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The Use of Occlusion

Training to Produce
Muscle Hypertrophy
Jeremy Paul Loenneke, BS and Thomas Joseph Pujol, EdD, CSCS
Department of Health, Human Performance, and Recreation, Southeast Missouri State University, Cape Girardeau,
Missouri

SUMMARY muscle hypertrophy or strength gains The purpose of this article will be to
(2). Occlusion training can provide cover the cause and effect of occlusion
LOW-INTENSITY OCCLUSION (50–
a unique beneficial mode of exercise training on a practical and physiological
100 MM HG) TRAINING PROVIDES
in the clinical setting because it produ- level and to further describe populations
A UNIQUE BENEFICIAL TRAINING in which occlusion training is safe and
ces positive training adaptations, at the
MODE FOR PROMOTING MUSCLE appropriate (Table 1).
equivalent to physical activity of daily
HYPERTROPHY. TRAINING AT IN-
life (10–30% of maximal work capacity) PHYSIOLOGY OF OCCLUSION
TENSITIES AS LOW AS 20% 1
(1). Muscle hypertrophy has recently TRAINING
REPETITION MAXIMUM WITH MOD-
been shown to occur during exercise as Under normal conditions, slow-twitch
ERATE VASCULAR OCCLUSION low as 20% of 1RM with a moderate
RESULTS IN MUSCLE HYPERTRO-
fibers are recruited first, and as the
vascular occlusion (33). Low-intensity intensity increases, fast-twitch fibers
PHY IN AS LITTLE AS 3 WEEKS. A occlusion training has also been shown (FT) are recruited as needed. Under
TYPICAL EXERCISE PRESCRIPTION to be quite beneficial to athletes (35), ischemic conditions, FT fibers are
CALLS FOR 3 TO 5 SETS TO patients in postoperative rehabilitation recruited even if the intensity is low
VOLITIONAL FATIGUE WITH SHORT specifically anterior cruciate ligament (24). Aerobic motor units, which are
REST PERIODS. THE METABOLIC (ACL) injuries, cardiac rehabilitation normally recruited at light loads, would
BUILDUP CAUSES POSITIVE patients, and the elderly (34,37). Some be expected to fatigue more rapidly
PHYSIOLOGIC REACTIONS, SPE- research indicates that occlusion train- during blood flow restriction. Exercise
CIFICALLY A RISE IN GROWTH ing might also be beneficial for astro- with occlusion requires the recruitment
HORMONE THAT IS HIGHER THAN nauts in space (12). of the larger fast motor units, which are
LEVELS FOUND WITH HIGHER IN- normally only recruited during stron-
Low-intensity occlusion training can
TENSITIES. OCCLUSION TRAINING ger efforts (22). Integrated electromy-
benefit many in and out of the clinical
IS APPLICABLE FOR THOSE WHO ography (iEMG) has shown that
setting. Occlusion training can be used
ARE UNABLE TO SUSTAIN HIGH occlusion causes the activation of
by athletes to give them a break from all
LOADS DUE TO JOINT PAIN, a sufficient number of FT fibers at
the stress associated with high-intensity
POSTOPERATIVE PATIENTS, CAR- these low intensities (35,38).
resistance training. It could be an
DIAC REHABILITATION, ATHLETES effective stimulus to use during an Madarame et al. (19) sought to de-
WHO ARE UNLOADING, AND AS- unloading phase for athletes because it termine whether occlusion training
TRONAUTS. results in a positive training adaptation, causes a crossover effect as is seen
although causing little to no muscle with regular (nonoccluded) resistance
INTRODUCTION damage (35). Many people are unable training. The subjects in both groups
to withstand the high mechanical stress performed an unrestricted single arm
he American College of Sports

T Medicine recommends lifting


a resistance of at least 65% of
one’s 1 repetition maximum (1RM) for
placed upon the joints during heavy
resistance training, namely, the elderly.
Low-intensity resistance training with
bicep curl at 50% 1RM for 3 sets of 10.
The rest between sets was 180 seconds
to diminish the hormonal response to
6–12 repetitions to achieve muscle occlusion may help decrease the risk of
KEY WORDS:
hypertrophy under normal conditions. sarcopenia by allowing the elderly to
train their musculoskeletal system while blood flow restriction; low intensity;
It is believed that anything below this
resistance exercise; sarcopenia
intensity rarely produces substantial keeping the overall intensity very low.

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Occlusion Training

Table 1
Effects of occlusion training

Marker Effect (4,Y,[) Reference


Mechanisms for muscle hypertrophy (human)
Lactate [ (10,28,34,35,38)
Growth hormone (GH) [ (1,9,19,27,28,34,35,39)
Ribosomal S6 kinase 1 (S6K1) [ (9)
Norepinephrine (NE) [ (35)
Insulin growth factor-1 (IGF-1) [ (34)
Noradrenaline (NA) [ (12,19)
Muscle-specific ring finger 1 (MuRF1) [ (7)
Myogenic differentiation 1 (MyoD) [ (7)
Cyclin-dependent kinase inhibitor 1A (p21) [ (7)
Eukaryotic translation elongation factor 2 (eEF2) [ (9)
Myostatin (GDF-8) Y (7)
Measures of strength and muscle (human)
One repetition maximum [ (1,19,23)
Isometric strength [ (1,23,32,36,39)
Isokinetic strength [ (5,33,36,38,39)
Isometric torque [ (19,23,32)
Isokinetic torque [ (34,38,39)
Muscular endurance [ (13,33,36)
Postactivation potentiation [ (23)
iEMG [ (23,35,38)
Cross-sectional area (CSA) [ (1,19,36,38,39)
Effects of chronic occlusion in rats
Heat shock protein 72 (HSP 72) [ (14)
Nitric oxide synthase-1 (NOS-1) [ (14)
Lactate [ (15,14)
Cross-sectional area (CSA) [ (15,14)
Myostatin (GDF-8) Y (15)
Fiber-type switch Slow!fast (15)
Markers for muscle damage
Creatine kinase 4 (35)
Lipid peroxide 4 (35)
Myoglobin 4 (1)

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exercise. After the arm curl, both groups area (CSA) (3,14,21,20,25,31,40). Kawa- training even though hypoxia-inducible
performed a knee extension and knee da and Ishii (15) found that 2 weeks of factor-1 alpha (HIF-1a) is elevated.
flexion exercise, with one group per- chronic occlusion in rats caused a fiber- A reduced REDD1 mRNA expression
forming the exercises with and the type shift from slow to fast. They may prove to be important because
other without blood flow restriction. attributed this to the additional recruit- a reduction in REDD1 would relieve
They found that resistance exercise ment of large motor units and their inhibition on mTOR, promoting a stim-
with occlusion for leg muscles caused associated type II fibers at the expense of ulation of mTOR signaling, mRNA
increases in the size and strength of arm rapid fatigue in slow oxidative fibers translation, and muscle cell growth
muscles that had undergone normal during blood flow restriction. (7). Possible explanations for the in-
resistance training, even though the crease in HIF-1a without the increase
HSP 72 levels have been shown to
intensity was much lower than that, in REDD1 might be that there is an-
be increased in response to occlusion
which would cause muscle hypertrophy other unknown factor that influences the
training (14). HSP 72 is induced by such
under normal conditions. The authors transcription of REDD1, so although
stressors as heat, ischemia, hypoxia, and
also found that occlusion exercise for HIF-1a may upregulate REDD1, an-
free radicals. HSP 72 acts as a chaperone
leg muscles did not cause any changes other factor that is increased to a
to prevent misfolding or aggregation of greater extent by exercise may result
in untrained arm muscle, which they
proteins. An increase in HSP 72 content in downregulation of HIF-1a, resulting
suggested could be attributed to any
has been shown to attenuate atrophy so in a net decrease in REDD1. There
systemic factors (growth hormone
that it may play a role in occlusion- might also be a factor that inhibits or
[GH] and noradrenaline) released after
induced muscle hypertrophy (25). In- stimulates HIF-1a effects on REDD1
the occlusive exercise. These factors
creased expression of NOS-1 has also expression, so even though HIF-1a
might be involved in this cross-transfer
been shown to stimulate muscle growth expression is higher, its activity is not.
effect, but local exercise stimulus, even
through increased satellite cell activation Also, occlusion training itself may
at low intensity, is absolutely necessary
(3,40). Myostatin is a negative regulator increase HIF-1a but then reperfusion
for muscle hypertrophy.
of muscle, and mutations of this gene after exercise may inhibit its action.
Physiologically, occlusion training re- result in overgrowth of musculature in
sults in several changes to the body in mice, cattle, and humans (21,20,31). STUDIES DEMONSTRATING THE
both human and animal models. Met- Myostatin gene expression is signifi- EFFICACY OF OCCLUSION
abolic by-product accumulation seems cantly decreased in response to occlu- TRAINING
to be the primary mechanism behind sion training (14). Although there have been numerous
the benefits seen with occlusion training. studies of occlusion training, the 3
Fujita et al. (9) have shown that low-
Whole blood lactate (10,34), plasma described below clearly identify the
intensity resistance training increases
lactate (9,28,34,38), and muscle cell benefits and the mechanisms involved.
ribosomal S6 kinase 1 (S6K1) phosphor- Kawada and Ishii sought to investigate
lactate (15,14) accumulation due to the
ylation and muscle protein synthesis. the effects of occlusion on muscular size
blood flow restriction results in in-
They suggest that enhanced mamma- at either the cellular or subcellular level
creased GH. This is significant because
lian target of rapamycin (mTOR) sig- on a rat model. Veins from the rat’s hind
GH has shown to be stimulated by an
naling may be another important leg were occluded followed by 14 days
acidic intramuscular environment (38).
cellular mechanism that may in part of normal cage time. At the conclusions
Evidence indicates that a low pH
explain the hypertrophy induced by of the experimental period, fiber CSA
stimulates sympathetic nerve activity
low-intensity occlusion training. S6K1 increased 34% in the occluded group
through a chemoreceptive reflex medi-
is involved in the regulation of messen- compared with the control. HSP 72 and
ated by intramuscular metaboreceptors
ger RNA (mRNA) translation initiation NOS-1 were both significantly elevated
and group III and IV afferent fibers (41).
Consequently, the same pathway has and seems to be a critical regulator of above control, whereas myostatin was
recently been shown to play an impor- exercise-induced muscle protein synthe- significantly decreased. They found no
tant role in the regulation of hypophy- sis and training-induced hypertrophy change in insulin growth factor-1 (IGF-
seal secretion of GH (11,41). One study (4,29). Signaling to S6K1 also inhibits 1), which they suggest could mean that
showed an increase in GH approxi- eukaryotic translation elongation factor IGF-1 may not always be essential for
mately 290 times greater than baseline 2 (eEF2) kinase, which reduces eEF2 muscle hypertrophy if HSP 72, NOS-1,
measurements (35). This increase in GH phosphorylation and thus promotes and myostatin change in favor of
levels is higher than what is typically translation elongation (42). muscular growth (14). Abe et al. (1)
seen with regular resistance training A follow-up study showed that REDD1 have also suggested that IGF-1 may not
(18,17). Heat shock protein 72 (HSP (regulated in development and DNA be increased with occlusion training due
72), nitric oxide synthase-1 (NOS-1), damage responses 1), which is normally to the low intensity of the exercise.
and myostatin seem to also contribute to expressed in states of hypoxia, is not Abe et al. (1) wanted to determine the
the increase in muscle cross-sectional increased in response to occlusion acute and chronic effects daily physical

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Occlusion Training

activity combined with vascular occlu- lactate. The concentration of GH was generation. The authors concluded
sion would have on muscle size, approximately 290 times as high as that an extremely light resistance
maximum dynamic and isometric that before exercise (35). This magni- exercise combined with occlusion
strength, and blood hormonal parame- tude of increase in GH concentration greatly stimulates the secretion of
ters. Acutely, they compared the effects was larger by a factor of approximately GH through regional accumulation of
of a single bout of walking with and 1.7 than that previously reported for metabolites without considerable tis-
without occlusion on 11 healthy un- high-intensity resistance exercise with sue damage (35).
trained men (n = 6 for occlusion and a short rest period, indicating that the
OCCLUSION EXERCISE
n = 5 for control). For the chronic study, exercise with occlusion can provoke PRESCRIPTION
they compared the effects of walking strong endocrine responses even at an Occlusion training was originally de-
with and without occlusion on 18 extremely low intensity (18,17). veloped in Japan where it is better
healthy untrained men (n = 9 for There were no changes in creatine known as KAATSU training (30). The
occlusion and n = 9 for control). The kinase or lipid peroxide levels between occlusion training system seems most
subjects walked on a treadmill 6 d/wk groups, which suggested that no seri- effective when used with the lower
for 3 weeks using 5 sets of 2-minute ous muscle damage occurred. They did limbs due to the large muscle groups.
bouts at 50 m/min, with a 1-minute rest find that the concentration of interleu- The biceps brachii are much smaller in
between bouts with occlusion and kin-6 (IL-6) gradually increased but CSA than the quadriceps, and the
without occlusion. Occlusion training was only slightly higher than in control metabolic stress induced by partial
increased thigh muscle CSA and vol- (35). They thought that the slight vascular occlusion would be less wide-
ume in just 3 weeks with occluded elevation could mean microdamage, spread and might potentially attenuate
walking. The estimated muscle–bone but IL-6 has been shown previously some of the lactate responses to
CSA continually increased in the oc- to increase with the contraction of a muscular work (28). Although not as
cluded group, and the resultant increase muscle (8,26). IL-6 concentration mea- effective, Takarada et al. have demon-
was constant throughout the training sured 90 minutes after exercise was still strated that low-intensity occlusion
period, increasing by approximately 2% less than one fourth of that reported for training can also provide benefits in
per week. Isometric strength of the knee eccentric exercise. iEMG activity was the upper body as well (38). Occlusion
extensors was also increased in the significantly higher in the occluded can occur from using a KAATSU
occluded group. Blood markers of group compared with control, and this apparatus or more practically through
muscle damage were unchanged as elevated activation level of the muscle elastic knee wraps. Elastic knee wraps
measured by creatine phosphokinase at a low level of force generation may can be wrapped around the proximal
and myoglobin. Although there was no be related to a hypoxic intramuscular part of the target muscle (Figures 1–4).
change in IGF-1 and cortisol, GH environment, in which motor units of The pressure can be relatively low
increased immediately after and 15 more glycolytic fibers are to be acti- as Sumide et al. (33) have showed
minutes post exercise compared with vated to keep the same level of force beneficial effects occurring at levels as
the control (1).
Occlusion has been shown to cause an
increase in GH (1,9,19,27,28,34,35,39).
However, Takarada et al. (35) showed
the largest rapid increase when they
investigated the hormonal and inflam-
matory responses to low-intensity
resistance exercise with vascular
occlusion in male athletes. Subjects
performed bilateral leg extension exer-
cise occluded. They found an increase
in whole blood lactate that was twice
as large as the control group, which
was likely caused by local hypoxia and
the suppression of lactate clearance
within the muscle subjected to the
occlusion. Norepinephrine (NE) was
also elevated in the occluded group,
and the time course of changes in
concentrations of both NE and GH
seemed to be closely similar to that of Figure 1. How to begin the occlusion for the knee extensors.

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APPLICABLE POPULATIONS
Patients who are injured, specifically
ACL injuries, have been shown to
benefit from an occlusive stimulus.
With knee surgery, suppressing the
disuse atrophy of thigh muscles has
been regarded as important because
the rehabilitation usually takes a pro-
longed period to regain the original
muscular strength. Takarada et al. (37)
showed that when an occlusion was
present even without an exercise
stimulus, it was effective in diminishing
the disuse atrophy of knee extensors
3 days after surgical operation. Because
occlusion training allows individuals to
train at much lower intensities with the
Figure 2. Completion of the practical occlusion. benefits of higher intensity training, it
may be highly useful for other post-
operative populations and for improv-
low as 50 mm Hg, although most will fatigue. This is done to ensure that
ing muscular function in the bedridden
use a pressure of 100 mm Hg because it there is a high metabolic buildup. The older population.
is a sufficient stimulus to restrict venous rest periods are 30 seconds to 1
blood flow, which causes pooling of minute in length and occur between Low-intensity occlusion training may
blood in capacitance vessels distal to every set, with the occlusion still also be useful in the cardiac rehabilita-
the cuff, ultimately restricting arterial being applied (5,6,27,35,36,39). At tion setting because occlusion has been
blood flow (23). the conclusion of the last set, blood shown to significantly stimulate the
flow is restored to the muscle. Cook exercise-induced GH, IGF, and vascular
A typical low-intensity prescription
et al. (6) compared different protocols endothelial growth factor responses with
would involve an intensity of 20–50%
the reduction of cardiac preload during
of 1RM with a 2-second cadence for of occlusion using percent maximal
exercise (34). GH and IGF-1 have been
both the concentric and eccentric voluntary contraction (%MVC) and
established as regulators of cardiac
actions. The 1RM is calculated from found that 20% MVC with contin-
growth, structure, and function, and
the maximum amount of weight you uous partial occlusion was the only
GH has been applied for treatment of
can lift once under normal blood flow protocol that elicited significantly
congestive heart failure (16). In a study
conditions. Three to five sets of each more fatigue than the higher
by Takano et al. (34), low-intensity
exercise are completed to volitional intensity protocol.
exercise with occlusion induced signifi-
cant exercise-induced GH responses as
compared with exercises at the same
intensity without occlusion. Further re-
search should be done with occlusion in
this setting, but it does appear promising.
Astronauts are also a unique population
that could benefit from occlusion train-
ing. During spaceflight, several health
concerns arise due to the changes in
cardiovascular function that occur due
to weightlessness. When gravitational
hydrostatic gradients are abolished,
there is a shift of intravascular fluid
from the capacitance vessels of the legs
and lower body centrally toward the
head. Elevations of capillary blood
pressure and increased capillary perfu-
sion pressure in tissues of the head have
Figure 3. The practical occlusion after wrapping. been shown to cause facial intracranial

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Occlusion Training

36,39). Occlusion can be applied with


a KAATSU apparatus or more practi-
cally through elastic knee wraps. The
pressure only needs to be high enough to
block venous return (~50–100 mm Hg)
(23,33). Occlusion training can be ap-
plied to athletes; patients in postopera-
tive rehabilitation, specifically ACL
injuries; cardiac rehabilitation patients;
the elderly; and even astronauts to
combat atrophy and when applied with
exercise to induce muscle hypertrophy
(12,34,35,37).

Jeremy Paul
Loenneke is a
graduate student
Figure 4. Practical occlusion for the knee extensors. in Nutrition and
Exercise Science at
Southeast Missouri
edema and headache. After spaceflights, risks associated with long-term use and State University in
regardless of the duration, almost every determine populations in which this the Department of
astronaut experiences orthostatic hypo- type of training may be contraindicated Health, Human
tension and reduced upright exercise (6). Although the research has yet to Performance, and
capacity, which is likely attributed to define populations in which occlusion Recreation.
the microgravity-induced hypovolemia, training is dangerous, we postulate that
decreased baroreflex responsiveness, those with endothelial dysfunction Thomas Joseph
decreased skeletal muscle tone, and should not use occlusion training Pujol is the chair
increased venous compliance. Iida because of the reduction in blood flow. of the Department
et al. (12) showed that when occlusion Research should also further study the of Health, Human
was applied on both thighs in supine microdamage to blood vessels and Performance, and
subjects, it induced the hemodynamic, subtle changes in blood flow, both of Recreation and
hormonal, and autonomic alterations which may stimulate thrombosis (38). professor of Exer-
that were very similar to standing. They Also, one should seek to evaluate the cise Science at
conclude that occlusion training may be gene expression at later stages of Southeast Missouri
a promising and safe method to counter postexercise recovery after occlusion State University.
symptoms of orthostatic intolerance and in response to occlusion training
and muscle atrophy in astronauts. (7). Finally, studies should begin to
focus on the local regulators of mus-
CONCLUSIONS REFERENCES
cular growth, such as growth factors
In conclusion, low-intensity occlusion and reactive oxygen species, to eluci- 1. Abe T, Kearns C, and Sato Y. Muscle size
training offers a unique beneficial date the mechanism for the present and strength are increased following walk
training mode for promoting muscle cooperative effects of exercise and
training with restricted venous blood
hypertrophy. Training at intensities of flow from the leg muscle, Kaatsu-walk
occlusive stimuli (39). training. J Appl Physiol 100: 1460–1466,
20% 1RM and receiving the equivalent
2006.
benefit of training at 65% 1RM have PRACTICAL APPLICATION
positive implications for a variety of 2. American College of Sports Medicine.
Low-intensity occlusion training pro- Position stand: progression models in
populations, particularly the elderly vides a unique beneficial training mode resistance training for healthy adults. Med
who physically cannot handle high for several different populations. Re- Sci Sports Exerc 34: 364–380, 2002.
mechanical loads (33). This is also search has shown us that moderate
unique because studies are showing 3. Anderson J. A role for nitric oxide in muscle
vascular occlusion causes numerous repair: nitric oxide-mediated activation of
hypertrophy in as little as 3 weeks with positive physiologic adaptations at loads muscle satellite cells. Mol Biol Cell 11:
GH increases of 290 times over as low as 10–30% of maximal work 1859–1874, 2000.
baseline (35). capacity (1). Typically, 3 to 5 sets to 4. Baar K and Esser K. Phosphorylation of
Future research on occlusion training volitional fatigue with 30-second to 1- p70(S6k) correlates with increased
should focus on studying the health minute rest between sets (5,6,27,35, skeletal muscle mass following resistance

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exercise. Am J Physiol Cell Physiol 276: 15. Kawada S and Ishii N. Changes in skeletal 27. Pierce J, Clark B, Ploutz-Snyder L, and
C120–C127, 1999. muscle size, fiber-type composition and Kanaley J. Growth hormone and muscle
capillary supply after chronic venous function responses to skeletal muscle
5. Burgomaster K, Moore D, Schofield L,
occlusion in rats. Acta Physiol 192: ischemia. J Appl Physiol 101: 1588–1595,
Phillips S, Sale D, and Gibala M.
541–549, 2008. 2006.
Resistance training with vascular
occlusion: metabolic adaptations in human 16. Khan A, Sane D, Wannenburg T, and 28. Reeves G, Kraemer R, Hollander D, Clavier J,
muscle. Med Sci Sports Exerc 35: 1203– Sonntag W. Growth hormone, insulin-like Thomas C, Francois M, and Castracane V.
1208, 2003. growth factor-1 and the aging Comparison of hormone responses
cardiovascular system. Cardiovasc Res following light resistance exercise with
6. Cook S, Clark B, and Ploutz-Snyder L.
54: 25–35, 2002. partial vascular occlusion and moderately
Effects of exercise load and blood-flow
17. Kraemer W, Gordon S, Fleck S, difficult resistance exercise without
restriction on skeletal muscle function.
Marchitelli J, Mello R, Dziados J, Friedl K, occlusion. J Appl Physiol 101: 1616–
Med Sci Sports Exerc 39: 1708–1713,
Harman E, Maresh C, and Fry A. 1622, 2006.
2007.
Endogenous anabolic hormonal and 29. Reynolds T, Bodine S, and Lawrence J Jr.
7. Drummond M, Fujita S, Abe T, Dreyer H, growth factor responses to heavy Control of Ser2448 phosphorylation in the
Volpi E, and Rasmussen B. Human muscle resistance exercise in males and females. mammalian target of rapamycin by insulin
gene expression following resistance Int J Sports Med 12: 228–235, 1991. and skeletal muscle load. J Biol Chem 277:
exercise and blood flow restriction.
18. Kraemer W, Marchitelli L, Gordon S, 17657–17662, 2002.
Med Sci Sports Exerc 40: 691–698,
Harman E, Dziados J, Mello R, Frykman P, 30. Sato Y. The history and future of KAATSU
2008.
McCurry D, and Fleck S. Hormonal and training. Int J Kaatsu Train Res 1: 1–5,
8. Febbraio M and Pedersen B. Muscle- growth factor responses to heavy 2005.
derived interleukin-6: mechanisms for resistance exercise protocols. J Appl
activation and possible biological roles. 31. Schuelke M, Wagner K, Stolz L, Hubner C,
Physiol 69: 1442–1450, 1990.
Riebel T, Komen W, Braun T, Tobin J,
FASEB J 16: 1335–1347, 2002.
19. Madarame H, Neya M, Ochi E, Nakazato K, and Lee S. Myostatin mutation
9. Fujita S, Abe T, Drummond M, Cadenas J, Sato Y, and Ishii N. Cross-transfer effects associated with gross muscle hypertrophy
Dreyer H, Sato Y, Volpi E, and of resistance training with blood flow in a child. N Engl J Med 350: 2682–2688,
Rasmussen B. Blood flow restriction during restriction. Med Sci Sports Exerc 40: 258– 2004.
low-intensity resistance exercise increases 263, 2008.
32. Shinohara M, Kouzaki M, Yoshihisa T,
S6K1 phosphorylation and muscle protein
20. McPherron A, Lawler A, and Lee S. and Fukunaga T. Efficacy of tourniquet
synthesis. J Appl Physiol 103: 903–910, Regulation of skeletal muscle mass in mice ischemia for strength training with low
2007. by a new TGF-B superfamily member. resistance. Eur J Appl Physiol 77:
10. Gentil P, Oliveira E, and Bottaro M. Time Nature 387: 83–90, 1997. 189–191, 1998.
under tension and blood lactate response 21. McPherron A and Lee S. Double muscling 33. Sumide T, Sakuraba K, Sawaki K,
during four different resistance training in cattle due to mutations in the myostatin Ohmura H, and Tamura Y. Effect of
methods. J Physiol Anthropol 25: 339– gene. Proc Natl Acad Sci U S A 94: resistance exercise training combined
344, 2006. 12457–12461, 1997. with relatively low vascular occlusion.
11. Gosselink K, Grindeland R, Roy RR, 22. Meyer R. Does blood flow restriction J Sci Med Sport 12: 107–112,
Zhong H, Bigbee A, Grossman E, and enhance hypertrophic signaling in skeletal 2009.
Edgerton V. Skeletal muscle afferent muscle? J Appl Physiol 100: 1443–1444, 34. Takano H, Morita T, Iida H, Asada K, Kato
regulation of bioassayable growth 2006. M, Uno K, Hirose K, Matsumoto A,
hormone in rat pituitary. J Appl Physiol 84: Takenaka K, Hirata Y, Eto F, Nagai R,
23. Moore D, Burgomaster K, Schofield L,
1425–1430, 1998. Sato Y, and Nakaajima T. Hemodynamic
Gibala M, Sale D, and Phillips S.
12. Iida H, Kurano M, Takano H, Kubota N, Neuromuscular adaptations in human and hormonal responses to a short-term
Morita T, Meguro K, Sato Y, Abe T, muscle following low intensity resistance low-intensity resistance exercise with
Yamazaki Y, Uno K, Takenaka K, Hirose K, training with vascular occlusion. Eur J Appl the reduction of muscle blood flow.
and Nakajima T. Hemodynamic and Physiol 92: 399–406, 2004. Eur J Appl Physiol 95: 65–73,
neurohumoral responses to the restriction 2005.
24. Moritani T, Michael-Sherman W,
of femoral blood blow by KAATSU in Shibata M, Matsumoto T, and Shinohara M. 35. Takarada Y, Nakamura Y, Aruga S, Onda T,
healthy subjects. Eur J Appl Physiol 100: Oxygen availability and motor unit activity in Miyazaki S, and Ishii N. Rapid increase in
275–285, 2007. humans. Eur J Appl Physiol 64: 552–556, plasma growth hormone after low-intensity
13. Kaijser L, Sundberg C, Eiken O, Nygren A, 1992. resistance exercise with vascular
Esbjornsson M, Sylven C, and Jannson E. occlusion. J Appl Physiol 88: 61–65,
25. Naito H, Powers S, Demirel H, Sugiura T,
Muscle oxidative capacity and work 2000.
Dodd S, and Aoki J. Heat stress attentuates
performance after training under local leg skeletal muscle atrophy in hindlimb- 36. Takarada Y, Sato Y, and Ishii N. Effects of
ischemia. J Appl Physiol 69: 785–787, unweighted rats. J Appl Physiol 88: 359– resistance exercise combined with
1990. 363, 2000. vascular occlusion on muscle function in
14. Kawada S and Ishii N. Skeletal muscle 26. Pedersen B and Fischer C. Beneficial athletes. Eur J Appl Physiol 86: 308–314,
hypertrophy after chronic restriction of health effects of exercise-the role of IL-6 as 2002.
venous blood flow in rats. Med Sci Sports a myokine. Trends Pharmacol Sci 28: 37. Takarada Y, Takazawa H, and Ishii N.
Exerc 37: 1144–1150, 2005. 152–156, 2007. Application of vascular occlusion diminish

Strength and Conditioning Journal | www.nsca-lift.org 7


Occlusion Training

disuse atrophy of knee extensor muscles. 39. Takarada Y, Tsuruta T, and Ishii N. pH and nitric oxide. Mol Biol Cell 13:
Med Sci Sports Exerc 32: 2035–2039, Cooperative effects of exercise and 2909–2918, 2002.
2000. occlusive stimuli on muscular function in
41. Victor R and Seals D. Reflex stimulation of
low-intensity resistance exercise with
38. Takarada Y, Takazawa H, Sato Y, sympathetic outflow during rhythmic
moderate vascular occlusion. Jpn J Physiol
Takebayashi S, Tanaka Y, and Ishii N. 54: 585–592, 2004. exercise in humans. Am J Physiol 257:
Effects of resistance exercise combined H2017–H2024, 1989.
40. Tatsumi R, Hattori A, Ikeuchi Y, Anderson J,
with moderate vascular occlusion on and Allen R. Release of hepatocyte 42. Wang X and Proud C. The mTOR pathway
muscle function in humans. J Appl Physiol growth factor from mechanically stretched in the control of protein synthesis.
88: 2097–2106, 2000. skeletal muscle satellite cells and role of Physiology 21: 362–369, 2006.

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