James (2016) Ischaemic preconditioning does not alter the determinants of endurance running performance in the heat

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Eur J Appl Physiol
DOI 10.1007/s00421-016-3430-y
ORIGINAL ARTICLE
Ischaemic preconditioning does not alter the determinants
of endurance running performance in the heat
Carl A. James1
· Ashley G. B. Willmott1
· Alan J. Richardson1
· Peter W. Watt1
·
Neil S. Maxwell1

Received: 8 April 2016 / Accepted: 5 July 2016
© Springer-Verlag Berlin Heidelberg 2016
or affect blood glucose concentration throughout the
trial [mean (±SD); CON 5.03 (0.94) mMol L−1
, IP
5.47 (1.38) mMol L−1
, p = 0.260). There was no differ-
ence in ˙VO2max [CON 55.5 (3.7) mL kg−1
min−1
, IP 56.0
(2.6) mL kg−1
min−1
, p = 0.436], average running econ-
omy [CON 222.3 (18.0) mL kg−1
km−1
, IP 218.9 (16.5)
mL kg−1
km−1
, p = 0.125], or total running time during
graded exercise [CON 347 (42) s, IP 379 (68) s, p = 0.166].
The IP procedure did not change muscle temperature [CON
∆ = 0.55 (0.57) °C, IP ∆ = 0.78 (0.85) °C, p = 0.568], but
did reduce TCORE during exercise (~−0.1 °C, p = 0.001).
Conclusion The novel application of IP prior to exercise
in the heat does not enhance the determinants of endurance
performance. For events where IP appears ergogenic, mus-
cle warming strategies are unnecessary as IP does not influ-
ence deep muscle temperature.
Keywords Ischaemic preconditioning · Occlusion ·
Hyperthermia · Endurance · Lactate threshold · ˙VO2max
Abbreviations
ANOVA Analysis of variance
CON Control group
GXT Graded exercise test
HR Heart rate
IP Ischaemic preconditioning
LTP Lactate turnpoint
PSI Physiological strain index
RE Running economy
RER Respiratory exchange ration
RPE Rating of perceived exertion
TCORE Core temperature
TSKIN Skin temperature
TS Thermal sensation
VE Ventilation rate
Abstract
Purpose Ischaemic preconditioning (IP) has been shown to
be ergogenic for endurance performance in normothermic
conditions and alleviate physiological strain under hypoxia,
potentially through haemodynamic and/or metabolic mech-
anisms. Exertional hyperthermia is characterised by com-
petition for blood flow between the muscles and skin, an
enhanced metabolic strain and impaired endurance perfor-
mance. This study investigated the effect of IP on the deter-
minants of endurance performance, through an incremental
exercise test in the heat.
Method Eleven males completed two graded exercise tests
in the heat (32 °C, 62 % RH) until volitional exhaustion,
preceded by IP (4 × 5 min 220 mmHg bilateral upper
leg occlusion) or a control (CON) condition (4 × 5-min
50 mmHg bilateral).
Result IP did not improve running speeds at fixed blood
lactate concentrations of 2 and 4 mMol L−1
(p = 0.828),
Communicated by Narihiko Kondo.
* Carl A. James
carlos_james@hotmail.co.uk
Ashley G. B. Willmott
a.willmott@brighton.ac.uk
Alan J. Richardson
a.j.richardson@brighton.ac.uk
Peter W. Watt
p.watt@brighton.ac.uk
Neil S. Maxwell
N.maxwell@brighton.ac.uk
1
Environmental Extremes Laboratory, Centre for Sport
and Exercise Science and Medicine (SESAME), University
of Brighton, Welkin Laboratories, Denton Road,
Eastbourne BN20 7SN, UK

Eur J Appl Physiol
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˙VO2max Maximum oxygen consumption
v˙VO2max Velocity at ˙VO2max
Introduction
Repeated bouts of occlusion and reperfusion, termed
ischaemic preconditioning (IP), are established within
clinical practice to prepare cardiac muscle for subsequent
stresses arising from surgically induced hypoxia, infarc-
tion and reperfusion (Hausenloy and Yellon 2008). Skeletal
muscle may also be exposed to modest exercise-induced
arterial hypoxemia and ischaemic threat (Noakes 2000).
Therefore, this simple, acute intervention has been utilised
prior to a range of exercise protocols and shown to offer
meaningful improvements in both high intensity and endur-
ance exercise (Salvador et al. 2016).
Of note, Crisafulli et al. (2011) reported a 4 % increase
in maximal power output and a ~40 s increase in total exer-
cise time during an incremental cycling test to exhaustion
immediately following IP, whilst de Groot et al. (2010)
observed a 3 % increase in ˙VO2max, alongside a 1.6 %
increase in maximal power output during incremental
cycling. Few studies have considered endurance running,
however, Bailey et al. (2012a) reported lower blood lactate
concentration (mean difference −1.07 mMol L−1
) through-
out an incremental submaximal running test, although no
subsequent effect on maximum oxygen consumption (˙V
O2max) was observed. This was followed by improved 5 km
running time with a mean improvement of 34 s (2.5 %,
p = 0.03), highlighting the potential for use prior to endur-
ance running. In swimming, IP may provide a particular
benefit by mitigating against the relative exercise-induced
hypoxia that occurs as a result of specified breathing pat-
terns (Noakes 2000), that elicit a decreased arterial partial
pressure of oxygen and decreased blood pH (Craig 1986;
Sharp et al. 1991). Accordingly, Jean-St-Michel et al.
(2011) reported a meaningful and statistically significant
0.7 s improvement in 100 m swim time (−1.1 %, p = 0.02)
following IP, improving personal best times within a highly
trained cohort. Exercising in extreme environments may
also elicit a heightened physiological strain and as such, IP
has been shown to be beneficial under hypoxia (Foster et al.
2011, 2014), but has yet to be adopted under heat stress.
Bushell et al. (2002) have mimicked the protective
effects of IP through adenosine infusion. Adenosine may
proffer beneficial clinical and exertional effects by act-
ing as a vasodilator (Gustafsson et al. 1993), and/or open-
ing potassium (KATP) channels, which in turn preserves
energy (Pang et al. 1997; Cohen et al. 2000). This may
occur in reduced mitochondrial oxygen consumption
(Cooper and Brown 2008), although a reduced oxygen
consumption for a given submaximal exercise intensity is
not uniformly observed (De Groot et al. 2010). There is
also likely an effect of IP in promoting endothelial nitric
oxide biosynthesis (Kimura et al. 2007), which appears to
maintain vascular function that may be impaired follow-
ing high intensity exercise (Bailey et al. 2012b). In turn,
such changes will serve to maintain the supply of oxygen
and energy substrates, whilst removing metabolites during
exercise. Collectively, these haemodynamic and/or meta-
bolic ischaemic responses may present a more efficient
muscular action, facilitating greater work to be completed
for the same energy expenditure (Crisafulli et al. 2011;
Pang et al. 1995). Clevidence et al. (2012) speculated that
IP appears to be effective when an ischaemic event is most
likely and may require a minimum metabolic stress to be
achieved during the exercise bout to be effective during
exercise. Thus, extreme environmental conditions, higher
intensity exercise (Crisafulli et al. 2011) and/or activities
such as running (Bailey et al. 2012a) and swimming (Jean-
St-Michel et al. 2011), that elicit significant physiological
strain, warrant investigation.
Environmental heat stress provides an additional stressor
to exercise performance (Galloway and Maughan 1997).
Indeed, endurance running in the heat is characterised by
competition for blood flow between the muscles and skin
as individuals become hyperthermic (Gonzalez-Alonso
et al. 2008) and the potential for hyperthermia-induced
central fatigue (Nybo and Nielsen 2001), alongside meta-
bolic alterations that include increased blood lactate pro-
duction, carbohydrate oxidation and glycogen depletion
(Hargreaves 2008). Collectively, these alterations contrib-
ute towards the widely reduced exercise duration and inten-
sity during exercise under heat stress (Nybo et al. 2014),
whilst an increase in glycogenolysis may have implica-
tions for prolonged exercise or regular training in the heat
(Hargreaves 2008). Mechanisms underpinning the shift
towards carbohydrate metabolism may relate to compro-
mised blood flow due to enhanced skin blood flow for
thermoregulation, a Q10 effect upon glycolysis enzymes
and/or elevated plasma adrenaline levels (Febbraio 2001).
Alongside these changes, the lactate turnpoint (Lorenzo
et al. 2011) the exercise intensity that elicits an exponen-
tial increase in blood lactate concentration (Jones 2006),
and ˙VO2max (Nybo et al. 2014) are impaired in the heat.
These markers help to determine endurance performance,
when combined with running economy (Bassett and How-
ley 2000). These changes are significant given that the lac-
tate turnpoint (LTP) remains a strong predictor of time trial
performance in hot environments (Lorenzo et al. 2011) and
appears sensitive to the effects of IP (Bailey et al. 2012a),
whilst ˙VO2max is considered the best individual predictor
of performance, explaining 90.2 % of the total variance in
a 16-km run (McLaughlin et al. 2010). Furthermore, evi-
dence exists that occlusion may modify thermoregulatory

Eur J Appl Physiol
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responses, through the muscle metaboreflex, independently
of body temperature (Kondo et al. 1999). Thus, through
effecting a change in the peripheral vasculature, muscle
metaboreflex and/or influence mitochondrial function, IP
may ameliorate some of the metabolic changes and ther-
moregulatory responses under heat stress, in turn influenc-
ing markers such as LTP and ˙VO2max, thereby reducing the
fractional utilisation of ˙VO2max. Theoretically, therefore, IP
may be a beneficial acute intervention for athletes to con-
sider in addition to traditional techniques such as precool-
ing (James et al. 2015; Randall et al. 2015) and heat accli-
mation (Gibson et al. 2015; Mee et al. 2015; Willmott et al.
2016), that seek to alleviate the significant impairment to
endurance performance afforded by heat stress (Guy et al.
2015).
This study investigated the effect of IP across a range
of submaximal and maximal physiological markers during
incremental exercise in the heat. It was hypothesised that
IP would ameliorate the decline in the lactate turnpoint
and ˙VO2max during endurance running in the heat, provid-
ing potential as a simple, acute ergogenic technique for use
prior to competition.
Methods
Participants
Eleven male, recreational club runners volunteered as par-
ticipants [mean (±SD)]: age 37 (12) years, stature 178.3
(5.9) cm, mass 74.4 (6.1) kg, sum of four skinfolds 25.1
(3.3) mm, ˙VO2max 57.6 (3.2) mL kg−1
min−1
. All partici-
pants trained at least three times per week and had run a
sub 22 min 5 km in the previous month [mean (±SD) 20:06
(1.0) min]. Each participant provided written informed con-
sent and institutional ethical approval was issued in accord-
ance with the Declaration of Helsinki 1964, as revised in
2013. Participants arrived hydrated, having refrained from
intense exercise for 48 h preceding trials, as well as avoid-
ing alcohol, caffeine and replicating their diet for 24 h prior
to each test, as is common in similar trials (James et al.
2014; Hayes et al. 2014). Finally, participants were asked
to prepare for each trial as they would for a competition.
Experimental design
A repeated measures crossover design was used to inves-
tigate the effect of a brief period of IP on the determinants
of endurance performance in the heat, with two conditions;
IP and control (CON). All participants undertook a prior,
cooler familiarisation trial [24 °C, 50 % relative humidity
(RH)], containing no treatment, before two experimen-
tal trials in the heat (32 °C, 60 % RH). Testing occurred
during the UK spring (mean ambient temperature of 12 °C)
therefore, participants had been absent from repeated exter-
nal heat exposure across during previous months. All tri-
als were separated by 7–10 days to prevent an acclimation
effect from repeated heat exposures (Barnett and Maughan
1993), and occurred at the same time of the day (±2 h) to
minimise fluctuation in thermoregulatory responses as a
result of circadian variation (Reilly and Waterhouse 2009).
Ischaemic preconditioning
In both IP and CON trials, whilst in the supine position,
participants were fitted with automated tourniquet thigh
cuffs (10 × 30 cm), positioned around the upper thigh of
both legs. Each leg was exposed to 5 min of occlusion with
the cuff inflated to 220 mmHg (IP) or 50 mmHg (CON),
followed by 5 min of reperfusion and rest for four consecu-
tive cycles, as has previously been shown to be effective
(Jean-St-Michel et al. 2011; Bailey et al. 2012a). An over-
view of the preconditioning protocol and subsequent graded
exercise test (GXT) is shown in Fig. 1. The occlusion pres-
sure of 220 mmHg was chosen following pilot testing to
identify the limb occlusion pressure when blood flow traces
within the popliteal artery ceased, utilising Doppler ultra-
sound (Shenzhen Delicate Electronics Co. Ltd., Shenzhen,
China). Occlusion pressure for the group was between 160
and 170 mmHg, therefore, 220 mmHg ensured the pressure
was at least 50 mmHg above systolic blood pressure. This
pressure is supported by similar IP literature (Bailey et al.
2012a; de Groot et al. 2010; Sharma et al. 2015), how-
ever, recent near infrared spectroscopy data indicates arte-
rial pulses may be observed up to 300 mmHg (Kido et al.
2015). Pilot data, collected using Doppler ultrasound, as
well as published literature (Gibson et al. 2013) identified
50 mmHg as an appropriate control pressure, as it provides
a sensation of pressure without impairing arterial flow. As
IP cannot be truly blinded, participants were informed both
conditions had the potential to be equally effective. Partici-
pants completed an extended rest period during the famil-
iarisation trial, prior to exercise. As shown in Fig. 1, partic-
ipants began a low intensity five min warm-up ten min after
IP. Following the warm-up there was a 5 min break before
the exercise test began.
Graded exercise tests
A graded exercise test, split into two parts; GXT 1 and
GXT 2, was adopted as displayed in Fig. 1. Participants
entered the thermostatically controlled environmen-
tal chamber (WatFlow control system TISS, Hampshire,
UK) within which conditions were continuously moni-
tored throughout the trial using a heat stress meter (HT30,
Extech Instruments, USA). GXT 1 was similar to that

Eur J Appl Physiol
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adopted by James et al. (2015), initially a submaximal
incremental speed protocol followed by GXT 2, an incre-
mental gradient protocol to volitional exhaustion. Starting
speeds were between 8 and 11 km h−1
(1 % gradient, Jones
and Doust 1996) depending upon recent running perfor-
mance, with each participant completing a minimum of six
stages, using speed increments of 1 km h−1
. Each stage was
4 min, consisting of 3 min running and 1 min for capillary
blood sampling, analysed using a YSI 2300 Glucose and
Lactate analyser (YSI, Hampshire, UK, 2 % typical error
at 2 mMol L−1
, 1.4 % typical error at 4 mMol L−1
). Exer-
cise continued until blood lactate concentration exceeded
4 mMol L−1
. The same number of exercise stages and run-
ning speeds completed during the familiarisation trial were
replicated during all subsequent trials. Following a 10 min
rest, GXT 2 began at a speed 2 km h−1
below the previous
GXT 1 final speed, with gradient increasing by 1 % each
min and continuing until volitional exhaustion. Participants
were not permitted to drink and were blinded to all forms
of feedback throughout the duration of the trial.
Physiological measures
During the familiarisation trial, anthropometric data were
collected for stature, body mass and a four site skin fold
calliper assessment (Harpenden, Burgess Hill, UK) across
iliac crest, subscapular, triceps and biceps (Durnin and
Womersley 1974). During all trials, a urine sample was
provided upon arrival for assessment of hydration sta-
tus. Euhydration was achieved when urine osmolality and
urine specific gravity were below 700 mOsmol kg−1
H2O
and 1.020, respectively (Sawka et al. 2007). Single-use
rectal probes (Henleys Medical, UK, Meter logger Model
401, Yellow Springs Instruments, Missouri, USA) were
inserted 10 cm beyond the anal sphincter for core tempera-
ture (TCORE) measurement. Telemetry thermistors (U-Type
connected to Gen II GD38 transmitter, Eltek, UK) were
attached to the mid-belly of the pectoralis major, biceps
brachii, rectus femoris and gastrocnemius for measurement
of skin temperature (TSKIN) with data transmitted wirelessly
to a datalogger (RX250AL 1000 series Wireless Squirrel
Logger, Eltek) as per James et al. (2014). Heart rate was
monitored continuously using a Polar 810i heart rate moni-
tor (Kempele, Finland). Pre and post the IP protocol, mus-
cle temperature was measured through a needle thermistor
probe (Type MLA connected to DM 852 Medical Precision
Thermometer, Ellab A/S, Hilleroad, Denmark) inserted to
a depth of two centimetres into the right thigh at the mid-
point between the greater trochanter and tibial tuberosity, in
the vastus lateralis.
Heart rate (HR), TCORE, TSKIN, rating of perceived
exertion (RPE, Borg 1998) and thermal sensation (TS,
0 = unbearably cold to 8 = unbearably hot, Gagge et al.
1969) were noted every 5 min during rest and the IP pro-
tocol, and at the end of each stage during exercise. The
following physiological responses were calculated; lactate
Fig. 1 Protocol overview. The entire protocol was completed in a hot
environment. ‘R’ and ‘L’ represent occlusion of right and left legs,
respectively. ‘GXT 1’ denotes 3 min exercise stages with increments
of 1 km h−1
. ‘GXT 2’ denotes gradient based test to exhaustion, incor-
porating 1 min stages with increments of 1 %

Eur J Appl Physiol
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thresholds, running economy (RE), ˙VO2max and velocity at
˙VO2max (v˙VO2max). Fixed blood lactate concentrations of 2
and 4 mMol L−1
were used to denote the lactate threshold
and lactate turnpoint, respectively, by solving the polyno-
mial regression equation for blood lactate concentration
versus speed at 2 and 4 mMol L−1
as per Saunders and
Green (2013) and previously adopted (James et al. 2015).
This approach accounted for differences in the number of
stages completed, removed subjectivity of experimenter
identification and provided precision to less than 1 km h−1
.
Ventilatory gases were measured using 30 s averaging from
a Metalyzer 3B analyser (Cortex, Leipzig, Germany) and
the two values from the final min of each stage used for
measuring RE, ventilation (VE) and respiratory exchange
ratio (RER). Average running economy across the first five
exercise stages is presented, although the data from each
individual stage was used for analysis. During the ˙VO2max
test, the highest 30 s moving average represented ˙VO2max.
A ˙VO2max, not ˙VO2peak, was accepted when a ˙VO2 plateau
(2 mL kg−1
min−1
across two successive 30 s fixed-time
averages) was observed. Whilst a subsequent verification
phase is recommended for the robust assessment of ˙VO2max
(Midgley and Carroll 2009), the precise consequences
of heat strain cannot not be accurately replicated, which
would be necessary, given the strong relationship between
heat strain and ˙VO2max decrement (Nybo et al. 2014).
Therefore, in the absence of a plateau, a test was deemed
maximal if three out of the following four criteria were
met; blood lactate concentration 8 mMol L−1
, HR within
ten beats of age predicted maximum, respiratory exchange
ratio 1.1, and RPE at or above 19 (Edvardsen et al. 2014).
Velocity at ˙VO2max (v˙VO2max) was calculated by multiply-
ing ˙VO2max (mL kg−1
min−1
) by 60 and dividing by the
mean running economy (mLO2 kg−1
km−1
) determined
during the first five stages of the treadmill test as per Jones
(2006). Sweat rate (L h−1
) was calculated from the differ-
ence in pre and post nude body mass divided by the indi-
vidual exercise duration.
Statistical analyses and derivative calculations
Mean skin temperature (TSKIN) (Ramanathan 1964):
Physiological Strain Index (PSI) (Moran et al. 1998):
T0
CORE and HR0
denote baseline and T1
CORE and HR1
denotes measurement taken at the respective time.
All outcome variables were assessed for normality
and sphericity prior to further analysis. Where assump-
tions of normality were not met, data was log transformed
as appropriate. Two way, repeated measures ANOVA
(treatment × time) were used to test for differences in
blood lactate indices, expired metabolic gases, TCORE,
TSKIN, PSI, RPE and TS. Where appropriate, Bonferroni
adjusted pairwise comparisons revealed where differences
occurred. Paired samples t tests were used to detect dif-
ferences between running time until ˙VO2max during GXT
2, v˙VO2max sweat rate, environmental conditions and mus-
cle temperature. Data were analysed using SPSS (Version
21, SPSS Inc, Illinois, USA) with statistical significance
set at p 0.05 and data presented as means and standard
deviation (SD). Effect sizes for main effects and interac-
tion effects are presented as partial eta squared (η2
), whilst
differences between two related samples were evaluated
through Cohen’s dav (d) in accordance with Lakens (2013).
Results
Environmental conditions did not differ between con-
ditions; CON 32.6 (0.3) °C, 61.8 (3.1) % RH, IP 32.4
(0.3) °C, 60.8 (3.6) % RH [wet bulb globe temperature
CON 28.2 (0.5) °C, IP 27.8 (0.6) °C, t = 1.531, p = 0.157].
Similarly, comparisons of physiological variables between
CON and IP, at rest prior to cuff inflation, did not reveal
differences between conditions (Table 1).
During GXT 1, IP did not improve running speeds at
fixed blood lactate concentrations of 2 and 4 mMol L−1
as
shown in Figs. 2 and 3. At 2 mMol L−1
, the mean running
speed in CON was 11.6 (1.2) km h−1
and 11.7 (1.4) km h−1
Mean TSKIN = 0.3(TCHEST + TARM) + 0.2(TTHIGH + TCALF),
PSI = (5 × (T1
CORE−T0
CORE))/((39.5−T0
CORE)
+ (5 × (HR1
−HR0
) × (180 − HR0
)),
Table 1 Comparisons of physiological variables at rest during CON
and IP, prior to cuff inflation (mean ± SD)
TCORE core temperature, TSKIN skin temperature, TTHIGH thigh tem-
perature, TCALF calf temperature, TMUSC muscle temperature, t t test
value, p significance value, d Cohen’s d effect size
CON IP t p d
Hydration
(mOsmol kg−1
H2O)
247 (191) 322 (208) 0.842 0.419 0.37
Blood lactate
(mMol L−1
)
0.85 (0.38) 0.80 (0.29) 0.533 0.605 0.11
Blood glucose
(mMol L−1
)
5.17 (0.94) 5.08 (1.26) 0.432 0.675 0.11
Heart rate
(b min−1
)
55 (6) 52 (8) 2.138 0.058 0.52
TCORE (°C) 37.00 (0.28) 37.04 (0.36) 0.463 0.654 0.11
TSKIN (°C) 34.15 (0.74) 34.13 (0.36) 0.107 0.918 0.03
TTHIGH (°C) 33.90 (0.69) 33.84 (0.57) 0.274 0.792 0.10
TCALF (°C) 33.69 (0.74) 33.54 (0.58) 0.605 0.564 0.23
TMUSC (°C) 34.82 (0.69) 34.50 (0.96) 0.732 0.483 0.39

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in IP. At 4 mMol L−1
running speed in CON was 13.6
(1.0) km h−1
and 13.5 (1.2) km h−1
in IP. There were no
main effects between conditions (F = 0.050, p = 0.828,
partial η2
= 0.005), or interaction effects across the levels
of blood lactate concentration (F = 1.319, p = 0.277, par-
tial η2
= 0.117). Similarly, during exercise, no main effect
of treatment on blood glucose concentration was observed
[CON 5.03 (0.94) mMol L−1
, IP 5.47 (1.38) mMol L−1
,
F = 1.423, p = 0.260, partial η2
= 0.125], nor an interac-
tion effect (F = 2.056, p = 0.087, partial η2
= 0.171).
There was no main effect for treatment in RE [CON
222.3 (18.0) mL kg−1
km−1
, IP 218.9 (16.5) mL kg−1
km−1
,
F = 2.806, p = 0.125, partial η2
= 0.219], nor an interac-
tion effect (F = 0.446, p = 0.774, partial η2
= 0.043). No
main effect was observed on VE for treatment (F = 0.013,
p = 0.910, partial η2
= 0.001), nor an interaction effect
(F = 0.843, p = 0.477, partial η2
= 0.078). Similarly, there
was no main effect for RER (F = 1.593, p = 0.236, partial
η2
= 0.137), or an interaction effect (F = 1.318, p = 0.272,
partial η2
= 0.116).
˙VO2max, as defined by specified criteria, was achieved
in 16 trials, with the remaining 6 trials demonstrating ˙V
O2peak. There were 7 ˙VO2max and 4 ˙VO2peak in CON, and
9 ˙VO2max and 2 ˙VO2peak following IP. There was no differ-
ence in ˙VO2max [CON 55.5 (3.7) mL kg−1
min−1
, IP 56.0
(2.6) mL kg−1
min−1
, t = −0.812, p = 0.436, d = 0.17],
as shown in Fig. 4, nor in total running time during GXT
2 [CON 347 (42) s, IP 379 (68) s, t = 1.496, p = 0.166,
d = 0.58] (Fig. 5). However, differences in v˙VO2max were
observed (Fig. 6), with IP demonstrating a greater predicted
running speed [CON 15.0 (1.2) km h−1
, 15.4 (1.2) km h−1
,
t = 2.727, p = 0.021, d = 0.33].
Resting HR was not different between groups (Table 1),
however, HR as noted at the end of each 5 min occlu-
sion period, was consistently lower whilst undergoing
IP, compared with CON [CON 60 (10) b min−1
, IP 56
(10) b min−1
, F = 9.977, p = 0.010, partial η2
= 0.499].
The lower pre-exercise heart rate did not continue during
exercise, with HR similar throughout GXT 1 (F = 0.132,
p = 0.724 partial η2
= 0.13), and at maximum during GXT
8
9
10
11
12
13
14
15
16
PIlortnoCPIlortnoC
Runningspeed(km.h-1)
4 mMol.L-12 mMol.L-1
Fig. 2 Running speed at 2 and 4 mMol L−1
, respectively. Grey col-
umns represent group means (±SD), with individual data shown by
grey lines
0.0
0.5
1.0
1.5
2.0
2.5
3.0
3.5
4.0
4.5
5.0
5.5
6.0
6.5
7.0
7.5
3 7 11 15 19 23
Bloodlactate(mmo.L-1)
Time (min)
Control IP Famil
Fig. 3 Mean (±SD) blood lactate concentration during GXT 1 for IP
and CON. ‘Famil’ represents cooler familiarisation, and is presented
in grey, without error bars for clarity
46
48
50
52
54
56
58
60
62
64
Famil Control IP
VO2max(mL.kg-1.min-1)
Fig. 4 ˙VO2max during familiarisation, Control and IP. Grey columns
represent group means (±SD), with individual data shown by grey
lines. ‘Famil’ represents normothermic familiarisation
200
250
300
350
400
450
500
550
IPControl
RunningƟme(seconds)
Fig. 5 Total running time during GXT 2. Grey columns represent
group means (±SD), with individual data shown by grey lines

Eur J Appl Physiol
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2 [CON 186 (10) b min−1
, 186 (11) b min−1
, t = 0.341,
p = 0.740, d = 0.03]. A main effect for PSI was observed,
with PSI lower following IP (F = 5.548, p = 0.043, par-
tial η2
= 0.381), with no interaction effect (F = 1.380,
= 0.133). No differences were
observed between IP and CON for RPE (F = 0.028,
= 0.003), or thermal sensation
(F = 0.054, p = 0.821, partial η2
= 0.005).
There were no differences in thermoregulatory variables
at rest, as shown in Table 1. There was also no main effect
for treatment on TCORE during the preconditioning phase
(F = 0.666, p = 0.433, partial η2
= 0.062). However, there
was a progressive decrease in TCORE during this phase,
which was not matched in CON, providing an interaction
effect (F = 6.098, p = 0.009, partial η2
= 0.379) as shown
in Fig. 7. However, Bonferroni post hoc did not detect dif-
ferences at any time points. The IP phase did not elicit a
change in muscle temperature [CON ∆ = 0.55 (0.57) °C,
IP ∆ = 0.78 (0.85) °C, t = −0.593, p = 0.568, d = 0.33].
There was also no main effect for treatment on mean TSKIN
throughout the IP phase (F = 2.177, p = 0.184, partial
η2
= 0.237) and no differences in localised skin tempera-
tures of the legs at the calf (F = 0.001, P = 0.971, par-
tial η2
= 0.000) or thigh (F = 4.522, p = 0.071, partial
η2
= 0.392).
The reduced TCORE following IP continued during GXT
1, with IP lower throughout (F = 27.886, p = 0.001, par-
tial η2
= 0.756), however, the rate of increase was simi-
lar between the groups, so no interaction effect was seen
(F = 3.308, p = 0.05, partial η2
= 0.269). No difference
in mean TSKIN during exercise was observed between tri-
als (F = 0.001, p = 0.976, partial η2
= 0.000). Similarly,
calf (F = 0.804, p = 0.400, partial η2
= 0.103) and thigh
(F = 0.475, p = 0.513, partial η2
= 0.064) skin tempera-
tures did not differ between conditions during exercise.
Finally, sweat loss did not differ between conditions [CON
2.76 (0.54), IP 2.87 (0.83) L h−1
, t = −0.471, p = 0.648,
d = 0.15].
Discussion
This study investigated the effect of IP on the primary
physiological determinants of endurance running, notably
the lactate turnpoint, ˙VO2max and running economy, under
heat stress. Whilst an enhanced cardiovascular and meta-
bolic strain are not limiting factors leading to the cessation
of exercise during submaximal exercise in the heat (Gon-
zalez-Alonso et al. 2008), the competition for blood flow
between the skin and the muscles during exercise leads to
impaired performance in competition or training, relative to
cooler conditions. It was hypothesised that the novel appli-
cation of IP in the heat would alleviate some of the deleteri-
ous physiological consequences of heat strain, possibly by
enhancing skeletal muscle vasodilation and/or influencing
muscle metabolism, leading to a mediated metabolic strain,
as has been demonstrated under normothermic conditions.
11
12
13
14
15
16
17
18
19
20
PIlortnoC
vVO2max(km.h-1)
*
Fig. 6 v˙VO2max during GXT 2 between conditions. Grey columns
represent group means (±SD), with individual data shown by grey
lines. Asterisk represents a statistical difference (p 0.05)
Fig. 7 Mean (±SD) Core
temperature throughout the
protcocol. Exercise data is taken
from GXT 1 only. Error bars
represent one standard devia-
tion. IP-R ischaemic precondi-
tioning of the right leg, IP-L the
left leg
36.5
36.8
37.1
37.4
37.7
38.0
38.3
38.6
38.9
39.2
REST IP-R IP-L IP-R IP-L IP-R IP-L IP-R IP-L 3 7 11 15 19 23
Coretemperature(°C)
Exercise Ɵme (min)
Control IP

Eur J Appl Physiol
1 3
Moreover, occlusion has previously been shown to initiate
thermoregulatory responses independently of changes in
body temperature (Kondo et al. 1999). However, these data
indicate IP does not provide any benefit to the determinants
of endurance performance in the heat.
The lack of difference in blood lactate accumulation
during GXT 1 is distinctly different from the results of Bai-
ley et al. (2012a). They reported a reduced blood lactate
concentration throughout an incremental, submaximal run
and attributed subsequent improved 5 km performance to
improvements in vascular function, facilitating enhanced
removal and transport of lactate for uptake and use. Bailey
et al. (2012a) speculated that such changes may increase
lactate oxidation in the mitochondria of working skeletal
muscles, and/or reflect energy sparing, through augmented
mitochondrial flux or increased excitation–contraction
coupling efficiency, as has previously been observed in
preconditioned pig muscle (Pang et al. 1995). Recently,
observed improvements in endurance exercise of the fore-
arm suggests such alterations in muscle metabolism may
occur without concomitant haemodynamic changes (Bar-
bosa et al. 2015). Previously, the improvements to vascu-
lar function following IP have been attributed to biochemi-
cal changes that follow ATP degradation during periods of
occlusion. For example, the accumulation of intracellular
adenosine interacts with adenosine receptors A1 and A2
(Marongiu and Crisafulli 2014), and ultimately mediates
vasodilation (Riksen et al. 2008). Adenosine accumulation
has also been suggested to maintain endothelium function,
when it is normally impaired following strenuous exercise
(Bailey et al. 2012b). Alongside adenosine, ischaemia stim-
ulates increased endothelial nitric oxide (NO) release that
attenuates sympathetic vasoconstriction, inducing smooth
muscle relaxation as part of the secondary plateau phase
of the bimodal cutaneous response to local hyperthermia
(Kellogg et al. 1998). It is possible that under heat stress,
any reduction in skeletal muscle energy consumption were
too small for these measures to detect or, from a haemody-
namic perspective, skeletal muscle may not be sensitive to
further increases in NO following IP, due to the apparently
greater role of prostaglandins, relative to NO for inducing
vasodilation (Kellogg et al. 2005). Moreover, it is possible
that blood vessels are already maximally dilated from heat
stress (Lorenzo and Minson 2010).
Muscle temperature was measured pre and post IP to
quantify the thermal effects of such large, cyclical altera-
tions in major limb blood flow. This measurement would
appear to be novel within IP studies and the lack of change
in muscle temperature suggests passive heating or rewarm-
ing of muscles to be unnecessary when IP is adopted, in
order that muscle temperature is maintained for the start
of an anaerobic exercise bout. While muscle temperature
did not change following IP, interestingly IP appeared to
elicit a small change in resting TCORE (~0.1 °C). This may
reflect a redistribution of blood away from the core to the
periphery as part of recovery for the previously occluded
limb. Alternatively, this could be explained through the
central integration and command of peripheral inputs, with
changes in muscle metaboreflex having previously initiated
thermoregulatory responses in the absence of changes in
body temperature (Kondo et al. 1999). During exercise this
difference was maintained, presenting a small, but consist-
ent change in TCORE, which in turn influenced PSI. How-
ever, the small magnitude of difference in TCORE between
conditions (~0.1 °C) explains the lack of an independent
effect of body temperature on performance measures such
as ˙VO2max and blood lactate indices. Furthermore, the per-
formance implications of this reduced TCORE are likely
negligible, given the subsidiary role of TCORE, relative to
TSKIN, for influencing perceived thermal strain (Flouris
and Schlader 2015), which was unchanged following IP.
Alongside perceived thermal strain, cardiovascular strain
may be considered a primary determinant of endurance
performance in the heat (Schlader et al. 2011; Périard and
Racinais 2015), however, the small reduction in TCORE did
not elicit a change in HR. However, it should be acknowl-
edged that modest changes in TCORE have the potential to
modify effector thresholds such as vasomotor and sudomo-
tor sensitivity or sweat rate (Kondo et al. 2009), however,
this effect may necessitate sweating to have commenced,
which is unlikely during IP at rest, and may explain why
neither TSKIN nor sweat rate subsequently differed. Whilst
the observed reduction in TCORE may be considered small
in comparison to that following precooling techniques
(Bongers et al. 2015; Tyler et al. 2015), future research may
also consider how this could complement a cooling strategy
prior to competing in the heat. Moreover, future research
should investigate changes in whole-body blood flow to
understand the observed change in TCORE, that appears
to be independent of changes in both muscle and skin
temperatures.
Among other studies to have found no significant effect
from IP during submaximal exercise, Clevidence et al.
(2012) suggested their incremental cycling exercise pro-
tocol may not have provided sufficient ischaemic chal-
lenge to realise the benefits of IP, although the authors also
acknowledge they may not have achieved full occlusion
during the IP procedure. Notwithstanding, the elevated
physiological and metabolic strain observed during sub-
maximal running in the heat, compared with familiarisation
data collected under cooler conditions (Fig. 3) is support-
ive of an ischaemic challenge, especially given the dis-
tinct improvements following IP observed by Bailey et al.
(2012a) during a similar normothermic incremental run-
ning protocol. However, Febbraio (2001) has highlighted
that oxygen availability is not the main factor mediating

Eur J Appl Physiol
1 3
the augmented glycogenolysis and elevated blood lactate
concentration during moderate exercise under heat stress,
although they did not rule out a role for decreased muscu-
lar blood flow influencing metabolic processes in an oxy-
gen independent manner. Indeed, Febbraio et al. (1994)
have previously highlighted a strong relationship between
reduced body temperature and reduced plasma adrena-
line levels in explaining metabolic changes following heat
acclimation, notably a reduced RER, indicating greater
fatty acid or ketone oxidation and less glycogenolysis.
These findings were in the apparent absence of changes in
fibre type recruitment and with changes far exceeding that
expected from a Q10 effect on glycogenolytic and glyco-
lytic processes. Therefore, despite potentially greater blood
flow to the muscle following IP, metabolic alterations and
metabolite production by the muscle were maintained. This
is in keeping with elevated muscle temperature and adrena-
line being the prominent drivers of increased intramuscular
carbohydrate utilisation in the heat, rather than localised
ischemia (Febbraio 2001), although it is acknowledged
these were not directly measured in the current study.
˙VO2max is attenuated in the heat (Nybo et al. 2014), as
a consequence of cardiovascular strain and insufficient
muscular blood flow at maximal intensities (Gonzalez-
Alonso et al. 2008). Given that mean finishing TCORE
in both conditions was elevated (39.0 °C CON, 38.9 °C
IP), and ˙VO2max was lower than the cooler familiarisation
(~−2 mL kg−1
min−1
, Fig. 4), it is probable ˙VO2max was
indeed impaired in this cohort. Notwithstanding that IP was
applied under different environmental conditions, effects
of IP on ˙VO2max appear equivocal (Marocolo et al. 2015).
A potential explanation for such variability in ˙VO2max fol-
lowing IP are methodological differences between exercise
protocols, time of exercise following IP, training status of
participants, as well as data analysis techniques, such as ˙V
O2 averaging time. Furthermore, it is unclear if other stud-
ies adopted ˙VO2max criteria as in this study, or may in fact
be reporting ˙VO2peak. Although the adoption of ˙VO2max cri-
teria is not without criticism (Poole et al. 2008), verification
phases are supported to reaffirm the attainment of ˙VO2max
(Midgley and Carroll 2009), however, this is not reported
across the IP literature. In this study, a verification phase
would be confounded by the environmental conditions,
given ˙VO2max impairments are determined by the progres-
sive influence of heat strain (Gonzalez-Alonso et al. 2008).
Interestingly there was a statistical difference in v˙VO2max
(+0.4 km h−1
), a composite measure of running economy
and ˙VO2max, which could indicate small improvements in
both of these variables, which were not substantial enough
to be seen individually, but is apparent from the combined
calculation. However, the mean difference of 0.4 km h−1
,
does not exceed our calculated typical error of 0.5 km h−1
established during pilot across a series of similar studies
under the same conditions, indicating that changes may not
be meaningful.
Crisafulli et al. (2011) has highlighted a role for altered
fatigue perception to explain enhanced performance fol-
lowing IP, after observing no differences in physiologi-
cal parameters including ˙VO2max, maximal stroke volume
and maximal cardiac output. These data cannot support,
or refute this, as testing occurred under different environ-
mental conditions. However, no differences were found
in RPE and whilst a mean improvement in total running
time of 32 s during GXT 2 could be considered mean-
ingful, this was not statistically significant, nor did it far
exceed our own laboratory typical measurement error of
27 s derived from a larger cohort of similar standard run-
ners under the same environmental conditions. Recently,
Tocco et al. (2015) did not observe an effect from IP with
highly trained athletes during free paced 5 km time trials
on a track. They also suggested altered fatigue sensations
could account for some of the benefits observed by IP
and that training status may modify the sensitivity to this
alteration. Such a suggestion would help explain the dif-
ference between effects in sub-elite (Bailey et al. 2012a)
and elite runners (Tocco et al. 2015), but does not appear
to be universal, with Jean-St-Michel et al. (2011) having
reported improvements in elite swimmers. Furthermore,
the influence of a ‘placebo effect’ should be considered,
as IP is difficult to blind. Although we tried to maintain
participant naivity, the potential for a placebo effect to
influence performance remains a limitation across all IP
research.
In conclusion, this study investigated the novel applica-
tion of IP during exercise in the heat. These data indicate IP
does not provide any benefit to the determinants of endur-
ance performance in the heat. Furthermore, four cycles of
IP did not influence deep muscle temperature, but elicited a
modest influence on TCORE during subsequent exercise.
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