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Abstract and Figures

Background Ischemic preconditioning (IPC) is the exposure to brief periods of circulatory occlusion and reperfusion in order to protect local or systemic organs against subsequent bouts of ischemia. IPC has also been proposed as a novel intervention to improve exercise performance in healthy and diseased populations. Objective The purpose of this systematic review is to analyze the evidence for IPC improving exercise performance in healthy humans. Methods Data were obtained using a systematic computer-assisted search of four electronic databases (MEDLINE, PubMed, SPORTDiscus, CINAHL), from January 1985 to October 2015, and relevant reference lists. Results Twenty-one studies met the inclusion criteria. The collective data suggest that IPC is a safe intervention that may be capable of improving time-trial performance. Available individual data from included studies demonstrate that IPC improved time-trial performance in 67 % of participants, with comparable results in athletes and recreationally active populations. The effects of IPC on power output, oxygen consumption, rating of perceived exertion, blood lactate accumulation, and cardiorespiratory measures are unclear. The within-study heterogeneity may suggest the presence of IPC responders and non-responders, which in combination with small sample sizes, likely confound interpretation of mean group data in the literature. Conclusion The ability of IPC to improve time-trial performance is promising, but the potential mechanisms responsible require further investigation. Future work should be directed toward identifying the individual phenotype and protocol that will best exploit IPC-mediated exercise performance improvements, facilitating its application in sport settings.
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SYSTEMATIC REVIEW
The Effects of Ischemic Preconditioning on Human Exercise
Performance
Anthony V. Incognito
1
Jamie F. Burr
1
Philip J. Millar
1
ÓSpringer International Publishing Switzerland 2015
Abstract
Background Ischemic preconditioning (IPC) is the
exposure to brief periods of circulatory occlusion and
reperfusion in order to protect local or systemic organs
against subsequent bouts of ischemia. IPC has also been
proposed as a novel intervention to improve exercise per-
formance in healthy and diseased populations.
Objective The purpose of this systematic review is to
analyze the evidence for IPC improving exercise perfor-
mance in healthy humans.
Methods Data were obtained using a systematic com-
puter-assisted search of four electronic databases (MED-
LINE, PubMed, SPORTDiscus, CINAHL), from January
1985 to October 2015, and relevant reference lists.
Results Twenty-one studies met the inclusion criteria. The
collective data suggest that IPC is a safe intervention that
may be capable of improving time-trial performance.
Available individual data from included studies demon-
strate that IPC improved time-trial performance in 67 % of
participants, with comparable results in athletes and recre-
ationally active populations. The effects of IPC on power
output, oxygen consumption, rating of perceived exertion,
blood lactate accumulation, and cardiorespiratory measures
are unclear. The within-study heterogeneity may suggest
the presence of IPC responders and non-responders, which
in combination with small sample sizes, likely confound
interpretation of mean group data in the literature.
Conclusion The ability of IPC to improve time-trial
performance is promising, but the potential mechanisms
responsible require further investigation. Future work
should be directed toward identifying the individual phe-
notype and protocol that will best exploit IPC-mediated
exercise performance improvements, facilitating its appli-
cation in sport settings.
Key Points
This systematic review examined the effects of
ischemic preconditioning (IPC) on exercise time-
trial performance, power output, and oxygen
consumption in healthy individuals.
Although, large between-study variability exists, the
most consistent benefit of IPC is for an improvement
in time-trial performance in exercise tests of
predominantly lactic anaerobic and aerobic capacity.
Future trials must strive to determine the optimal IPC
and sham-control protocols and to limit the presence
of known confounders.
1 Introduction
Ischemic preconditioning (IPC) is the exposure to brief
periods of circulatory occlusion and reperfusion to protect
local or systemic (remote IPC) organs against subsequent
ischemia-reperfusion injury [14]. Since the discovery of this
&Philip J. Millar
pmillar@uoguelph.ca
1
Department of Human Health and Nutritional Sciences,
University of Guelph, 50 Stone Road East, Guelph, ON
N1G2W1, Canada
123
Sports Med
DOI 10.1007/s40279-015-0433-5
phenomenon in 1986 [2], research has focused primarily on
the clinical utility of IPC to protect against organ damage and
cellular injury, such as during myocardial infarction or
perioperative periods [57]. Although the mechanisms
responsible for these actions are incompletely understood,
IPC has been shown to improve metabolic efficiency by
attenuating ATP depletion [810], glycogen depletion [11],
and lactate production [8,9] during prolonged ischemia. In
addition, IPC may improve skeletal muscle blood flow by
inducing conduit artery vasodilation [12], enhancing func-
tional sympatholysis [13], and preserving endothelial and
microvascular function during stress [1,1416]. Based on
these findings, IPC has garnered interest as a novel inter-
vention to improve exercise capacity and performance.
The most common IPC protocol involves three or four
cycles of 5 min circulatory occlusion and reperfusion [2,
17,18]. As this method is easily administered, non-inva-
sive, and inexpensive, it would represent an attractive
ergogenic aid for athletes to improve exercise performance
and gain a competitive advantage [1820]. Although the
first proof-of-concept study reported that IPC increased
maximal oxygen consumption (VO
2max
) and peak power
output in trained cyclists during graded maximal cycling
[17], the benefit of IPC on exercise capacity and perfor-
mance in subsequent studies remains equivocal.
With adherence to the Preferred Reporting Items for
Systematic Reviews and Meta-Analyses (PRISMA)
guidelines [21,22], the objective of this systematic review
is to examine the current state of evidence for IPC
improving exercise performance. We investigate both
mean and individual data in order to better capture the
impact of IPC on exercise capacity and performance, and
attempt to elucidate factors delineating responders and
non-responders. In addition, we discuss potential mecha-
nisms responsible for the reported improvements and
conclude with recommendations for future investigations
required for advancing IPC into sport practice.
2 Methods
2.1 Literature Search
Potential studies were identified by two unbiased reviewers
using MEDLINE, PubMed, SPORTDiscus, and CINAHL
databases. Common search terms used to address exercise
performance and IPC were ‘‘sports’’, ‘‘exercise’’, and ‘‘per-
formance’’, and ‘‘ischemic preconditioning’’, ‘‘ischemic
conditioning’’, and ‘‘preconditioning’’, respectively. For both
sets of search terms, relevant predefined database-specific
terms were added to broaden the search. For each database,
the date range was limited to January 1, 1985 (since the first
discovery of IPC was in 1986 [2]) to October 18, 2015. The
language was limited to English. Reference lists of articles
retrieved were manually checked for additional articles.
2.2 Eligibility Criteria for Potential Studies
Primary research studies published in or accepted by peer
reviewed journals were eligible for review. Animal studies,
case studies, study proposals, and review articles were
excluded. No restrictions were placed on participant age or
fitness level. Studies in disease populations were excluded to
yield a more focused review and to avoid confounding
conclusions that may arise from grouping participants with
different health status. IPC interventions were defined as any
procedure that performed multiple cycles of skeletal muscle
blood flow occlusion and reperfusion prior to exercise. These
protocols have been shown to be effective for cytoprotection
from ischemia-reperfusion injury [2]. Occlusion to both
exercising (IPC) and non-exercising (remote IPC) limbs were
included in the analysis since both have been shown to elicit
comparable cytoprotective effects [14]. Further, although
remote IPC requires a neurohumoral signal transduction
factor, considerable overlap in mechanisms between the two
forms of conditioning exist (e.g., triggering stimuli: nitric
oxide, adenosine, bradykinin, opioids; intracellular media-
tors: protein kinase C, hypoxia-inducible factor-1a,reper-
fusion injury salvage kinase, microRNA-144; intracellular
effectors: mitochondria ATP-dependent potassium channel;
see Heusch [23]). Studies were only eligible if participants
were randomized into the IPC or control/sham interventions
(i.e., randomized control or crossover designs).
2.3 Study Selection
All studies investigating the effects of IPC on exercise
capacity or performance and meeting the eligibility criteria
indicated above were selected. Studies were first screened
by title and/or abstract, and then the manuscript was
reviewed if the study appeared to satisfy the eligibility
criteria and purpose of this systematic review (Fig. 1). This
process was conducted independently by two reviewers
(A.V.I. and P.J.M).
2.4 Data Collection
The primary study outcomes related to exercise capacity or
performance included measures of time-trial performance,
power output, VO
2
[maximal (VO
2max
) or peak (VO
2peak
)],
rating of perceived exertion (RPE), and blood lactate
accumulation. Secondary study outcomes included relevant
cardiorespiratory variables (e.g., heart rate, blood pressure,
and ventilation). Studies investigating the effect of IPC on
time-trial performance and power output were classified
A. V. Incognito et al.
123
based on the predominant energy systems utilized during
the test. This was determined based on test duration, with
alactic anaerobic capacity predominating between exercise
initiation and 10 s, lactic anaerobic capacity predominating
between 10 and 75 s, and aerobic capacity predominating
for exercise longer than 75 s [24]. An exception was made
for activities requiring breath holds, which were defined as
tests of predominately lactic anaerobic capacity. Studies
investigating the effects of IPC on VO
2
were subdivided
into tests of VO
2max/peak
and tests of submaximal VO
2
.
Authors were contacted if their article examined time-
trial performance or VO
2max/peak
but had unreported or
unclear individual participant data on responders and non-
responders. Five [2529] out of nine contacted authors
responded to our request for individual participant data.
These data are presented in Table 1and are included in
response rate calculations.
3 Results
3.1 Study Selection
Following article screening, 21 studies were selected for
review, totaling 374 participants (309 men, 65 women).
All major study characteristics are summarized in
Table 2. Twenty studies were designed as randomized
crossover trials, 12 of which used a sham-control and
eight of which used a time-control; the remaining study
was a randomized control trial with a parallel design.
Individual participant responses were obtained from 13 of
the 21 studies (through the article and/or authors) and
used to calculate the proportion of IPC responders and
non-responders (Table 1).
3.2 Effects of Ischemic Preconditioning (IPC)
on Exercise Performance
3.2.1 Time-Trial Performance
3.2.1.1 Tests of Predominantly Alactic Anaerobic Capac-
ity IPC had no effect on 30 m running sprint time [27].
3.2.1.2 Tests of Predominantly Lactic Anaerobic Capac-
ity IPC improved (-1.1 % [18]) and had no effect [30]
on 100 m swim sprint time. IPC also improved under-
water swimming distance (?8.2 % [31]) and mean static
breath hold duration (?17.2 % [31]). IPC had no effect
on three sets of submaximal bilateral knee extension to
failure [32].
Fig. 1 Flow diagram of the
study selection process based on
eligibility criteria for a
systematic review examining
the effects of ischemic
preconditioning (IPC) on
exercise performance
Ischemic Preconditioning and Exercise Performance
123
3.2.1.3 Tests of Predominantly Aerobic Capacity IPC
improved 5 km treadmill running time (-2.5 % [19]), 1 km
rowing sprint time (-0.4 % [31]), time to failure during
graded maximal cycling (*?3.6 % [33]) and constant load
cycling (*?15.8 % [28] and ?7.9 % [26]), and time to
failure during submaximal rhythmic handgrip (?10.6 %
[34]). IPC had no effect on 5 km outdoor running time [29],
time to failure during graded maximal cycling [19,25]or
constant load cycling at 130 % of peak power [33], or time
needed to cycle 100 kJ of total work [35].
3.2.1.4 Overall Findings IPC improved time-trial per-
formance in nine of 17 exercise performance tests. After
examination of the available individual responses,
improvements and no effects in 118 and 57 participants
(Fig. 2a), respectively, were noted, which corresponds to a
67 % response rate [18,19,25,2731,33,34]. Dividing
the studies on the basis of exercise test duration demon-
strated improvements in 11 and no effects in 14 partici-
pants [27], respectively, in tests of predominantly alactic
anaerobic capacity (44 % response rate). There were
improvements in 32 and no effects in 11 participants [18,
31] within tests of lactic anaerobic capacity (74 % response
rate), and 75 and 32 participants [19,25,26,28,29,31,33,
34], respectively, in tests of predominantly aerobic capac-
ity (70 % response rate).
3.2.2 Power Output
3.2.2.1 Tests of Predominantly Alactic Anaerobic Capac-
ity IPC increased (?2.3 % [36]) and had no effect [37,
38] on peak power output during repeated 6 s cycling
sprints.
3.2.2.2 Tests of Predominantly Lactic Anaerobic Capac-
ity IPC had no effect [38] and detrimental effects [39]on
peak power output during a Wingate test.
3.2.2.3 Tests of Predominantly Aerobic Capacity IPC
increased (?3.7 % [17]and?1.6 % [33]) and had no effect
[40] on peak power output during graded maximal cycling
tests. Additionally, IPC had no effect on submaximal
cycling workload required to reach target heart rate [41].
3.2.2.4 Overall Findings IPC increased peak power in
three of eight exercise tests, and had no effect on sub-
maximal power output in one exercise test.
3.2.3 Oxygen Consumption
3.2.3.1 Tests of Maximal Oxygen Consumption IPC
increased (?2.8 % [17]) and had no effect [33]onVO
2max
determined using a graded maximal cycling test. Addi-
tionally, IPC had no effect on VO
2max/peak
during a graded
maximal treadmill test when tested acutely [19] or after
8 weeks of repeated IPC treatments [42]. IPC was also
shown to increase (?2.8 %) VO
2max/peak
during constant
load cycling to failure at 100 % peak power [26] but had no
effect at 130 % peak power [33]orat89%VO
2peak
[28].
3.2.3.2 Tests of Submaximal Oxygen Consumption IPC
had no effect on mean VO
2
during a 5 km running time
Table 1 Responders vs. non-responders to ischemic preconditioning (IPC) in studies reporting individual differences in time-trial performance
and maximal oxygen uptake
References Effects of IPC IPC benefit IPC null
de Groot et al. [17]:VO
2max
12 3
Jean-St-Michel et al. [18];100 m swim time 14 3
Crisafulli et al. [33]:Time to failure 10 7
$VO
2max
69
Clevidence et al. [25]$Time to failure 6 6
Bailey et al. [19];5 km running time 11 2
Gibson et al. [27]$30 m sprint time 11 14
Kjeld et al. [31];1 km row time 11 3
:Underwater swim distance 9 2
Tocco et al. [29]$Mean 5 km running speed 5 6
Barbosa et al. [34]:Handgrip time to failure 9 4
Kido et al. [28]:Time to failure 13 2
Marocolo et al. [30]$100 m swim time 9 6
Cruz et al. [26]:Time to failure 10 2
:VO
2peak
84
:Increase, ;decrease, $no change, max maximal, VO
2
oxygen consumption
A. V. Incognito et al.
123
Table 2 Summary of study characteristics and exercise performance and physiology changes with ischemic preconditioning (IPC)
Study Study design Population IPC protocol IPC limb Exercise test Effects of IPC
de Groot
et al. [17]
Randomized,
controlled
crossover
12 M, 3 F; 27 ±6 years;
trained cyclists
395 min at
220 mmHg
Bilateral upper
leg
Graded max cycling :VO
2max
:W
peak
$BL 2 min post cycling
Jean-St-
Michel
et al. [18]
Randomized, sham-
controlled
crossover
9 M, 9 F for 100 m swim;
19 ±3 years; 8 M, 8 F for
200 m intervals;
19 ±3 years; elite swimmers
495 min at 15 mmHg
above resting SBP
Unilateral
upper arm
100 m swim ;100 m swim time
79200 m swim intervals $BL 2 min post each 200 m
Crisafulli
et al. [33]
Randomized,
controlled
crossover
17 M; 35 ±9 years;
recreationally active
395 min at 50 mmHg
above resting SBP
Bilateral upper
leg
Graded max cycling :Time to failure
:W
peak
and W
total
$VO
2max
All out cycle sprint at 130 %
W
peak
to failure (W
determined by a graded max
cycling test)
$Time to failure
$VO
2max
$W
total
$BL post cycle sprint
Foster et al.
[35]
Randomized,
controlled
crossover
6 M, 2 F; 39 ±10 years;
experienced cyclists
495 min at 20 mmHg
above resting SBP
Unilateral
upper leg
Cycle sprint to 100 kJ $Cycle sprint time
Clevidence
et al. [25]
Randomized,
controlled
crossover
12 M; 27 ±9 years;
competitive amateur cyclists
395 min at 220
mmHg
Alternate
unilateral
upper leg
Graded max cycling $Time to failure
$BL 5 min post cycling
Bailey et al.
[19]
Randomized, sham-
controlled
crossover
13 M; 25 ±6 years; healthy,
moderately trained
495 min at 220
mmHg
Bilateral upper
leg
5 km treadmill run ;5 km running time
;RPE during first 1000 m
;BL during submax running
Graded max treadmill running $Time to failure
$VO
2max
$BL 3 min post graded max running
El Messaoudi
et al. [41]
Randomized,
controlled
crossover
10 M, 10 F; 22 ±4 years;
healthy volunteers
395 min at 200
mmHg
Bilateral upper
arm
70 min cycling at 80 % HR
max
or reserve; 15 min or until
failure at 95 % HR
max
or
reserve
$W required for target HR
Gibson et al.
[27]
Randomized, sham-
controlled
crossover
16 M, 9 F; 23 ±3 years;
competitive team sport
athletes
395 min at
220 mmHg
Alternate
unilateral
upper leg
3930 m running sprints $30 m sprint time
Paixa
˜o et al.
[39]
Randomized, sham-
controlled
crossover
15 M; 30 ±7 years;
competitive amateur cyclists
495 min at 250
mmHg
Alternate
unilateral
upper leg
3 Wingate tests separated by
10 min rest
;W
peak
in the first Wingate and W
total
in first and second Wingate tests
$BL 6 min post each Wingate
Kjeld et al.
[31]
Randomized,
controlled
crossover
10 M, 4 F; 23 years; elite
oarsmen; 10 M, 1 F;
29 years; elite free divers
495 min at 40 mmHg
above resting SBP
Unilateral
upper arm
1 km row ;1 km row time
Static breath hold; underwater
distance swim
:Static breath hold time and
underwater swim distance
Ischemic Preconditioning and Exercise Performance
123
Table 2 continued
Study Study design Population IPC protocol IPC limb Exercise test Effects of IPC
Jones et al.
[42]
Randomized,
controlled
18 M; 22 ±2 years IPC,
26 ±5 years control; healthy
volunteers
495 min at
220 mmHg, 39/
week, 8 weeks
Unilateral
upper arm
Graded max treadmill running $VO
2peak
Patterson
et al. [36]
Randomized, sham-
controlled
crossover
14 M; 30 ±4 years;
recreational team sport
athletes
495 min at 220
mmHg
Bilateral upper
leg
12 96 s cycle sprints :W
peak
and W
mean
for sprints 1, 2, 3
$RPE
$BL immediately post sprint 4, 8, 12
Hittinger
et al. [40]
Randomized,
controlled
crossover
15 M; 30 ±7 years;
competitive cyclists and
triathletes
495 min at 15 mmHg
above resting SBP
Bilateral upper
leg
Graded max cycling $W
peak
$RPE
Lalonde and
Curnier
[38]
Randomized, sham-
controlled
crossover
8 M, 9 F; 29 ±8 years; healthy
students and amateur
triathletes
495 min at 50 mmHg
above resting SBP
Unilateral
upper arm
696 s cycle sprints; Wingate
test
$W
peak
and W
mean
for either test
;RPE during Wingate
Tocco et al.
[29]
Randomized, sham-
controlled
crossover
11 M; 35 ±8 years;
competitive runners
395 min at 50 mmHg
above resting SBP
Bilateral upper
leg
5 km run $5 km running time
$BL 1 min post running
Gibson et al.
[37]
Randomized, sham-
controlled
crossover
7 M, 9 F; 24 ±3 years;
competitive team sport
athletes
395 min at 220
mmHg
Alternate
unilateral
upper leg
596 s cycle sprints $W
peak
and W
total
$RPE
;BL 3 min post fifth sprint in women
Barbosa et al.
[34]
Randomized, sham-
controlled
crossover
13 M; 25 ±4 years;
recreationally active
395 min at
200 mmHg
Bilateral upper
leg
Rhythmic handgrip at 45 %
MVC to failure (60
contractions/min)
:Time to failure
Kido et al.
[28]
Randomized,
controlled
crossover
15 M; 24 ±1 years; habitually
active
395 min at
[300 mmHg
Bilateral upper
leg
3 min cycling at 30 W, 4 min
cycling at 90 % GET, until
failure at 70 % of difference
between GET and VO
2peak
:Time to failure
$VO
2peak
$BL during submax and
immediately post cycling
Marocolo
et al. [30]
Randomized, sham-
controlled
crossover
15 M; 21 ±4 years;
competitive amateur
swimmers
495 min at 220
mmHg
Alternate
unilateral
upper arm
100 m swim $100 m swim time
Cruz et al.
[26]
Randomized, sham-
controlled
crossover
12 M; 20–36 years;
recreationally trained cyclists
495 min at 220
mmHg
Bilateral upper
leg
100 % W
peak
to failure (W
determined by a graded max
cycling test)
:Time to failure
:VO
2peak
;RPE
$BL immediately post cycling
Marocolo
et al. [32]
Randomized sham-
controlled
crossover
13 M; 26 ±5 years; resistance
trained
495 min at 220
mmHg
Alternate
unilateral
upper leg
3 sets of bilateral leg extension
to failure (12 repetition max
load)
$Repetitions per set
$RPE
$BL 4 min post set 3
Age data are mean ±SD
:Increase, ;decrease, $no change, BL blood lactate, Ffemale, GET gas exchange threshold, HR heart rate, Mmale, max maximum/maximal, MVC maximal volitional contraction, post after,
RPE rating of perceived exertion, SD standard deviation, submax submaximal, SBP systolic blood pressure, VO
2
oxygen consumption, Wworkload or power
A. V. Incognito et al.
123
trial [29], repeated 6 s cycle sprints and associated recov-
ery periods [36], or submaximal VO
2
during graded cycling
[17,25] or during 4 min of cycling at a workload corre-
sponding to *55 % of VO
2max
[28].
3.2.3.3 Overall Findings IPC increased VO
2max
in two of
seven exercise tests, and had no effect on mean or sub-
maximal VO
2
in five exercise tests. Examination of the
available individual responses noted VO
2max/peak
improve-
ments and no effects in 26 and 16 participants (62 %
response rate; Fig. 2b), respectively [17,33].
3.2.4 Rating of Perceived Exertion
IPC decreased RPE during a Wingate test (*1 point on a
Borg 1–10 scale [38]), during the first 1000 m of a 5 km
treadmill time trial (*1–2 points on a Borg 6–20 point scale
[19]), and during the first 4 min of cycling to failure at
100 % power output (0.8 points on a Borg 6–20 point scale
[26]), but had no effect during a graded maximal cycling test
[40], three sets of submaximal bilateral knee extension to
failure [32], or repeated 6 s cycling sprints [37,43].
3.2.5 Blood Lactate
IPC attenuated blood lactate accumulation during sub-
maximal treadmill running (-1.07 mmol
-1
or -25.4 %
[19]), but had no effect during submaximal cycling [28].
IPC decreased blood lactate 6 min post cycling exercise in
women (-1.4 mmol
-1
or -15.9 % [37]), but had no effect
on post-exercise blood lactate accumulation in all other
studies, though the non-statistically significant mean results
ranged from 7.1 % lower to 8.7 % higher [1719,25,26,
28,29,32,33,39,43].
3.3 Effects of IPC on Cardiorespiratory Variables
During Exercise
3.3.1 Heart Rate
IPC increased (*?2.4 % [32]) and had no effect [17,28]
on maximal heart rate during graded maximal cycling; no
effect on maximal [26,28] or submaximal [28] heart rate
during constant load cycling to failure; no effect on max-
imal or submaximal heart rate during cycling to 100 kJ of
total work [35]; and no effect on maximal [19] or mean
heart rate [29] during a 5 km running time trial. Similarly,
IPC had no effect on peak heart rate during rhythmic
handgrip exercise to failure [34] or during a 100 m swim
time trial [18]. IPC had no effect on heart rate during
submaximal interval swims [18], submaximal cycling
workloads [17,28], submaximal treadmill running [19], or
submaximal rhythmic handgrip [34]. IPC did increase heart
rate at a submaximal intensity of 30 % maximal cycling
power output (?5.1 % [25]).
3.3.2 Blood Pressure
IPC had no effect on submaximal mean arterial pressure, but
increased maximal mean arterial pressure (?11 mmHg or
?9.2 % [34]) during rhythmic handgrip exercise to failure,
compared with control conditions. IPC had no effect on
maximal mean arterial pressure [33]orsystolicordiastolic
blood pressure [17] during graded maximal cycling. Addi-
tionally, IPC attenuated hypoxia-induced increases in pul-
monary artery systolic pressure at rest (-22.5 % [35]).
3.3.3 Respiratory Variables
IPC had no effect on respiratory exchange ratios during a
5 km running time trial [29], nor during graded maximal
cycling [25]. IPC increased (*?8.1 % [33]) and had no
effect on maximal minute ventilation during graded max-
imal cycling [17,25], and no effect on maximal or sub-
maximal pulmonary VO
2
during submaximal cycling to
failure [28]. Additionally, IPC had no effect on maximal or
submaximal minute ventilation during graded maximal
treadmill running [19] or on mean pulmonary ventilation
during a 5 km running time trial [29].
3.4 Safety and Tolerability
Although no studies sought specifically to investigate the
safety of IPC, no adverse clinical events were reported in
Fig. 2 Number of responders
and non-responders to ischemic
preconditioning (IPC)-mediated
effects on atime-trial
performance, and bmaximal
oxygen consumption
Ischemic Preconditioning and Exercise Performance
123
any of the reviewed studies. The IPC procedure has been
reported to elicit a score of ‘‘4’’ on a 1–10 pain scale in
healthy participants [38], suggesting it is uncomfortable but
not painful for the average participant.
4 Discussion
4.1 Summary of Findings
IPC has been proposed as a novel intervention to increase
exercise capacity and performance [20,44]. The results of
this systematic review highlight the considerable equipoise
in the literature and variability in IPC-mediated exercise
benefits between studies. The most consistent evidence was
for an improvement in time-trial performance (nine of 17
exercise tests; 67 % individual response rate), detected
only in exercise modes lasting 10–75 s (three of five
exercise tests; 74 % individual response rate) and [75 s
(six of 11 exercise tests; 70 % individual response rate),
which were characterized in this review as tests of pre-
dominantly lactic anaerobic and aerobic capacity, respec-
tively. The effects on power output, VO
2
, RPE, and blood
lactate accumulation were less clear; as were changes in
cardiorespiratory measures. An examination of individual
participant data supports the hypothesis that IPC respon-
ders and non-responders may exist [45], which could
explain the large variability observed in exercise perfor-
mance responses within and between studies. The present
results are best used to catalyze future research questions,
study designs, and hypotheses, to establish the utility of
using IPC as an ergogenic aid. Future research must aim to
determine the phenotype most likely to respond to IPC,
optimal IPC protocols, and the mechanisms involved in
mediating the potential beneficial effects on exercise
performance.
4.2 Potential IPC Responders and Non-Responders
The responsiveness to any therapy or treatment can vary
between individuals on the basis of genetic, pathological,
and/or environmental profiles. It is acknowledged that such
heterogeneity even exists in the responsiveness to exercise
training [46]. Whether a similar range of responsiveness
exists to IPC has recently been postulated [45] to explain
the discrepancy between the widespread cytoprotective
success in experimental models [2,4,811] and the
inconsistency of benefits in clinical trials [47,48]. Exam-
inations of clinical IPC responsiveness have reported
reduced or absent cardioprotection in women, diabetics,
and older patients with coronary artery disease [48,49],
suggesting a phenotype for ‘‘responders’’ and ‘‘non-re-
sponders’’ may exist. This could explain the large
variability observed in exercise performance responses
within and between studies (Table 1and 2) and highlights
the potential limitation of conventional statistical approa-
ches based on aggregate data.
4.3 Potential Sources of Between-Study Variability
In addition to potential differences in IPC responsiveness,
it is difficult to compare results between studies as partic-
ipant characteristics (e.g., sex, training status) and study
methods (e.g., exercise mode, pre-study restrictions, IPC
protocol) differ widely. The following sections will assess
the potential impact that this between-study variability may
have on the results.
4.3.1 Study Participants
Participant characteristics differed widely between stud-
ies. Females were not included in eight of 21 studies and
only represent 17 % of participants overall, raising the
question of whether a sex-based difference in IPC
responsiveness may exist. To our knowledge, this has not
been investigated formally in humans. Peak exercise
capacity and training status were also highly variable. We
attempted to classify the studies into categories based on
one or a combination of participant VO
2max/peak
,peak
power output, and author-reported fitness status. We
identified five studies with highly trained participants [18,
29,31,39,40], 12 studies with trained participants [17,
19,2527,30,32,33,3538], and four studies with
recreationally active participants [28,34,41,42]. Within
the highly trained population, two of five studies (40 %)
reported improvements in exercise performance following
IPC [18,31], compared with five of 12 studies (42 %) in
the trained population [17,19,26,33,36] and two of four
studies (50 %) in the recreationally active population [28,
34]. Available individual participant time-trial response
rates were 81, 57, and 79 % for the highly trained, trained,
and recreationally active population, respectively. It must
be acknowledged that although we attempted to catego-
rize participant fitness status, we only identified two elite
athlete populations [18,31]. Broadening the continuum of
fitness status is required to understand the role of fitness
and/or sport-specific training status on IPC efficacy.
Understanding these potential trends may explain vari-
ability in results and give insight into the IPC responder
phenotype.
4.3.2 Exercise Mode
The mode of exercise performed differed dramatically
between studies (Table 2). To help stratify the results, we
A. V. Incognito et al.
123
grouped exercise mode by duration and predominant
energy systems. With respect to time-trial performance, the
results demonstrate clearly that the majority of observed
benefits were in exercise tests lasting longer than 10 s,
although no differences in IPC responsiveness were
observed between tests of predominantly lactic anaerobic
and aerobic capacity. While the large variability in exercise
modes makes it difficult to compare directly between
studies, the reported benefits across a variety of tests pro-
vide support for a generalized effect.
4.3.3 IPC Protocols
The optimal methodology for implementing IPC is
unknown [50], with variability in the size (muscle mass)
of the occluded limb, the number of ischemia-reperfusion
cycles or cycle length, and the time lag between IPC and
the start of exercise. The protective effects of remote IPC
against brachial artery endothelial ischemia-reperfusion
injury have been shown to be similar when occlusion was
completed three times in the arms and legs [51]; however,
whether the effects on exercise performance are propor-
tional to the muscle mass is uncertain. No clear rela-
tionships were evident from the present data as time-trial
performance was improved byimplementingIPCtothe
arm [18,31]orleg[19,26,33,34]. The number of
ischemia-reperfusion cycles may also be important, and
interact with the amount of muscle mass. Two cycles of
5 min circulatory occlusion in the legs, but not the arms,
prevents brachial artery endothelial ischemia-reperfusion
dysfunction [51]. All of the studies included in this review
completed either three or four cycles of 5 min occlusion
and reperfusion; however, no clear relationships with
exercise performance were present. Lastly, IPC is known
to exert an early (1–2 h) and late (12–72 h) window of
effectiveness on ischemia-reperfusion injury [52]. The
optimal time lag between IPC and the start of exercise has
not been investigated. Current studies ranged from 5–105
min, with no clear relationships with exercise perfor-
mance. Future investigations establishing optimal proto-
cols for the implementation of IPC prior to exercise are
warranted.
4.3.4 Pre-Study Restrictions
A notable limitation of the existing literature is the
inconsistency in limiting confounders known to modulate
the effects of IPC, such as caffeine, alcohol, and physical
activity [33,5355]. Of the 21 studies, only 14 reported
pre-study instructions, 13 restricted caffeine, 12 restricted
alcohol, and 11 restricted physical activity. The timelines
for these restrictions were also not standardized.
With respect to caffeine, studies implemented 48 h
(n=2), 24 h (n=7), 12 h (n=1), 6 h (n=2), and 2 h
(n=1) restrictions. A plasma concentration of *6mg/L,
the equivalent of drinking two to four cups of coffee, has
been shown to abolish the cytoprotective effects of IPC
compared with plasma concentrations of *0.2 mg/L,
achieved by asking participants to abstain from caffeine for a
minimum of 24 h [55]. Given that caffeine is reported to
have a half-life in plasma of roughly 5.5 h [56], two to four
cups of coffee would take roughly 27.5 h to reduce to con-
centrations of 0.2 mg/L. This information should encourage
caffeine restriction for at least 24 h prior to IPC testing.
The captured studies implemented a 48 h (n=2) and
24 h (n=10) abstinence from alcohol. The protective
effects of IPC against myocardial ischemia have been
shown to be abolished when blood ethanol concentrations
were between 16 and 34 mg/dL, 30 min after oral admin-
istration of 40 g of ethanol (approximately three standard
alcoholic drinks in North America) compared with the
placebo group [54]. As alcohol has a clearance rate of
*13 mg/dL/h [57], the commonly used 24 h abstinence
prior to IPC testing is likely sufficient.
With regards to physical activity, studies implemented a
pre-study restriction of 5 days (n=1), 48 h (n=2), and
24 h (n=7). One study restricted physical activity for 1
week between crossover study visits, but did not commu-
nicate a pre-study restriction. Since physical activity may
elicit a similar preconditioning response to IPC [33,53],
and the effects of IPC can persist for up to 48 h [1],
restrictions on physical activity should extend for a mini-
mum of 48 h prior to IPC testing.
It is acknowledged that the implementation of these
restrictions may compromise the practicality of research in
athletes. For example, caffeine represents a common
ergogenic aid employed by endurance athletes to improve
performance [58], while restricting exercise for 48 h (or
longer) would likely alter the training schedule of most
athletes and lead to sub-optimal performances during
subsequent testing. It is recommended that careful docu-
mentation of these confounders be collected and reported
in all future research.
4.4 Potential Mechanisms for IPC-Mediated
Improvements in Exercise Performance
Whether the factors regulating the clinical benefits of IPC
for protecting organs against prolonged ischemia are
the same as those needed for potential improvements in
exercise performance is unclear. In animal models testing
ischemic tolerance, IPC acts via a blood-borne sub-
stance(s) that requires the presence of adenosine [59,60],
nitric oxide [60], and an intact nervous system [60,
61]. The following sections briefly review potential
Ischemic Preconditioning and Exercise Performance
123
mechanisms that may be responsible for IPC’s ability to
alter exercise performance.
4.4.1 Metabolic Efficiency
With the exception of Patterson et al. [43], IPC-mediated
improvements were observed in exercise performance tests
classified as predominantly utilizing lactic anaerobic or
aerobic energy systems [1719,28,31,33,34]. This sug-
gests that IPC may not have as strong of an impact on
alactic anaerobic capacity [24]. In support of a metabolic
mechanism, animal-based investigations using prolonged
ischemia of skeletal muscle have demonstrated that IPC
attenuates ATP depletion [810,62] secondary to mito-
chondrial ATP-sensitive potassium (mKATP) channel
opening [51,62], skeletal muscle opioid receptor activation
[8], and preservation of ischemia-induced reductions in
muscle energy charge potential [9]. IPC has also been
shown to attenuate ischemia-induced mitochondrial dys-
function [63,64]. This may be the result of IPC-mediated
increases in nitric oxide [6567], as nitrate supplementa-
tion in humans has been shown to improve basal mito-
chondrial efficiency through enhancement of ADP
sensitivity [68]. Furthermore, IPC has been observed to
reduce ischemia-induced glycogen depletion [11] and lac-
tate production [8,9] in skeletal muscle. These studies
suggest that IPC can reduce muscle energy demand and
improve metabolic efficiency in times of ischemic stress.
Evidence of IPC improving metabolic efficiency in
humans is scarce. Bailey et al. [19] reported attenuations in
submaximal exercise blood lactate accumulation in healthy
participants, but whether this was due to reduced produc-
tion or increased clearance is unclear. IPC has been shown
to increase peak forearm deoxygenation during handgrip
exercise to failure [34] and mean forearm deoxygenation
during a static breath hold [31], which may represent
increased oxygen extraction by the muscle. However, both
of these investigations also reported increased time to task
failure following IPC; therefore, the enhanced deoxy-
genation reported with IPC may reflect the greater time
available for oxygen extraction [31,34]. When compared
at equal time points during submaximal exercise, IPC does
not alter the magnitude of deoxygenation, rather, it alters
the kinetics, speeding up deoxygenation at the onset of
moderate cycling exercise [28], which would reduce the
oxygen deficit. In addition, IPC has recently been shown to
increase VO
2peak
partially through increasing the amplitude
(not the delay) of the slow component of whole body VO
2
[26]. This change may have been driven by the recruitment
of additional motor units towards the end of exercise [26].
Overall, human evidence for IPC improving metabolic
efficiency requires further investigation.
4.4.2 Blood Flow
IPC has been observed to increase muscle oxygen satura-
tion during 6 s cycle sprints [43] and rhythmic handgrip
exercise at 25 % maximal volitional contraction [13],
reflecting a disproportional increase in muscle blood flow
compared with oxygen demand. IPC-mediated increases in
muscle blood flow during exercise are likely secondary to
the ability of IPC to protect against exercise-induced and
ischemia-induced endothelial [1,15,19] and microvascular
[16] dysfunction. Additionally, IPC can induce conduit
artery vasodilation of the contralateral limb [12]. IPC can
also enhance functional sympatholysis [13], likely medi-
ated by increases in nitric oxide [6567] or decreases in
sympathetic activity [12,69]. Therefore, IPC may improve
skeletal muscle blood flow by preserving endothelial and
microvascular function, as well as attenuating neurogenic
restraint on peripheral vasculature. Since endothelial and
microvascular function and sympathetic activity are
impacted by nitric oxide [16,65,70], these mechanisms
may work in concert to enhance skeletal muscle blood flow
during exercise. Arguing against increases in blood flow,
remote IPC failed to increase brachial artery diameter or
blood flow compared with control during rhythmic hand-
grip, even though time to failure was increased [34]. Fur-
ther work in humans is required to confirm that IPC-
mediated vascular effects are involved in improving exer-
cise performance.
4.5 Potential Clinical Benefits
The value of IPC for improving exercise performance in
clinical populations remains largely unstudied. In patients
with coronary [44] or peripheral artery disease [71,72], IPC
had no effect on exercise time to failure or oxygen uptake,
but did alter clinically relevant markers, such as increasing
time to claudication [71] and cardiac ischemia [44], and
lowering peak systolic blood pressure and rate pressure
product [44]. The ability of IPC to prolong the onset of
myocardial ischemia during exercise [44] may be due to
improved metabolic efficiency and increases in myocardial
blood flow, similar to the above mechanisms described in
skeletal muscle. Compared with control conditions, remote
IPC was shown to preserve mitochondrial respiration in
atrial [73] and ventricular [74] tissue after aortic cross-
clamping in patients undergoing coronary artery bypass graft
surgery. Furthermore, remote IPC has been shown to
increase coronary artery blood flow in animals [75]and
humans [76]. Together, these results suggest that prolonged
onset of exercise-induced cardiac ischemia following IPC
may be due to improved myocardial oxygen utilization or
delivery.
A. V. Incognito et al.
123
One important unanswered question is whether clinical
patients fully respond to IPC. In patients with heart failure
[77], IPC had no effect on VO
2peak
, exercise duration, or
power output. Blood drawn from these heart failure
patients following IPC did not attenuate infarct size in a
mouse heart Langendorff model of infarction [77], com-
pared with a 38.6 % reduction previously reported with
healthy athletes [18]. Further, IPC does not protect against
endothelial ischemic-reperfusion injury in heart failure
patients [78]. The reduced efficacy in patients with heart
failure with reduced ejection fraction may highlight the fact
that these patients are already preconditioned due to
chronic exposure to a low flow state. Although potential
disease-specific differences in IPC responsiveness may
exist, the therapeutic benefits of IPC on exercise capacity
and performance for clinical populations warrant further
study. It is known that exercise capacity is a strong marker
of overall mortality in cardiovascular disease [7982] and
that the benefits of exercise rehabilitation are dose/volume
dependent [83]. Interventions to increase exercise duration
or tolerance may allow patients to perform more exercise
and reap greater overall benefits.
4.6 Future Directions
To better establish the effects of IPC on human exercise
performance, more strictly controlled and mechanistic
studies are needed. Overall, sample sizes need to be
increased to account for the large variability in between-
subject IPC responsiveness and to detect the modest 1–3 %
improvements in exercise performance that have been
reported to date. Additionally, there is a need for a direct
comparison between different IPC protocols, exercise
modalities, individual fitness levels, and sport-specific
backgrounds to determine if these factors play a role in IPC
effectiveness and to better understand the potential IPC
responder and non-responder phenotypes. Pre-study
restrictions on caffeine, alcohol, and physical activity are
recommended to be implemented for a minimum of 24, 12,
and 48 h, respectively. In athletes, these restrictions may
not be practical, and it is recommended that careful data
collection on these confounders be reported. Further, a
major confounder with all human studies remains the
inability to effectively sham-control IPC treatments.
Highlighting the potential influence of placebo effects on
results, a recent study noted that 67 % of participants
improved 100 m swim time following a sham-IPC condi-
tion compared with a time-controlled condition when they
were told that sham-IPC would improve exercise perfor-
mance [30]. At a minimum, studies should seek to record
participants’ knowledge of IPC-mediated exercise effects
[38], while the use of deception may be required.
5 Conclusion
Current evidence suggests that IPC may be efficacious as
an ergogenic aid to improve exercise performance and gain
a competitive advantage. Of the 21 investigations
reviewed, 10 reported statistically significant exercise
performance benefits such as improved time-trial perfor-
mance, increased VO
2max/peak
, increased power output, or
reduced ratings of perceived exertion. The mechanisms
responsible for these improvements are unknown, but
likely involve changes in both metabolic and vascular
pathways. However, despite these positive findings, 11
studies demonstrated no effect of IPC on exercise perfor-
mance, three of which were completed with short-duration
exercise modes utilizing predominantly alactic anaerobic
metabolism. The large between-subject variability of
results may be impacted by populations of IPC responders
and non-responders, and therefore caution should be used
in the interpretation of mean group changes in exercise
performance. Future IPC research should focus on (1)
increasing the statistical power to detect the modest
changes in exercise performance and account for the
variability in IPC responsiveness, (2) improving our
understanding of the physiological mechanisms involved,
(3) identifying the participant phenotype or IPC protocol
mediating beneficial exercise responses, and (4) deter-
mining the applicability for clinical populations engaged in
exercise rehabilitation. Overall, the application of IPC as
an ergogenic aid and adjunct clinical rehabilitation therapy
is promising, but requires further investigation.
Compliance with Ethical Standards
Funding Anthony Incognito is supported by a Fredrick Banting and
Charles Best Canada Graduate Scholarship. Jamie Burr and Philip
Millar are both supported by National Science and Engineering
Research Council (NSERC) Discovery Grants.
Conflicts of interest Anthony Incognito, Jamie Burr, and Philip
Millar declare that they have no conflicts of interest relevant to the
content of this review.
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... Several studies [7][8][9] have demonstrated significant improvements in functional capacity in this deteriorated population after a period of strength training with BFR and low loads, compared to a control group. In this same context, another method of vascular occlusion, ischemic preconditioning (IPC), has been reported to be ergogenic for musculoskeletal recovery [10,11] and sports performance [12]. However, IPC has not yet been investigated in an elderly population. ...
... Although we did not assess any physiological responses to exercise previous IPC studies have reported varied and complex physiological mechanisms that can explain the remote ergogenic effects observed here [12,46]. In fact, shear stress and local tissue hypoxia induced by the maneuver increase nitric oxide (NO) levels, a potent vasodilator [47], and activate vascular endothelial growth-factor (VEGF-α) gene expression [48]. ...
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Background: Aging decreases some capacities in older adults, sarcopenia being one of the common processes that occur and that interfered with strength capacity. The present study aimed to verify the acute effect of IPC on isometric handgrip strength and functional capacity in active elderly women. Methods: In a single-blind, placebo-controlled design, 16 active elderly women (68.1 ± 7.6 years) were randomly performed on three separate occasions a series of tests: (1) alone (control, CON); (2) after IPC (3 cycles of 5-min compression/5-min reperfusion at 15 mmHg above systolic blood pressure, IPC); and (3) after placebo compressions (SHAM). Testing included a handgrip isometric strength test (HIST) and three functional tests (FT): 30 s sit and stand up from a chair (30STS), get up and go time (TUG), and 6 min walk distance test (6MWT). Results: HIST significantly increased in IPC (29.3 ± 6.9 kgf) compared to CON (27.3 ± 7.1 kgf; 7.1% difference; p = 0.01), but not in SHAM (27.7 ± 7.9; 5.5%; p = 0.16). The 30STS increased in IPC (20.1 ± 4.1 repetitions) compared to SHAM (18.5 ± 3.5 repetitions; 8.7%; p = 0.01) and CON (18.5 ± 3.9 repetitions; 8.6%; p = 0.01). TUG was significantly lower in IPC (5.70 ± 1.35 s) compared to SHAM (6.14 ± 1.37 s; -7.2%; p = 0.01), but not CON (5.91 ± 1.45 s; -3.7%; p = 0.24). The 6MWT significantly increased in IPC (611.5 ± 93.8 m) compared to CON (546.1 ± 80.5 m; 12%; p = 0.02), but not in SHAM (598.7 ± 67.6 m; 2.1%; p = 0.85). Conclusions: These data suggest that IPC can promote acute improvements in handgrip strength and functional capacity in active elderly women.
... The concept of IPC has been observed throughout the medical literature for a number of years and can be defined as the exposure to brief periods of circulatory occlusion and reperfusion to protect local or systemic organs against subsequent bouts of ischemia. 110 Furthermore, we have seen studies find an improvement in VO 2 max, increased sports performance, and increased strength/endurance. [110][111][112][113][114][115] Franz et al. 116 also found that IPC may blunt exercise-induced muscle damage when performed before bouts of eccentric exercise of the muscle flexors. ...
... 110 Furthermore, we have seen studies find an improvement in VO 2 max, increased sports performance, and increased strength/endurance. [110][111][112][113][114][115] Franz et al. 116 also found that IPC may blunt exercise-induced muscle damage when performed before bouts of eccentric exercise of the muscle flexors. Tanaka et al. 117 theorize that the origin of the beneficial effects from IPC may likely be the enhancement of mitochondrial metabolism in skeletal muscle. ...
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The use of blood flow restriction (BFR) within rehabilitation is rapidly increasing as further research is performed elucidating purported benefits such as improved muscular strength and size, neuromuscular control, decreased pain, and increased bone mineral density. Interestingly, these benefits are not isolated to structures distal to the occlusive stimulus. Proximal gains are of high interest to rehabilitation professionals, especially those working with patients who are limited due to pain or postsurgical precautions. The review to follow will focus on current evidence and ongoing hypotheses regarding physiologic responses to BFR, current clinical applications, proximal responses to BFR training, potential practical applications for rehabilitation and injury prevention, and directions for future research. Interestingly, benefits have been found in musculature proximal to the occlusive stimulus, which may lend promise to a greater variety of patient populations and conditions. Furthermore, an increasing demand for BFR use in the sports world warrants further research for performance research and recovery. Level of Evidence Level V, expert opinion.
... For example, for cycling exercise, LIPC refers to application of blood flow occlusion to the legs, whereas RIPC refers to application of blood flow occlusion to the arms. At present, it is thought that both LIPC and RIPC may improve functioning of the mitochondrial ATP-dependent potassium channel, attenuate ATP depletion, promote phosphocreatine (PCr) resynthesis, enhance metabolic efficiency, and increase vasodilation, oxygen delivery and extraction, thereby enhancing subsequent endurance performance [2,3]. However, the acute effect of IPC on the performance of repeated or interval sprints, in which aerobic contribution is predominant [4], remains controversial. ...
... Thus, LIPC and RIPC can improve the total work and the fatigue resistance of SIE without contributing to the acidic environment in the body, which indicates that LIPC and RIPC can improve the metabolic efficiency of SIE. Similarly, Incognito et al. [2] reported that, by increasing metabolic efficiency, IPC can improve the performance of subsequent exercises. Since LIPC and RIPC can escalate metabolic efficiency and total work, they can strengthen the training quality of a sprint interval training (SIT) program. ...
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The aim of this study was to investigate the effects of local (LIPC) and remote (RIPC) ischemic preconditioning on sprint interval exercise (SIE) performance. Fifteen male collegiate basketball players underwent a LIPC, RIPC, sham (SHAM), or control (CON) trial before conducting six sets of a 30-s Wingate-based SIE test. The oxygen uptake and heart rate were continuously measured during SIE test. The total work in the LIPC (+2.2%) and RIPC (+2.5%) conditions was significantly higher than that in the CON condition (p < 0.05). The mean power output (MPO) at the third and fourth sprint in the LIPC (+4.5%) and RIPC (+4.9%) conditions was significantly higher than that in the CON condition (p < 0.05). The percentage decrement score for MPO in the LIPC and RIPC condition was significantly lower than that in the CON condition (p < 0.05). No significant interaction effects were found in pH and blood lactate concentrations. There were no significant differences in the accumulated exercise time at ≥80%, 90%, and 100% of maximal oxygen uptake during SIE. Overall, both LIPC and RIPC could improve metabolic efficiency and performance during SIE in athletes.
... The IPC has traditionally been performed at rest (IPC-rest) by placing a pressure cuff or an elastic bandage around the arms or legs to repeatedly compromise muscle blood perfusion for several minutes, separated by rest with an intact blood supply. 3 Studies have shown that IPC-rest can improve the ability to perform short-term (1-3 min) maximal exercise by 2% to 3% in recreationally active men. 4,5 Trained subjects are also reported to benefit from IPCrest in the competitive time domain from 3 to 22 minutes; however, improvements are typically smaller (∼0.5% to 1%). ...
Article
Purpose: This study tested the hypothesis of whether ischemic exercise preconditioning (IPC-Ex) elicits a better intense endurance exercise performance than traditional ischemic preconditioning at rest (IPC-rest) and a SHAM procedure. Methods: Twelve men (average V˙O2max ∼61 mL·kg-1·min-1) performed 3 trials on separate days, each consisting of either IPC-Ex (3 × 2-min cycling at ∼40 W with a bilateral-leg cuff pressure of ∼180 mm Hg), IPC-rest (4 × 5-min supine rest at 220 mm Hg), or SHAM (4 × 5-min supine rest at <10 mm Hg) followed by a standardized warm-up and a 4-minute maximal cycling performance test. Power output, blood lactate, potassium, pH, rating of perceived exertion, oxygen uptake, and gross efficiency were assessed. Results: Mean power during the performance test was higher in IPC-Ex versus IPC-rest (+4%; P = .002; 95% CI, +5 to 18 W). No difference was found between IPC-rest and SHAM (-2%; P = .10; 95% CI, -12 to 1 W) or between IPC-Ex and SHAM (+2%; P = .09; 95% CI, -1 to 13 W). The rating of perceived exertion increased following the IPC-procedure in IPC-Ex versus IPC-rest and SHAM (P < .001). During warm-up, IPC-Ex elevated blood pH versus IPC-rest and SHAM (P ≤ .027), with no trial differences for blood potassium (P > .09) or cycling efficiency (P ≥ .24). Eight subjects anticipated IPC-Ex to be best for their performance. Four subjects favored SHAM. Conclusions: Performance in a 4-minute maximal test was better following IPC-Ex than IPC-rest and tended to be better than SHAM. The IPC procedures did not affect blood potassium, while pH was transiently elevated only by IPC-Ex. The performance-enhancing effect of IPC-Ex versus IPC-rest may be attributed to a placebo effect, improved pH regulation, and/or a change in the perception of effort.
... Positive effects of (r)IPC on exercise performance were related to a promoted phosphocreatine resynthesis, improved functioning of the mitochondrial ATP-dependent potassium channels, attenuated ATP depletion, enhanced metabolic efficiency, and increased vasodilation by the above-mentioned NO-dependent pathways. Thus, oxygen delivery and extraction were enhanced, and subsequent physical performance was ameliorated [20,21]. The remaining heterogeneity of the results might be explained by the differences in the reported study settings, including variations in the number of applied I/R cycles, the applied pressure within the blood pressure cuff, the application site (arm(s) or leg(s) or both), the study cohort, and the associated performance test [16][17][18]. ...
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Beneficial effects of (remote) ischemia preconditioning ((r)IPC), short episodes of blood occlusion and reperfusion, are well-characterized, but there is no consensus regarding the effectiveness of (r)IPC on exercise performance. Additionally, direct comparisons of IPC and rIPC but also differences between reflow modes, low reflow (LR) and high reflow (HR) in particular, are lacking, which were thus the aims of this study. Thirty healthy males conducted a performance test before and after five consecutive days with either IPC or rIPC maneuvers (n = 15 per group). This procedure was repeated after a two-week wash-out phase to test for both reflow conditions in random order. Results revealed improved exercise parameters in the IPC LR and to a lesser extent in the rIPC LR intervention. RBC deformability increased during both rIPC LR and IPC LR, respectively. Pulse wave velocity (PWV) and blood pressures remained unaltered. In general, deformability and PWV positively correlated with performance parameters. In conclusion, occlusion of small areas seems insufficient to affect large remote muscle groups. The reflow condition might influence the effectiveness of the (r)IPC intervention, which might in part explain the inconsistent findings of previous investigations. Future studies should now focus on the underlying mechanisms to explain this finding.
... Es probable que esta mayor expresión de la proteína NOS expresada en el músculo esquelético (nNOSμ) esté asociada con una mayor producción de NO por el músculo esquelético, que es menos dependiente del oxígeno localmente (McConell et al., 2007). El NO parece ser un factor clave en la respuesta mecanicista a la oclusión arterial (Incognito et al., 2016). el problema es que este hecho no ha sido comprobado en este estudio, ya que su medición es poco práctica para usar como indicador de rendimiento en futbolistas; sin embargo, es una posible explicación del menor consumo de oxígeno muscular al final de la pretemporada. ...
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Introducción: El desarrollo de dispositivos portátiles de espectroscopia de infrarrojo cercano no invasivo (NIRS) ha permitido que las mediciones de oxígeno muscular se realicen fuera de un entorno de laboratorio para investigar cambios musculares locales en pruebas campo para guiar el entrenamiento. En general, durante el ejercicio los NIRS portátiles utiliza la saturación de oxígeno muscular (SmO2) como parámetro principal para el estudio de la hemodinámica porque proporciona información sobre el rendimiento y el metabolismo muscular durante el ejercicio. Un uso novedoso de NIRS portátil, es la medición de la oxigenación muscular en reposo a través del método de oclusión arterial (AOM). AOM consiste en realizar breves oclusiones arteriales para conocer el consumo de oxígeno muscular en reposo (mVO2). En la actualidad, AOM es una técnica para obtener información de la capacidad oxidativa del músculo en reposo, lo cual significa que el atleta no realiza ningún esfuerzo físico. Sin embargo, existe poca literatura científica de cómo está implicado el mVO2 en el proceso de entrenamiento. Por otro lado, el monitoreo de la acumulación de fatiga pre y post competencia es importante dentro de la planificación del entrenamiento. Uno de los roles de los científicos del deporte es conocer el perfil de fatiga y recuperación con el fin de optimizar los procesos de entrenamiento para buscar un mejor rendimiento deportivo. Pero existen limitaciones, debido a que el estudio de la fatiga es un fenómeno multifactorial que envuelve diferentes mecanismos fisiológicos. En cuanto a la relación que pueda tener NIRS portátil y la medición de SmO2 con la fatiga dentro de un contexto deportivo se desconoce, debido a que es una variable que no se ha puesto en práctica en el deporte, pero con un gran potencial. En el contexto de la salud, existen numerosas investigaciones que han asociado la SmO2 a enfermedades cardiovasculares, respiratorias y metabólicas como el sobrepeso y obesidad, que son patologías que afectan la entrega de oxígeno durante la actividad física. Uno de los factores claves para prescribir el ejercicio físico es conocer las zonas de metabólica, es decir la intensidad de ejercicio donde existen cambios metabólicos y que se aplica según el objetivo de la sesión de entrenamiento en personas que realizan actividad física para la salud. Por último, existen algunos vacíos científicos de la aplicación de NIRS portátil en contextos de fatiga, rendimiento y salud. Por lo tanto, con esta tesis podemos brindar nuevos aportes científicos del metabolismo muscular a través de la medición de la SmO2 en reposo y durante el ejercicio, necesario para conocer estados de condición física de un deportista, fatiga, recuperación y la prescripción de ejercicio de ejercicio físico. Objetivos: La tesis presenta como objetivo general: Utilizar la saturación de oxígeno muscular y estudiar su implicación en la fatiga, rendimiento y salud. Para realizar el objetivo general se llevó a cabo los siguientes objetivos específicos: 1. Examinar la relación de la saturación de oxígeno muscular en reposo con marcadores de fatiga en futbolistas femeninos. 2. Interpretar el rol de la saturación de oxígeno muscular como un marcador de rendimiento deportivo durante una prueba de alta intensidad (sprint-repetidos) en futbolistas femeninos. 3. Evaluar los cambios de oxigenación muscular en reposo después de un periodo de entrenamiento y correlacionarlos con la composición corporal y la potencia de salto en futbolistas. 4. Comparar y correlacionar los parámetros fisiológicos en función de la saturación de oxígeno muscular por zonas metabólicas durante una prueba de esfuerzo en personas con sobrepeso/obesidad y normo-peso. Métodos: Los cuatro objetivos de esta tesis fueron investigados con cuatro estudios científicos. Los participantes fueron futbolistas femeninos y masculinos que competían en segunda y tercera división respectivamente, y mujeres con sobrepeso/obesidad y normo-peso. En todas las pruebas se utilizó un NIRS portátil marca MOXY colocado en el músculo gastrocnemio y músculo vasto lateral. El primer estudio consistió en medir marcadores de fatiga neuromuscular, escalas psicológicas y marcadores sanguíneos utilizados para medir fatiga a nivel biológico. En conjunto se midió la prueba de oxígeno muscular en reposo (mVO2 y SmO2) mediante la técnica AOM. Todas las mediciones se realizaron pre, post y post 24 h tras un partido de futbol femenino. El segundo estudio consistió en que los futbolistas femeninos realizaran una prueba de sprint repetidos, donde se evaluó la frecuencia cardiaca, velocidad y SmO2 en conjunto. El tercer estudio consistió en observar cambios de SmO2 en reposo después de un periodo de pretemporada en jugadores de futbol y relacionarlo con la composición corporal y la potencia de salto. El cuarto estudio consistió en realizar una prueba de esfuerzo incremental con detección de zonas metabólicas: fatmax, umbrales de entrenamiento VT1 y VT2 y potencia aeróbica máxima para compararlo y relacionarlo con la SmO2. Resultados y Discusión: En base a los objetivos de la tesis: Primero, en las jugadoras de futbol se encontró un aumento de mVO2 y SmO2 en reposo a las 24 h post partido oficial [(mVO2: 0.75 ± 1.8 vs 2.1± 2.7 μM-Hbdiff); (SmO2: 50 ± 9 vs 63 ± 12 %)]. Principalmente, este aumento es resultado de la correlación de la vasodilatación mediada por el flujo sanguíneo y el trasporte de oxígeno muscular que es un mecanismo implicado en los procesos de recuperación de la homeostasis del músculo esquelético y la restauración del equilibrio metabólico. El aumento del consumo de oxígeno se relacionó con la disminución de la potencia de salto (r= −0.63 p <0.05) y el aumento del lactato deshidrogenada (LDH) (r = 0.78 p <0.05) como marcadores de fatiga. Seguidamente en el segundo estudio, encontramos que la disminución del rendimiento durante una prueba de sprint repetidos, comienza con el aumento gradual de la SmO2, debido al cambio de la presión intramuscular y la respuesta hiperémica que conlleva, mostrando una disminución en la respuesta inter-individual [desaturación desde el cuarto sprint (Δ= 32%) y re-saturación después del sexto sprint (Δ= 89%)]. Además, la extracción de oxígeno por parte del músculo tiene una asociación no-lineal con la alta velocidad (r = 0.89 p <0.05) y con la fatiga mostrada el % decremento del sprint (r = 0.93 p <0.05). En el estudio 3 se encontró que la dinámica de SmO2 en reposo es sensible a cambios después de un periodo de pretemporada (SmO2-Pendiente de recuperación: 15 ± 10 vs. 5 ± 5). Asimismo, se mostró que la SmO2 en reposo está relacionado paralelamente con el porcentaje de grasa del cuerpo (r= 0,64 p <0.05) y una relación inversa con la potencia de salto a una sola pierna (r = -0,82 p<0.01). Esto significa que a través del entrenamiento se mejoró el metabolismo y hemodinámica muscular con un tránsito más rápido del oxígeno muscular, y se asoció a las mejoras del peso corporal, somatotipo, CMJ y SLCMJ. En el cuarto estudio, basado en los parámetros fisiológicos de una prueba de esfuerzo para prescribir ejercicio: se encontró una relación entre la SmO2 y el VO2max durante la zona fatmax y VT1 (r=0,72; p=0,04) (r=0,77; p=0,02) en mujeres con normo-peso. Sin embargo, en el grupo sobrepeso obesidad no se encontró ninguna correlación ni cambios de SmO2 entre cada zona metabólica. Conclusión: La investigación de esta tesis ha demostrado avances en la medición de la SmO2. El uso de mVO2 y SmO2 en reposo es una variable de carga de trabajo que se puede utilizar para el estudio de la fatiga después de un partido de futbol femenino. Asimismo, la SmO2 en reposo puede ser interesante tomarlo en cuenta como un parámetro de rendimiento en futbolistas. Siguiendo el contexto, en el rendimiento durante una prueba de sprint repetidos, la SmO2 debe interpretarse basado en la respuesta individual del porcentaje de extracción de oxígeno muscular (∇%SmO2). El aporte de ∇%SmO2 es un factor de rendimiento limitado por la capacidad de velocidad y soporte de la fatiga de los futbolistas femeninos. Respecto a los aspectos de salud y prescripción del ejercicio, proponemos utilizar la SmO2 como un parámetro fisiológico para controlar y guiar el entrenamiento en zonas fatmax y VT1, pero solo en mujeres normo-peso. En patologías metabólicas como el sobrepeso y obesidad se necesitan más estudios. Como conclusión general, esta tesis muestra nuevas aplicaciones prácticas de cómo utilizar la SmO2 y su implicación en la fatiga, en contraste la adaptación al entrenamiento, pruebas de rendimiento y prescripción de la actividad física para la salud.
... Intermittent BFR is used only during the exercise and released upon completion of the set [11]. Furthermore, ischemic preconditioning is also differentiated as a method utilizing occlusion only before the exercise [12,29,44]. Thus, the duration of occlusion may vary substantially between used protocols [44]. ...
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Introduction. Athletes, as well as recreationally trained individuals are increasingly looking for innovative techniques and methods of resistance training to provide an additional stimulus to break through plateaus, prevent monotony and achieve various training goals. Partial or total blood flow restriction (BFR) to the working muscles during resistance exercise has been used as a complementary training modality, aiming to further increase muscle mass and improve strength. BFR is usually used during low-load resistance exercise and has been shown to be effective in enhancing long-term hypertrophic and strength responses in both clinical and athletic populations. However, recently some attention has been focused on the acute effects of BFR on strength and power performance during highload resistance exercise. Aim of Study. This article provides an overview of available scientific literature and describes how BFR affects the 1-repetition maximum (1RM), the number of repetitions performed, time under tension and kinematic variables such as power output and bar velocity. Material and Methods. Available scientific literature. Results. As a result, BFR could be an important tool in eliciting greater maximal load, power output and strength-endurance performance during resistance exercise. Conclusions. BFR as a training tool can be used as an additional factor to help athletes and coaches in programming varied resistance training protocols.
... A growing number of experimental studies demonstrated a positive effect of IP on subsequent endurance performance measured during various tasks such as cycling, running, and swimming (Incognito et al. 2016;Caru et al. 2019). The mechanisms through which IP might induce an ergogenic effect are still unclear and numerous hypotheses are proposed to explain its positive effect on endurance performance. ...
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Purpose This study investigated the effect of ischemic preconditioning (IP) on metaboreflex activation following dynamic leg extension exercise in a group of healthy participants. Method Seventeen healthy participants were recruited. IP and SHAM treatments (3 × 5 min cuff occlusion at 220 mmHg or 20 mmHg, respectively) were administered in a randomized order to the upper part of exercising leg’s thigh only. Muscle pain intensity (MP) and pain pressure threshold (PPT) were monitored while administrating IP and SHAM treatments. After 3 min of leg extension exercise at 70% of the maximal workload, a post-exercise muscle ischemia (PEMI) was performed to monitor the discharge group III/IV muscle afferents via metaboreflex activation. Hemodynamics were continuously recorded. MP was monitored during exercise and PEMI. Results IP significantly reduced mean arterial pressure compared to SHAM during metaboreflex activation (mean ± SD, 109.52 ± 7.25 vs. 102.36 ± 7.89 mmHg) which was probably the consequence of a reduced end diastolic volume (mean ± SD, 113.09 ± 14.25 vs. 102.42 ± 9.38 ml). MP was significantly higher during the IP compared to SHAM treatment, while no significant differences in PPT were found. MP did not change during exercise, but it was significantly lower during the PEMI following IP (5.10 ± 1.29 vs. 4.00 ± 1.54). Conclusion Our study demonstrated that IP reduces hemodynamic response during metaboreflex activation, while no effect on MP and PPT were found. The reduction in hemodynamic response was likely the consequence of a blunted venous return.
Article
Purpose: Whilst pre-exercise ischaemic preconditioning (IPC) can improve lower-body exercise performance, its impact on upper-limb performance has received little attention. This study examines the influence of IPC on upper-body exercise performance and oxygen uptake (⩒O2) kinetics. Methods: Eleven recreationally-active males (24 ± 2 years) completed an arm-crank graded exercise test to exhaustion to determine the power outputs at the ventilatory thresholds (VT1 and VT2) and ⩒O2peak (40.0 ± 7.4 ml·kg-1·min-1). Four main trials were conducted, two following IPC (4 × 5-min, 220 mmHg contralateral upper-limb occlusion), the other two following SHAM (4 × 5-min, 20 mmHg). The first two trials consisted of a 15-minute constant work rate and the last two time-to-exhaustion (TTE) arm-crank tests at the power equivalents of 95% VT1 (LOW) and VT2 (HIGH), respectively. Pulmonary ⩒O2 kinetics, heart rate, blood-lactate concentration, and rating of perceived exertion were recorded throughout exercise. Results: TTE during HIGH was longer following IPC than SHAM (459 ± 115 vs 395 ± 102 s, p = 0.004). Mean response time and change in ⩒O2 between 2-min and end exercise (Δ⩒O2) were not different between IPC and SHAM for arm-cranking at both LOW (80.3 ± 19.0 vs 90.3 ± 23.5 s [p = 0.06], 457 ± 184 vs 443 ± 245 ml [p = 0.83]) and HIGH (96.6 ± 31.2 vs 92.1 ± 24.4 s [p = 0.65], 617 ± 321 vs 649 ± 230 ml [p = 0.74]). Heart rate, blood-lactate concentration, and rating of perceived exertion did not differ between conditions (all p≥0.05). Conclusion: TTE was longer following IPC during upper-body exercise despite unchanged ⩒O2 kinetics.
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RESUMO: O pré-condicionamento isquêmico [do termo em inglês ischemic preconditioning (IPC)] é uma estratégia caracterizada por breves ciclos de restrição do fluxo sanguíneo seguidos de reperfusão, realizados nos membros superiores ou inferiores com o objetivo de melhorar o desempenho físico. Essa intervenção tem chamado atenção devido a sua característica não invasiva, seu baixo custo e a fácil aplicação. Uma vez que não há um consenso sobre a sua efetividade como uma estratégia ergogênica, o objetivo deste estudo foi investigar o seu estado atual de produção científica, o efeito sobre o desempenho físico e o efeito do nível de treinamento dos participantes e diferentes exercícios/testes utilizados para avaliação do desempenho. Sessenta e sete artigos, envolvendo 984 participantes (177 mulheres) de diferentes níveis de treinamento, preencheram os critérios de inclusão. Sete exercícios (ciclismo, exercício resistido, corrida, natação, patinação, futebol, remo) e cinco níveis de treinamento (destreinados, recreacionalmente treinados, treinados, bem treinados, profissional) foram identificados. A maioria da produção científica sobre IPC e desempenho físico foi publicada a partir de 2015. Mais da metade dos estudos apresentaram um efeito positivo do IPC sobre o desempenho físico (59,7%, n=40). O teste exato de Fischer mostrou que existe uma relação entre o efeito do IPC sobre o desempenho físico e o nível de treinamento dos participantes [X2(8) = 15,149; p = 0,026], mas não entre o efeito do IPC e exercício/teste [X2(12) = 19,528; p = 0,129]. Na última década, houve um aumento substancial na produção cientifica sobre IPC e desempenho físico. Nossos achados sustentam um efeito benéfico do IPC na melhora do desempenho físico, sendo este efeito mais pronunciado em indivíduos destreinados e recreacionalmente treinados, independente do exercício/teste realizado.
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This study evaluated the effect of ischemic preconditioning (IPC) on resistance exercise (RE) performance in the lower limbs. Thirteen men participated in a randomized crossover design that involved 3 separate sessions (ischemic preconditioning, placebo and control). A 12-RM load for the leg extension exercise was assessed through test and retest sessions prior to the first experimental session. The IPC session consisted of 4 cycles of 5 minutes occlusion at 220 mmHg of pressure alternated with 5 minutes of reperfusion at 0 mmHg for a total of 40 minutes. The PLACEBO session consisted of 4 cycles of 5 minutes of cuff administration at 20 mmHg of pressure alternated with 5 minutes of pseudo-reperfusion at 0 mmHg for a total of 40 minutes. The occlusion and reperfusion phases were conducted alternately between the thighs, with subjects remaining seated. No ischemic pressure was applied during the control (CON) session and subjects sat passively for 40 minutes. Eight minutes following IPC, PLACEBO or CON, subjects performed three repetition maximum sets of the leg extension (2min rest between sets) with the pre-determined 12-RM load. Four minutes following the third set for each condition, blood lactate was assessed. The results showed that for the first set, the number of repetitions significantly increased for both the IPC (13.08 ± 2.11; p = 0.0036) and PLACEBO (13.15 ± 0.88; p = 0.0016) conditions, but not the CON (11.88 ± 1.07; p > 0.99) condition. Additionally, the IPC and PLACEBO conditions resulted insignificantly greater repetitions versus the CON condition on the 1set (p=0.015; p=0.007) and 2set (p=0.011; p=0.019), but not the 3 set (p=0.68; p>0.99). No difference (p=0.465) was found in the fatigue index and lactate concentration between conditions. These results indicate that IPC and PLACEBO ischemic preconditioning may have small beneficial effects on repetition performance over a CON condition. Due to potential for greater discomfort associated with the IPC condition, it is suggested that ischemic pre-conditioning might be practiced gradually to assess tolerance and potential enhancements to exercise performance.
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Systematic reviews and meta-analyses are essential to summarize evidence relating to efficacy and safety of health care interventions accurately and reliably. The clarity and transparency of these reports, however, is not optimal. Poor reporting of systematic reviews diminishes their value to clinicians, policy makers, and other users.Since the development of the QUOROM (QUality Of Reporting Of Meta-analysis) Statement--a reporting guideline published in 1999--there have been several conceptual, methodological, and practical advances regarding the conduct and reporting of systematic reviews and meta-analyses. Also, reviews of published systematic reviews have found that key information about these studies is often poorly reported. Realizing these issues, an international group that included experienced authors and methodologists developed PRISMA (Preferred Reporting Items for Systematic reviews and Meta-Analyses) as an evolution of the original QUOROM guideline for systematic reviews and meta-analyses of evaluations of health care interventions.The PRISMA Statement consists of a 27-item checklist and a four-phase flow diagram. The checklist includes items deemed essential for transparent reporting of a systematic review. In this Explanation and Elaboration document, we explain the meaning and rationale for each checklist item. For each item, we include an example of good reporting and, where possible, references to relevant empirical studies and methodological literature. The PRISMA Statement, this document, and the associated Web site (http://www.prisma-statement.org/) should be helpful resources to improve reporting of systematic reviews and meta-analyses.
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The acute effect of ischemic preconditioning (IPC) on the maximal performance in the 100-m freestyle event was studied in recreational swimmers. 15 swimmers (21.0±3.2 years) participated in a random crossover model on 3 different days (control [CON], IPC or SHAM), separated by 3-5 days. IPC consisted of 4 cycles of 5-min occlusion (220 mmHg)/5-min reperfusion in each arm, and the SHAM protocol was similar to IPC but with only 20 mmHg during the occlusion phase. The subjects were informed that both maneuvers (IPC and SHAM) would improve their performance. After IPC, CON or SHAM, the volunteers performed a maximal 100-m time trial. IPC improved performance (p=0.036) compared to CON. SHAM performance was only better than CON (p=0.059) as a tendency but did not differ from IPC performance. The individual response of the subjects to the different maneuvers was very heterogeneous. We conclude that IPC may improve performance in recreational swimmers, but this improvement could mainly be a placebo effect. © Georg Thieme Verlag KG Stuttgart · New York.
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Ischemic preconditioning (IPC) improves maximal exercise performance. However, the potential mechanism(s) underlying the beneficial effects of IPC remain unknown. The dynamics of pulmonary oxygen uptake (VO2) and muscle deoxygenation during exercise is frequently used for assessing O2 supply and extraction. Thus, this study examined the effects of IPC on systemic and local O2 dynamics during the incremental step transitions from low- to moderate- and from moderate- to severe-intensity exercise. Fifteen healthy, male subjects were instructed to perform the work-to-work cycling exercise test, which was preceded by the control (no occlusion) or IPC (3 × 5 min, bilateral leg occlusion at >300 mmHg) treatments. The work-to-work test was performed by gradually increasing the exercise intensity as follows: low intensity at 30 W for 3 min, moderate intensity at 90% of the gas exchange threshold (GET) for 4 min, and severe intensity at 70% of the difference between the GET and VO2 peak until exhaustion. During the exercise test, the breath-by-breath pulmonary VO2 and near-infrared spectroscopy-derived muscle deoxygenation were continuously recorded. Exercise endurance during severe-intensity exercise was significantly enhanced by IPC. There were no significant differences in pulmonary VO2 dynamics between treatments. In contrast, muscle deoxygenation dynamics in the step transition from low- to moderate-intensity was significantly faster in IPC than in CON (27.2 ± 2.9 vs. 19.8 ± 0.9 sec, P < 0.05). The present findings showed that IPC accelerated muscle deoxygenation dynamics in moderate-intensity exercise and enhanced severe-intensity exercise endurance during work-to-work test. The IPC-induced effects may result from mitochondrial activation in skeletal muscle, as indicated by the accelerated O2 extraction. © 2015 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of the American Physiological Society and The Physiological Society.
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Permissions and Reprints Correction to Acute Effect of Ischemic Preconditioning is Detrimental to Anaerobic Performance in CyclistsInt J Sports Med eFirst DOI: 10.1055/s-0034-1384588 Erratum R. C. Paixão, G. Ribeiro da Mota, M. Marocolo Acute Effect of Ischemic Preconditioning is Detrimental to Anaerobic Performance in Cyclists Int J Sports Med 2014. DOI http://dx.doi.org/10.1055/s-0034-1372628 Published online: May 26, 2014. The E-First-version contains an error in Authors. The correct name of the 2nd author is da Mota GR, not G. Ribeiro da Mota.
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Purpose: This study investigated the effects of ischemic preconditioning (IPC) on the ratings of perceived exertion (RPE), surface electromyography (EMG), and pulmonary oxygen uptake (V̇O2) onset kinetics during cycling until exhaustion at the peak power output attained during an incremental test (PPO). Methods: A group of 12 recreationally trained cyclists volunteered for this study. After determination of PPO, they were randomly subjected on different days to a performance protocol preceded by intermittent bilateral cuff pressure inflation to 220 mm Hg (IPC) or 20 mm Hg (control). To increase data reliability, the performance visits were replicated, also in a random manner. Results: There was an 8.0% improvement in performance after IPC (Control: 303 s, IPC 327 s, factor SDs of ×/÷1.13, P = 0.01). This change was followed by a 2.9% increase in peak V̇O2 (Control: 3.95 L·min(-1), IPC: 4.06 L·min(-1), factor SDs of ×/÷ 1.15, P = 0.04) owing to a higher amplitude of the slow component of the V̇O2 kinetics (Control: 0.45 L·min(-1), IPC: 0.63 L·min(-1), factor SDs of ×/÷ 2.21, P = 0.05). There was also an attenuation in the rate of increase in RPE (P = 0.01) and a progressive increase in the myoelectrical activity of the vastus lateralis muscle (P = 0.04). Furthermore, the changes in peak V̇O2 (r = 0.73, P = 0.007) and the amplitude of the slow component (r = 0.79, P = 0.002) largely correlated with performance improvement. Conclusion: These findings provide a link between improved aerobic metabolism and enhanced severe-intensity cycling performance after IPC. Furthermore, the delayed exhaustion after IPC under lower RPE and higher skeletal muscle activation suggest they have a role on the ergogenic effects of IPC on endurance performance.
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Remote ischaemic preconditioning (RIPC) protects tissues against ischaemia-reperfusion (I/R) injury, a common occurrence in several clinical settings. To evaluate whether RIPC has a beneficial impact on walking disability in arterial intermittent claudication. A total of 20 patients with proven intermittent claudication underwent two treadmill walking tests with a 7-day interval in between; they were randomized according to the order in which they received either RIPC or a control procedure before the first treadmill test, with a crossover at the second test. Patients received three cycles of alternating 5-minute inflation and 5-minute deflation of blood-pressure cuffs on both arms, with inflation to a pressure of 200mmHg in the RIPC procedure or 10mmHg in the control procedure. Walking distances and limb oxygenation data, assessed with transcutaneous oximetry and near infrared spectroscopy measurements, were obtained during both RIPC and control procedures in all patients. Similar exercise intensities were achieved after the control and RIPC procedures. Walking distances did not significantly differ after the control and RIPC procedures (204 [141-259]m vs 215 [162-442]m, respectively; P=0.22). Similarly, no difference was observed in terms of transcutaneous oxygen pressure change and near infrared spectroscopy measurements during exercise between the two procedures. RIPC did not improve walking distance or limb ischaemia variables in patients with peripheral artery disease and intermittent claudication. Copyright © 2015 Elsevier Masson SAS. All rights reserved.
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Background— Ischemic preconditioning reduces local tissue injury caused by subsequent ischemia-reperfusion (IR), but may also have a salutary effect on IR injury of tissues remote from those undergoing preconditioning. We tested the hypothesis that limb ischemia induces remote preconditioning, reduces endothelial IR injury in humans, and reduces experimental myocardial infarct size. Methods and Results— Endothelial IR injury of the human forearm was induced by 20 minutes of upper limb ischemia (inflation of a blood pressure cuff to 200 mm Hg) followed by reperfusion. Remote preconditioning was induced by three 5-minute cycles of ischemia of the contralateral limb. Venous occlusion plethysmography was used to assess forearm blood flow in response to acetylcholine at baseline and 15 minutes after reperfusion. Experimental myocardial infarction was achieved by 40 minutes of balloon occlusion of the left anterior descending artery in 15-kg pigs. Remote preconditioning was induced by four 5-minute cycles of lower limb ischemia. Triphenyltetrazolium staining was used to assess the extent of myocardial infarction. In the human study, the response to acetylcholine was significantly attenuated in the control group after 15 minutes’ reperfusion, but remote preconditioning prevented this reduction. Limb ischemia caused a significant reduction in the extent of myocardial infarction relative to the area at risk compared with control (26±9% versus 53±8%, P<0.05). Conclusion— Remote ischemic preconditioning prevents IR-induced endothelial dysfunction in humans and reduces the extent of myocardial infarction in experimental animals. Transient limb ischemia is a simple preconditioning stimulus with important potential clinical applications.