Potential safety issues with blood flow restriction training

Abstract

The focal point of previous literature was establishing the efficacy of blood flow restriction training with respect to muscular strength, muscular hypertrophy, and muscular endurance. After mounting evidence supporting the efficacy of low-intensity blood flow restriction training, research has shifted to the overall safety of this training modality. The aim of this review was to summarize the research on the overall safety of blood flow restriction training, focusing on the cardiovascular system (central and peripheral), muscle damage, oxidative stress, and nerve conduction velocity responses compared with those observed with regular exercise. Although still sparse, the blood flow restriction training research thus far is promising with respect to safety outcomes. Individuals respond similarly to blood flow restriction training and to regular exercise; however, longer term studies are required to better understand the chronic effects of low-intensity blood flow restriction training and possible safety issues.

Full text

Review
Potential safety issues with blood flow restriction training
J. P. Loenneke
1
, J. M. Wilson
2
, G. J. Wilson
3
, T. J. Pujol
4
, M. G. Bemben
1
1
Department of Health and Exercise Science, The University of Oklahoma, Norman, Oklahoma, USA,
2
Department of Exercise
Science and Sport Studies, University of Tampa, Tampa, Florida, USA,
3
Department of Nutritional Sciences, University of Illinois,
Champaign-Urbana, Illinois, USA,
4
Department of Health, Human Performance, and Recreation, Southeast Missouri State
University, Cape Girardeau, Missouri, USA
Corresponding author: Jeremy Paul Loenneke, 1401 Asp Avenue, Room 104, Norman, Oklahoma 73019-0615, USA. Tel: 11
405 325-5211, Fax: 11 405 325-0594, E-mail: jploenneke@ou.edu
Accepted for publication 13 December 2010
The focal point of previous literature was establishing the
efficacy of blood flow restriction training with respect to
muscular strength, muscular hypertrophy, and muscular
endurance. After mounting evidence supporting the efficacy
of low-intensity blood flow restriction training, research has
shifted to the overall safety of this training modality. The
aim of this review was to summarize the research on the
overall safety of blood flow restriction training, focusing on
the cardiovascular system (central and peripheral), muscle
damage, oxidative stress, and nerve conduction velocity
responses compared with those observed with regular ex-
ercise. Although still sparse, the blood flow restriction
training research thus far is promising with respect to safety
outcomes. Individuals respond similarly to blood flow re-
striction training and to regular exercise; however, longer
term studies are required to better understand the chronic
effects of low-intensity blood flow restriction training and
possible safety issues.
The American College of Sports Medicine (ACSM)
recommends weight training at 70% or greater of
one’s one repetition maximum (1RM) in order to
achieve muscular hypertrophy under normal condi-
tions. Exercise intensities below 70% 1RM rarely
produce substantial muscle hypertrophy or strength
gains (ACSM, 2009). However, many individuals
such as the elderly and rehabilitating athletes are
unable to withstand the high mechanical stresses
placed upon the joints during heavy resistance train-
ing; therefore, professionals have sought lower
intensity training alternatives.
One such alternative is training with low intensities
in combination with blood flow restriction, also
known as KAATSU training. Blood flow restriction
training, as the name implies, involves decreasing
blood flow to a muscle by application of a wrapping
device, such as a blood pressure cuff or specially
designed restrictive straps. Evidence indicates that
this style of training can provide a unique, beneficial
mode of exercise, even in clinical settings, because it
produces positive training adaptations equivalent to
the physical activity of daily life (10–30% of maximal
work capacity) (Abe et al., 2006). Muscle hypertro-
phy has recently been shown to occur even during
exercise with intensities as low as 20% 1RM
with moderate vascular restriction ( 100 mmHg)
(Yasuda et al., 2005), which could be quite beneficial
to athletes (Takarada et al., 2000a) and patients in
post-operation rehabilitation, particularly those with
ACL injuries (Takarada et al., 2000b; Ohta et al.,
2003), the elderly (Fry et al., 2010; Karabulut et al.,
2010), and even astronauts (Iida et al., 2007; Loen-
neke & Pujol, 2010). Published studies hypothe-
size that blood flow restriction training induces
skeletal muscle hypertrophy through a variety of
mechanisms (for a review, please see (Loenneke
et al., 2010); however, a definitive mechanism has
yet to be elucidated.
The focal point of previous literature was estab-
lishing the efficacy of blood flow restriction training
with respect to muscular strength, muscular hyper-
trophy, and muscular endurance (for reviews, please
see (Wernbom et al., 2008; Loenneke & Pujol, 2009,
2010; Manini & Clark, 2009; Loenneke et al., 2010).
After demonstrating the efficacy of blood flow
restriction training, the literature now has shifted
more toward the overall safety issues of training with
moderately restricted blood flow (Clark et al., 2010;
Madarame et al., 2010; Renzi et al., 2010). Therefore,
the purpose of this manuscript is to provide an
updated review on several measures of safety with
respect to blood flow restriction training, and
compare those responses to regular exercise.
Scand J Med Sci Sports 2011 &2011 John Wiley & Sons A/S
doi: 10.1111/j.1600-0838.2010.01290.x
1

Cardiovascular
Peripheral blood flow changes
Because blood flow dynamics are manipulated with
blood flow restriction training, there are obvious
potential safety concerns for practitioners with
respect to blood flow changes post-exercise (PO
bf
).
The congestion and distension of veins that can
occur from the pooling of blood with blood flow
restriction could potentially result in valve damage
within the veins. The cardiovascular responses to
regular exercise are partially dependent upon the
type of muscle contraction, with differing intensities
and types of contraction (isometric, dynamic, ec-
centric, etc.) producing different patterns of blood
flow. Alomari and Welsch (2007) reported increased
peak PO
bf
with dynamic handgrip exercise; how-
ever, others have reported decreased PO
bf
follwing
isometric contractions (McGowan et al., 2006,
2007).
Studies investigating PO
bf
following blood flow
restriction exercise are sparse. Renzi et al. (2010)
reported decreased flow-mediated vasodilation fol-
lowing 14 min of blood flow restriction walking. In
contrast to this acute study, Patterson and Ferguson
(2010) reported that chronic (4 weeks) plantar flexion
exercise with blood flow restriction resulted in an
enhanced PO
bf
compared with resistance exercise
alone, suggesting that the blood flow with restrictive
exercise is acutely impaired post-exercise but en-
hanced over repeated bouts of exercise.
The exact mechanism for the increase in PO
bf
with
chronic blood flow restriction exercise remains un-
known. Patterson and Ferguson (2010) postulated
that perhaps an increased venous compliance from
the pooling of blood associated with blood flow
restriction training could explain the increase in
PO
bf
(Convertino et al., 1988). Other potential ex-
planations include the restriction of oxygen and/or
accumulation of metabolites, specifically vasoactive
metabolites (e.g. adenosine) (Loenneke et al., 2010).
The accumulation of metabolites and the decreased
availability of oxygen results in the recruitment of
fast twitch (FT) fibers at lower than expected exercise
intensities (Loenneke et al., 2010). FT fibers have
demonstrated preferential capillarization compared
with slow twitch fibers in certain situations (Adair et
al., 1990). Local metabolic changes may also play an
important signaling role for vascular endothelial
growth factor (VEGF) upregulation (Roca et al.,
1998), possibly initiated through the VEGF/NO
cascade (Milkiewicz et al., 2005), because at least
one study reported VEGF increased in response to
resistance training with blood flow restriction (Ta-
kano et al., 2005). Additionally, capillary shear stress
facilitates angiogenesis, thus reperfusion of blood
flow post-exercise might also contribute to the en-
hancement of blood flow following blood flow re-
striction exercise (Suzuki et al., 2000; Hudlicka &
Brown, 2009). Further support comes from Evans et
al. (2010) who recently reported that 4 weeks of
blood flow restriction exercise (plantar flexion) en-
hanced microvascular filtration, an index of capillar-
ity, supporting the hypothesis that an increase in
capillarization can occur.
Like PO
bf
, research is equivocal regarding the
changes in peripheral pulse wave velocity (PWV)
from regular exercise. PWV is an indirect measure
of peripheral arterial stiffness, determined by mea-
suring waveforms from the common femoral and
posterior tibial artery of the ankle (Clark et al.,
2010). PWV increases as arterial stiffness increases.
Collier et al. (2008) found that 4 weeks of resis-
tance training (65% 1RM) increased peripheral
PWV; however, several studies have shown no
deliterious effect of resistance training on arterial
stiffness (PWV) (Cortez-Cooper et al., 2005; Casey
et al., 2007; Yoshizawa et al., 2009). The Collier et
al. (2008) study investigated pre- and stage 1
hypertensive patients, which might explain the
disparity in findings (elevated sympathetic out-
flow). Clark et al. (2010) found no changes in
PWV following 4 weeks of bilateral knee extensor
training with either low-intensity blood flow re-
striction training (30% 1RM) or high-intensity
exercise (80% 1RM).
Other indices of peripheral resistance, total per-
ipheral resistance (TPR) and ankle brachial index
(ABI), have also been investigated with blood flow
restriction training. Takano et al. (2005) found peak
TPR to be similar between blood flow restricition
exercise and a work matched control group; how-
ever, more recently, Renzi et al. (2010) found TPR to
be significantly higher (BFR 512% vs
CON 540%) during walking with blood flow
restriction. These different intensities might be attri-
butable to the different exercise modes or the overall
volume of exercise. ABI appears to remain un-
changed following both acute (Renzi et al., 2010)
and chronic blood flow restriction exercise (Clark
et al., 2010).
In summation, the peripheral blood flow response
to blood flow restriction training appears to respond
in a similar fashion as regular exercise, and future
research efforts might be better served to focus on the
time course of the PO
bf
impairment observed with
acute blood flow restriction exercise. In addition,
chronic blood flow restriction training studies should
be designed to measure both the chronic effects of
training, as well as the acute responses observed on
the last training day of a program, and the exercise
should include more than one muscle group being
trained in a session in order to better reflect a real-
world setting.
Loenneke et al.
2

Central responses of the cardiovascular system
In general, dynamic exercise results in a simultaneous
decrease in peripheral resistance with a concomitant
increase in heart rate and stroke volume (Mayo &
Kravitz, 1999). These responses result in only slight
increases in mean arterial pressure (MAP). During
high-intensity double leg resistance training, based on
ACSM guidelines (70–100% 1RM), there is complete
occlusion of the skeletal muscle vasculature from
mechanical compression and increases in intrathoracic
pressure. Extensive research from MacDougall’s lab
using a high-intensity (80–100% 1RM) double leg
press model demonstrated peak systolic and diastolic
pressures as high as 480/350mmHg and a doubling of
MAP (114–212 mmHg) (MacDougall et al., 1985,
1992; Haslam et al., 1988; Lentini et al., 1993).
Additionally, heart rates reached values of 170 beats
per minute or higher. End-diastolic and end-systolic
volumes declined by 30% and 50%, respectively, with
a concomitant 17–35 mL decline in stroke volume. In
comparison with low-intensity non-occlusion exercise
(20% 1RM), low-intensity blood flow restriction
training (20% 1RM) with the lower body (bilateral
leg extensions) has been found to result in slightly
greater values for heart rate (109 vs 96 bpm), and
systolic (182 vs 155 mmHg), diastolic (105 vs
99 mmHg), and mean arterial blood pressures (127
vs 113 mmHg) (Takano et al., 2005); however, these
values are all well below changes that occur during
high-intensity resistance training. While end-diastolic
and end-systolic volumes have yet to be measured
with blood flow restriction training, slight declines in
stroke volume (12%), but not cardiac output, have
been observed with blood flow restriction training
(Takano et al., 2005). Because these central cardio-
vascular responses are generally lower than traditional
resistance training, they suggest that low-intensity
blood flow restriction training is a safe alternative.
It should be noted that although Takano et al.
(2005) observed central cardiovascular values lower
than traditional resistance training studies, different
exercises were used. Central cardiovascular responses
to double leg press with blood flow restriction have
yet to be investigated. In addition, although tradi-
tional resistance training results in acute spikes in
blood pressure, research has observed a beneficial
post-exercise hypotensive response (MacDonald et
al., 1999; Fisher, 2001; Simao et al., 2005; de Salles et
al., 2010), even observed at intensities as low as 50%
1RM (Fisher, 2001). Furthermore, evidence exists to
indicate that chronic traditional resistance training
might also lower resting blood pressure (Cornelissen
& Fagard, 2005). Future blood flow restriction
research should investigate the post-exercise blood
pressure response into recovery as well as the effect of
chronic training on resting blood pressure.
Blood coagulation
Hemostasis is maintained through a balance between
coagulation and fibrinolytic activity and exercise has
been shown to affect activation of both processes
(Nakajima et al., 2007). Regular exercise preferen-
tially activates fibrinolysis, while strenuous exercise
may increase activity of the coagulation system,
resulting in venous thrombosis. Research demon-
strates that complete vascular occlusion can cause
the formation of a thrombus and can induce a
microvascular occlusion even after reperfusion.
This post-reperfusion occlusion can result in both
muscle damage and cell necrosis (Harman, 1948;
Strock & Majno, 1969). Furthermore, the literature
has suggested that metabolic and/or adrenergic fac-
tors may play some role in exercise-induced throm-
bin production. To illustrate, Herren et al. (1992)
reported a positive correlation between post-exercise
blood lactate and thrombin–antithrombin III com-
plex (TAT) concentrations and Wallen et al. (1999)
found that an adrenaline infusion, as well as fati-
guing exercise, also increased plasma TAT.
Nakajima et al. (2006) first investigated the ques-
tion of thrombosis in a survey of Asian facilities
implementing blood flow restriction training. Only
0.06% out of 300 000 training sessions resulted in an
incidence of venous thrombosis, which is lower rate
than that reported for the general Asian population
(0.2–0.26%) (Klatsky et al., 2000). Nakajima
confirmed their survey findings with a study measur-
ing various blood markers such as D-dimer and
fibrin degradation product (FDP), markers of intra-
vascular clot formation, which were not increased
following low-intensity blood flow restriction exer-
cise (30% 1RM). Prothrombin time (PT) and throm-
bin time, markers of coagulation activity, were also
unaffected with low-intensity blood flow restriction
exercise. However, blood flow restriction training did
result in increased tissue plasminogen activity (tPA),
a fibrinolytic protein that catalyzes the conversion of
plasminogen to plasmin, without affecting plasmino-
gen activator of inhibitor-1, the principle inhibitor of
tPA (Nakajima et al., 2007).
Clark et al. (2010) further investigated the coagu-
lation effects of blood flow restriction exercise and
found that neither PT nor D-dimer increased acutely
or chronically following 4 weeks of low-intensity
blood flow restriction training (30% 1RM) in 20–30
year olds. Fry et al. (2010) also found that D-dimer
was unaffected in elderly subjects (70 years of age)
performing an acute blood flow restriction exercise
bout (20% 1RM). However, one study (Zaar et al.,
2009) found that plasma TAT, a marker of thrombin
generation, increased after a 10 min bout of lower
body negative pressure at 30 mmHg, despite plasma
D-dimer not increasing (Zaar et al., 2009). To
Safety of blood flow-restricted exercise
3

address this concern, Madarame et al. (2010) inves-
tigated all previous blood markers of the coagulation
system as well as TAT, and reported that neither
markers of intravascular clot formation (D-dimer,
FDP) nor TAT were increased with low-intensity
blood flow restriction exercise (30% 1RM).
In summation, coagulation activity does not ap-
pear to increase following low-intensity blood flow
restriction exercise. In contrast, fibrinolytic potential
(tPA) appears to be enhanced with blood flow
restriction exercise as it is with traditional resistance
training. Protocols that have investigated coagula-
tion activity have implemented cuff sizes ranging
from 50 to 60 mm, restriction pressures of 150–
200 mmHg and exercise intensities ranging from
20% to 30% 1RM for up to four sets of lower
body exercise ( 10–15 min total time under restric-
tion) (Nakajima et al., 2007; Clark et al., 2010; Fry
et al., 2010; Madarame et al., 2010). Thus, these
findings are specific to studies using similar protocols
and are not necessarily applicable to all blood flow
restriction training models. Interestingly, vascular
compressions alone have long been associated with
an increase in fibrinolytic activity without elevation
of the coagulation cascade (Holemans, 1963; Robert-
son et al., 1972; Shaper et al., 1975; Stegnar &
Pentek, 1993). Thus, it is currently unknown if the
fibrinolytic response is from the exercise bout, the
moderate restriction stimulus, or the combination of
both. Future research should examine what effects
longer duration low-intensity blood flow restriction
exercise might have on the coagulation system.
Oxidative stress
Oxidative stress is a biological phenomenon marked
by an imbalance between reactive free radicals and
antioxidant defenses (Halliwell & Gutteridge, 1999).
The term oxidative stress indicates a combination of
increased free radical production and/or exhaustion
of antioxidant defenses (local water-soluble than fat-
soluble antioxidants). Severe acute or prolonged
chronic oxidative stress can lead to oxidatively mod-
ified lipids, proteins, and DNA (Hudson et al., 2008).
An acute exercise bout under normal conditions is
typically associated with a transient increase in
oxidative stress, with the response being proportional
to exercise intensity. The literature demonstrates that
high-intensity exercise ( 70% 1RM) involving a
large muscle mass consistently elicits a measurable
increase in blood oxidative stress markers (Lee et al.,
2002; Bloomer et al., 2005, 2006, 2007; Hudson et al.,
2008), but the responses to lower intensity resistance
exercise (o60% 1RM) have been mixed (McBride
et al., 1998; McAnulty et al., 2005). Not only is the
oxidative stress response affected by exercise intensity,
it has also been shown to increase with ischemic
reperfusion (IR) models (Tsutsumi et al., 2007). IR
in muscle results in an increased vascular permeability,
attributed to an increase of xanthine oxidase activity
during the hypoxic condition resulting in elevated
reactive oxygen species (ROS) (Korthuis et al., 1985).
Although IR models increase ROS levels, this has
not been observed with exercise in combination with
moderate vascular restriction. Takarada et al.
(2000a) provided the first study looking at oxidative
stress following low-intensity (20% 1RM) knee ex-
tensor exercise with moderate blood flow restriction
(214 mmHg). Using thiobarbituric acid reactive
substances (TBARS) as the measure, Takarada et al.
(2000a) found no increases in TBARS with either
low-intensity exercise or low-intensity exercise with
blood flow restriction (20% 1RM). One limitation of
this study was the measurement of TBARS, which is
a non-specific and insensitive measure of lipid per-
oxidation. To address this, Goldfarb et al. (2008)
followed up with a study measuring protein carbo-
nyls and blood glutathione status, both of which are
sensitive indicators of oxidative stress. They found
that neither was increased with low-intensity blood
flow restriction exercise (30% 1RM); however, eleva-
tions were seen with the moderate resistance exercise
(70% 1RM) and during blood flow restriction
without exercise.
Goldfarb et al. (2008) cited two possible explana-
tions for why oxidative stress remained unchanged
with respect to blood flow restriction and exercise.
The first possibility is that the muscle contractions
during the partial occlusion were able to overcome
the resistance to venous outflow and thus helped
remove the oxidative stress markers from the circula-
tion. The second possibility is that the pressures
during the contractions were sufficient to enhance
blood flow during the muscle contractions, which
enabled adequate blood flow delivery to overcome
the partial vascular restriction.
Other explanations could be that the partial occlu-
sion with exercise causes oxidative stress markers to
peak much later than the 15 min post-exercise time
point measured in the Goldfarb study (Goldfarb et
al., 2008). The protein carbonyl levels, while not
statistically significant, did increase from post-exer-
cise to 15 min post-exercise. Previous investigations
have found that protein carbonyls do not always
peak immediately following exercise, but instead
continued to increase for over an hour post-exercise
(Bloomer et al., 2005). One other possibility may be a
protective effect from heat shock proteins (HSP) as
they are known inhibitors of oxidative stress (Polla
et al., 1996) and researchers using a rat model have
shown that vascular blood flow restriction increases
HSPs (Kawada & Ishii, 2005). This HSP response
has been investigated only once with respect to blood
Loenneke et al.
4

flow restriction exercise in humans, and that study
found no increase in HSPs (Fry et al., 2010); how-
ever, this study involved an elderly population in
which the HSP response is known to be blunted
(Hamada et al., 2005; Vasilaki et al., 2006).
In summation, oxidative stress has not been shown
to increase in response to low-intensity blood flow
restriction training ( 30% 1RM). Despite this,
research on this topic is sparse, and much more
research is warranted before a definitive opinion
can be made on the effects of low-intensity blood
flow restriction training on damage from oxidative
stress. Research should focus on measuring blood
markers of oxidative stress out to at least 24 h post-
exercise and ideally up to 48 h. HSPs, known inhibi-
tors of free radicals, should also be measured in
younger populations to see what role, if any, they
play in the antioxidant defense system.
Muscle damage
Muscle damage occurs during and after unaccus-
tomed exercise, particularly if the exercise involves a
large amount of eccentric contractions (Wilson et al.,
2009). It is currently thought that the initial muscle
damage is proportional to the relative load and thus
mechanical perturbations in skeletal muscle, while
the inflammatory response that occurs later may
explain additional damage following exercise (Clark-
son & Hubal, 2002). Because of the inherent errors in
assessing whole muscle damage from small biopsy
samples, as well as the invasive nature of these
techniques, investigators have sought more indirect
indices. According to Warren et al. (1999), the three
most frequently utilized measures include subjec-
tively estimated soreness from a pain rating scale,
strength decrements, and changes in blood protein
levels (e.g. creatine kinase and lactate dehydrogen-
ase) (Warren et al., 1999). Our data and others have
found that muscle soreness peaks at approximately
24–72 h following exercise (White et al., 2008; Wilson
et al., 2009). In general, isokinetic knee extensions
result in approximately a marking of 4–5 on a scale
of 10 with soreness, while maximal eccentric contrac-
tions result in scores as high as 7–8 (Clarkson &
Hubal, 2002). However, low-intensity blood flow
restriction knee extensor exercise (35% MVC) only
resulted in peak soreness scores of 2.8 at 24 h, with no
increases in perceived soreness at any other time
points (Umbel et al., 2009). In two independent
studies, we reported increases in creatine kinase
from 140 U/L at rest to values as high as 1100 U/L
following leg extension exercise (White et al., 2008;
Wilson et al., 2009); however, others have found
post-exercise values 45000 U/L using primarily
eccentric downhill exercise (Clarkson & Hubal,
2002). In contrast, low-intensity blood flow restric-
tion training has not been shown to result in changes
in either creatine kinase or myoglobin content fol-
lowing acute bouts of resistance exercise at 20%
1RM (Takarada et al., 2000a) or walk training at
50 m/min (Abe et al., 2006). While more extensive
research needs to be conducted, to this point it
appears that low-intensity blood flow restriction
training causes only minimal muscle damage.
Nerve conduction velocity
Nakajima et al. (2006) found from their survey of 105
facilities that used blood flow restriction as a training
technique that numbness was sometimes reported in
response to a blood flow restrictive exercise bout.
Although only 1.6% out of 30 000 sessions reported
the transient side effect, it raised an important safety
question, with respect to the numbness and possible
nerve conduction blockage which is often seen fol-
lowing surgery (Lundborg, 1988) or when external
compressions are applied to a limb causing both
ischemia and a slowing of nerve conduction velocity
(NCV) (Denny-Brown & Brenner, 1944; Pedowitz
et al., 1991; Mittal et al., 2008).
Clark et al. (2010) investigated the overall integrity
of sensory motor nerve conduction by estimating
NCV from the latency responses in H-reflex record-
ings. NCV was unchanged after 4 weeks of low-
intensity blood flow restriction training (30% 1RM).
This was an expected outcome because the overall
length of the restrictive exercise bout only lasted
approximately 10–15 min. Surgery, which requires
much longer durations of occlusion, is associated
with a transient slowing in NCV, which is rapidly
reversed and rarely results in permanent nerve
damage (Lundborg, 1988).
In summation, low-intensity blood flow restriction
training (30% 1RM) does not seem to have a chronic
negative effect on NCV in healthy human subjects.
Future research should investigate the NCV effects of
an acute blood flow restriction training bout to see if
any short-term impairment occurs, and if so, the time
course of that impairment. In addition, focus should
be placed on long-term studies greater than 4 weeks,
to determine what effect longer term training has on
H-reflex amplitudes during blood flow restriction
exercise because increases have been noted following
chronic resistance training (Aagaard et al., 2002;
Lagerquist et al., 2006; Holtermann et al., 2007).
Pressure recommendations for future research
Following a careful review of the literature, numer-
ous pressures have been used for restricting blood
flow. These restrictive pressures generally range from
Safety of blood flow-restricted exercise
5

approximately 1.3 times greater than systolic blood
pressure ( 160 mmHg) to upwards of 200 mmHg.
In most published reports, the width of the belt used
to restrict blood flow is often times ignored. How-
ever, the width of the restrictive device is of impor-
tance because wider cuffs transmit pressure
differently than narrow cuffs (Crenshaw et al.,
1988), thus applying 200 mmHg across 50 mm with
a KAATSU Master cuff which will likely produce a
different stimulus than 200 mmHg applied over
135 mm with a different cuff. Crenshaw et al. (1988)
demonstrated that wider cuffs restrict blood flow at a
lower overall pressure than a narrow belt. Addition-
ally, Shaw and Murray (1982) observed that limb
circumference is also a determining factor in the level
of blood flow restriction from a given pressure,
especially with a narrow cuff. They demonstrated
using an 80 mm wide cuff, a consistent decrease in the
mean maximal tissue-fluid pressure as the circumfer-
ence of the limb increased. However, although a
wider cuff may produce a greater level of restriction
with lower pressures, Mittal et al. (2008) has shown
that a wider cuff also produces a greater reduction in
NCV when compared with a narrow cuff (140 vs
70 mm).
In summary, perhaps the pressures used to restrict
blood flow should to some degree be determined by
the width of the cuffs and limb circumference, and
not necessarily by pressures previously used in the
literature. Investigators should also consider the
possible NCV impairments that may occur from
using a wider cuff (Mittal et al., 2008).
Perspectives
This review focused on what is currently known
about the safety of blood flow restriction training
and how this compares to exercise under normal
blood flow conditions (Fig. 1). The research, while
positive, is limited and more research should be
completed to better determine under what conditions
this type of training can be safely used. In addition,
the width of the belt and limb circumference should
be accounted for when applying the restrictive sti-
mulus to each subject. In conclusion, the current
research on blood flow restriction training with
respect to safety outcomes confirms earlier reports
that blood flow restriction exercise, when used in a
controlled environment by trained and experienced
personnel, provides a safe training alternative for
most individuals regardless of age and training
status.
Key words: KAATSU, cardiovascular, muscle
damage, hypertrophy.
Fig. 1. Summary of the potential safety issues with blood flow restriction (BFR) compared with high-intensity resistance
training (HIT-RT). Responses for each were as follows: ", increases; #, decreases; $, no change.
Loenneke et al.
6

Acknowledgements
This review was not supported by funding from an outside
source. The only affiliation that one of the co-authors, M. G.
Bemben, has with Sato Sports Plaza is that he is the current
Chair for the Kaatsu Training Interest Group within the
American College of Sports Medicine.
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