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A Mechanistic Approach to Blood Flow Occlusion

  • 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
Published online:
November 2, 2009
Int J Sports Med 2010; 31:
1 – 4 © Georg Thieme
Verlag KG Stuttgart · New York
ISSN 0172-4622
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
Key words
HSP 72
growth hormone
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
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
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
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
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
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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Review 3
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.
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 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.
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
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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... È stato inoltre dimostrato che anche l'ossido nitrico sintasi-1 (nitric oxide synthase-1, NOS-1) e la miostatina sono influenzati dalla stimolazione indotta dall'occlusione del flusso sanguigno. 40 of the cuff. Therefore, the energy accumulated and produced by the cuff could explain the results. ...
... Nitric oxide synthase-1 and myostatin have also been shown to be affected by occlusion stimulation. 40 ...
BACKGROUND: This study aimed to analyze the effects of different arterial occlusion pressure (AOP) percentages of blood flow restriction (BFR) training combined with squat exercise (SQ) on acute exercise. METHODS: Seventeen male volunteers (24.94±5.64 years) were included in the study. Participants underwent adaptation sessions and a one-repetition maximum (1-RM) test. Participants were randomly assigned to three groups: resistance training (RT) only without blood flow restriction (BFR 0%) and two different AOP groups with BFR (80% and 150%) applied to the lower limb; the groups were termed BFR0, BFR80, and BFR150, respectively. SQ was applied as a back semi-squat in all exercise sets. The acute effects of the exercise on strength and endurance performance were evaluated by repetition number, mean and peak power, mean and peak velocity, and rate of perceived exertion (REP). RESULTS: BFR0-150 had the highest scores in terms of repetition number, mean power, mean velocity, and REP among all three groups (P≤0.05). The number of repetitions, mean power, and mean velocity were significantly higher in the BFR80 and BFR150 groups than in the BFR0 group (P<0.05). However, REP was significantly lower in BFR80 compared to the BFR150 and BFR0 groups (P<0.05). CONCLUSIONS: Performing back squat all-out exercise with BFR150 resulted in the best acute exercise effects. This suggests that BFR training can provide trainers and athletes with more benefits in performing sports programs in terms of the number of repetitions with the same loads and power outputs as traditional strength training. KEY WORDS: Muscle strength; Resistance training; Ischemia
... Neto et al. 33 also performed a set of 80% 1RM highintensity squats with 60% AOP, and the results showed that the MF values of the VM and VL decreased by 18.5% and 18.2%, respectively. Previous studies have shown that BFR training induces fatigue mainly by stimulating protein synthesis of the Akt/mTOR signaling pathway, and the decrease in MF values is sensitive to biochemical changes in type II muscle fibers 34 . Combined with the above results, it can be concluded that neuromuscular fatigue is affected by the intermittent mode and the external BFR intensity. ...
Full-text available
We aimed to investigate acute changes before and after low-intensity continuous and intermittent blood flow restriction (BFR) deep-squat training on thigh muscle activation characteristics and fatigue level under suitable individual arterial occlusion pressure (AOP). Twelve elite male handball players were recruited. Continuous (Program 1) and intermittent (Program 2) BFR deep-squat training was performed with 30% one-repetition maximum load. Program 1 did not include decompression during the intervals, while Program 2 contained decompression during each interval. Electromyography (EMG) was performed before and after two BFR training programs in each period. EMG signals of the quadriceps femoris, posterior femoral muscles, and gluteus maximus, including the root mean square (RMS) and normalized RMS and median frequency (MF) values of each muscle group under maximum voluntary contraction (MVC), before and after training were calculated. The RMS value under MVC (RMSMVC) of the rectus femoris (RF), vastus medialis (VM), vastus lateralis (VL), and gluteus maximus (GM) decreased after continuous and intermittent BFR training programs, and those of the biceps femoris (BF) and semitendinosus (SEM) increased; The RMS standard values of the VL, BF, and SEM were significantly increased after continuous and intermittent BFR training (P < 0.05), The RMS value of GM significantly decreased after cuff inflating (P < 0.05). The MF values of RF, VM, VL, and GM decreased significantly after continuous BFR training (P < 0.05). Continuous BFR deep-squat training applied at 50% AOP was more effective than the intermittent BFR training program. Continuous application of BFR induces greater levels of acute fatigue than intermittent BFR that may translate into greater muscular training adaptations over time.
... However, the recruitment of fast muscle fibres during KT is facilitated by a hypoxic environment caused by metabolite accumulation, which is unsuitable for the mobilisation of slow muscle fibres (Meyer, 2006). Decreased oxygen supply and metabolite accumulation in muscle fibres can stimulate type afferents and inhibit alpha-motor neurons, thereby promoting the recruitment of fast muscle fibres to maintain muscle strength (Loenneke et al., 2010). Similar to traditional high-intensity training, low-intensity KT has similar fast muscle motor units and discharge frequency and can activate fast muscle fibres that participate in muscle activities. ...
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Objective: This study aimed to investigate the effect of whole-body vibration training (WBVT) combined with KAATSU training (KT) on lower limb joint muscle strength and to provide a reference for improving muscle strength in older women. Methods: A total of 86 healthy older people was randomly divided into WBVT group (WG, n = 21), KT group (KG, n = 22), combined intervention group (CIG, n = 20) and control group (CG, n = 23). WG and CIG subjects underwent WBVT, and KG and CIG subjects underwent 150 mmHg and lower limb joint and local compression intervention for 16 weeks (three times per week, about 15 min/time). The peak torque (PT) and endurance ratio (ER) of joint flexion or extension were tested for all subjects. Results: 1) Results at 16 weeks were compared with the baseline data. The knee extension and ankle flexion PT (60°/s) in CIG increased by 14.3% and 15.3%, respectively ( p < 0.05). The knee extension PT (180°/s) increased by 16.9, 18.4% and 33.3% in WG, KG and CIG ( p < 0.05), respectively, and the ankle extension PT (180°/s) in CIG increased by 31.1% ( p < 0.05). The hip, knee extension and ankle flexion ER increased by 10.0, 10.9% and 5.7% in CIG ( p < 0.05), respectively. 2) Results were compared among groups at 16 weeks. The relative changes were significantly lower in WG, KG and CG compared to CIG in the knee extension and ankle flexion PT (60°/s) ( p < 0.05). The relative changes were significantly greater in WG, KG and CIG compared to CG in the knee extension PT (180°/s) ( p < 0.05). The relative changes were significantly lower in WG, KG and CG compared to CIG in the ankle extension PT (180°/s) ( p < 0.05). The relative changes were significantly lower in WG, KG and CG compared to CIG in the hip extension ER ( p < 0.05). The relative changes were significantly lower in CG compared to CIG in the knee extension ER ( p < 0.05). Conclusion: Sixteen-week WBVT and KT increased the knee extensor strength in older women. Compared with a single intervention, the combined intervention had better improvements in the knee extensor and ankle flexor and extensor strength and hip extension muscle endurance. Appears to be some additional benefit from combined intervention above those derived from single-interventions.
... Muscular adaptation due to BFR training has been attributed to the greater accumulation of metabolites, additional muscle fiber recruitment, and the resultant muscle protein synthesis [55]. Conversely, in research conducted on individuals diagnosed with breast cancer, sarcopenia was shown to be a risk factor for mortality in women with early-stage breast cancer [56]. ...
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Background: Cancer, being a highly widespread disease on a global scale, has prompted researchers to explore innovative treatment approaches. In this regard, blood flow restriction has emerged as a promising procedure utilized in diverse clinical populations with favorable results including improvements in muscle strength, cardiovascular function, and postoperative recovery. The aim of this systematic review was to assess the efficacy of blood flow restriction in cancer survivors. Methods: An investigation was carried out using various databases until February 2023: PubMed, Scientific Electronic Library Online, Physiotherapy Evidence Database, Scopus, Web of Science, Cochrane Plus, SPORTDiscus, Physiotherapy and Podiatry of the Complutense University of Madrid, ScienceDirect, ProQuest, Research Library, Cumulative Index of Nursing and Allied Literature Complete Journal Storage, and the gray literature. To assess the methodological quality of the studies, the PEDro scale was utilized, and the Cochrane Collaboration tool was employed to evaluate the risk of bias. Results: Five articles found that blood flow restriction was beneficial in improving several factors, including quality of life, physical function, strength, and lean mass, and in reducing postoperative complications and the length of hospital stay. Conclusion: Blood flow restriction can be a viable and effective treatment option. It is important to note that the caution with which one should interpret these results is due to the restricted quantity of articles and significant variation, and future research should concentrate on tailoring the application to individual patients, optimizing load progression, ensuring long-term follow-up, and enhancing the methodological rigor of studies, such as implementing sample blinding.
... The implementation of high intensity exercise programs is not feasible in some situations, for instance for older persons with joint restrictions such as osteoarthritis, herniated discs, and vertebral fractures. 10 Thus, much of the scientific community has been looking for alternatives that use low intensity exercises for such individuals to improve bone health. ...
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Introduction The preservation of bone mass in elderly women is associated with better levels of practice of systematic physical exercises. Aerobic training combined with blood flow restriction seems to be a new alternative that determines this process, but knowledge gaps are still observed when referring to exercise associated with blood flow restriction (BFR) and adaptations on bone variables. Objective To analyze the chronic effects of aerobic training with and without BFR on bone mineral density and bone biomarker osteocalcin concentrations in older women. Methods Thirty women were randomized into the following groups: walking on a treadmill at low intensity with BFR; moderate treadmill walking with no BFR; only BFR (no exercise) for 20 minutes, twice a week, for 24 weeks. Bone mineral density was measured before and 24 weeks after intervention. Blood serum osteocalcin concentrations were measured before, 12 and 24 weeks after intervention. Results There were no differences between groups in bone mineral density (femoral neck, p = 0.31; total femur, p = 0.17; lumbar spin, p = 0.06) and osteocalcine (W(2) = 0.27; p = 0.87) ouctomes after 24 weeks of intervention. Conclusion There was no difference between walking training, blood flow restriction only, or walking+blood flow restriction on bone mineral density and osteocalcin concentrations after 24-weeks of intervention in older women with osteopenia/osteoporosis.
... Jeremy P. Loenneke et al. suggest that the combination of BFR and 20%-30% 1RM low-intensity resistance training can significantly increase the volume and strength of muscles and achieve the effect of high-intensity resistance training, while higher intensity load does not bring more benefits (Loenneke, et al., 2012a). Training at an intensity as low as 20% 1RM and combined with blood flow restriction will lead to muscle hypertrophy in just 3 weeks, providing a unique beneficial training mode for promoting muscle hypertrophy (Loenneke, et al., 2010). The characteristic of blood flow restriction training is to use low-intensity exercise load for training, which can also achieve the effect of high-intensity exercise load for training and reduce the risk of sports injury during exercise. ...
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As an emerging training method, blood flow restriction training has been proved to promote the growth of muscle mass and strength. In recent years, it has been gradually applied in different populations. However, there are few studies on how blood flow restriction training affects muscle mass and strength in the elderly. The relevant literature is compiled and summarized in this study. Through the comparison of blood flow restriction training with traditional training methods and its application in the elderly, it shows that blood flow restriction training can effectively increase muscle mass and strength, prevent muscle atrophy, improve cardiopulmonary function, facilitate injury and postoperative rehabilitation, and intervene in related degenerative diseases as a training method suitable for the elderly,. The main mechanism of blood flow restriction training promoting muscle mass and strength growth is metabolic stress response, including muscle fiber recruitment, protein synthesis signal pathway activation, hormone secretion, etc., and is also related to cell swelling caused by pressure. At present, although the application of blood flow restriction training in the elderly population is increasing, there is a lack of personalized programs. In the future, more research on the dose effect and safety of blood flow restriction training is needed to develop more accurate personalized training programs.
... A diminuição do aporte sanguíneo produz um ambiente isquêmico dentro dos músculos, e acarreta elevado estresse metabólico (Pearson & Hussain, 2015) resultado do aumento do lactato e dos íons de hidrogênio e assim como, aumenta o fator de crescimento endotelial vascular, aumentando assim a biodisponibilidade de NO 2 intracelular; nesse tipo de treinamento. De forma a ocasionar o aumento da força por maior ativação de contração das fibras de contração rápida (tipo II) (Loenneke, Wilson, Wilson, Pujol, & Bemben, 2011;Woollard et al., 2011), a elevação da secreção de hormônios do crescimento, da síntese proteica e da hipertrofia muscular (Takarada et al., 2000;Loenneke, Wilson, & Wilson, 2010). Tais fatos viabilizam o uso da RFS para populações clínicas (Buford et al., 2015). ...
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The aim of the study was to systematically review the effect of resistance training with blood flow restriction on muscle strength and functional capacity of clinical populations. This research used SCOPUS, WEB OF SCIENCE and MEDLINE/PubMed databases from the first records until November 2021 and in English. The terms (“blood flow restriction” or “vascular occlusion” or “kaatsu training” and “low intensity”) and (“strength training” or “resistance training” or “strength”) and (“clinical populations” or “elderly” or “old” or “hypertension” or “diabetes” or “myositis” or “obesity” and “chronic diseases”) and (“functional capacity” or “functionality” or “muscle function”) were used. Clinical trials (randomised and non-randomised) were included when compared to high-intensity resistance training, low-intensity resistance training, low-intensity resistance training with blood flow restriction and a control group without physical exercise. The quality of the evidence was assessed using the Testex scale. During the research, 122 articles were pre-selected and analysed, and at the end of the selection, nine articles met all the inclusion criteria and established specifications. We conclude that resistance training associated with blood flow restriction has been an effective and tolerable alternative in improving muscle strength and functional capacity and, therefore, a potential tool for the clinical population.
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O treinamento com oclusão vascular se encontra numa constante crescente no que diz respeito a estudos acadêmicos acerca da técnica, devido à sua popularização nos últimos anos, tanto no âmbito visando hipertrofia quanto como tratamento de recuperação para indivíduos com lesão articular. Outro tema que acumula pesquisas na área da saúde é relativo à reabilitação de ruptura do LCA, trauma sofrido por praticantes esportivos. O presente estudo tem como objetivo mapear o que se tem produzido cientificamente sobre a utilização de treinamento com oclusão vascular na reabilitação de indivíduos com ruptura de LCA. Uma pesquisa sistemática foi realizada nos dias 25 e 26 de maio de 2023, para o escopo desta investigação foi utilizada a base de dados da PubMed, alguns termos foram utilizados para a composição da string utilizada na busca: Vascular occlusion training, rehabilitation" AND "anterior cruciate ligament. Sinônimos foram consultados na literatura para compor a string de busca. A pesquisa bibliográfica resultou em um total de 39 estudos. Na sequência, 20 estudos foram excluídos durante a revisão de títulos, 6 retirados após a leitura do resumo, restando 13 artigos completos para a avaliação da elegibilidade. Os resultados comprovam que o método é de fato eficaz, desde que aplicado aos exercícios corretos, em consonância à pressurização ideal para o membro do utente e carga. Comprovou-se que o treinamento com oclusão vascular a indivíduos submetidos à reconstrução de LCA apresenta resultados positivos aos utentes, respeitando 80% de restrição do fluxo sanguíneo executados exercícios de até 30% de 1 RM.
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Purpose Constant blood flow occlusion (BFO) superimposed on aerobic exercise can impair muscle function and exercise tolerance; however, no study has investigated the effect of intermittent BFO on the associated responses. Fourteen participants (n = 7 females) were recruited to compare neuromuscular, perceptual, and cardiorespiratory responses to shorter (5:15s, occlusion-to-release) and longer (10:30s) BFO applied during cycling to task failure. Methods In randomized order, participants cycled to task failure (task failure 1) at 70% of peak power output with (i) shorter BFO, (ii) longer BFO, and (iii) no BFO (Control). Upon task failure in the BFO conditions, BFO was removed, and participants continued cycling until a second task failure (task failure 2). Maximum voluntary isometric knee contractions (MVC) and femoral nerve stimuli were performed along with perceptual measures at baseline, task failure 1, and task failure 2. Cardiorespiratory measures were recorded continuously across the exercises. Results Task failure 1 was longer in Control than 5:15s and 10:30s (P < 0.001), with no differences between the BFO conditions. At task failure 1, 10:30s elicited a greater decline in twitch force compared to 5:15s and Control (P < 0.001). At task failure 2, twitch force remained lower in 10:30s than Control (P = 0.002). Low-frequency fatigue developed to a greater extent in 10:30s compared to Control and 5:15s (P < 0.047). Dyspnea and Fatigue were greater for Control than 5:15s and 10:30s at the end of task failure 1 (P < 0.002). Conclusion Exercise tolerance during BFO is primarily dictated by the decline in muscle contractility and accelerated development of effort and pain.
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American College of Sports Medicine Position Stand on Progression Models in Resistance Training for Healthy Adults. Med. Sci. Sports Exerc. Vol. 34, No. 2, 2002, pp. 364-380. In order to stimulate further adaptation toward a specific training goal(s), progression in the type of resistance training protocol used is necessary. The optimal characteristics of strength-specific programs include the use of both concentric and eccentric muscle actions and the performance of both single- and multiple-joint exercises. It is also recommended that the strength program sequence exercises to optimize the quality of the exercise intensity (large before small muscle group exercises, multiple-joint exercises before single-joint exercises, and higher intensity before lower intensity exercises). For initial resistances, it is recommended that loads corresponding to 8-12 repetition maximum (RM) be used in novice training. For intermediate to advanced training, it is recommended that individuals use a wider loading range, from 1-12 RM in a periodized fashion, with eventual emphasis on heavy loading (1-6 RM) using at least 3-min rest periods between sets performed at a moderate contraction velocity (1-2 s concentric. 1-2 s eccentric). When training at a specific RM load, it is recommended that 2-10% increase in load be applied when the individual can perform the current workload for one to two repetitions over the desired number. The recommendation for training frequency is 2-3 d.wk(-1) for novice and intermediate training and 4-5 d.wk(-1) for advanced training. Similar program designs are recommended for hypertrophy training with respect to exercise selection and frequency. For loading, it is recommended that loads corresponding to 1-12 RM be used in periodized fashion, with emphasis on the 6-12 RM zone using 1- to 2-min rest periods between sets at a moderate velocity. Higher volume, multiple-set programs are recommended for maximizing hypertrophy. Progression in power training entails two general loading strategies: 1) strength training, and 2) use of light loads (30-60% of 1 RM) performed at a fast contraction velocity with 2-3 min of rest between sets for multiple sets per exercise. It is also recommended that emphasis be placed on multiple-joint exercises, especially those involving the total body. For local muscular endurance training, it is recommended that light to moderate loads (40-60% of 1 RM) be performed for high repetitions (> 15) using short rest periods (< 90 s). In the interpretation of this position stand, as with prior ones, the recommendations should be viewed in context of the individual's target goals, physical capacity, and training status.
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Six men were studied to determine the interrelationships among blood supply, motor unit (MU) activity and lactate concentrations during intermittent isometric contractions of the hand grip muscles. The subjects performed repeated contractions at 20% of maximal voluntary contraction (MVC) for 2 s followed by 2-s rest for 4 min with either unhindered blood circulation or arterial occlusion given between the 1st and 2nd min. The simultaneously recorded intramuscular MU spikes and surface electromyogram (EMG) data indicated that mean MU spike amplitude, firing frequency and the parameters of surface EMG power spectra (mean power frequency and root mean square amplitude) remained constant during the experiment with unhindered circulation, providing no electrophysiological signs of muscle fatigue. Significant increases in mean MU spike amplitude and frequency were, however, evident during the contractions with arterial occlusion. Similar patterns of significant changes in the surface EMG spectra parameters and venous lactate concentration were also observed, while the integrated force-time curves remained constant. These data would suggest that the metabolic state of the active muscles may have played an important role in the regulation of MU recruitment and rate coding patterns during exercise.
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Heat shock protein 70 (Hsp70) is a highly conserved and ubiquitous protein that is reported to provide cytoprotection in various cell types and tissues. However, the importance of Hsp70 expression during skeletal muscle atrophy, when Hsp70 levels are significantly decreased, is not known. The current study aimed to determine whether plasmid-mediated overexpression of Hsp70, in the soleus muscle of rats, was sufficient to regulate specific atrophy signaling pathways and attenuate skeletal muscle disuse atrophy. We found that Hsp70 overexpression prevented disuse muscle fiber atrophy and inhibited the increased promoter activities of atrogin-1 and MuRF1. Importantly, the transcriptional activities of Foxo3a and NF-kappaB, which are implicated in the regulation of atrogin-1 and MuRF1, were abolished by Hsp70. These data suggest that Hsp70 may regulate key atrophy genes through inhibiting Foxo3a and NF-kappaB activities during disuse. Indeed, we show that specific inhibition of Foxo3a prevented the increases in both atrogin-1 and MuRF1 promoter activities during disuse. However, inhibition of NF-kappaB did not affect the activation of either promoter, suggesting its requirement for disuse atrophy is through its regulation of other atrophy genes. We conclude that overexpression of Hsp70 is sufficient to inhibit key atrophy signaling pathways and prevent skeletal muscle atrophy.
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To examine endogenous anabolic hormonal responses to two different types of heavy resistance exercise protocols (HREPs), eight male and eight female subjects performed two randomly assigned protocols (i.e. P-1 and P-2) on separate days. Each protocol consisted of eight identically ordered exercises carefully designed to control for load, rest period length, and total work (J) effects. P-1 utilized a 5 RM load, 3-min rest periods and had lower total work than P-2. P-2 utilized a 10 RM load, 1-min rest periods and had a higher total work than P-1. Whole blood lactate and serum glucose, human growth hormone (hGH), testosterone (T), and somatomedin-C [SM-C] (i.e. insulin-like growth factor 1, IGF-1) were determined pre-exercise, mid-exercise (i.e. after 4 of the 8 exercises), and at 0, 5, 15, 30, and 60 min post-exercise. Males demonstrated significant (p less than 0.05) increases above rest in serum T values, and all serum concentrations were greater than corresponding female values. Growth hormone increases in both males and females following the P-2 HREP were significantly greater at all time points than corresponding P-1 values. Females exhibited significantly higher pre-exercise hGH levels compared to males. The P-1 exercise protocol did not result in any hGH increases in females. SM-C demonstrated random significant increases above rest in both males and females in response to both HREPs.(ABSTRACT TRUNCATED AT 250 WORDS)
There are forms of growth hormone (GH) in the plasma and pituitary of the rat and in the plasma of humans that are undetected by presently available immunoassays (iGH) but can be measured by bioassay (bGH). Although the regulation of iGH release is well documented, the mechanism(s) of bGH release is unclear. On the basis of changes in bGH and iGH secretion in rats that had been exposed to microgravity conditions, we hypothesized that neural afferents play a role in regulating the release of these hormones. To examine whether bGH secretion can be modulated by afferent input from skeletal muscle, the proximal or distal ends of severed hindlimb fast muscle nerves were stimulated ( approximately 2 times threshold) in anesthetized rats. Plasma bGH increased approximately 250%, and pituitary bGH decreased approximately 60% after proximal nerve trunk stimulation. The bGH response was independent of muscle mass or whether the muscles were flexors or extensors. Distal nerve stimulation had little or no effect on plasma or pituitary bGH. Plasma iGH concentrations were unchanged after proximal nerve stimulation. Although there may be multiple regulatory mechanisms of bGH, the present results demonstrate that the activation of low-threshold afferents from fast skeletal muscles can play a regulatory role in the release of bGH, but not iGH, from the pituitary in anesthetized rats.
Eight men cycled for 5 min at 120 +/- 6 W (mean +/- SE) at which O2 uptake was 50% of its maximal normoxic value, breathing room air (21% O2; normoxia) on one occasion and 11% O2 in N2 (respiratory hypoxia/hypoxic--Resp. Hx.) on the other. Biopsies were taken from the quadriceps femoris muscle. Oxygen uptake during exercise was not significantly different between Resp. Hx (1.59 +/- 0.08 1 min-1) and normoxia (1.55 +/- 0.08 1 min-1). At rest, muscle lactate was the same under both conditions but was four times higher after Resp. Hx (33.2 +/- 5.2 mmol kg-1 dry wt) than normoxic cycling (8.6 +/- 1.0 mmol kg-1 dry wt; P less than 0.01). The muscle lactate/pyruvate (which is proportional to cytosolic NADH/NAD) was significantly higher after Resp. Hx.(76 +/- 19) than after normoxic cycling (26 +/- 2; P less than 0.05). At rest, analytically determined NADH averaged 0.14 +/- 0.02 mmol kg-1 dry wt under both conditions. However, exercise during Resp. Hx. resulted in a significantly higher NADH content (0.17 +/- 0.01) than exercise during normoxia (0.12 +/- 0.01; P less than 0.01). Indirect evidence indicates that the difference in muscle NADH reflects a difference in the mitochondrial redox state (Sahlin & Katz 1986). The increased muscle NADH during Resp. Hx. therefore indicates a relative lack of O2 at the cellular level (muscle hypoxia). It is suggested that the increased lactate production during Resp. Hx. is a consequence of the cellular adaptation to muscle hypoxia (i.e. increases in cytosolic ADP, AMP, Pi and NADH).
Twelve male subjects were tested to determine the effects of motor unit (MU) recruitment and firing frequency on the surface electromyogram (EMG) frequency power spectra during sustained maximal voluntary contraction (MVC) and 50% MVC of the biceps brachii muscle. Both the intramuscular MU spikes and surface EMG were recorded simultaneously and analyzed by means of a computer-aided intramuscular spike amplitude-frequency histogram and frequency power spectral analysis, respectively. Results indicated that both mean power frequency (MPF) and amplitude (rmsEMG) of the surface EMG fell significantly (P less than 0.001) together with a progressive reduction in MU spike amplitude and firing frequency during sustained MVC. During 50% MVC there was a significant decline in MPF (P less than 0.001), but this decline was accompanied by a significant increase in rmsEMG (P less than 0.001) and a progressive MU recruitment as evidenced by an increased number of MUs with relatively large spike amplitude. Our data suggest that the surface EMG amplitude could better represent the underlying MU activity during muscle fatigue and the frequency powers spectral shift may or may not reflect changes in MU recruitment and rate-coding patterns.
The regulation of the energy metabolism in contracting skeletal muscle is under close control, and several regulating factors have been reported. The aim of this study was to investigate the importance of the oxygen supply as a limiting factor for muscle performance during contractions and recovery from contractions. To perform well-controlled standardized experiments on contracting skeletal muscle, the perfused rat hind limb model was developed. The 31P NMR technique was adapted to the rat hind limb model. This enabled continuous nondestructive monitoring of the energy state at various levels of muscular activity. Significant correlations were found between oxygen delivery and oxygen consumption, lactate release, and glucose uptake, respectively. An increased degree of fatigue was observed at lower oxygen deliveries. In both soleus and gastrocnemius muscles, oxygen delivery correlated with the intramuscular concentrations of phosphocreatine (PCr), lactate, and glycogen. The 31P NMR experiments showed a correlation between oxygen delivery and the steady-state level of PCr/inorganic phosphate (Pi) during the contraction period. The rate of recovery in PCr/Pi after the contraction was also dependent on oxygen delivery. The results demonstrate a causal relationship between oxygen supply and energy state in contracting as well as recovering skeletal muscles.
Shear stress enhances expression of Ca(2+)-calmodulin-sensitive endothelial cell nitric oxide synthase (ecNOS) mRNA and protein in bovine aortic endothelial cells (BAEC). The present studies were performed to investigate mechanisms responsible for regulation of ecNOS mRNA expression by shear stress and to determine if this induction of ecNOS mRNA is accompanied by an enhanced nitric oxide (NO) production. Shear stresses of 15 dyn/cm2 for 3-24 h resulted in a two- to threefold increase of ecNOS mRNA content quantified by Northern analysis in BAEC. Shear stresses (1.2-15 dyn/cm2) for 3 h resulted in an induction of ecNOS mRNA in a dose-dependent manner. In human aortic endothelial cells, shear stresses of 15 dyn/cm2 for 3 h also resulted in ecNOS mRNA induction. In BAEC, this induction in ecNOS mRNA was prevented by coincubation with actinomycin D (10 micrograms/ml). The K+ channel antagonist tetraethylammonium chloride (3 mM) prevented increase in ecNOS mRNA in response to shear stress. The ecNOS promotor contains putative binding domains for AP-1 complexes, potentially responsive to activation of protein kinase C (PKC). However, selective PKC inhibitor calphostin C (100 nM) did not inhibit ecNOS induction by shear stress. Finally, production of nitrogen oxides under both basal conditions and in response to the calcium ionophore A-23187 (1 microM) by BAEC exposed to shear stress was increased approximately twofold compared with cells not exposed to shear stress. These data suggest that ecNOS mRNA expression is regulated by K+ channel opening, but not by activation of PKC, and that shear not only enhances ecNOS mRNA expression but increases capacity of endothelial cells to release NO.
The transforming growth factor-beta (TGF-beta) superfamily encompasses a large group of growth and differentiation factors playing important roles in regulating embryonic development and in maintaining tissue homeostasis in adult animals. Using degenerate polymerase chain reaction, we have identified a new murine TGF-beta family member, growth/differentiation factor-8 (GDF-8), which is expressed specifically in developing and adult skeletal muscle. During early stages of embryogenesis, GDF-8 expression is restricted to the myotome compartment of developing somites. At later stages and in adult animals, GDF-8 is expressed in many different muscles throughout the body. To determine the biological function of GDF-8, we disrupted the GDF-8 gene by gene targeting in mice. GDF-8 null animals are significantly larger than wild-type animals and show a large and widespread increase in skeletal muscle mass. Individual muscles of mutant animals weigh 2-3 times more than those of wild-type animals, and the increase in mass appears to result from a combination of muscle cell hyperplasia and hypertrophy. These results suggest that GDF-8 functions specifically as a negative regulator of skeletal muscle growth.