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©Journal of Sports Science and Medicine (2020) 19, 761-771
http://www.jssm.org
Received: 17 September 2020 / Accepted: 10 November 2020 / Published (online): 01 December 2020
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Similar Recovery of Maximal Cycling Performance after Ischemic
Preconditioning, Neuromuscular Electrical Stimulation or Active Recovery in
Endurance Athletes
Pénélope Paradis-Deschênes 1, 2, Julien Lapointe 1, Denis R. Joanisse 1, 2 and François Billaut 1, 2
1 Department of Kinesiology, Laval University, and 2 Quebec Heart and Lung Institute, Quebec, QC, Canada
Abstract
This study investigated the efficacy of ischemic preconditioning
(IPC) on the recovery of maximal aerobic performance and phys-
iological responses compared with commonly used techniques.
Nine endurance athletes performed two 5-km cycling time trials
(TT) interspersed by 45 minutes of recovery that included either
IPC, active recovery (AR) or neuromuscular electrical stimula-
tion (NMES) in a randomized crossover design. Performance,
blood markers, arterial O2 saturation (SpO2), heart rate (HR), near-
infrared spectroscopy-derived muscle oxygenation parameters
and perceptual measures were recorded throughout TTs and re-
covery. Differences were analyzed using repeated-measures
ANOVAs and Cohen’s effect size (ES). The decrement in chron-
ometric performance from TT1 to TT2 was similar between re-
covery modalities (IPC: -6.1 sec, AR: -7.9 sec, NMES: -5.4 sec,
p = 0.84, ES 0.05). The modalities induced similar increases in
blood volume before the start of TT2 (IPC: 13.3%, AR: 14.6%,
NMES: 15.0%, p = 0.79, ES 0.06) and similar changes in lactate
concentration and pH. There were negligible differences between
conditions in bicarbonate concentration, base excess of blood and
total concentration of carbon dioxide, and no difference in SpO2,
HR and muscle O2 extraction during exercise (all p > 0.05). We
interpreted these findings to suggest that IPC is as effective as AR
and NMES to enhance muscle blood volume, metabolic by-prod-
ucts clearance and maximal endurance performance. IPC could
therefore complement the athlete’s toolbox to promote recovery.
Key words: Blood flow restriction, endurance, lactate, muscle
oxygenation, NIRS.
Introduction
Strategies for adequate acute recovery can make the differ-
ence between failure and success in many sports situations.
This is particularly relevant when athletes have to perform
maximal efforts interspersed with short recovery times (<1
h) that limit a complete return to homeostasis (e.g. track
cycling or cross-country sprint skiing events) (Barnett,
2006). The inability to maintain subsequent performance is
multifactorial (Knicker et al., 2011), but blood flow ap-
pears determinant during recovery by optimizing oxygen
(O2) and nutrient delivery and clearing away metabolic by-
products from active muscles (Borne et al., 2017; Malone
et al., 2014b). Active recovery (AR) is highly used by ath-
letes (Ortiz et al., 2019; Van Hooren and Peake, 2018) and
has been reported to improve subsequent performance
compared to passive rest (Connolly et al., 2003;
Greenwood et al., 2008; Weltman et al., 1977). For exam-
ple, performing AR at 30% of maximal aerobic power
(MAP) between two maximal aerobic efforts reduced
blood lactate and led to greater performance in trained cy-
clists, compared to passive recovery and neuromuscular
electrical stimulation (NMES) of quadriceps muscle
(Malone et al., 2014a). While AR can readily maintain both
the arterial inflow to and venous return from fatigued mus-
cles, two main determinants of a successful recovery strat-
egy, some authors have sugges-ted that the use of a passive
approach with similar effects on blood flow could limit in-
tramuscular glycogen store depletion and thereby further
improve the overall reco-very process (Barnett, 2006;
Monedero and Donne, 2000). The quest to optimize recov-
ery strategies has led to investigations of varied passive
modalities that could reproduce the benefits of AR on limb
blow flow with the benefits of limiting exercise (Borne et
al., 2017; MacRae et al., 2011; Malone et al., 2014a).
Among these recovery interventions, NMES repre-
sents an efficient alternative, particularly when the stimu-
lations are executed on the calf muscles, which have been
termed the “peripheral venous heart” (Borne et al., 2017;
Izumi et al., 2010). For example, both NMES of the calf
muscles for 15 min and AR, but not passive recovery, were
found beneficial to speed up the return of pH, blood lactate
and bicarbonate concentrations to initial values and to
maintain running shuttle performance (Bieuzen et al.,
2014). Furthermore, NMES performed for ~25-30 min in-
creased calf arterial inflow, measured by plethysmography,
and performance recovery between 30-s supramaximal ef-
forts (Borne et al., 2017) and 1000-m kayak time trials (TT)
(Borne et al., 2015). The NMES modality can be mixed
with other strategies, such as hydration and nutritional in-
take, and represents an alternative during competitive
events where a proper AR protocol is unfeasible, for exam-
ple due to space or equipment availability. However,
NMES suffers from some pitfalls (Barnett, 2006; Borne et
al., 2015; Malone et al., 2014b). This recovery modality
requires specific equipment that is not always available to
large teams, requires drying of the skin, and stimulating
electrodes must be worn beneath a skinsuit to be in direct
contact with the athlete’s skin, which is not practical in
some situations. Thus, there is a scope to investigate the
efficacy of other non-invasive, affordable and simple mo-
dalities for inclusion in the athlete’s toolbox for enhanced
recovery in order to face varied situations.
Ischemic preconditioning (IPC) is a strong candi-
date in this respect. This manoeuver involves repeated ep-
isodes of muscle ischemia administered via compression of
a pressure cuff wrapped proximally around a limb, fol-
Research article
IPC as a recovery modality
762
lowed by rapid reperfusion. IPC can acutely improve per-
formance shortly after the manoeuver, particularly during
maximal aerobic exercise where the oxidative system is
fully taxed (Bailey et al., 2012; Paradis-Deschênes et al.,
2018; Salvador et al., 2016). Though the precise mecha-
nisms of action are still under investigation, performance
enhancement has been associated with improvements in lo-
cal vasodilation, blood flow and, ultimately, O2 uptake
(Bailey et al., 2012; Enko et al., 2011; Kilding et al., 2018;
Paradis-Deschênes et al., 2016). Clinical studies have also
reported slowing acidosis, reduced lactate production, as
well as lesser adenosine triphosphate and glycogen deple-
tion during, or after prolonged ischemia preceded by IPC
(Andreas et al., 2011; Salvador et al., 2016). Taken to-
gether, these results suggest a potential impact of IPC on
recovery processes, but this has received very little experi-
mental attention. Four cycles of intermittent bilateral cuff
inflation performed before successive 50-m swimming
sprints led to better performance 2 h (1.0%) later, com-
pared to a SHAM procedure (Lisboa et al., 2017). In con-
trast, when IPC was performed after a simulated rugby
match, it did not improve performance during an agility T-
test and vertical jumps, compared to passive rest (Garcia et
al., 2017). To the best of our knowledge, no study has doc-
umented this potency during endurance exercise, which
could benefit the most from IPC.
This study therefore aimed to investigate the poten-
tial of IPC to enhance the recovery of performance and spe-
cific physiological responses, including blood markers, ar-
terial O2 saturation (SpO2), h eart rat e (HR), mu scle o xygen-
ation parameters (i.e., blood volume, O2 extraction, tissue
saturation index) during two simulated 5-km TT separated
by a short (< 1 hr) resting period. A major limitation of IPC
studies is the difficulty to blind participants to the experi-
mental procedure, which involves high pressures, and
which often leads to placebo effect. We therefore used a
cross-over design to evaluate IPC against two other modal-
ities that also enhance blood flow and performance and that
are commonly used by trained athletes, namely active re-
covery and NMES. We hypothesized that the three modal-
ities would impact muscle blood volume, but that IPC
would further increase O2 uptake and performance during
a subsequent maximal effort.
Methods
Ethics approval
The study was approved by the Ethics Committee of the
University, and adhered to the principles established in the
Declaration of Helsinki. Participants provided written in-
formed consent after being explained the experimental pro-
cedures, associated risks and potential benefits.
Participants
Thirteen trained male road cyclists, runners and triathletes
volunteered. Two dropped out due to external commit-
ments or injuries unrelated to the study protocol, 2 were
excluded due to their maximal O2 consumption (VO2max)
being < 50.0 mLꞏkg-1ꞏmin-1 as an initial selection criterion,
and 9 completed the study (mean±standard error, age 26.4
± 1.6 years; body mass 75.5 ± 3.5 kg; body height 1.80 ±
0.02 m; body fat 9.6 ± 1.4 %; VO2max 61.9 ± 3.2 mLꞏkg-
1ꞏmin-1; MAP 397 ± 11 W). Subjects trained on average 8.0
± 0.6 h/week in an endurance sport at the time of the study
and had at least 2 years of training history in their respec-
tive sport. A minimal cycling experience was required for
runners. All participants were non-smokers, free of health
problems and injuries, and did not use any medication or
any other tobacco/nicotine products. None of them had pre-
viously used IPC or NMES.
Study design
Participants visited the laboratory for two preliminary vis-
its (for a maximal incremental step test and familiarization
of the recovery interventions, and for a5-km TT practice)
and then for three experimental trials conducted in a ran-
domized crossover design. During all experimental ses-
sions, participants performed two TTs interspersed by one
of the three recovery modalities, and measurements were
made before, during and after the two TTs. The timeline
for every experimental session was as follows: 5-min su-
pine rest (near-infrared spectroscopy (NIRS) baseline:
BSTT1), 10-min standardized self-paced warm-up, 2-min
rest seating on bike, 5-km TT (TT1), 2-min rest seating on
bike (recovery measurements every 30 sec), blood samples
(Post-TT1), 3-min cool down, 30-min recovery interven-
tion (IPC, AR, NMES), 15-min rest (including blood sam-
ples, BSTT2, transition and equipment adjustments), 3-min
standardized self-paced re-activation, 2-min rest seating on
bike, 5-km TT (TT2), 2-min rest seating on bike (recovery
measurements), blood samples (Post-TT2), 3-min cool
down, 5 min supine rest and arterial occlusion (AO, see
Near-infrared spectroscopy). All sessions were performed
at the same time of the day to avoid potentially confound-
ing circadian rhythm effects and were separated by a min-
imum of 3 days to avoid residual fatigue and a maximum
of 7 days. Temperature (22.1 ± 0.1°C) and humidity (31.5
± .2%) were kept constant in the laboratory. Prior to each
testing day, participants were asked to record and replicate
their dietary intake and physical activity respectively for 24
h and 72 h before testing, vigorous exercise was avoided
for 48 h and alcohol and caffeine were refrained from for
24 h. The handlebars and seat settings of each device (Ex-
calibur Sport, Velotron Elite) were individualized and rep-
licated throughout the study.
Experimental protocol
Preliminary testing: During the first visit, resting HR and
blood pressure (inclusion criteria: <100 beats per minute,
<140/90 mmHg) were recorded in a seated position and
baseline characteristics (body height, body mass and body
fat) were measured. The percentage body fat was measured
by bioelectrical impedance (Tanita TBF-310; Tanita Corp.
of America Inc., Arlington). Thigh skinfold thickness
(mean 6.4 ± 0.6 mm) and thigh circumference (mean 57.5
± 1.5 cm) were also measured as there are known factors
to respectively influence the penetration of near-infrared
light through muscle tissue (see Near-infrared spectros-
copy) (McCully and Hamaoka, 2000) and the occlusion of
arterial blood flow (Loenneke et al., 2012). The percentage
body fat was measured by bioelectrical impedance (Tanita
TBF-310; Tanita Corp. of America Inc., Arlington Heights,
Paradis-Deschênes et al.
763
IL). The participant was then familiarized, for 5 to 10 min
per modality, to IPC by progressively inflating blood pres-
sure cuffs to 220 mmHg (1 cycle per lower limb), and to
NMES by increasing transcutaneous electrical impulses
until visible contraction of the calf muscles. After the fa-
miliarization, the participant was positioned on an electro-
magnetically-braked cycle ergometer (Excalibur Sport,
Lode, the Netherlands) for a 2-min baseline in a seated po-
sition and a 5 min warm-up at 100 W before the maximal
incremental step test (30 W per min until volitional exhaus-
tion) to assess the VO2max and the MAP. Expired gases
were analyzed breath-by-breath throughout the test (Breez-
esuite, MedGraphics Corp., Minnesota, Saint Paul, USA).
The second preliminary visit started with a 10-min
self-paced warm-up during which power output, speed and
gear were continuously noted by the experimenter and
strictly reproduced thereafter. After a 2-min bike seated
rest, the participant performed a 5-km TT.
5-km ergometer time trial: The 5-km TTs were ex-
ecuted on a computer-controlled electrically braked cycle
ergometer (Velotron Elite, RacerMate, Seattle, WA, USA).
The 10-min warm-up before TT1 and the 3-min re-activa-
tion phase before TT2 were self-paced and standardized for
each athlete, so that power output, speed and gear from the
first session were strictly reproduced in every experimental
session. This ensured minimum effect of warm-up on pri-
mary variables of investigation between trials. Participants
were instructed to complete the 5-km distance as quickly
as possible and to remain seated, with the distance travelled
as the only available information to them. They were
strongly verbally encouraged during all exercise protocols
and were warned to give a maximal effort in the first TT1
without pacing. The 3-min cool down was performed at a
load individually adjusted from the results of their maximal
incremental step test (30% MAP) after each TT.
Recovery modalities: The delay between both TTs
was timed and reproduced at every session (IPC: 54 ± 1
min; NMES: 54 ± 1 min; AR: 53 ± 1 min). Recovery inter-
ventions were specifically applied to replicate as much as
possible the procedures commonly employed by athletes in
the field and in research studies and were matched for total
resting duration (30 min). They were as follows:
1) IPC: In a supine position, non-elastic nylon blood
pressure cuffs (WelchAllyn, Skaneateles Falls, NY, USA,
width: 21 cm) were positioned around each upper thigh un-
der the gluteal line and rapidly inflated to 220 mmHg for 5
min to prevent arterial inflow. This was repeated three
times per limb, alternately, with each compression episode
separated by 5 min of reperfusion (cuff release). This pro-
tocol has previously been shown to completely occlude
vascular arterial inflow (Sabino-Carvalho et al., 2016), al-
ter physiological responses and enhance acute endurance
performance (Bailey et al., 2012; Paradis-Deschênes et al.,
2018). The intervention lasted 30 min.
2) AR: The participant remained seated on the bike after
the 3-min cool down and cycled at 30% MAP for an addi-
tional 10 min in order to simulate a practical AR phase (i.e.,
often <15 min) that athletes would typically perform in the
field when two maximal efforts are repeated close to each
other (for review see (Van Hooren and Peake, 2018)).
Then, they remained seated quietly for 20 min on a bed ad-
jacent to the bike to complete the 30-min period.
3) NMES: In a prone position, two self-adhesive elec-
trodes (Veinopack, Ad Rem Technology, Paris, France,
surface 8 x 13 cm) were placed on the medio-central part
of both calves and connected to an electrical stimulator
(Veinoplus Sport, Ad Rem Technology, Paris, France).
The stimulation voltage ranged from 9 to 18 Vpeak (corre-
sponding level selected by the participants in the current
study: 27 ± 2) and was adjusted manually depending on
participant tolerance (i.e., comfortable sensation) and the
investigator (minimal threshold: visible contraction of the
calf muscles). The specific stimulation modulation pattern
of the Veinoplus Sport automatically changed every 5 min
and resulted in 60 to 90 calf muscles contractions per mi-
nute for 30 minutes. Although NMES has been applied for
varied periods of time, this stimulation pattern has been
previously described and successfully used on the calf
muscles to optimize venous return and performance in var-
ied recovery studies using maximal endurance exercise in-
cluding cycling (Bieuzen et al., 2014; Borne et al., 2017;
Borne et al., 2015; Izumi et al., 2010).
Instrumentation and measurements analysis
Power output: The power output was continuously rec-
orded from the Velotron ergometer and was averaged over
a period of 10 sec leading up to every 250 m.
Near-infrared spectroscopy: A portable spatially
resolved, dual wavelength NIRS apparatus (PortaMon, Ar-
tinis Medical Systems BV, The Netherlands) was installed
on the distal part of the right vastus lateralis muscle belly
(approximately 15 cm above the proximal border of the pa-
tella), parallel to muscle fibres, to quantify changes in the
absorption of near-infrared light by oxy-hemoglobin
(HbO2) and deoxy-hemoglobin (HHb). The skinfold thick-
ness (6.4 ± 0.6 mm) was measured at the site of the appli-
cation of the NIRS using a Harpenden skinfold caliper
(British Indicators Ltd, West Sussex, Great Britain) during
the first session, and was less than half the distance be-
tween the emitter and t he detector ( i.e., 20 mm). Th is thick-
ness allows adequate penetration of near-infrared light into
muscle tissue for valid measurements (McCully and
Hamaoka, 2000). The device was packed in transparent
plastic wrap to protect it from sweat and fixed with tape.
Black bandages were used to cover the device from inter-
fering background light. The position of the apparatus on
the thigh was marked with an indelible pen for reposition-
ing during the subsequent visit. The pressure cuff used to
induce IPC was positioned above the NIRS device and did
not affect the placement of the device.
A modified form of the Beer-Lambert law, using
two continuous wavelengths (760 and 850 nm) and a dif-
ferential optical path length factor of 4.95 was used to cal-
culate micromolar changes in tissue [HbO2], [HHb] and to-
tal hemoglobin ([THb] = [HbO2] + [HHb]). Changes in tis-
sue saturation index (TSI = [HbO2]/[THb]) were also used
as an index of tissue oxygenation since it reflects the dy-
namic balance between O2 supply and consumption in the
IPC as a recovery modality
764
tissue microcirculation (Ferrari et al., 2004; van Beekvelt
et al., 2001). This parameter is independent of near-infra-
red photon path length in tissue. Before the first TT, one
minute of baseline values was analyzed once the signal was
stabilized (BSTT1). Muscle oxygenation changes (∆[HHb],
∆[THb] and ∆TSI) during exercise and recovery were then
normalized to this resting baseline in order to exclude the
effects of TT1 and recovery on subsequent muscle oxygen-
ation changes. ∆[HHb] was expressed in percentage of the
average of the maximal amplitude calculated during the
AO (∆[HHb], %AO). The AO was performed after each
experimental session by inflating the cuff on the right thigh
at 220 mmHg for ∼3–5 min to obtain a physiological cali-
bration of the NIRS signals. The cuff pressure was released
after reaching a plateau in the [HHb] and TSI signal.
Δ[ HHb] w as take n as an inde x of mu scle O2 extraction (van
Beekvelt et al., 2002), Δ[THb] as a change in regional
blood volume (van Beekvelt et al., 2001), and the differ-
ence between BSTT1 and BSTT2 (∆BS) as an index of change
in muscle oxygenation parameters induced by the recovery
modalities. NIRS data were acquired continuously at 10 Hz
and were averaged over 10 sec for every 250 m of the TT,
and every 30 sec for a 2-min period immediately after ex-
ercise. A 10th order zero-lag low-pass Butterworth filter
was applied to smooth NIRS signal (Paradis-Deschênes et
al., 2018).
Arterial O2 saturation and heart rate: SpO2 and HR,
measured from an adhesive forehead sensor secured with a
headband connected a pulse oximeter (Nellcor Bedside,
Nellcor Inc. Hayward, CA), were recorded every 250 m
during TT and every 30 sec for a 2-min period immediately
after exercise. This technique has been shown to be in good
agreement with hemoglobin O2 saturation based on arterial
blood analysis over the 70-100% range (Romer et al.,
2007). The SpO2 measured at the forehead is also highly
correlated with the O2 saturation measured by direct arte-
rial blood measurements (R2 = 0.90, P < 0.0001) and has
significantly lower bias and greater precision for SpO2 (0.3
± 1.5%) and HR (1.8 ± 5.5%) than finger probes in athletes
(Yamaya et al., 2002).
Blood sampling: Blood samples (92-µL) were
drawn from fingertips using disposable lancets (Safety-
Lancet Neonatal, Sarstedt, Germany) at rest at the first ex-
perimental session (baseline), and at three additional time
points during others testing sessions: 2 min after each TT
and immediately after the 30-min period of each recovery
modality. Samples were collected into a capillary tube
(Epoc ® Care-fillTM, Siemens Healthinners, Germany) and
immediately transferred into the sample well of a test card
(Epoc ® Test Card, Siemens Healthinners, Germany) for
analysis with the Epoc® device (Epoc ® Blood Analysis
System, Siemens Healthinners, Germany). This device was
used to measure pH, carbon dioxide and O2 partial pres-
sure, concentrations of sodium, potassium, ionized cal-
cium, chloride, glucose, lactate, and hematocrit. Moreover,
concentrations of hemoglobin, bicarbonate, total carbon di-
oxide, arterial blood O2 saturation, base excess of extracel-
lular fluid, and base excess of blood were calculated in de-
vice. Prior to data collection, the analyzer was calibrated
according to the manufacturer’s specifications (i.e., ther-
mal quality calibration with a buffered aqueous solution).
Perceptual measures: The rate of perceived exer-
tion (RPE) was recorded every 500 m of the TT using the
Borg 10-point scale to assess subjective perceived exer-
tion. Recovery intervention was evaluated by two ques-
tions immediately after each recovery modality (“How do
you rate the efficacy of this recovery intervention?” and
‘How did you like this recovery intervention?”) by means
of a 10-point Likert scale, ranging from 1 (not at all) to 10
(very, very much) (Bieuzen et al., 2014).
Statistical analysis
We evaluated the magnitudes of difference for perfor-
mance and physiological variables within condition (re-
covery vs. rest; TT2 vs. TT1). We also evaluated the per-
centage difference between IPC, AR and NMES for the
TT1, the recovery period and the changes between trials
(TT2 vs. TT1, ∆TT). Practical significance was evaluated
using Cohen’s effect sizes (ES) ± 90% confidence limits,
and compared to the smallest worthwhile change that was
calculated as the standardized mean difference of 0.2 be-
tween-subject standard deviations (Batterham and
Hopkins, 2006; Hopkins et al., 2009). Standardized effects
were classified as small (0.2-0.49), moderate (0.5-0.79) or
large (≥0.8) (Hopkins et al., 2009). The effect of IPC was
deemed “unclear” if chances of having better/greater and
poorer/lower changes in performance and physiological
variables were both >5% (Batterham and Hopkins, 2006;
Hopkins et al., 2009). All variables were log-transformed
before analysis (Hopkins et al., 2009), except for ∆TSI dur-
ing recovery, [BE(ecf)], and [BE(b)]. Furthermore, the dif-
ferences in performance and physiological responses
across the two time trials and between the three recovery
modalities were also analyzed using repeated-measures
ANOVA tests (three levels: IPC, NMES and AR). Tukey’s
HSD post-hoc analyses were used to locate differences
among pairs of means when ANOVAs revealed significant
F-ratio for main and interactive effects. The level of signif-
icance was set at P < .05. Raw data are reported as mean±
SE for clarity.
Results
Performance parameters
Average completion times and individual percentage dif-
ferences in the two TTs are displayed in Figures 1 and 2,
respectively. The calculated smallest worthwhile change
for TT time in IPC, NMES and AR equated to 4.4 sec, 5.5
sec and 4.7 sec, respectively. When every recovery modal-
ity was examined separately, TT2 was clearly slower than
TT1 after IPC (6.1 sec, ES 0.21) and AR (7.9 sec, ES 0.28),
whereas the TT1-TT2 change was less than the smallest
worthwhile change after NMES (5.4 sec, ES 0.19). Of note
is that TT1 was the slowest in NMES (clear difference vs.
AR: 2.5 sec, ES 0.21). However, when comparing perfor-
mance changes between modalities, there was no differ-
ence between conditions (IPC vs. AR: ES 0.07, p = 0.84;
IPC vs. NMES: ES -0.02, p = 0.97; AR vs. NMES: ES -
0.09, p = 0.72).
The power output profiles during the TTs are dis-
played in Figure 3. There were clear differences within
every condition with a lower power output in TT2
Paradis-Deschênes et al.
765
compared to TT1. The power output was higher in IPC and
AR conditions, compared to NMES, during the first half of
the TT1, but mirroring the chronometric performance,
there was no difference between conditions for perfor-
mance changes (IPC vs. AR: ES -0.03, p = 0.95; IPC vs.
NMES: ES 0.01, p = 0.99; AR vs. NMES: ES 0.04, p =
0.93.
Physiological responses
Muscle oxygenation values at baseline and changes follow-
ing TTs and recovery are displayed in Table 1. Figure 4
shows a schematic representation of these values over the
course of the trials and recovery. Overall, all modalities in-
creased local blood volume during the recovery period be-
tween the TTs, compared to resting baseline, and remained
higher during the second TT with no differences between
conditions (IPC vs. AR: ES 0.07, p = 0.81; IPC vs. NMES:
ES 0.09, p = 0.61; AR vs. NMES: ES 0.02, p = 0.94). Mus-
cle O2 extraction did not change and there were no differ-
ences between conditions.
Figure 1. Average completion times during the 5-km TTs in-
terspersed by IPC, AR or NMES. (*) denotes clear differences
within conditions when comparing TT2 to TT1 (IPC: 1.3%, ES 0.21; AR:
1.7%, ES 0.28). (⸹) denotes a clear difference between AR and NMES at
TT1 (1.4%, ES 0.23, 0.06;0.40). Values are mean ± SE.
Figure 2. Average (black line) and individual (grey lines) percentage differences between 5-km time trials inter-
spersed by IPC, AR or NMES. (*) denotes a clear difference within conditions at TT2 compared to TT1.
Figure 3. Power output profile during the 5-km time trials (TT1, dotted line; TT2, solid line) interspersed by IPC, AR or NMES
(*) denotes clear differences within conditions at TT2 for the first half (IPC: ↓8.2%, ES -0.52 ± 0.27; AR: ↓8.2%, ES -0.52 ± 0.21; NMES: ↓7.2%, ES
-0.46 ± 0.28), and the entire TT (AR: ↓3.5%, ES -0.22 ± 0.14), compared to TT1. Clear differences between IPC and NMES (-3.3%, ES -0.20 ± 0.32,
†) and AR and NMES (4.7%, ES -0.29 ± 0.32, ⸹) at TT1 are denoted. Values are mean ± SE.
IPC as a recovery modality
766
Table 1. Muscle oxygenation at baseline, and changes during time trials and recovery. Values are means (±SE).
IPC NMES AR
[HHb], μm [THb], μm TSI, % [HHb], μm [THb], μm TSI, % [HHb], μm [THb], μm TSI, %
BSTT1 29.5 (1.4)‡ 78.7 (3.2) 70.4 (2.3) 30.4 (1.5) 79.4 (3.7) 74.5 (3.3) 31.1 (1.6) 79.7 (4.2) 68.4 (2.5)
BSTT2 30.2 (1.4) 89.2 (3.7) 78.1 (1.9) 30.5 (1.6) 91.4 (4.3) 76.5 (1.2) 30.4 (1.5) 91.1 (4.4) 77.3 (0.9)
Muscle oxygenation changes during exercise and recovery (∆)
%AO μm % %AO μm % %AO μm %
TT1 101 (3)‡ 10.3 (1.4) 23.4 (2.5)† 96 (7) 9.4 (1.8) 27.1 (2.3) 96 (5) 9.0 (1.7) 24.3 (3.0)
R30 63.9 (5.4) 18.4 (2.4) 2.3 (3.4)† 65.4 (7.0) 18.3 (2.3) 8.7 (4.0) 59.0 (7.2) 17.0 (2.4) 3.4 (3.7)
R60 38.6 (4.1)‡ 20.1 (2.4) -5.7 (3.0) 37.3 (5.2)†21.4 (1.4) -1.0 (3.1) 29.9 (5.6) 18.2 (2.5) -5.9 (3.0)
R90 30.3 (3.9)†‡ 21.1 (2.1) -7.9 (2.5)† 23.8 (5.4) 19.5 (2.1) -2.2 (2.7) 19.8 (2.9) 19.5 (1.7) -7.8 (2.6)
R120 26.5 (4.0)†‡ 21.4 (2.3) -7.6 (2.7)† 19.7 (5.6) 19.7 (2.4) -3.3 (2.5) 14.3 (3.3) 19.5 (1.9) -8.8 (2.5)
TT2 103 (4) 13.3 (1.6) 22.2 (3.3) 102 (9) 12.9 (2.3) 25.7 (2.8) 98 (4) 13.7 (1.8) 20.9 (2.8)
R30 67.1 (5.5) 20.9 (2.7) 3.2 (3.7) 66.9 (8.4) 22.9 (3.1) 7.1 (3.2) 59.5 (5.2) 21.4 (2.4) 1.8 (3.4)
R60 41.9 (4.8) 25.3 (2.8) -5.8 (2.8) 35.3 (5.5) 24.5 (2.2) -1.2 (2.9) 31.4 (5.1) 23.7 (1.6) -7.0 (2.4)
R90 30.3 (3.7) 24.4 (2.4) -8.2 (2.7) 28.1 (5.9) 26.0 (2.2) -2.9 (2.7) 22.9 (3.6) 23.9 (1.8) -8.6 (2.6)
R120 25.1 (3.6) 23.3 (1.9) -8.6 (2.4) 22.9 (5.2) 24.4 (1.7) -3.0 (2.6) 20.1 (4.8) 24.2 (1.2) -8.5 (2.6)
% difference within conditions (TT2 compared to TT1)
∆BS 2.1%‡ 13.3%** 11.1%***† 0.1% 15.0%*** 3.3% -2.0% 14.6%*** 13.6%***
∆TT 2.0% 33.8%* -9.0%*‡ 5.5%* 55.9%** -6.7% 3.4% 45.6%* -16.7%*
∆R30 4.8% 20.2%* 34.4%† 1.8% 17.0% -20.2% 3.6% 22.3%* -59.5%
∆R60 9.1%† 31.2%**† -2.3% -11.2%* 11.9%* -23.5% 8.7% 68.0% -17.5%
∆R90 9.5%† 15.5%*† -3.3% 12.0% 38.4%** -28.0% 14.9%* 23.3%* -10.3%
∆R120 -15.3%*† 13.1%*† -12.6% 21.3%* 31.6%** 9.5% 15.0% 27.8%* 2.9%
Within-condition clear differences for changes (∆: TT2 compared to TT1) are denoted as small (0.20-0.49, *), moderate (0.50-0.79, **), or large (≥0.80,
***). Between-condition clear differences for the TT1 and recovery period and for changes are denoted for IPC vs. NMES (†) or IPC vs. AR (‡). For
small, moderate or large effects, symbols are presented in italics, bold, or underlined, respectively. Abbreviations : AR, active recovery; BS, baseline
preceding TT (BSTT1, BSTT2); ES, effect size; [HHb], deoxy-hemoglobin; IPC, ischemic preconditioning; NMES, neuromuscular electrical stimulation;
R(30 to 120), values after 30 to 120 sec of recovery; [THb], total haemoglobin; TSI, tissue saturation index; TT, time trial.
Figure 4. Average Δ[HHb], Δ[THb] and ΔTSI during the 5-km time trials and recovery (TT1, dotted line; TT2,
solid line) interspersed by IPC, AR or NMES. Values are mean ± SE.
Paradis-Deschênes et al.
767
Table 2. Blood parameters at baseline and after time trials and recovery.
BS Post-TT1 Post-recovery Post-TT2 ∆TT2 vs. ∆TT1
Mean (SE) %D within conditions
pH
IPC
NMES
AR
7.46
(0.02)
7.22 (0.01)*** †
7.28 (0.02)***
7.24 (0.02)***
7.44 (0.01)‡
7.44 (0.01)
7.48 (0.02)*
7.26 (0.02)*** †‡
7.31 (0.02)***
7.29 (0.02)***
0.4%*
0.7%***
0.7%***
PCO2
mmolꞏL-1
IPC
NMES
AR
34.7
(2.1)
29.3 (1.7)*** †
27.6 (1.8)***
28.0 (2.2)***
33.5 (1.6)
35.8 (1.1)*
31.7 (3.1)**
29.9 (1.2)*** †
27.1 (2.5)***
29.8 (1.8)***
2.9%‡
-4.0%
7.0%*
PO2
mmolꞏL-1
IPC
NMES
AR
86.8
(7.6)
95.5 (3.8)***
100.4 (4.0)
95.5 (4.5) **
70.3 (4.7)** ‡
66.8 (4.2)***
81.0 (7.2)
99.8 (2.5)*** ‡
100.5 (7.3)***
94.5 (4.2)
4.2%*
-0.2%
-1.0%
[Na+]
mmolꞏL-1
IPC
NMES
AR
147
(1)
144 (1)
144 (1)*
144 (1)**
144 (1)**
144 (1)**
146 (2)
142 (1)*** †
144 (1)**
143 (1)**
-0.9%*
0.0%
-0.1%
[K+]
mmolꞏL-1
IPC
NMES
AR
6.98
(0.50)
5.53 (0.41)**
5.95 (0.52)*
5.80 (0.64)
6.26 (0.69)
6.04 (0.70)
6.30 (0.67)
5.08 (0.39)***
6.44 (1.01)
5.73 (0.73)*
-6.9%
7.2%
-2.6%
[Ca2+]
mmolꞏL-1
IPC
NMES
AR
1.22
(0.02)
1.26 (0.02)
1.22 (0.03)
1.24 (0.02)
1.19 (0.02)
1.20 (0.02)
1.19 (0.02)***
1.22 (0.01)
1.23 (0.02)
1.23 (0.02)
-2.3%
0.6%
-0.6%
[Cl-]
mmolꞏL-1
IPC
NMES
AR
113
(2)
112 (1)
113 (1)
112 (2)
112 (2)
110 (1)
113 (2)
110 (1)
113 (3)
113 (3)
-2.5%*
-1.2%
-0.7%
[Glc]
mmolꞏL-1
IPC
NMES
AR
5.96
(0.30)
7.14 (0.29)*** ‡
6.42 (0.48)
6.94 (0.33)***
5.78 (0.31)†‡
6.30 (0.35)
6.81 (0.36)**
6.18 (0.36)†
5.60 (0.32)
5.97 (0.43)
-10.4%**
-15.3%***
-14.6%***
[Lact]
mmolꞏL-1
IPC
NMES
AR
3.50
(0.50)
14.6 (0.5)***
14.3 (0.7)***
14.6 (0.6)***
4.8 (0.4)*** †
4.1 (0.5)***
4.1 (0.5)***
12.5 (0.6)***
12.0 (0.8)***
12.4 (1.0)***
-11.8%*
-16.3%**
-16.6%**
Hct
%
IPC
NMES
AR
48.1
(1.3)
48.9 (0.8)†
49.8 (1.3)
49.3 (1.0)
44.0 (1.3)***
44.6 (1.2)***
44.9 (1.2)***
49.0 (1.0)†
51.6 (1.6)**
49.1 (0.6)
-0.4%
3.5%*
-0.2%
[HCO3-]
mmolꞏL-1
IPC
NMES
AR
24.3
(0.8)
12.0 (0.8)***
12.9 (1.0)***
11.9 (0.6)***
22.7 (0.6)* †
24.2 (0.3)
22.8 (1.1)**
13.3 (0.9)***
13.6 (1.3)***
14.3 (0.9)***
9.9%** ‡
8.6%*
19.2%***
[cTCO2]
mmolꞏL-1
IPC
NMES
AR
25.3
(0.9)
12.9 (0.8)***
13.7 (1.0)***
12.8 (0.7)***
23.8 (0.6)* †
25.3 (0.4)
23.8 (1.2)**
14.2 (1.0)***
14.4 (1.4)***
15.2 (0.9)***
9.6%** ‡
7.7%
18.2%***
[Be(ecf)]
mmolꞏL-1
IPC
NMES
AR
0.4
(0.8)
-15.6 (0.9)***
-14.0 (1.2)***
-15.4 (0.6)***
-1.4 (0.5)* †
0.1 (0.4)*
-0.8 (0.7)**
-13.9 (1.2)*** †‡
-12.7 (1.5)***
-12.3 (1.1)***
-10.6%** ‡
-14.6%**
-21.3%***
[Be(b)]
mmolꞏL-1
IPC
NMES
AR
1.0
(0.6)
-14.1 (0.8)***
-12.2 (1.1)***
-13.7 (0.6)***
-0.6 (0.4)** †
0.4 (0.4)*
0.2 (0.4)*
-12.5 (1.2)*** †‡
-10.7 (1.3)***
-10.7 (1.1)***
-11.0%** ‡
-18.0%***
-21.8%***
cSO2
%
IPC
NMES
AR
96.2
(0.7)
95.7 (0.5)
96.8 (0.5)
95.8 (0.7)
93.6 (1.3)**
92.9 (1.2)***
95.0 (2.0)
96.5 (0.4)* ‡
96.8 (0.5)
96.2 (0.7)
0.8%*
-0.2%
0.4%
[cHgb]
gꞏdL-1
IPC
NMES
AR
16.4
(0.4)
16.7 (0.3)†
17.0 (0.5)
16.8 (0.3)
14.9 (0.4)***
15.1 (0.4)***
15.3 (0.4)***
16.7 (0.3)†
17.5 (0.6)**
16.8 (0.2)
-0.9%
3.1%
-0.4%
Within-condition clear differences at time point (post-TT1, post-recovery, post-TT2), compared to baseline, and for changes (∆: TT2
compared to TT1) are denoted as small (0.20-0.49, *), moderate (0.50-0.79, **), or large (≥0.80, ***). Between-condition clear differ-
ences at time point, compared to baseline, and between changes are denoted for IPC vs. NMES (†) or IPC vs. AR (‡). For small,
moderate or large effects, symbols are presented in italics, bold, or underlined, respectively. Abbreviations: AR, active recovery; Be(b),
Be(ecf), base excess of blood and extracellular fluid; BS, baseline; Ca2+, ionized calcium; HCO3−, bicarbonate; cHgb, haemoglobin; Cl−,
chloride; cSO2, arterial blood O2 saturation; cTCO2, total CO2; %D, percentage difference; glc, glucose; Hct, hematocrit; IPC, ischemic
preconditioning; K+, potassium; lact, lactate; NMES, neuromuscular electrical stimulation; PCO2 and PO2, CO2 an d O2 partial pressure.
Mean values of blood parameters at rest and imme-
diately after TTs and recovery are displayed in Table 2.
There were some clear differences between changes in IPC
and AR. Specifically, differences between TT2 and TT1
were lower after IPC compared to AR, but not significant,
for carbon dioxide partial pressure (ES 0.28 ± 0.38, p =
0.85), total carbon dioxide (ES 0.42 ± 0.52, p = 0.25), and
concentrations of bicarbonates (ES 0.45 ± 0.56, p = 0.81)
and base excess of blood (ES 0.36 ± 0.56, p = 0.43) and
extracellular fluid (ES 0.38 ± 0.48, p = 0.28). However, no
IPC as a recovery modality
768
Table 3. Heart rate and arterial O2 saturation following time trials and during recovery. Values are means (±SE).
IPC NMES A
R
HeartrateandarterialO2saturationvalues
HR(bpm)SpO2(%)HR(bpm)SpO2(%)HR(bpm)SpO2(%)
TT1175 (3) 96.8 (0.5) 175 (4) 96.9 (0.5) 176 (3) 96.5 (0.6)
R30164 (3) 96.9(0.5) b 163 (5) 96.7 (0.5) 165 (5) 96.4 (0.5)
R60142 (4) 97.8 (0.5) 142 (5) 97.6 (0.4) 140 (4) 97.7 (0.5)
R90124 (4) 98.1 (0.4) 124 (5) 98.2 (0.4) 126 (4) 97.9 (0.5)
R120117 (5) 98.2(0.4) b 115 (4) 98.2 (0.4) 119 (5) 97.9 (0.6)
TT2171 (4) 97.8 (0.4) 172 (4) 97.8 (0.4) 171 (3) 97.6 (0.6)
R30166 (5) 97.0 (0.5) 167 (4) 97.4 (0.5) 167 (5) 97.8 (0.5)
R60144 (5) 98.0 (0.5) 143 (3) 98.6 (0.4) 147 (4) 98.3 (0.4)
R90125 (5) 98.2 (0.5) 125 (4) 98.3 (0.4) 127 (5) 98.0 (0.4)
R120118 (6) 98.4 (0.4) 111 (7) 98.4 (0.4) 118 (6) 98.4 (0.4)
%differencewithinconditions(TT2comparedtoTT1)
∆TT-2.7% * 1.0% ** -1.7% * 0.9% * -3.0% * 1.1% **
∆R300.8% 0.1% ab 2.6% * 0.8% ** 1.1% 1.2% **
∆R601.3% b 0.2% a 1.3% 1.0% ** 4.6% * 0.5% *
∆R900.5% 0.1% 0.9% 0.1% 0.8% 0.3%
∆R1200.4% 0.2% a -4.4% 0.2% 0.6% 0.6% *
Within-condition clear differences for changes (∆: TT2 compared to TT1) are denoted as small (*), moderate (**), or large (***). Between-condition
clear differences for the first TT and recovery period and for changes are denoted for IPC vs. NMES (a) or IPC vs. AR (b). For small (0.20-0.49),
moderate (0.50-0.79) or large (≥0.80) effects, symbols are presented in italics, bold, or underlined, respectively. Abbreviations: AR, active recovery;
bpm, beat per minute; ES, effect size; HR, heart rate; IPC, ischemic preconditioning; NMES, neuromuscular electrical stimulation; R(30, 60, 90, 120),
values after 30, 60, 90 or 120 sec of recovery; SpO2, arterial O2 saturation; TT, time trial.
approach appears to provide a systematically greater bene-
fit in the recovery of these measures overall, all appearing
to allow for a rapid clearance of metabolic by-products. In
all conditions, values remained within their normal clinical
range at all times.
Table 3 shows changes to HR and SpO2 values during TTs
and recovery. Overall, all modalities decreased HR and in-
creased SpO2 during the second TT, compared to TT1, with
no differences between conditions.
Perceptual measures
Mean RPE was not different within conditions (TT2 com-
pared to TT1) and there was no difference between the
three recovery modalities. There were, however, clear dif-
ferences between conditions for the perception of efficacy
(IPC: 8.3 ± 0.4; NMES: 7.6 ± 0.6; AR: 6.8 ± 0.8) and ap-
preciation of the technique (IPC: 6.6 ± 0.5; NMES: 6.9 ±
0.8; AR: 7.9 ± 0.5), with clearly higher scores for IPC
(compared to AR: ES 0.74 ± 0.79; NMES ES 0.31 ±0.26)
and AR (IPC: ES 0.65 ± 0.60; NMES: ES 0.59 ± 0.81),
respectively.
Discussion
This study examined the effects of IPC administered dur-
ing recovery on subsequent endurance performance and as-
sociated physiological responses compared to two other re-
covery modalities commonly used by athletes in the sport-
ing field (active recovery and neuromuscular electrical
stimulation). The main practical finding was that the per-
formance decrement in a second 5-km cycling time trial re-
peated after less than an hour of recovery was similar in the
three modalities. IPC did not outperform AR nor NMES in
preserving endurance performance. The increase in muscle
blood volume and metabolic by-products clearance after
recovery, as well as the physiological responses (i.e. mus-
cle O2 extraction, HR and SpO2) during the second 5-km
TT were also similar in the three modalities.
IPC has been reported to improve acute perfor-
mance shortly after the procedure in various contexts espe-
cially when the oxidative system contributes greatly to the
energy provision (Bailey et al., 2012; Paradis-Deschênes et
al., 2018; Salvador et al., 2016). However, studies where
IPC is applied during recovery are scarce, do not include
prolonged efforts and present conflicting results. For ex-
ample, IPC performed after a simulated rugby match did
not improve performance on an agility T-test and vertical
jumps, compared to passive rest (Garcia et al., 2017). On
the other hand, when compared to SHAM protocols, IPC
induced beneficial effects on 50-m swimming sprints 2 and
8 h later (Lisboa et al., 2017) and on power production and
sprint performance immediately and 24 h after IPC
(Beaven et al., 2012), emphasizing the potential of this
technique for recovery and the need for further investiga-
tions. Within the current cross-over randomised design, the
performance decrement from one TT to the other was sim-
ilar between the three recovery modalities (IPC: -6.1 sec;
NMES: -5.1 sec; AR: -7.9 sec, p=0.84, ES 0.05), indicating
that none of the tested strategies was more efficient than
the others in these trained endurance athletes. The decrease
in power output occurred mostly in the first half of the TT
(IPC: -24 W; NMES: -21 W; AR: -25 W) and was not dif-
ferent between modalities despite participants’ perception
of efficacy and preference for IPC and AR, respectively.
Corresponding to this reduce work rate, participants dis-
played higher SpO2 and lower HR and changes in blood
markers after the second TT. NMES was the only condition
with no clear within-group difference between TT1 and
TT2 (ES 0.19). However, it is important to mention that
TT1 was also the slowest in this condition (clearly different
from AR for completion time and from AR and IPC for
power output developed in the first half of the TT), likely
leading to this statistical artifact.
One of the main pitfalls of IPC research is the diffi-
culty to blind participants to the high cuff pressure exerted
Paradis-Deschênes et al.
769
on the limb. Thus, to avoid a potential placebo effect
derived from the intervention and to reduce the cumber-
someness of the protocol, we opted to not include a SHAM
condition, with a cuff inflated at ~20 mmHg as done in
many IPC studies, or a fourth “true” control condition with
passive rest between the two TTs. Instead, we chose to
compare IPC to two other modalities that are commonly
employed by athletes in training and competitive settings
and whose recovery benefits have been robustly demon-
strated and, like IPC, are also mainly derived from blood
flow improvement (Barnett, 2006; Bieuzen et al., 2014;
Borne et al., 2017; Greenwood et al., 2008; Malone et al.,
2014b; Monedero and Donne, 2000; Weltman et al., 1977).
Although it is difficult to ascertain whether IPC would re-
ally improve subsequent performance, the present design
compares its potential efficacy against proven ergogenic
methods, which were ultimately used as “practical con-
trols”. In fact, athletes do not use passive rest to accelerate
the recovery of physiological responses and performance
in real sport settings (Van Hooren and Peake, 2018), which
makes the conclusion of the current study more relevant
and applicable. Therefore, we interpreted these findings to
suggest that IPC was at least as efficient in maintaining
maximal endurance performance as the two other recovery
modalities, which adds to the current literature on the effi-
cacy of this technique for aerobic exercise when the choice
of a particular modality is limited by space, equipment
availability or other contextual reasons.
The similar effects of the three recovery modalities
on performance could be partly explained by their equiva-
lent effect on the increase of local blood volume (↑∆BS,
~14%), suggesting an enhancement of muscle perfusion
immediately before the second TT. IPC has been reported
to improve vasodilation and blood flow at rest (Enko et al.,
2011; Kraemer et al., 2011; Paradis-Deschênes et al.,
2016), and NMES and AR are typically used in recovery
for their “muscle pump effect” on the vascular system re-
sulting from low-frequency stimulation and voluntary
muscle contractions, respectively (Bangsbo et al., 1994;
Borne et al., 2017; Grunovas et al., 2007; Layec et al.,
2008). For example, Borne et al. reported a greater increase
in calf arterial inflow after NMES (~243%), compared to
passive rest (~66%), and this was positively correlated with
performance (Borne et al., 2017). This NMES-derived hy-
per-perfusion response has also been demonstrated to re-
duce the muscle blood flow limitations before exercise or
the spatial heterogeneities within the active muscles during
exercise (Layec et al., 2008). Thus, despite the fact that
NIRS does not offer a robust assessment of blood flow
since it does not detect change in blood velocity (DeLorey
et al., 2003), the increase in local blood volume in the pre-
sent study is in accordance with previous studies and sug-
gests enhanced perfusion following all three modalities.
The higher local blood volume in the quadriceps
muscle following all three modalities did not transfer into
higher muscle O2 extraction (estimated non-invasively
through [HHb] changes), which is in agreement with some,
but not all, studies. Indeed, IPC accelerated muscle deoxy-
genation dynamics and enhanced performance during
whole-body cycling (Kido et al., 2015), and increased mus-
cle perfusion and O2 uptake in strength-trained athletes, al-
beit during maximal contractions (Paradis-Deschênes et
al., 2016). However, IPC applied in hypoxia before 2 re-
peated 5-km cycling TTs, compared to SHAM, did not im-
prove the TT performed immediately after the intervention,
but prevented the performance decrement 2 h later, proba-
bly through greater O2 extraction (da Mota et al., 2019).
This is in accordance with the delayed positive effect of
IPC observed on sprint swimming performance at sea level
(Lisboa et al., 2017). Thus, one may argue that there may
exist a minimum time delay for the IPC-derived effects
(e.g., improved tissue perfusion and metabolism) to come
into play and enhance performance. The timing of the IPC
procedure before a subsequent exercise and the delayed
physiological effects should be investigated in future stud-
ies. It could also be argued that the subsequent TT in this
study could have been limited by factors other than O2 de-
livery and consumption (Amann, 2011; Knicker et al.,
2011).
Maintaining blood flow after exercise is also para-
mount to remove metabolic by-products (such as hydrogen
ions, inorganic phosphate) produced during high-intensity
exercise from the contraction sites and to convert lactate
back to glucose (Ament and Verkerke, 2009; Borne et al.,
2017; Malone et al., 2014b; Neric et al., 2009). The ergo-
genic effects of AR and NMES in that regards have already
been reported (Bieuzen et al., 2014; Borne et al., 2017) and
clinical studies on IPC have also reported slowing of aci-
dosis and reduced lactate production (Andreas et al., 2011;
Salvador et al., 2016). However, experimental effects may
be more easily detected when compared to a control condi-
tion with passive rest. In the present study, IPC was com-
pared to modalities that were reported to be ergogenic on
several occasions and, hence, displayed neither beneficial
nor detrimental effects on blood markers during recovery
and subsequent exercise. All TTs induced metabolic acido-
sis, and not surprisingly, a decrease in base excess, with no
differential impact of the recovery modality. Moreover, de-
spite some marginal differences between modalities after
30 min of recovery, values for pH (7.44 to 7.48) and the
concentrations of lactate (4.1 to 4.8 mmolꞏL-1), bicar-
bonates (22.7 to 24.2 mmolꞏL-1) as well as the base excess
of blood (-0.6 to 0.4 mmolꞏL-1) were within the normal
clinical range. Studies including more frequent blood sam-
ples during recovery are warranted to evaluate potential
differences between modalities in the time course of recov-
ery. These results combined with the fact that the perfor-
mance decrement was not different between conditions,
suggested that the three modalities allowed an equivalent
return to resting baseline conditions.
Conclusion
This study demonstrated that IPC enhanced muscle blood
volume and metabolic by-product clearance and main-
tained muscle oxygenation and performance during a sec-
ond 5-km time trial in endurance-trained athletes to the
same extent as active recovery and neuromuscular
IPC as a recovery modality
770
electrical stimulation. Thus, IPC may represent an afforda-
ble and easy technique for athletes when the choice of a
recovery strategy is limited by practical and/or meteorolog-
ical considerations.
Acknowledgements
The authors thank the athletes for their participation in this study. We also
sincerely thank all graduate and undergraduate students from our research
group for their assistance during sessions. This work was supported by a
research grant from the Institut national du sport du Québec (FO122232)
to FB, and PhD scholarships (Jean Aimé Simoneau and Claude Bouchard
– Monique Chagnon) from Laval University to PPD. The authors have no
conflict of interest to declare. The authors have no conflicts of interests to
declare. The experiments comply with the current laws of the country in
which they were performed.
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Key points
The impact of IPC on the recovery of maximal en-
durance performance and physiological responses to
exercise is unknown.
IPC appears as effective as active recovery and neu-
romuscular electrical stimulation to enhance muscle
blood volume and metabolic by-products clearance.
The performance decrement in a second 5-km cy-
cling time trial repeated after less than an hour of
recovery is similar in the three recovery modalities.
Ischemic preconditioning may complement the ath-
lete’s toolbox to promote recovery in particular set-
tings.
AUTHOR BIOGRAPHY
Pénélope PARADIS-DESCHÊNES
Employment
PhD student in the Department of Kine-
siology at Laval University.
Degree
MSc
Research interests
Physiological responses and the optimi-
zation of exercise performance with a
current emphasis on ischemic precondi-
tioning, training, altitude and recovery.
Julien LAPOINTE
Employment
A strength and conditioning specialist for provincial and na-
tional level athletes at Excellence Sportive Quebec Levis.
Degree
MSc
Research interests
Ischemic preconditioning, endurance exercise performance.
Denis JOANISSE
Employment
Professor of exercise physiology in the
Department of kinesiology at Laval Uni-
versity.
Degree
PhD
Research interests
The impact of exercise and training on
muscle peripheral adaptations.
François BILLAUT
Employment
Professor of sport physiology in the De-
partment of kinesiology at Laval Uni-
versity.
Degree
PhD
Research interests
Human adaptations to training and expo-
sure to hypoxia
E-mail: francois.billaut@kin.ulaval.ca
Prof. François Billaut
Department of Kinesiology, Faculty of Medicine, Laval Univer-
sity,2300 rue de la Terrasse, Quebec (QC) G1V 0A6, Canada
