15, 0.01); P = 0.05], skill control [SMD = −2.12; 95% CI (−3.01, −1.24); P < 0.00001], and RPE [SMD = 0.47; 95% CI (0.02, 0.92); P = 0.04]. Overall, total sleep deprivation primarily affected AE [SMD = −0.56; 95% CI (−1.08, −0.05); P = 0.03]. In terms of testing phases, p.m. tests had a significant impact on AE [SMD = −1.4; 95% CI (−2.47, −0.34); P = 0.01], EP [SMD = −0.68; 95% CI (−1.06, −0.31); P = 0.0004], MF [SMD = −0.3; 95% CI (−0.51, −0.09); P = 0.005], skill control [SMD = −2.12; 95% CI (−3.01, −1.24); P < 0.00001], and RPE [SMD = 0.72; 95% CI (0.20, 1.24); P = 0.007]. In contrast, a.m. tests primarily affected speed [SMD = −0.81; 95% CI (−1.52, −0.1); P = 0.03] and RPE [SMD = 0.44; 95% CI (0.01, 0.86); P = 0.04]. Conclusion Sleep deprivation significantly impairs athletes' performance across various domains, including AE, MF, speed, and skill control, while also exacerbating RPE. In contrast, although sleep deprivation also negatively affects the AE of healthy non-athletes. Furthermore, PSDE appears to have a more pronounced effect on sports performance overall. Additionally, performance assessments conducted in the p.m. have been shown to further impact sports performance. These findings are crucial for understanding how sleep deprivation impacts both athletes and non-athletes, particularly in the context of training and competitive settings.
Article
Pulmonary rehabilitation is a comprehensive, interdisciplinary intervention that aims to enhance the physical and psychological well-being of individuals with chronic respiratory diseases. This approach entails the implementation of tailored therapies, including exercise training, education, and behavioral modification. Sleep plays a crucial role in numerous physiological processes, including the regulation of inflammation and tissue repair, both of which are fundamental to the efficacy of rehabilitation. A paucity of optimal sleep health has been associated with deleterious effects on pivotal factors that are indispensable for favorable outcomes in pulmonary rehabilitation, including mental and physical health and immune function. This, in turn, may increase susceptibility to impaired pulmonary function. The integration of pulmonary rehabilitation protocols with healthy sleep practices is expected to yield significant improvements in lung function and overall health, which will, in turn, promote long-term adherence to rehabilitative behaviors. This study aims to examine the relationship between sleep health and pulmonary rehabilitation outcomes.
Article
Full-text available
Physical activity is a meaningful part of life, which starts before birth and lasts until death. There are many health benefits to be derived from physical activity, hence, regular engagement is recommended on a weekly basis. However, these recommendations are often not met. This raises the question: when and why are people motivated to be physically active? Attempts to explain the motivation for physical activity (or lack thereof) have been the research interest for many years and disciplines. In this review, we provide evidence suggesting that physical activity behavior and the psycho-physiological foundations thereof are influenced by evolution, genetics, life stage, and the environment. The psycho-physiological foundations in turn comprise motivational and volitional factors as described in traditional psychological theories, psychological states and traits such as affective and stress reactions, as well as physiological states and systems (e.g. anatomical development and neural networks and transmitters). Importantly, physical activity elicits differential physiological responses and subjective experiences, which may impact future physical activity behavior and motivation. In summary, the interplay of psycho-physiological mechanisms and the importance of examining the ultimate mechanism for physical activity behavior are emphasized. The synthesis of knowledge provided in this review provides impetus for theory development and can facilitate the promotion of physically active lifestyles.
Article
Full-text available
Background Information on sleep quality and insomnia symptomatology among elite athletes remains poorly systematised in the sports science and medicine literature. The extent to which performance in elite sport represents a risk for chronic insomnia is unknown. Objectives The purpose of this systematic review was to profile the objective and experienced characteristics of sleep among elite athletes, and to consider relationships between elite sport and insomnia symptomatology. Methods Studies relating to sleep involving participants described on a pre-defined continuum of ‘eliteness’ were located through a systematic search of four research databases: SPORTDiscus, PubMed, Science Direct and Google Scholar, up to April 2016. Once extracted, studies were categorised as (1) those mainly describing sleep structure/patterns, (2) those mainly describing sleep quality and insomnia symptomatology and (3) those exploring associations between aspects of elite sport and sleep outcomes. ResultsThe search returned 1676 records. Following screening against set criteria, a total of 37 studies were identified. The quality of evidence reviewed was generally low. Pooled sleep quality data revealed high levels of sleep complaints in elite athletes. Three risk factors for sleep disturbance were broadly identified: (1) training, (2) travel and (3) competition. Conclusion While acknowledging the limited number of high-quality evidence reviewed, athletes show a high overall prevalence of insomnia symptoms characterised by longer sleep latencies, greater sleep fragmentation, non-restorative sleep, and excessive daytime fatigue. These symptoms show marked inter-sport differences. Two underlying mechanisms are implicated in the mediation of sport-related insomnia symptoms: pre-sleep cognitive arousal and sleep restriction.
Article
Full-text available
IntroductionAttentional networks are sensitive to sleep deprivation and increased time awake. However, existing evidence is inconsistent and may be accounted for by differences in chronotype or time-of-day. We examined the effects of sustained wakefulness over a normal “socially constrained” day (following 18 h of sustained wakefulness), following a night of normal sleep, on visual attention as a function of chronotype. Methods Twenty-six good sleepers (mean age 25.58; SD 4.26; 54 % male) completed the Attention Network Test (ANT) at two time points (baseline at 8 am; following 18-h sustained wakefulness at 2 am). The ANT provided mean reaction times (RTs), error rates, and the efficiency of three attentional networks—alerting, orienting, and executive control/conflict. The Morningness–Eveningness Questionnaire measured chronotype. ResultsMean RTs were longer at time 2 compared to time 1 for those with increasing eveningness; the opposite was true for morningness. However, those with increasing morningness exhibited longer RT and made more errors, on incongruent trials at time 2 relative to those with increasing eveningness. There were no significant main effects of time or chronotype (or interactions) on attentional network scores. Conclusion Sustained wakefulness produced differential effects on visual attention as a function of chronotype. Whilst overall our results point to an asynchrony effect, this effect was moderated by flanker type. Participants with increasing eveningness outperformed those with increasing morningness on incongruent trials at time 2. The preservation of executive control in evening-types following sustained wakefulness is likely driven by differences in circadian phase between chronotypes across the day.
Article
Full-text available
Good sleep is essential for optimal performance, yet few studies have examined the sleep/wake behaviour of elite athletes. The aim of this study was to assess the impact of early-morning training on the amount of sleep obtained by world-class swimmers. A squad of seven swimmers from the Australian Institute of Sport participated in this study during 14 days of high-intensity training in preparation for the 2008 Olympic Games. During these 14 days, participants had 12 training days, each starting with a session at 06:00 h, and 2 rest days. For each day, the amount of sleep obtained by participants was determined using self-report sleep diaries and wrist-worn activity monitors. On nights that preceded training days, participants went to bed at 22:05 h (s�00:52), arose at 05:48 h (s�00:24) and obtained 5.4 h (s�1.3) of sleep. On nights that preceded rest days, participants went to bed at 00:32 h (s�01:29), arose at 09:47 h (s�01:47) and obtained 7.1 h (s�1.2) of sleep. Mixed model analyses revealed that on nights prior to training days, bedtimes and get-up times were significantly earlier (pB0.001), time spent in bed was significantly shorter (pB0.001) and the amount of sleep obtained was significantly less (pB0.001), than on nights prior to rest days. These results indicate that early-morning training sessions severely restrict the amount of sleep obtained by elite athletes. Given that chronic sleep restriction of B6 h per night can impair psychological and physiological functioning, it is possible that early-morning schedules actually limit the effectiveness of training.
Article
Full-text available
Background Autonomic regulation of heart rate (HR) as an indicator of the body’s ability to adapt to an exercise stimulus has been evaluated in many studies through HR variability (HRV) and post-exercise HR recovery (HRR). Recently, HR acceleration has also been investigated. Objective The aim of this systematic literature review and meta-analysis was to evaluate the effect of negative adaptations to endurance training (i.e., a period of overreaching leading to attenuated performance) and positive adaptations (i.e., training leading to improved performance) on autonomic HR regulation in endurance-trained athletes. Methods We searched Ovid MEDLINE, Embase, CINAHL, SPORTDiscus, PubMed, and Academic Search Premier databases from inception until April 2015. Included articles examined the effects of endurance training leading to increased or decreased exercise performance on four measures of autonomic HR regulation: resting and post-exercise HRV [vagal-related indices of the root-mean-square difference of successive normal R–R intervals (RMSSD), high frequency power (HFP) and the standard deviation of instantaneous beat-to-beat R–R interval variability (SD1) only], and post-exercise HRR and HR acceleration. Results Of the 5377 records retrieved, 27 studies were included in the systematic review and 24 studies were included in the meta-analysis. Studies inducing increases in performance showed small increases in resting RMSSD [standardised mean difference (SMD) = 0.58; P < 0.001], HFP (SMD = 0.55; P < 0.001) and SD1 (SMD = 0.23; P = 0.16), and moderate increases in post-exercise RMSSD (SMD = 0.60; P < 0.001), HFP (SMD = 0.90; P < 0.04), SD1 (SMD = 1.20; P = 0.04), and post-exercise HRR (SMD = 0.63; P = 0.002). A large increase in HR acceleration (SMD = 1.34) was found in the single study assessing this parameter. Studies inducing decreases in performance showed a small increase in resting RMSSD (SMD = 0.26; P = 0.01), but trivial changes in resting HFP (SMD = 0.04; P = 0.77) and SD1 (SMD = 0.04; P = 0.82). Post-exercise RMSSD (SMD = 0.64; P = 0.04) and HFP (SMD = 0.49; P = 0.18) were increased, as was HRR (SMD = 0.46; P < 0.001), while HR acceleration was decreased (SMD = −0.48; P < 0.001). Conclusions Increases in vagal-related indices of resting and post-exercise HRV, post-exercise HRR, and HR acceleration are evident when positive adaptation to training has occurred, allowing for increases in performance. However, increases in post-exercise HRV and HRR also occur in response to overreaching, demonstrating that additional measures of training tolerance may be required to determine whether training-induced changes in these parameters are related to positive or negative adaptations. Resting HRV is largely unaffected by overreaching, although this may be the result of methodological issues that warrant further investigation. HR acceleration appears to decrease in response to overreaching training, and thus may be a potential indicator of training-induced fatigue.
Article
Full-text available
Despite the perceived importance of sleep for elite footballers, descriptions of the duration and quality of sleep, especially following match play, are limited. Moreover, recovery responses following sleep loss remain unclear. Accordingly, the present study examined the subjective sleep and recovery responses of elite footballers across training days (TD) and both day and night matches (DM and NM). Sixteen top division European players from three clubs completed a subjective online questionnaire twice a day for 21 days during the season. Subjective recall of sleep variables (duration, onset latency, time of wake/sleep, wake episode duration), a range of perceptual variables related to recovery, mood, performance and internal training loads and non-exercise stressors were collected. Players reported significantly reduced sleep durations for NM compared to DM (-157 min) and TD (-181 min). In addition, sleep restfulness (SR; arbitrary scale 1 = very restful, 5 = not at all restful) and perceived recovery (PR; acute recovery and stress scale 0 = not recovered at all, 6 = fully recovered) were significantly poorer following NM than both TD (SR: +2.0, PR: -2.6), and DM (SR: +1.5; PR: -1.5). These results suggest that reduced sleep quantity and quality and reduced PR are mainly evident following NM in elite players.
Article
Full-text available
Recovery is essential for high athletic performance, and therefore especially sleep has been identified as a crucial source for physical and psychological well-being. However, due to earlymorning trainings, which are general practice in many sports, athletes are likely to experience sleep restrictions. Therefore, this study investigated the sleep–wake patterns of 55 junior national rowers (17.7 ± 0.6 years) via sleep logs and actigraphy during a four-week training camp. Recovery and stress ratings were obtained every morning with the Short Recovery and Stress Scale on a 7-point Likert-type scale ranging from 0 (does not apply at all) to 6 (fully applies). The first training session was scheduled for 6:30 h every day. With two to four training sessions per day, the training load was considerably increased from athletes’ home training. Objective sleep measures (n = 14) revealed less total sleep time (TST) in the first two weeks (409.6 ± 19.1 and 416.0 ± 16.3 min), while training volume and intensity were higher. In the second half of the camp, less training sessions were implemented, more afternoons were training free and TSTs were longer (436.3 ± 15.8 and 456.9 ± 25.7 min). A single occasion of 1.5-h delayed bedtime and usual early morning training (6:30 h) resulted in reduced ratings of Overall Recovery (OR) (M = 3.3 ± 1.3) and greater Negative Emotional State (NES) (M = 1.3 ± 1.2, p < .05), which returned to baseline on the next day. Following an extended night due to the only training-free day, sleep-offset times were shifted from ~5:30 to ~8:00 h, and each recovery and stress score improved (p < .01). Moreover, subjective ratings of the first six days were summarised as a baseline score to generate reference data as well as to explore the association between sleep and recovery. Intercorrelations of these sleep parameters emphasised the relationship between restful sleep and falling asleep quickly (r = .34, p < .05) as well as few awakenings (r = .35, p < .05). Overall, the findings highlight the impact of sleep on subjective recovery measures in the setting of a training camp. Providing the opportunity of extended sleep (and a day off) seems the most simple and effective strategy to enhance recovery and stress-related ratings.
Article
Full-text available
This review outlines recent advancements in the understanding of athlete immune health. Controversies discussed include whether high levels of athletic training and environmental stress (e.g. heat acclimation, cryotherapy and hypoxic training) compromise immunity and increase upper respiratory tract infection (URTI). Recent findings challenge early exercise immunology doctrine by showing that international athletes performing high-volume training suffer fewer, not greater, URTI episodes than lower level performers and URTI incidence decreases, not increases, around the time of competition compared with heavy training. Herein we raise the possibility of host genetic influences on URTI and modifiable behavioural and training related factors underpinning these recent observations. Continued controversy concerns the proportion of URTI symptoms reported by athletes that are due to infectious pathogens, airway inflammation or as yet unknown causes and indeed whether the proportion differs in athletes and non-athletes. Irrespective of the cause of URTI symptoms (infectious or non-infectious), experts broadly agree that self-reported URTI hinders high-volume athletic training but, somewhat surprisingly, less is known about the influence on athletic performance. In athletes under heavy training both innate and acquired immunity are often observed to decrease, typically 15-25%, but whether relatively modest changes in immunity increase URTI susceptibility remains a major gap in knowledge. With the exception of cell-mediated immunity that tends to be decreased, exercising in environmental extremes does not provide an additional threat to immunity and host defence. Recent evidence suggests that immune health may actually be enhanced by regular intermittent exposures to environmental stress (e.g. intermittent hypoxia training).Immunology and Cell Biology accepted article preview online, 13 November 2015. doi:10.1038/icb.2015.99.
Article
Purpose: Despite the perceived importance of sleep for athletes, little is known regarding athlete sleep quality, their prevalence of daytime sleepiness or risk factors for obstructive sleep apnoea (OSA) such as snoring and witnessed apnoeic episodes. The purpose of the present study was to characterise normative sleep quality among highly trained team sport athletes. Methodology: 175 elite or highly trained rugby sevens, rugby union and cricket athletes completed the Pittsburgh Sleep Quality Index (PSQI), Epworth Sleepiness Score (ESS) and Quality of Life questionnaires and an OSA risk factor screen. Results: On average, athletes reported 7.9 ± 1.3 h of sleep per night. The average PSQI score was 5.9 ± 2.6, and 50% of athletes were found to be poor sleepers (PSQI > 5). Daytime sleepiness was prevalent throughout the population (average global score of 8.5) and clinically significant (ESS score of ≥10) in 28% of athletes. OSA may be an important clinical consideration within athletic populations, as a considerable number of athletes (38%) defined themselves as snorers and 8% reported having a witnessed apnoeic episode. The relationship between self-rated sleep quality and actual PSQI score was strong (Pearson correlation of 0.4 ± 0.1, 90% confidence limits). Conclusion: These findings suggest that this cohort of team sport athletes suffer a preponderance of poor sleep quality, with associated high levels of daytime sleepiness. Athletes should receive education about how to improve sleep wake schedules, extend total sleep time and improve sleep quality.