Personalized Blood Flow Restriction

If you are struggling with putting on muscle and recovering

from your training session, or in pain and having to limit

your training sessions- leading to lost gains and goals; then

Lifters Clinic is here for you.

Recovery and post injury states are not to different in their requirements. With muscle growth signaling being an essential component of both, let’s learn a little about what future technology and programming can do for you.

Muscle growth signaling occurs over the span of 48-72 hours. Therefore a tapering effect happens even though your muscles may still be recovering.

Simply put, taking to many days from working a muscle group can lead to a loss in growth and strength.

This too occurs following an injury which leads to common occurrence of muscle atrophy.

The term anabolic resistance is used today to signify the decreased rate of muscle protein synthesis (building) which aids in balancing out the normal day to day muscle breakdown that is not only a product of weight lifting, rather a normal process of metabolism and fasting.

Blood flow restriction is becoming a common rehab practice modality and training recovery strategy that is safe and highly effective at increasing the muscle building signal for improved muscle size, strength and function.

Here at Lifters Clinic we believe in utilizing the highest in evidence to support all that we do to deliver an exceptional performance Physical Therapy experience and outcome.

Working with a Strength Performance Physical Therapist with understands your active lifestyle, health needs and fitness goals can help prevent injuries and get you back in the game if you have been injured.

 

Traditional training methods for muscle hypertrophy focus on progressively lifting heavier loads over time to induce muscular damage and repair. Interestingly blood flow restriction (BFR) training works almost exactly opposite. Recent research suggests that due to the low loads used during BFR training, skeletal muscle break down does not occur. The evident increase in muscle protein building thus appears to have a separate mechanism that is largely dependent on lactic acid as a primary driver for muscle adaptation. These recent findings demonstrate that due to the absence of exercise induced muscle breakdown and inflammation, BFR training methods can be performed more regularly for increased muscle adaptation which may also play a role in tissue regeneration and recovery.

 

Mechanical Trauma and BFR

For decades, skeletal muscle protein synthesis was thought to be largely dependent on muscle damage as the primary catalyst for adaptation and growth of muscle fiber proteins. It was from here that much validation in programming progressive loading took place and essentially built the foundation for periodization. In fact, the term de-loading came about through periodization as a means to allow the body, namely the joints to recover while minimizing the loss of training adaptations such as muscle strength and size.

[Periodization: The planed implementation of specific training periods or phases. Each phase or period builds on the one before; either increasing or decreasing the volume (total reps x sets) as well the intensity (load or percentage of 1RM)]

Progressive loading is a common method used to implement mechanical trauma to skeletal muscle in order to achieve muscle growth (hypertrophy). This method requires structured recovery periods in order to allow the process of inflammation and tissue regeneration/adaptation to occur. Therefore careful consideration in training frequency (how often you train heavy) to respect the recovery strategy. It should be quite clear to most that too much, too often can overwhelm the regenerative properties and lead to injury.

This disruption of cellular contents and subsequent inflammation leads to a rise in growth factors like growth hormone (GH), and insulin-like growth factor 1 (IGF-1). GH and IGF-1 together play a role in collagen synthesis which strengthens tendons and bones but they also play a prominent role in muscle recovery via the proliferation and fusion of muscle stem cells called myo-satellite cells (MSC).

Because muscle does not readily undergo cellular division (making a copy of itself known as hyperplasia), cellular repair is critical for tissue function. Muscle fibers contain muscle cells called myocytes. Each myocyte has a nuclei (nuclei or nucleus: the control center of a cell) which is directly involved with the repair of damage received to the muscle following daily function, resistance training, and or injury. Muscle fibers are specialized for this repair process by containing multiple myocytes along its fibers making it a multinucleated structure. With multiple myocytes present the rate and quality of recovery via protein synthesis can be increased.

The addition of myocytes to a muscle has been demonstrated as a direct effect from mechanical strain and damage as seen with high intensity training due to the GH and IGF-1. The specific roles of GH and IGF-1 are now understood to work collaboratively in the process.

In summary, GH specifically activates the satellite cell and IGF-1 then chaperones and fuses the satellite cell into the muscle fiber. All in all, the process if very energy consuming and again requires structured recovery (i.e. nutrition, sleep, and periodization) to reduce the likelihood of either, under-training secondary to pain or over-training leading to injury.

Direct protein synthesis without muscle breakdown

Recent scientific literature has demonstrated that myogenic satellite cells can be proliferated and fused to a muscle fiber without the need of neither heavy mechanical tension nor tissue breakdown via blood flow restriction training (BFR-training). BFR+ exercise appears to be similar to that of regular exercise when considering the increase in GH and IGF-1 leading to significant up regulation of protein synthesis without the observed muscle breakdown and inflammation post exercise.

BFR is a method whereby a pneumatic tourniquet is placed around a working upper or lower limb while performing exercise. The pneumatic tourniquet is inflated to either an estimated safe range for upper and lower limb pressures (50 %UE or 80% LE); or based off of the individual’s personal limb occlusion pressure (via Doppler). The underlying mechanism for experiencing positive training results of increased muscle strength, size, endurance, and other various bone, vascular, and tendon health adaptations is related to training in a low oxygen state.

BFR training is well established in the scientific 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.

In recent studies performed by Abe et al; Takarada et al; and Pederson et al. when participants performed partial occlusion BFR exercises at 20% 1 RM, there were no statistical increases in direct muscle breakdown via Creatine Kinase, myoglobin, and lipid peroxides markers; nor were there significant indirect measures of muscle breakdown such as soreness and a post 24 hour drop in maximum muscle contraction (MVC); this would indicate muscle tissue breakdown and a reduced force production.

Nielsen et al. in 2012 also demonstrated that following a 3 week study of matched low load (20%1RM) knee extensor exercise, the BFR group had significant increases in MSC proliferation (quantity) and fusion. Levels of MSC’s were observed to increase by 280% at mid-training, 250% post 3 days and 140% post 10 days of detraining.

What was observed following the 10 day detraining protocol was a 30-40% increase in muscle fiber (type 2 and 1) size as was measured with direct muscle fiber biopsy. This finding indicated BFR training methods could in-fact, bridge the gap between low load resistance training and positive muscle protein synthesis (growth) via MSC proliferation/fusion.

To put into perspective the magnitude of increased muscle fiber size with BFR vs HIT, following a 12-16 wk. HIT study, results demonstrated an increase of 15-20% muscle fiber size within untrained men and a 37% increase in men identified as “hypertrophy responders” (Aagaard 2001, Kadi 2004, Olsen 2006, Petrella 2008).

These findings indicate a faster turnaround of protein synthesis and recovery which would explain how many of the individuals who participate in BFR exercise can perform repeated bouts of BFR more frequently; up to 3 times per day with no notable muscle breakdown.

With the increase in acute training volume and frequency due to the lack of recovery time required, muscle hypertrophy has been noted to occur in as fast as 2 weeks with proper BFR protocol methods (Nielson 2012).

Mechanical tension and BFR

As demand increases on a working muscle higher threshold motor units (HTMU’s) are recruited. We call these HTMU’s type 2 muscle fibers, or fast twitch muscle fibers. These muscle fibers types are required to complete high demanding force output activities, such as sprinting, jumping, and weight lifting. The uniqueness of these fibers is how they perform work in the near absence of oxygen, and thereby produce a byproduct that plays a critical role in all cellular adaption known as lactate.

Muscles fibers are divided via energy demands and fatigue. Type 1 slow twitch (tonic) fibers, are used for posture, stability, and long endurance activities such as running, where power output demands are low and fatigue resistance is high. Type 2 fast twitch (phasic) fibers, are used for explosive, short duration activities where fatigue resistance is moderate to low (respective of fiber 2a, and 2x).

All muscle fibers in general require adenosine tri-phosphate (ATP), which is a high energy compound required for muscle contraction. The ATP required for slow twitch fibers is performed through aerobic respiration (Glycolysis, and Krebs cycle). The process for ATP formation is slow and not suited for fast movements but can permit increased oxygen to the working muscle, allowing for continued work.

Type 2 fibers (2a and 2x) rely on anaerobic respiration (glycolysis – lactic acid cycle) to create low amounts of fast produced ATP. Type 2 fibers on the other hand of aerobic respiration, produce the byproduct of lactate (lactic acid) which inhibits further aerobic respiration. What is rather interesting is that as lactate increases, further type 2 fibers within the available pool of other motor units (muscle fibers) to maintain muscle force production.

This follows what is known as the size principle, whereas work performed under heavy loads will require further recruitment of muscle fiber type 2 via central nervous system facilitation to complete the task. The additional recruitment of further muscle fibers known as the central drive effect is explained by the size principle and one other determinant; lactate.

As noted above, with the recruitment of anaerobic type 2 fibers lactate is produced. This increase in lactate and subsequent decrease in pH and oxygen lead to quick fatigue, which will require further muscle fiber recruitment to continue work which will lead to the completion of the task and recovery from the task.

Example: as the demand increases on the quads and lactate is produced, assistance via the Glutes, hip rotators, lower leg muscles (gastroc and soleus) and trunk with become recruited complete knee extension and end the task which results in recovery, and restoration of cellular respiration (ATP production). This assistance results via a mechanism known as central motor drive (CMD).

CMD is the communication between specialized muscle nerve fibers called type III and IV afferents and the brain that become active during exposure to lactate.

Therefore, by increasing lactate a ramping up effect can occur, further recruiting muscle motor units of both local and distal muscle groups. The increase in recruitment would lead to increases in power output and thereby increase in muscle strength.

Where BFR plays a role in increasing muscle strength is in its ability to dramatically increase the amounts of lactate and whole blood lactate (Yasuda 2010). Finding in a recent study from Yasuda et al demonstrate increases in not only strength via the central motor drive phenomenon, but also increases in muscle hypertrophy via enhanced up-regulation of mTORC1, IGF-1, MSC, and a rapid decline in Myostatin signaling.

In an 8 week study by Takarada et al. Quadriceps muscle fiber hypertrophy (confirmed via MRI cross sectional area CSA) and increased muscle strength were observed.

Metabolic stress and BFR

With increased workload, comes increased muscle recruitment of type 2 fibers and the production of the by produce lactate and other metabolites. This buildup of metabolites has demonstrated to have positive effects of promoting enhanced muscle cell adaptive gains.

Muscle cells undergo a checks and balance for growth or protein synthesis (the formation of new muscle fibers; also known as myogenesis) that is largely controlled by both local and systemic pathways. The process of building required energy and can therefore not occur indefinitely with muscle breakdown being inevitable. This means that we will at times be in a building state and at other times be in a breaking state. The term net protein balance defines the difference between these 2 processes and can be explained by the Net protein balance (NPB) equation.

Muscle protein synthesis – Muscle protein breakdown = Net protein balance

MPS – MPB = NPB

High intensity training (HIT) due to its progressive mechanical loading or stimuli, has been observed to increase in skeletal muscle hypertrophy as a result of a key anabolic signaling pathway known as the mammalian target of rapamycin complex 1 (mTORC1). mTORC1 is a protein complex that directly controls protein synthesis via growth factors, energy status, amino acids and mechanical stimuli (example: resistance training via HIT and now known BFR methods). How mTORC1 is involved in muscle hypertrophy has much to do with the other anabolic growth regulators such as Insulin like growth factor 1 receptor (IGF-1R), Protein Kinase B or Akt. These protein synthesis signaling pathways regulate growth directly but as well indirectly through the down regulation of a negative regulator of skeletal muscle growth known as Myostatin. Myostatin is a specific myokine or protein that is produced by muscle cells which inhibit protein synthesis or myogenesis.

This active process of undergoing muscle adaptations is in large part dependent on mTORC1 which in many accounts can be said to be the master controller of protein synthesis.

mTORC1 pathway has been demonstrated to be activated by:

Mechanical stress (from heavy training loads)
Growth factors (IGF, growth hormone, insulin, etc.)
Amino acids (particularly leucine)
High concentrations of whole blood lactate (from recruitment of high threshold motor units)

To recap, high concentrations of lactate demonstrated increased super structure of tissues (muscle, tendon, ligament, and bone) via GH and collagen synthesis, as demonstrated increased distal and proximal strength via the central motor drive and played a direct role with increasing mTORC1, IGF-1 up-regulation and Myostatin down-regulation which leads to increased protein synthesis.

Therefore, increased metabolic stress to a muscle cell via high exposures to lactic acid, and hydrogen appear to play a prominent role in all forms of adaptation. This is critical to understand as varied training styles of either HIT or BFR can play key roles in increasing muscle health and positive training adaptations; leading to additional programing that can be implemented to improve recovery, and performance.

Cellular swelling

Interestingly, tourniquet application without exercise as demonstrated by Dr. Haussinger in the early and late 90’s (Haussinger 1993, 1996) influenced muscles cells to reinforce their structure through the activation of mTORC1 to promote protein synthesis in order to avoid cell death (apoptosis). The same can be said for HIT as venous flow can be occlude to 100% with prolonged isometric holds and simply with progressively heavy weights.

The information provided in this article is fundamental in furthering our understanding of muscle growth triggers, and how best we should be prescribing exercise intensities and repetitions for muscle growth. If the presence of increased blood lactate is what is required to promote the up-regulations of growth factors, and inhibit the control of negative growth factors; then the cue for growth should always be to seek the burn when not performing exercise under BFR.

The burn of lactic acid, essential would indicate that the working muscle has exhausted its ability to perform continued work through the Krebs cycle; leaving it no other choice but to increase recruitment of additional muscle motor units through type II muscle. The subsequent recruitment of these type II fibers would then yield the much needed by-product of lactate to then augment the increase in protein synthesis.

Where BFR enhances this process is by decreasing the clearance of the lactic acid by-product. The lack of clearance via the tourniquet, has demonstrated to promote much higher levels of anabolic signaling hormones, both locally and systemically.

BFR application and tourniquet research

Hopefully, there has been some “aha” moments and learning moments throughout this article for you. The goal was to not only educate you on the benefits of BFR training, but also to shine light on the many advantages to training with intent on feel and feedback. Healthy individuals can train heavy and hard. With proper programming, injuries can be low to none. BFR in this population can play a role to assist in recovery strategies such as when de-loading to allow your joints to recovery, prior to stage competition to improve the pump via cell swelling, and in general to augment further muscle growth.

But, the most important time to use BFR is in the event of an injury. What BFR can promote is a methodology that is rooted in scientific evidence to enhance the effects of low intensity training. As there is no additional tissue breakdown, injured groups need not fear further damaging tissues during times of required protection such as post-operative, or general acute musculoskeletal injuries. This pathway can create so many positive effects not just too enhanced tendon repair, ligament strength, or bone remodeling after a fracture but it can also put the control back in your hands which plays profoundly with decreasing fear, anxiety and pain.

Here are some direct accounts of using BFR for rehabilitation purposes.
(http://www.owensrecoveryscience.com/blog/category/in-the-news/)

How to apply

With many so called “BFR” wrap products on the market (nylon straps, knee wraps, medical grade emergency tourniquets, and handheld pneumatic pumps) it is difficult to differentiate what is real science and what is knock off. What we can state with total confidence is that each person has their own individual compression levels known as their “personal limb occlusion pressure” (LOP). The LOP is the total amount of pressure required to cut off blood flow by 100%. This total number is important because current BFR methods demonstrate that key percentages of this total when adjusted correctly can provide the optimal and safe way to promote positive adaptations.

The current literature supports 80% LOP for lower body BFR exercise, and 50% LOP for upper body BFR exercise. The key with the % of LOP is the trapping of whole blood lactate (WBL). With percentages to low (80 to 50% LOP respectively) blood and lactate will again be pumped out leading to reduced WBL and effects.

This is the problem with products that cannot measure LOP which created varied effects, and potential negative side effects (redness, bruising, and pain). As was noted in a recent study by Loenneke et al in 2010, “This study does not support the use of knee wraps as a mode of blood-flow restriction”. So, buyers beware.

Therefore the gold standard in BFR training comes through the ability to measure individual LOP to estimate the proper training zone. Currently, Owens recovery Science is the only FDA approved cuff that contains a built in Doppler to allow for proper levels to be achieved. To find providers in your area that currently have a unit (as they require training and certification) check here (http://www.owensrecoveryscience.com/certified-providers/)

Programming for BFR

Using the best knowledge above for how you may want to proceed with BFR here is a list of certain populations that should consult with a physician before strapping a BFR cuff on.

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

How can PBFR Directly Impact My Training and Rehabilitation

BFR methods implement using low intensities to promote the highest concentration of lactic acid without pumping it all out of the muscle. Again, HIT methods can do the same but BFR can be used within a HIT program to further enhance your own bodies DNA. Look at BFR as a ways to manufacture your own endogenous steroids, such as mTORC1, IGF1 and MSC’s whenever you need them without the additional breakdown.

Training methods currently accepted for BFR are intensities around as low as 25% to 35% of your 1 rep max. This is sick to believe that lite weights can increase strength and especially muscle size even higher than HIT. Below is the provided RM calculator and instructions.

 

 

Example
10 RM test: 100lbs
100 x 1.33 = 133lbs Estimated 1 RM
133 x .25 = 33.25lbs
133 x .35 = 46.55lbs
BFR training intensity range of 25-35%1RM: 33.25 – 46.55lbs

Because BFR has demonstrated to have very little influence on inflammatory markers such as Creatine kinase, myoglobin and lipid peroxides (i.e. markers of direct muscle breakdown) (Takarada 2000, Abe 2005); BFR can be performed twice per day. Below is the recommended set/rep/rest scheme.

 

BFR training volume and time frame of application

• Total Volume = 75 Reps
• Total time = 7 min

Frequency

BFR can be performed with isolation exercises (i.e. Open chain) as well Compound exercises (i.e. Closed Chain).

Open chain example:

Training Program examples

Bodybuilding example
ABE et al. 2 week protocol, 2x/day AM/PM session @ 20-30% 1RM, for 2 weeks

Yasuda et al. 6 week protocol single session @ 30% 1RM, for 3x weeks for lagging body part

Strength athlete
Hypertrophy/endurance conditioning on off days to enhance growth and recovery.

De-load programming
Decrease loading on joints and spine while maintaining strength, size, and endurance adaptation

Prehab/Rehab
Maintain muscle mass, increase tendon repair, increase bone repair, maintain VO2max (muscle endurance), improve muscle fiber recruitment (strength), and improve functional independence and return to activity.

Book your appointment now and optimize your health today!

Inquiry about Personalized Blood Flow Restriction

 

 

References

Abe T, Sato Y, Inoue K, Midorikawa T, Yasuda T, Kearns CF, Koizumi K, Ishii N.
Muscle size and IGF-1 increased after two weeks of low-intensity “Kaatsu”
resistance training (Abstract). Med Sci Sports Exerc 36: S353, 2004.

Abe T, Kearns CF, Sato Y. Muscle size and strength are increased following walk
training with restricted venous blood flow from the leg muscle, Kaatsu-walk
training. J Appl Physiol 100: 1460–1466, 2006.

Abe T, Sakamaki M, Fujita S, Ozaki H, Sugaya M, Sato Y, Nakajima
T. Effects of low-intensity walk training with restricted leg blood flow on muscle
strength and aerobic capacity in older adults. J Geriatr Phys Ther 33: 34–40,
2010.

Drummond MJ, Fujita S, Takash A, Dreyer HC, Volpi E, Rasmussen BB. Human
muscle gene expression following resistance exercise and blood flow restriction.
Med Sci Sports Exerc 40: 691–698, 2008.

Gundermann, D. M., Walker, D. K., Reidy, P. T., Borack, M. S., Dickinson, J. M., Volpi, E., & Rasmussen, B. B. (2014). Activation of mTORC1 signaling and protein synthesis in human muscle following blood flow restriction exercise is inhibited by rapamycin. Am J Physiol Endocrinol Metab, 306(10), E1198-1204.

Haussinger D, Roth E, Lang F, Gerok W. Cellular hydration state: an important determinant of protein catabolism in health and disease. Lancet (1993); 341: 1330–1332.

Haussinger D. The role of cellular hydration in the regulation of cell function. Biochem J 1996;313(Pt 3):697–710.

Karabulut, M., Sherk, V. D., Bemben, D. A., & Bemben, M. G. (2013). Inflammation marker, damage marker and anabolic hormone responses to resistance training with vascular restriction in older males. Clin Physiol Funct Imaging, 33(5), 393-399.

Lieber RL, Friden J. Muscle damage is not a function of muscle force but active muscle strain. J Appl
Physiol 1993: 74: 520–526.

McCully KK, Faulkner JA. Characteristics of lengthening contractions associated with injury to skeletal
muscle fibers. J Appl Physiol 1986: 61: 293–299.

Meyer, R. A. (2006). Does blood flow restriction enhance hypertrophic signaling in skeletal muscle? J
Appl Physiol (1985), 100(5), 1443-1444.

Nielsen, J. L., Aagaard, P., Bech, R. D., Nygaard, T., Hvid, L. G., Wernbom, M. Frandsen, U. (2012).
Proliferation of myogenic stem cells in human skeletal muscle in response to low-load resistance
training with blood flow restriction. J Physiol, 590(Pt 17), 4351-4361.

Pedersen BK. Muscles and their myokines. J Exp Biol 2011: 214:337–346. Pedersen BK, Fischer CP. Beneficial health effects of exercise – the role of IL-6 as a myokine. Trends Pharmacol Sci 2007: 28: 152–156.

Mikuki Sudo, Soichi Ando, David C. Poole, Yutaka Kano Blood flow restriction prevents muscle damage but not protein synthesis signaling following eccentric contractions Physiological Reports Jul 2015, 3 (7)

Thiebaud, R. S., Yasuda, T., Loenneke, J. P., & Abe, T. (2013). Effects of low-intensity concentric and eccentric exercise combined with blood flow restriction on indices of exercise-induced muscle
damage. Interv Med Appl Sci, 5(2), 53-59.

Yasuda T, Fujita S, Ogasawara R, Sato Y, Abe T. Effects of low intensity bench
press training with restricted arm muscle blood flow on chest muscle
hypertrophy: a pilot study. Clin Physiol Funct Imaging 30: 338–343, 2010.

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