Blood flow

restriction
training
Manual
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 The Lifters Clinic
BFR training manual

Blood flow
restriction
training
Manual
By: Dr. Mario G. Novo, DPT, PT

Copyright 2016 liftersclinic.com

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BFR training manual

Legal Disclaimer:

Information provided in this guide is in no way intended to substitute

medical guidance or counselling. This information should be
consulted with the guidance and care from your physician. As with
any training or nutritional program please consult with your physician
before starting. If you decide to not obtain physician consent
and/or decide to not work with your physician throughout the
duration of applying the recommendations within the program, you
are agreeing to accept full responsibility for your actions.

Continuing with execution of the program concepts included in this

training manual, despite precautions on the part of Dr. Mario Novo,
confirms your recognition of risks associated with injury or illness
which can occur because of your use of the aforementioned
information which you expressly assume such risks and waive,
relinquish and release any claim which you may have against Dr.
Mario Novo, as a result of any future physical injury or illness incurred
in connection with, or as a result of, the use or misuse of the
program.

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Introduction
This EBook is designed to take you the trainer
to the next level in evidence based training
methods within the application of Blood
Flow Restriction (BFR). Following this EBook
you will further understand the current
scientific evidence behind blood flow
occlusion training, the various methods of
application, the safety/efficacy and how to
realistically apply it in the training
environment for increased Image: Delfi PTS Owens Recovery Science Unit

hypertrophy/strength gains.

Author
Dr. Mario Novo, DPT, PT is a results driven sports orthopedic physical therapist
who specializes in strength and conditioning. Known well by his clients/patients
as a mentor and educator, Marios passion is to unify the highest levels of rehab
science with successful mind and body strength coaching. With Marios
research having focused on new advancements in muscle hypertrophy
periodization and joint health, his goals are to share his knowledge and improve
on the human condition through personalized cutting edge program design.
Mario currently resides in middle TN where he plans on integrating his skills and
knowledge in resistance exercise and rehab to empower and inspire those
individuals ready to make a change in their lives through health and fitness.

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BFR training manual

Main chapters
Guide to Bfr Application
The Science of Blood Flow
Chapter 1 Restriction

Image: Delfi PTS Owens Recovery Science Unit

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BFR training manual

Chapter 1
The Science of Bfr

Image: Delfi PTS Owens Recovery Science Unit

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BFR training manual
What is Blood flow restriction
(Bfr) training?
Blood Flow Restriction (BFR) training is a
form of safe low intensity resistance
exercise (LIRE) that when applied has
demonstrated enhanced muscle growth,
muscle strength, oxygen delivery and
utilization (VO2Max), collagen dependent
tissue repair, and increased bone healing
following a fracture.

Currently two methods of BFR training exist,

one of which is known as practical blood
flow restriction (PBFR), with the second Image: Delfi PTS Owens Recovery Science Unit

being pneumatic controlled BFR.

Both methods employ wrapping and

systematically compressing a working limb, in order to partially occlude blood
flow to the working muscle and trap or restrict the clearance of muscle
byproducts from escaping working muscle during rest periods. The partial
occlusion of blood flow to the working muscle rapidly leads to muscle fatigue of
low threshold muscle fibers, which when unable to continue work recruit higher
threshold muscle fibers. The recruitment of these high threshold motor units
product a byproduct know as lactate. Lactate is a form of muscle byproduct
that has been demonstrated to up-regulate the specific muscle growth
pathways that lead to adaptation both in size and strength. These pathways
traditionally have only been seen to activate and achieve muscle adaptation
with repeated bouts of High Intensity training (HIT).

HIT style training via the American Sports College of Medicine (ACSM) has been
defined as intensity levels of 65% up to 85% of a single repetition maximum
(1RM). BFR training can achieve similar if not better results for inducing muscle

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growth when compared to what has been traditionally observed with higher
intensity training (HIT). Historically muscle adaptations such as Muscle
Hypertrophy (muscle cell growth), Muscle Strength (increased motor unit
recruitment of higher threshold motor units), and VO2Max (Functional measure
of oxygen deliver and oxygen uptake), have been seen with high intensity bouts
of exercises repeated over a duration of time. What BFR training has shown, is
that similar if not enhanced effects of muscle hypertrophy, muscle strength, and
VO2Max, can be achieved with as little 20-35% of 1 RM and 40% VO2Max
settings respectively.

BFR training is well established in the research literature to be a safe for the
general population with similar responses seen in blood pressure (BP), blood
coagulation, delayed onset of muscle soreness (DOMS) and oxidative stress that
has been observed during regular resistance training.

Certain populations should consult with a physician before application as

contraindications include:

History of deep-vein thrombosis

pregnancy
varicose veins
high blood pressure
Cardiac disease

When appropriate, BFR is an effective exercise modality that has

demonstrated never before seen combined increases to performance
adaptations and may yield more undiscovered positive results.

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How does BFR work?
Blood flow restriction training research has been around for the last decade and
has looked at everything from using BFR in individuals that are immobilized to
reduce atrophy (Kubota et al. 2008) all to way to NASA investigating how to use
BFR in order to protect skeletal muscle integrity while in the confines of zero G
(Hackney et al. 2012).

BFR has some known mechanism and they are as follows.

Lactic acid metabolite mechanism: When a working muscle is placed under

low intensity stress such as with walking, energy for motion is being contributed
by an oxygen and glucose dependent system for cellular respiration known as
the citric acid (Krebs) cycle. With adequate calorie input and available oxygen,
the Krebs cycle can go on indefinitely producing muscle energy known as ATP.
While in the Krebs cycle, oxygen dependent muscle fibers known as slow twitch
or type 1 release CO2 as a byproduct. As the demand on that working muscle
increases secondary to external resistance/torque or acceleration; an equal rise
in energy demands must also occur. For higher demand tasks, specialized
muscle fibers known as fast twitch or types 2 are recruited. These specialized
muscle fibers operate within a separate energy system that is not dependent on
O2 known as the cori (lactic acid) cycle. Due to the absence of oxygen, this
energy system is limited to short burst and is therefore used only when demands
are high enough to reach the thresholds required to recruit type 2, higher
threshold motor units.

BFR training enhances the effects of the lactic acid cycle via the application of
a tourniquet around a limb. Although the tourniquet can cut off complete
blood flow to the working limb which is still considered safe under the care of a
certified medical provider and FDA compliant equipment; BFR implements
partial occlusion which is safe and less demanding on the circulatory system as
compared HIT. Once the tourniquet it placed around a proximal limb a specific
and often individual limb occlusion pressure (LOP) is used.

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Current literature demonstrates that safe compression ranges between 90-110
mmHg for upper extremity and 110-130 mmHg for Lower extremity can be used
to safely target the current best evidence for reaching occlusion ranges of 50%
(UE) and 80% (LE) of total limb occlusion. These ranges though are not
individualized which should therefore be taken as estimates for BFR training. To
achieve the gold standard in safety a Doppler must be used as is seen in 3rd
generation cuff systems.

While the individual is working with BFR and the respective % of LOP has been
achieved the extremity will begin to accumulate muscle metabolic byproduct
such as lactic acid, and hydrogen ions (H+). Lactic acid is the key metabolite
responsible for cascade of anabolic signaling pathways. As these positive
anabolic signaling pathways, namely mTORC1 become activated, the negative
muscle anabolic pathways, such as Myostatin will become inhibited. Equally,
Lactate will later play a role systemically in the up-regulation of growth
hormone, which is directly involved in collagen synthesis; and thus providing
additional super structure to tendons, ligaments, bone, and muscle.

Cell swelling mechanism: As a direct result of venous blood flow occlusion, there
continues to be an increase in fluid into the working muscle. This leads to a
characteristic swelling or pump. While muscles are contracting they push fluid
away from themselves much like a sponge being squeezed. As the fluid pressing
decreasing in the working muscle, upon relaxation of the contraction, fluid
rushes inward. As there is an accumulation of fluid and metabolite build up
which attracts more fluid, the muscle cells begin to engorge. As they increase in
size there is a stress placed on the cellular walls. This stress leads to a protective
response again leading to adapt and grow.

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Growth Hormone
As a direct result of increased lactate, the pituitary gland up regulates the
formation of endogenous growth hormone (GH). Growth hormone is currently
understood to play more of an indirect role with post exercise recovery than
with direct muscle growth via protein synthesis. What is agreed upon is that GH
promotes and increases the super structure of muscle, tendon, ligaments,
cartilage, blood vessels and bone.

How GH affects muscle and tendon is through the formation of new collagen
structures known as collagen synthesis. Following a bout of HIT, soft tissue
disruption and micro-damage are present. The cascade of inflammation and
lower oxygenation, which to the casual observer may be seen as negative do
play a critical role in the release of GH and subsequent collage synthesis. It
would be of upmost importance for the body to promote collagen synthesis as
collagen promotes soft tissue compliance, elasticity, and load tolerability.

What is most interesting with BFR+LIRE is the absence of inflammation and tissue
breakdown all while demonstrating the same if not better effects of increased
whole blood lactate, GH, and collagen synthesis. In fact, the data has
demonstrated that following BFR+LIRE, increases in GH have been seen to rise
up to 300% from baseline. The data further demonstrates that with the rise in GH
and subsequent collagen synthesis BFR+LIRE would improve in tissue recovery
and regeneration following an acute injury or post-operative rehabilitation
treatment program.

The application of BFR+LIRE within the rehabilitation setting can also be seen
with its positive effects on bone regeneration/remodeling. Following a bone
fracture a clot is formed, which aids in the formation of new blood vessels. The
process of building new vessels is known as angiogenesis and in bone requires
the increased expression of a growth factor known as vascular endothelial
growth factor (VEGF). VEGF is stimulated via hypoxia and lactate which also
occur with BFR+LIRE. As loading is required for healing yet contraindicated,
BFR+LIRE can play an early role in promoting increased bone healing.

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Myogenic stem cells
Myogenic stem cells: (MSC) also play a critical role in inducing protein synthesis.

IGF-1: Insulin like growth factor 1plays the role of aiding with fusion of MSC
(satellite cells) to muscle fibers.

MSCs under normal conditions respond to prolonged heavy resistance training

and play a role in amplifying muscle protein
synthesis. MSCs are thought to play a role in the
donation of additional myonuclei to a muscle cell,
which has been observed to be accompanied by
substantial muscle contractile protein synthesis.

MSCs donate additional myonuclei to improve

capacity for myofibrillar gene transcription. These
changes increase in myofibre area (MFA).
Increased MFA plays a role with enhancing the
activity of cellular protein synthesis. The increase in
MFA has demonstrated to play a direct role with
elevating maximal voluntary contraction (MVC) or
strength.

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The key anabolic signaling
pathway
Until recently, Insulin-Like
Growth Factor (IGF-1) was
through to be the key
anabolic signaling pathway.
What is currently agreed
upon, is that IGF-1 a muscle
growth mediator play but a
part in the larger anabolic
signaling pathway that is the
mammalian target of
rapamycin complex 1, or
better known as the
mTOR1C pathway.

As stated above IGF-1 plays an role with the fusion of satellite cells into a muscle
fiber. This fusion can allow for the satellite cell to mature into a muscle specific
cell (myocyte) which can now undergo protein synthesis and other cellular
processes. For protein synthesis to occur, certain inhibiting growth pathways
must be deactivated.

With increased work demand on a muscle as seen with HIT there is a rise in the,
there is direct increase in motor unit recruitment. This means that as

mTOR1C is the anabolic signaling pathway that directly controls the pathways
associated with muscle growth. This complex is regulated by insulin, growth
factors, key amino acids (e.g., leucine, -hydroxy -methylbutyrate), fatty acids
(phosphatidic acid) as well mechanical stimuli, and oxidative stress.

It is within the oxidative stress/metabolic stress pathway, that mTOR1C is

activated. Cellular swelling again plays a critical role in activating endogenous
phosphatidic acid (PA), which has shown to increase the mTOR1C pathway.

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What is interesting is that ingestion of exogenous PA and leucine, that when
combined with resistance training such as BFR, can increased the activation of
the mTOR1C pathway.

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Exercise + Blood
Flow Restriction
Training

LE 80% LOP UE 50% LOP

LE 110-130 mmHg UE 90-110 mmHg

Protocols

Strength/Hypertrophy Endurance
20-35% 1 RM
40% Vo2Max
Sets: 4 (30,15,15,15)
Rest: 30 sec /set
15 min total time

Frequency Frequency
3-4 days/wk 4-6 days/wk

Energy
systems

Krebs Cycle
Cori Cyle
Oxidative
No Lactate
Non-Oxidative
No increased goals present Lactate
Increased goals

Increased GH Increased mTORC1 Increased Alpha motor

Type III/IV Afferent Decreased Myostatin Increased recruitment
Pituitary Response Decreased TGF-B Type II HTMU

Increased Collagen Increased Skeletal

synthesis Muscle Protein Synthesis Increased i EMG
IGF-1 Decreased Scar tissue Increased 1 RM Strength
VEGF formation

Tendon regeneration
Bone Remodeling
Super structure of muscle
cappilary angio-genesis

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Table: Lifters Clinic

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BFR training manual

Get certified
Medical provider certification and FDA compliant BFR
pneumatic unit through Owens Recovery Science

http://www.owensrecoveryscience.com/certification/

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BFR training manual

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References
Kacin A, & Strazar K (2011). Frequent low-load ischemic resistance exercise to
failure enhances muscle oxygen delivery and endurance capacity. Scand J
Med Sci Sports, 21, e231-241.

Wilson JM, Lowery RP, Joy JM, Loenneke JP, & Naimo MA (2013). Practical Blood
Flow Restriction Training Increases Acute Determinants of Hypertrophy Without
Increasing Indices of Muscle Damage. J Strength Cond Res, epub ahead of
print.

Loenneke JP, Abe T, Wilson JM, Ugrinowitsch C, & Bemben MG (2012) Blood flow
restriction: how does it work? Front Physiol, 3, 392.

Loenneke JP, Wilson JM, Marin PJ, Zourdos MC, & Bemben MG (2012). Low
intensity blood flow restriction training: a meta-analysis. Eur J Appl Physiol, 112(5),
1849-1859.

Loenneke JP, Fahs CA, Wilson JM, & Bemben MG (2011). Blood flow restriction:
the metabolite/volume threshold theory. Med Hypotheses, 77(5), 748-752.

Loenneke JP, Fahs CA, Rossow LM, Abe T, & Bemben MG (2011). The anabolic
benefits of venous blood flow restriction training may be induced by muscle cell
swelling. Med Hypotheses, 78(1) , 151-154.

Loenneke JP, Wilson GJ, & Wilson JM (2010) A mechanistic approach to blood
flow occlusion. Int J Sports Med, 31(1) , 1-4.

Schoenfeld, BJ (2013). Potential mechanisms for a role of metabolic stress in

hypertrophic adaptations to resistance training. Sports Med, 43(3), 179-194.

Loenneke JP, Abe T, Wilson JM, Thiebaud RS, Fahs CA, Rossow LM, & Bemben
MG (2012) Blood flow restriction: an evidence-based progressive model. Acta
Physiol Hung, 99(3) , 235-250.

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Thiebaud RS, Yasuda T, Loenneke JP, Abe T (2013). Effects of low-intensity
concentric and eccentric exercise combined with blood flow restriction on
indices of exercise-induced muscle damage. Interven Med Appl Sci, 5, 53-59.

Lowery RP, Joy JM, Loenneke JP, Oliveira de Souza E, Weiner S, McCleary S, &
Wilson JM (2013). Practical blood flow restriction training increases muscle
hypertrophy during a periodized resistance training program. National Strength
and Conditioning Conference, J Strength Cond Res supplement.

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