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A Mechanistic Approach to Blood Flow Occlusion

Authors:
  • Applied Science and Performance Institute

Abstract and Figures

Low-Intensity occlusion training provides a unique beneficial training mode for promoting muscle hypertrophy. Training at intensities as low as 20% 1RM with moderate vascular occlusion results in muscle hypertrophy in as little as three weeks. The primary mechanisms by which occlusion training is thought to stimulate growth include, metabolic accumulation, which stimulates a subsequent increase in anabolic growth factors, fast-twitch fiber recruitment (FT), and increased protein synthesis through the mammalian target of rapamycin (mTOR) pathway. Heat shock proteins, Nitric oxide synthase-1 (NOS-1) and Myostatin have also been shown to be affected by an occlusion stimulus. In conclusion, low-intensity occlusion training appears to work through a variety of mechanisms. The research behind these mechanisms is incomplete thus far, and requires further examination, primarily to identify the actual metabolite responsible for the increase in GH with occlusion, and determine which mechanisms are associated to a greater degree with the hypertrophic/anti-catabolic changes seen with blood flow restriction.
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Review 1
Loenneke JP et al. A Mechanistic Approach to Blood Flow Int J Sports Med 2010; 31: 1 4
accepted after revision
August 17, 2009
Bibliography
DOI http://dx.doi.org/
10.1055/s-0029-1239499
Published online:
November 2, 2009
Int J Sports Med 2010; 31:
1 – 4 © Georg Thieme
Verlag KG Stuttgart · New York
ISSN 0172-4622
Correspondence
J. P. Loenneke
Southeast Missouri State
University Health, Human
Performance and Recreation
One University Plaza
63701 Cape Girardeau
United States
Tel.: 573-450-2952
Fax: 573-651-5150
jploenneke1s@semo.edu
Key words
HSP 72
growth hormone
lactate
mTOR
hypertrophy
myostatin
A Mechanistic Approach to Blood Flow Occlusion
rehabilitation, speci cally ACL injuries, cardiac
rehabilitation patients, the elderly [33, 36] and
even astronauts [12] . Although muscle hypertro-
phy would likely bene t those special populations,
more research should be done to further our
understanding of the proposed bene ts to each.
The primary mechanisms by which occlusion
training stimulates growth include: metabolic
accumulation which stimulates a subsequent
increase in anabolic growth factors, fast-twitch
ber recruitment (FT), and increased protein
synthesis through the mammalian target of
rapamycin (mTOR) pathway. Increases in heat
shock proteins (HSP), Nitric oxide synthase-1
(NOS-1), and decreased expression of Myostatin
have also been observed [15] . The purpose of this
manuscript is to describe the physiologic mecha-
nisms by which vascular occlusion leads to skel-
etal muscle hypertrophy.
Metabolic Accumulation and Growth
Hormone
&
Whole blood lactate [8, 34] , plasma lactate
[7, 28, 33] and muscle cell lactate [14, 15] are all
increased in response to exercise with blood ow
Introduction
&
The American College of Sports Medicine (ACSM)
recommends lifting a weight of at least 65 % of
one s one repetition maximum (1RM) to achieve
muscular hypertrophy under normal conditions.
It is believed that anything below this intensity
rarely produces substantial muscle hypertrophy
or strength gains [17] . However, some individu-
als are unable to withstand the high mechanical
stress placed upon the joints during heavy resist-
ance training. Therefore, scientists have sought
lower intensity alternatives such as blood occlu-
sion training, also known as KAATSU training.
Blood occlusion training, as the name implies,
involves decreasing blood ow to a muscle, by
application of a wrapping device, such as a blood
pressure cu . Evidence indicates that this style of
training can provide a unique, bene cial mode of
exercise in clinical settings, as it produces posi-
tive training adaptations at the equivalent to
physical activity of daily life (10 – 30 % of maximal
work capacity) [1] . Muscle hypertrophy has
recently been shown to occur during exercise as
low as 20 % of 1RM with moderate vascular occlu-
sion ( ~ 100 mmHg) [32] , which could be quite ben-
e cial to athletes [34] , patients in post operation
Authors J. P. Loenneke
1 , G. J. Wilson
2 , J. M. Wilson
3
A liations 1 Southeast Missouri State University, Health, Human Performance, and Recreation, Cape Girardeau, United States
2 University of Illinois, Division of Nutritional Sciences, Champaign-Urbana, United States
3 Florida State University, Department of Nutrition, Food, and Exercise Science, Tallahassee, United States
Abstract
&
Low-Intensity occlusion training provides a
unique bene cial training mode for promoting
muscle hypertrophy. Training at intensities as
low as 20 % 1RM with moderate vascular occlu-
sion results in muscle hypertrophy in as little as
three weeks. The primary mechanisms by which
occlusion training is thought to stimulate growth
include, metabolic accumulation, which stimu-
lates a subsequent increase in anabolic growth
factors, fast-twitch ber recruitment (FT), and
increased protein synthesis through the mam-
malian target of rapamycin (mTOR) pathway.
Heat shock proteins, Nitric oxide synthase-1
(NOS-1) and Myostatin have also been shown to
be a ected by an occlusion stimulus. In conclu-
sion, low-intensity occlusion training appears
to work through a variety of mechanisms. The
research behind these mechanisms is incomplete
thus far, and requires further examination, pri-
marily to identify the actual metabolite respon-
sible for the increase in GH with occlusion, and
determine which mechanisms are associated to a
greater degree with the hypertrophic / anti-cata-
bolic changes seen with blood ow restriction.
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Loenneke JP et al. A Mechanistic Approach to Blood Flow Int J Sports Med 2010; 31: 1 4
restriction. This is signi cant, as growth hormone (GH) has
shown to be stimulated by an acidic intramuscular environment
[34] . Evidence indicates that a low pH stimulates sympathetic
nerve activity through a chemoreceptive re ex mediated by
intramuscular metaboreceptors and group III and IV a erent b-
ers [38] . Consequently, this same pathway has recently been
shown to play an important role in the regulation of hypophy-
seal secretion of GH [9, 38] .
However, changes in blood lactate are not always predictive of
changes in GH. To illustrate, Reeves et al. [28] showed that while
occlusion training resulted in a greater GH response than a non-
occluded control, there were no signi cant di erences in blood
lactate concentrations between groups. One possibility for the
disparity is that occluding blood ow resulted in a slower di u-
sion of lactate out of muscle tissue, resulting in a more pro-
nounced intramuscular acidic environment and therefore, a
greater local stimulation of group IV a erents prior to its di u-
sion out of the cell. It is also possible that additional intramuscu-
lar metabolites stimulated changes in GH as group III and IV
a erents are sensitive to changes in adenosine, K + , H + , hypoxia,
and AMP. Increases in these metabolites during exercise is
thought to drive the pressor re ex leading to increased heart
rate and blood pressure, and it is postulated that this may also
facilitate increases in GH following occlusion training [27] .
Although there is no evidence that GH enhances muscle protein
synthesis when combined with traditional resistance exercise in
humans [40] , occlusion training may be di erent. Occlusion
training elevates GH to levels over that seen with traditional
resistance training [18, 19] . One study showed an increase in GH
~ 290 times greater than baseline measurements [34] . Research
on the e ects of supraphysiologic dosing of GH with traditional
resistance training in humans is limited. And while this research
has not yet demonstrated increased hypertrophy, it does appear
to indicate that GH administration elevates both the liver iso-
form of IGF-1 (Ea) in muscle as well as mechano-growth factor
[6] . More recently Ehrenborg and Rosen [6] have in an extensive
analysis of the literature on GH concluded that the majority of
the improvement with GH is due to the stimulation of collagen
synthesis which could provide a protective e ect in transferring
force from skeletal muscle externally and thus protect against
ruptures.
It is unclear if IGF-1 activity is increased in response to occlusion
training. More speci cally, Takano et al. [33] found a signi cant
increase, whereas two other studies found no increase [1, 15] .
Possible reasons as to why there was no increase could be related
to the low intensity of the exercise. Kawada and Ishii [15] postu-
late that IGF-1 may not be necessary for muscle hypertrophy
when other factors such as Myostatin, heat shock protein 72
(HSP-72), and nitric oxide synthase-1 (NOS-1) are changed in
favor of muscle growth.
Fiber Type Recruitment
&
The size principle suggests that under normal conditions slow
twitch bers (ST) are recruited rst and as the intensity increases,
fast twitch bers (FT) are recruited as needed. The novel aspect
of occlusion training is that FT are recruited even though the
training intensity is low. Moritani et al. [25] postulated that
since the availability of oxygen is severely reduced during occlu-
sion, that a progressive recruitment of additional motor units
(MU) may take place to compensate for the de cit in force devel-
opment. Previous studies have shown signi cant increases in
MU ring rate and MU spike amplitude associated with arterial
occlusion suggesting that the recruitment of high threshold MU
is not only a ected by the force and speed of contraction but also
the availability of oxygen [11, 13, 24] . Results from the use of
Integrated electromyography (iEMG) are consistent with these
ndings, demonstrating no practical di erence in iEMG activity
between low intensity occlusion and high intensity non occlu-
sion training suggesting that a greater number of FT bers are
activated at low intensities [34 – 36] .
mTOR Pathway
&
Increased rates of protein synthesis help to drive the skeletal
muscle hypertrophy response [39] . S6K1 phosphorylation a
critical regulator of exercise-induced muscle protein synthesis
has been demonstrated to increase with occlusion training.
Phosphorylation of S6K1 at Thr389 was increased by three-fold
immediately post exercise with occlusion training, and remained
elevated relative to control at three hours post exercise [7] .
Moreover research demonstrates that REDD1 (regulated in
development and DNA damage responses), which is normally
expressed in states of hypoxia, is not increased in response to
occlusion training even though hypoxia-inducible factor-1 alpha
(HIF-1 α ) is elevated. Normally HIF-1 α mRNA expression corre-
lates with a corresponding elevation in REDD1 [5] . The lack of
increases in REDD1 mRNA expression may prove to be impor-
tant as REDD1 works to reduce protein synthesis through inhibi-
tion of the mammalian target of rapamycin (mTOR), responsible
for the regulation of translation initiation [5] .
Currently there is no clear explanation for this paradox. How-
ever it is conceivable that an unknown factor is increased with
occlusion training, which in uences the transcription of HIF-1 α
and REDD1.
Heat Shock Proteins
&
HSPs are induced by stressors such as heat, ischemia, hypoxia,
free radicals, and act as chaperones to prevent misfolding or
aggregation of proteins. HSPs also appears useful to slowing
atrophy [15] , as HSP-72 plays a protective role in preventing pro-
tein degradation during periods of reduced contractile activity
[26] , by inhibiting key atrophy signaling pathways [4, 31] . The
primary pathway involved in mediating protein degradation is
the ubiquitin proteasome pathway. Recent in vivo data, demon-
strate that increased levels of HSP-70 is su cient to prevent
skeletal muscle disuse atrophy by inhibiting the promoter acti-
vation of atrogin-1 / muscle atrophy F-box (MAFbx) and muscle-
speci c RING nger 1 (MuRF1) as well as the transcription
factors which regulate their expression, forkhead box O (Foxo)
and nuclear factor of P + NF-P + . Senf et al. [4] also observed that
Foxo3a, a member of the Foxo family upregulated during atro-
phy, not NF-P + is necessary for the increase in MAFbx and
MuRF1 promoter activities during disuse. Regardless both tran-
scriptional factor activities, Foxo and NF-P + are inhibited with
elevated HSP-70 levels. Incidentally, occlusion training has been
shown to increase HSP-72 in a rat model [15] , and Kawada and
Ishii [15] postulated that the increase in HSP-72 could be a
potential mechanism by which occlusion increases skeletal mus-
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Loenneke JP et al. A Mechanistic Approach to Blood Flow Int J Sports Med 2010; 31: 1 4
cle hypertrophy and attenuates atrophy [36] , likely by inhibiting
the mediating pathways of the ubiquitin proteasome pathway.
NOS-1
&
Nitric oxide synthase is an enzyme responsible for converting
L-arginine into nitric oxide (NO), a small and electrically neutral
molecule capable of moving with ease through tissues [3] . Neu-
ronal NOS (nNOS) is found in the transmembrane / dystrophin
protein complex of skeletal muscle [29] . At rest, nNOS continu-
ally produces low levels of NO which appear to maintain satellite
cell quiescence. During exercise-induced contraction nNOS is
thought to be activated by mechanical shear forces, as well as
increased intracellular Ca
2 + concentrations [37] . nNOS is
increased in conjunction with occlusion training, possibly medi-
ated by the increased ux of Ca
2 + , as well as reperfusion [15] .
According to Anderson et al., [2, 3] a spike in NO production trig-
gers the release of hepatocyte growth factor (HGF) from its bind-
ing to the muscle extracellular matrix followed by co-localization
with its c-MET receptor on satellite cells leading to their activa-
tion. This model is supported by a number of ndings demon-
strating the inhibition of satellite cells in response to short-term
L-arginine methyl ester (L-NAME) treatment following injury or
mechanical stretch [3] .
Interestingly, Kawada and Ishii [15] did not show an increase in
NO, only nNOS, which could be due to the short life span of NO.
In this study, NO concentration was measured indirectly by its
oxidation products, therefore the obtained values might have
resulted from the production and breakdown of NO, both of
which might be in uenced by the occlusion of blood ow.
Myostatin
&
Myostatin is a negative regulator of muscle growth and muta-
tions of this gene result in overgrowth of musculature in mice,
cattle, and humans [21, 22, 30] . Myostatin appears to inhibit sat-
ellite cell proliferation because Myostatin-null mice display
muscle hypertrophy and increased postnatal muscle growth,
which have been linked to increase satellite cell activity
[10, 20, 23] . McCroskery et al. [20] conclude that Myostatin is
expressed in adult satellite cells and that Myostatin regulates
satellite cell quiescence and self-renewal, showing it does play a
role in adult myogenesis.
Muscle Myostatin gene expression has been shown to decrease
as a result of mechanical overloading [16] , as well as in low
intensity exercise with occlusion [15] . Occlusion may cause
favorable hypertrophic changes in Myostatin as a result of
hypoxia and / or the accumulation of metabolic subproducts.
Conclusion
&
In conclusion low-intensity occlusion training works through a
variety of mechanisms, with the most prominent being meta-
bolic accumulation, ber type activation, and mTOR signaling.
The research behind these mechanisms is incomplete thus far,
and more studies should be included to elucidate the actual
metabolite(s) responsible for the increase in GH with occlusion.
Furthermore, research should be directed towards determining
which particular mechanism(s) is associated to a greater degree
with the hypertrophic / anti-catabolic changes seen with blood
ow restriction. While we have a base foundation of possibili-
ties, controlled studies addressing each proposed mechanism
Fig. 1 Mechanisms by which blood occlusion training increases strength and muscular Hypertrophy. Arrows indicate stimulation, and blocked lines
indicate inhibition. HSP = Heat shock proteins, GH = Growth Hormone, NO = Nitric oxide, IGF-1 = Insulin like growth factor, GHRH = Growth Hormone
Releasing Hormone.
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Loenneke JP et al. A Mechanistic Approach to Blood Flow Int J Sports Med 2010; 31: 1 4
would provide a better understanding of each. For example, the
paradox of REDD1 and HIF-1 α should be examined to determine
if there is another factor that is increased in response to blood
ow restriction. As postulated earlier, perhaps there is an
unknown factor that in uences the transcription of HIF-1 α and
REDD1 leading to the paradoxical increase in HIF-1 α with a
decrease in REDD1 expression. HSPs may also play an important
role, speci cally in attenuating skeletal muscle atrophy. While
animal studies show promise, human studies should be per-
formed to try and con rm the initial ndings of Kawada and
Ishii.
The mechanisms described in this paper have all been shown to
potentially induce skeletal muscle hypertrophy in response to
blood- ow restriction. Although some mechanisms may be
more prominent than others, all the mechanisms described
likely play at least some part in the enhanced skeletal muscle
hypertrophy response associated with occlusion training.
Fig. 1 summarizes the mechanisms by which blood occlusion
training may stimulate muscular hypertrophy.
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... 1,2 Whilst the exact mechanisms which underpin the adaptations associated with BFRE are not fully understood, it has been proposed that the mechanical stress from the cuff occlusion, and the decline in oxygen delivery and metabolite clearance associated, contribute to blood pooling in the capillary beds of the musculature distal to the device, resulting in intramuscular acidosis. 3,4 When BFRE is combined with low-load resistance training (LLRT), it has been shown to increase systemic growth hormone production, 5 fast-twitch muscle fibre recruitment, 6 protein synthesis, 6 intramuscular anabolic and anti-catabolic signalling, 7 and reactive hyperaemia. 8 Additionally, when undertaken in conjunction with aerobic exercise, BFRE has been shown to elicit acute increases in exercising heart rate, blood lactate concentrations, and measures of endothelial function. ...
... 1,2 Whilst the exact mechanisms which underpin the adaptations associated with BFRE are not fully understood, it has been proposed that the mechanical stress from the cuff occlusion, and the decline in oxygen delivery and metabolite clearance associated, contribute to blood pooling in the capillary beds of the musculature distal to the device, resulting in intramuscular acidosis. 3,4 When BFRE is combined with low-load resistance training (LLRT), it has been shown to increase systemic growth hormone production, 5 fast-twitch muscle fibre recruitment, 6 protein synthesis, 6 intramuscular anabolic and anti-catabolic signalling, 7 and reactive hyperaemia. 8 Additionally, when undertaken in conjunction with aerobic exercise, BFRE has been shown to elicit acute increases in exercising heart rate, blood lactate concentrations, and measures of endothelial function. ...
... Implementing blood flow restriction (BFR) during walking is gaining momentum, with a benefit of this approach being reduced absolute external training intensity, still resulting in chronic adaptations to aerobic fitness (1) and muscular strength (2). BFRwalking leads to acute systemic and local physiological adjustments (3,4). Systemically, hemodynamic stability is reduced, decreasing venous return, cardiac preload, and stroke volume (5). ...
... To compensate, heart rate increases to maintain cardiac output (6) while minute ventilation simultaneously increases as the demand for oxygen rises (2). Locally, reductions in oxygen delivery and removal of metabolic waste create a localized hypoxic environment, lowering muscular pH (3). Consequently, BFR-walking is considered a suitable exercise for load-compromised individuals such as older adults, injured athletes, and patients with chronic musculoskeletal disorders (7). ...
... The recruitment of type I muscle fibers is decreased in the hypoxic environment of the muscle, but type II muscle fibers, which rely on anaerobic metabolism, are more easily recruited and activated (27). Previous research indicates that LL-BFRT can effectively stimulate type II muscle fibers, similar to HL-RT (28). Consequently, there is a similar muscle fiber activation effect between HL-RT and LL-BFRT. ...
... Peak torque at high-speed reflects the ability to generate force rapidly (43). At 120 • /s, extensors PT/BW was increased significantly, likely because the hypoxic environment created by BFRT is more effective for recruiting type II muscle fibers, which are responsible for faster force generation (28). However, HL-RT showed more remarkable improvement in lowspeed isokinetic movements assessing maximal torque values. ...
Article
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Objective The objective of this study is to compare the effectiveness of low-load blood flow restriction training (LL-BFRT) to heavy-load resistance training (HL-RT) in male collegiate athletes with chronic non-specific low back pain (CNLBP). Methods Twenty-six participants were randomly assigned to LL-BFRT (n = 13) or HL-RT (n = 13). All participants supervised exercises (deep-squat, lateral pull-down, bench-press and machine seated crunch) cycled 4 times per week for 4 weeks (16 sessions). LL-BFRT was done at 30% 1-repetition maximum (1RM) with 70% arterial occlusion pressure (AOP). HL-RT was done at 70% 1-RM. The outcomes were isokinetic core strength, isometric core endurance, pain intensity, and lumbar function disability level, measured at baseline and 4 weeks. Intra-group differences were evaluated using t-tests. Results Pain intensity and function disability level in LL-BFRT had extremely significant improvement at 4 weeks (p < 0.001, ES = 1.44–1.84). Participants in LL-BFRT and HL-RT showed significant differences in core extensors peak torque-body weight ratio (PT/BW) at isokinetic 120°/s and 30°/s, respectively (LL-BFRT: p = 0.045, ES = 0.62; HL-RT: p = 0.013, ES = 0.81). Isometric core extensor endurance was significantly increased in both groups (LL-BFRT: p = 0.016, ES = 0.78; HL-RT: p = 0.011, ES = 0.83). Conclusion Four weeks of LL-BFRT significantly reduced pain and functional disability while inducing similar strength gains as HL-RT in male collegiate athletes with CNLBP. Thereby, BFRT may qualify as a valuable training strategy for people with physical limitations.
... Blood flow restriction (BFR) training has gained increasing popularity in the fields of sports and rehabilitation (Hughes et al., 2017;Loenneke et al., 2010). This method involves applying an external constricting device to the proximal limbs to partially restrict venous return, thereby creating a hypoxic and stressful environment that promotes physical adaptations (Jessee et al., 2018). ...
... Although this study did not find a significant effect of AT-BFR on muscle mass, the analysis showed that AT-BFR significantly enhanced maximal strength. This phenomenon can be attributed to the mechanisms of blood flow restriction training, which involves recruitment of fast-twitch fibers, stimulation of protein synthesis, and activation of anabolic growth factors, all of which play a key role in strength improvement (Crane et al., 2013;Loenneke et al., 2010;Markov et al., 2022). However, the lack of significant muscle mass improvement may be due to the limitations of low-intensity aerobic training in promoting muscle hypertrophy. ...
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Aerobic training with blood flow restriction (AT-BFR) has shown promise in enhancing both aerobic capacity and exercise performance. The aim of this review was to systematically analyze the evidence regarding the effectiveness of this novel training method on aerobic capacity, muscle strength, and hypertrophy in young adults. Studies were identified through a search of databases including PubMed, Scopus, Web of Science, SPORTDiscus, CINAHL, Cochrane Library, and EMBASE. A total of 16 studies, involving 270 subjects, were included in the meta-analysis. The results revealed that AT-BFR induced greater improvements in VO2max (SMD = 0.27, 95%CI: [0.02, 0.52], p < 0.05), and muscle strength (SMD = 0.39, 95%CI: [0.09, 0.69], p < 0.05), compared to aerobic training with no blood flow restriction (AT-noBFR). However, no significant effect was observed on muscle mass (SMD = 0.23, 95%CI: [-0.09, 0.56], p = 0.162). Furthermore, no moderating effects on the outcomes were found for individual characteristics or training factors. In conclusion, AT-BFR is more effective than AT-noBFR in improving aerobic capacity and muscle strength, making it a promising alternative to high-intensity training. Systematic Review Registration https://www.crd.york.ac.uk/prospero/, identifier CRD42024559872.
... Twenty men with at least 1 year of RT experience (age: 24 All of them were accustomed to performing the SQ exercise with a proper technique. Participants were encouraged to maintain their daily routine and sleep patterns and to take the same dietary intake 24 hours before the intervention. ...
... The implementation of BFR exacerbates fatigue development, leading to earlier muscle failure and altered physiological responses compared with FF-RT. 11,12,21 This accelerated fatigue is attributed to reduced oxygen delivery to active muscles and subsequent metabolic accumulation (eg, hydrogen ion, blood deoxyhemoglobin concentration), [22][23][24] which could also contribute to the volitional termination of exercise via sensory input from III/IV afferents. 25 Moreover, moderate increases in perceived discomfort have been observed when BFR-RT is implemented, which may influence exercise tolerance. ...
Article
Purpose : To compare the acute effects on mechanical, metabolic, neuromuscular, and muscle contractile responses to different velocity-loss (VL) thresholds (20% and 40%) under distinct blood-flow conditions (free [FF] vs restricted [BFR]) in full squat (SQ). Methods : Twenty strength-trained men performed 4 SQ protocols with 60% 1-repetition maximum that differed in the VL within the set and in the blood-flow condition (FF20: FF with 20% VL; FF40: FF with 40% VL; BFR20: BFR with 20% VL; and BFR40: BFR with 40% VL). The level of BFR was 50% of the arterial occlusion pressure. Before and after the SQ protocols, the following tests were performed: (1) tensiomyography, (2) blood lactate, (3) countermovement jump, (4) maximal voluntary isometric SQ contraction, and (5) performance with the load that elicited a 1 m·s ⁻¹ at baseline measurements in SQ. Results : No “BFR × VL” interactions were observed. BFR protocols resulted in fewer repetitions and lower increases in lactate concentration than FF protocols. The 40% VL protocols completed more repetitions but resulted in lower mechanical performance and electromyography median frequency during the exercise than the 20% VL protocols. At postexercise, the 40% VL protocols also experienced greater blood lactate concentrations, higher alterations in tensiomyography-derived variables, and accentuated impairments in SQ and countermovement-jump performances. The 20% VL protocols showed an increased electromyography median frequency at postexercise maximal voluntary isometric contraction. Conclusions : Despite BFR-accelerated fatigue development during exercise, a given VL magnitude induced similar impairments in the distinct performance indicators assessed, regardless of the blood-flow condition.
... The significant improvement in the athletes' aerobic capacity with aerobic training combined with BFR is consistent with previous findings [14,16]. BFR training increases muscle tissue oxygen uptake [74], affecting metabolic adaptations [75][76][77] and enhancing oxygen utilization during aerobic exercises [29,62,78]. Furthermore, BFR training may improve vascular endothelial functions, increase nitric oxide release and promote vasodilation [79,80], enhance muscle perfusion [81,82] and improve microcirculation [83]. ...
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This systematic review and meta-analysis evaluated the effects of blood flow restriction (BFR) training on strength and aerobic capacity in athletes, examining how training variables and participant characteristics influenced outcomes. Four databases were searched for peer-reviewed English-language studies, and the risk of bias and quality of evidence were assessed using RoB 2 and GRADEpro GDT. We evaluated pre- and post-test differences by a three-level meta-analysis using the meta and metafor packages. Subgroup analyses and both linear and nonlinear meta-regression methods were used to explore moderating factors. Sixteen studies with 'some concerns' risk of bias and low evidence level were included. Combining BFR with low-intensity resistance training produced an effect size (ES) of 0.25 for strength, while combining BFR with aerobic training had an ES of 0.42. For aerobic capacity, the ES of combining BFR with aerobic training was 0.58. Subgroup and regression analyses showed no significant differences. While BFR with low-intensity resistance training enhances strength, it does not result in additional gains. Adding BFR with aerobic training enhances both strength and aerobic capacity. Overall, BFR appears to offer the most benefits for male athletes in improving strength and aerobic capacity.
... The main goal of BFR-RE is to trigger multiple hypertrophic pathways (5,55) performing a lower mechanical work than low-load training with free-flow (non-BFR-RE) (29). In this regard, the decrease in work capacity is because of the oxygen reduction availability and subsequent metabolic by-product accumulation (6,29,31). Furthermore, it has been shown that BFR-RE yields greater enhancements in both muscle strength and hypertrophy when compared with non-BFR-RE with low loads (1,2,50,51). This enhanced response is likely because of the hypoxic environment created during BFR-RE (38). ...
Article
Cornejo-Daza, PJ, Sánchez-Valdepeñas, J, Páez-Maldonado, J, Rodiles-Guerrero, L, Sánchez-Moreno, M, Gómez-Guerrero, G, León-Prados, JA, and Pareja-Blanco, F. Acute responses to different lifting velocities during squat training with and without blood flow restriction. J Strength Cond Res XX(X): 000-000, 2024-The aims of the research were to compare the acute mechanical, metabolic, neuromuscular, and muscle mechanical responses to different lifting velocities (maximal vs. half-maximal) under distinct blood flow conditions (free [FF] vs. restricted [BFR]) in full-squat (SQ). Twenty resistance-trained males performed 4 protocols that differed in the velocity at which loads were lifted (MaxV: maximal velocity vs. HalfV: half-maximal velocity) and in the blood flow condition (FF: free-flow vs. BFR: 50% of arterial occlusion pressure). The relative intensity (60% 1 repetition maximum), volume (3 sets of 8 repetitions), and resting time (2 minutes) were matched between protocols. Mean propulsive force (MPF), mean propulsive velocity (MPV), mean propulsive power (MPP), and electromyography (EMG) values were recorded for each repetition. Tensiomyography (TMG), blood lactate, countermovement jump (CMJ), maximal voluntary isometric contraction in 90° SQ, and performance with the load that elicited a 1-m·s-1 velocity at baseline measurements (V1-load) in SQ were assessed at pre-exercise and postexercise. The MaxV protocols showed significantly greater MPF, MPV, MPP, and EMG amplitude during the exercise than the HalfV protocols (velocity effect, p < 0.05). The FF protocols achieved higher MPF and MPP during exercise than BFR (BFR effect, p < 0.05). The BFR protocols induced greater blood lactate after exercise (BFR × time interaction, p = 0.02), along with higher postexercise impairments in mechanical performance (BFR × time interaction, p < 0.05). The MaxV protocols elicited superior performance and greater muscle activation during exercise. The BFR protocols resulted in lower force and power production during exercise and exhibited higher performance impairments and increased metabolic stress postexercise.
... This view is supported by previous studies reporting that (i) changes in cerebral oxygenation are sensitive indicators of changes in cerebral blood flow (Alosh et al. 2016;Hoshi et al. 2001;Perrey 2009); (ii) cerebral blood flow increases as a result of enhanced brain activity and metabolism (Ogoh and Ainslie 2009;Secher et al. 2008);and (iii) there is a linear relationship between brain activity and the amplitude of cerebral hemodynamic response (Gratton et al. 2001). Whether the increased cortical activity in boys during exercise with blood flow occlusion may lead to changes in motor unit recruitment (Liu et al. 2003;Sander et al. 2010), such as the activation of additional motor units and/or greater recruitment of higher-threshold motor units, as reported in men (Loenneke et al. 2010;Moritani et al. 1992), warrants further examination. ...
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Purpose To examine whether the children’s superiority, over adults, to resist fatigue during repeated maximal-efforts depends on their often-cited oxidative advantage, attributed to greater muscle blood flow and O2-delivery. We also investigated the mechanisms underlying child–adult differences in muscle-oxygenation (due to O2-supply or O2-utilization) and examined if there are age-differences in cerebral-oxygenation response (a brain-activation index). Methods Eleven men (23.3 ± 1.8yrs) and eleven boys (11.6 ± 1.1 yrs) performed 15 maximal-effort handgrips (3-s contraction/3-s rest) under two conditions: free-flow circulation (FF) and arterial-occlusion (OCC). Force, muscle-oxygenation (TSImuscle) and cerebral-oxygenation (oxyhemoglobin-O2Hbcerebral; total hemoglobin-tHbcerebral; deoxyhemoglobin-HHbcerebral) were assessed. Results In boys, force declined less (− 26.3 ± 2.6 vs. − 34.4 ± 2.4%) and at slower rate (− 1.56 ± 0.16 vs. − 2.24 ± 0.17%·rep⁻¹) vs. men in FF (p < 0.01–0.05; d = 0.60–1.24). However, in OCC there were no age-differences in the magnitude (− 38.3 ± 3.0 vs. − 37.8 ± 3.0%) and rate (− 2.44 ± 0.26 vs. − 2.54 ± 0.26%·rep⁻¹) of force decline. Boys compared to men, exhibited less TSImuscle decline in both protocols, and lower muscle VO2 (p < 0.05). Boys, also, presented a smaller O2Hbcerebral and tHbcerebral rise than men in FF; exercising with OCC increased the O2Hbcerebral and tHbcerebral response in boys. Using MVIC as a covariate in FF condition, abolished boys-men differences in force and TSImuscle decline and O2Hbcerebral rise. Conclusion During repeated maximal-efforts: (i) blood flow is a significant contributor to children’s superiority over adults to resist fatigue; (ii) age-difference in muscle hypoxia/deoxygenation is rather attributed to men’s greater metabolic demand than to lower muscle-perfusion; and (iii) cerebral oxygenation/blood volume increase more in men than boys under free circulation, implying greater brain activation.
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