Personalized Blood Flow Restriction: The Athlete Dewey Joern PT, DPT Giancarlo Bonifazi PT, DPT There are no conflicts of interest to announce during this presentation Objectives Discuss guidelines for strength training Quickly review muscle and exercise physiology Compare anaerobic versus aerobic muscle pathways
Gain an introductory understanding as to the science behind how blood flow restriction works Analyze theories behind BFR including Metabolite and Cellular Swelling theories Describe satellite cells, IGF, HGH contributions from BFR Review how up-regulation of GH, satellite cells, IGF and MTORC1 with concomitant down-regulation of myostatin promote protein synthesis and hypertrophy Perform quick overview of research on BFR Explain its clinical uses and application, especially for the injured/rehabbing athlete
Strength and Hypertrophy Training ACSM: 8-10 upper/lower body exercises. These exercises should target major muscle groups 2-3 d/wk at a training intensity of more than 65% of the subjects one-repetition maximum. (Donnelly 2009) Good rule of thumb is 70% of 1-RM for maximal hypertrophy gains per ACSM Strength Training Early on in the training, strength changes are
made due to neurological adaptations vs hypertrophy Efficiency of nerve firing patterns Increase in # of motor units recruited Around 10 weeks+, shift from neuro muscular adaptations Hypertrophy vs cellular swelling! Strength Training
Neural and muscular adaptations to strength training over time, according to Moritani and deVries (1979). Anabolic Resistance Resistance from numerous factors against protein anabolism More pronounced in elderly - sarcopenia, but can impact athletes INFLAMMATION DISUSE
**Net Protein Balance** Muscle Protein Synthesis (MPS) Muscle Protein Breakdown (MPB) In post-surgical or acute injury populations, the drive for protein breakdown often surpasses the stimulus provided for protein synthesis = strength and CSA loss! What Does that Mean for Us? Often in the sports setting, we work with athletes that are unable to work under resistances as high as 70% 1-RM due to postoperative restrictions, general weakness, and/
or pain post-injury What Does that Mean for Us? In these patients, we are restricted to utilizing low-load exercises that have minimal effect on fast-twitch fibers Muscle Physiology and Size Principle Muscle Physiology and Size Principle
Cori Cycle (Anaerobic Metabolism) Krebs Cycle (Aerobic) So What Can We Do? Since we cannot affect loading restrictions that are in place post-operatively/traumatically, or what the patient can tolerate due to weakness/pain, how do we get them better, quicker if we are relegated to light resistances? How do we get to recruiting those large, fast-twitch
Type II fibers for force production if we use lowloading exercises? The Answer: Personalized Blood Flow Restriction With use of occlusion cuff/tourniquet/band, we restrict venous flow out of a limb while allowing partial arterial flow into the limb Cuff placed on proximal extremity LE thigh as close to hip as possible Ideal Limb Occlusion Pressure of 80%
UE arm as close to shoulder as possible Ideal Limb Occlusion Pressure of 50% While actively engaged in BFR, low-intensity exercise performed 20-30% 1-RM, high repetitions, 30 seconds rest between sets Personalized Blood Flow Restriction
Has been well-validated in the research over 20+ years from muscle physiology standpoint Multiple studies demonstrate comparable results between low-intensity plus BFR to highintensity exercise including CSA and strength gains 2017 systematic review by Hughes et al 20 eligible studies (3 ACLR, 3 knee OA, 13 with sarcopenia, 1 inclusion-body myositis) Low-load with BFR was more effective, tolerable than low-load exsc alone
Personalized Blood Flow Restriction Awesome results, but how does it work? Not 100% understood, but prevailing thoughts are: **Metabolite theory** Muscle protein synthesis activation Increased fiber type recruitment Cellular swelling Metabolite Theory
With higher load exercises, due to mechanical tension across muscle and neurological adaptations, very easy to recruit higher order, more powerful motor units With lower load exercises, not so much How do we recruit type-II fibers then? Metabolite Theory Answer: Create a hypoxic environment As long as we are maintaining low-load exercise and have adequate oxygen (and
fuel), we will preferentially utilize the Krebs cycle (aerobic) With BFR, we limit the amount of oxygen being delivered to the muscles Should theoretically force a switch to anaerobic pathway CORI CYCLE type II fibers Metabolite Theory Credit: Owens Recovery Science
Metabolite Theory Takarada 2000 Metabolite Theory Takarada 2000 Metabolite Theory Credit: Owens Recovery Science Metabolite Theory
Takeaways: BFR plus low-load consistently shown to increase lactate production over controls, similar levels to HIT Affirms we are in Cori Cycle BFR with moderate to high loads no added benefits for blood lactate concentrations Loenneke 2012 15-30% 1-RM with BFR most ideal
Also found no significant increase in use of BFR and exercise with knee wraps more on this later Why the hype about lactate? Metabolite Theory As lactate accumulates in muscle fibers, it decreases their ability to generate forceful contractions Thus, in order to maintain activity at the same level, additional motor units must be recruited SIZE PRINCIPLE
Fast, type II fibers! Numerous studies demonstrate increase in iEMG muscle activity with addition of BFR compared to controls: Yasuda 2008, 2012 Manini 2012 Labarbera 2013 Cook 2013 Metabolite Theory These changes result in a cascade of anabolic
responses that give Blood Flow Restriction the bang for its buck Increase in Growth Hormone Increase in IGF-1 Promotion of protein synthesis Down-regulation of myostatin Growth Hormone Accumulation of lactate and H+ ions results in augmented GH release in response to exercise Goto 2005, Takarada 2000
Sodium bicarbonate, McArdles Syndrome = decreased lactate production, less GH release following exsc If lactate production = GH release, and BFR = lactate production, does BFR increase GH production? YES! Growth Hormone Takarada 2000
Growth Hormone Pierce 2006 BFR with exercises versus tourniquet only Only BFR had significant increase in GH secretion Kraemer et al 1990, 1991 100 fold increase in GH release after HIT with 1 minute rest breaks vs 3 min rest breaks Metabolite accumulation during short rest!
More later on Inagaki 2011 BFR with NMES vs NMES alone BFR with NMES led to increase GH production Growth Hormone Pierce 2006 BFR with exercises versus tourniquet only Only BFR had significant increase in GH secretion Kraemer et al 1990, 1991 100 fold increase in GH release after HIT with 1 minute rest breaks
vs 3 min rest breaks Metabolite accumulation during short rest! More later on Inagaki 2011 BFR with NMES vs NMES alone BFR with NMES led to increase GH production Growth Hormone So Human Growth Hormone will result in muscle anabolism and increased performance right? Wrong
Liu 2008 - no effect of exogenous HGH on athletic performance, muscle CSA, strength Growth Hormone If exercise is one of the most potent stimulators of GH, what is GHs purpose? RECOVERY through collagen synthesis Doessing 2010 exogenous GH for 14 days 3.9 fold increase in tendon mRNA, 5.8 fold increase in muscle collagen synthesis
Kurtz et al 1999 rats with Achilles tendon transection Rats with local GH injection had faster functional recovery Acromegaly increased GH secretions Soft-tissue hypertrophy and excess cartilage synthesis Growth Hormone Growth Hormone What does that mean for ATCs, PTs?
Promote healing of injured tendons, bones, muscle through collagen synthesis Collagen matrix surrounding mm often disrupted after injury Giles et al 2017 Quad strengthening with and without BFR in patients with PFP 93% pain reduction in group with BFR compared to non-BFR
As BFR is performed with low-load exercise, no muscular breakdown so we have positive collagen turnover Metabolite Theory BFR induces hypoxic environments Hypoxia anaerobic pathways Anaerobic pathways increase lactate production Lactate production stimulates GH release GH release is helpful for recovery
Hypertrophy and strength gains? IGF-1 and Satellite Cells Growth Hormone stimulates production of Insulin-like growth factor (IGF-1) IGF-1 critical for bone and tendon health, correlated with mm hypertrophy, but not protein synthesis Main hypertrophic role is for fusion of satellite cells into mm fibers Satellite cells are stem cells of muscle
precursors to skeletal mm cells Usually stimulated with high-load exercise, but can be stimulated with BFR too! IGF-1 and Satellite Cells Abe 2005, Takano 2005, Fujita 2007 all demonstrate increases in IGF-1 with BFR vs controls Credit: Owens Recovery Science
IGF-1 and Satellite Cells Credit: Owens Recovery Science IGF-1 and Satellite Cells Nielsen 2012 280% increase in satellite cells at mid-training, 250% 3 days out, 140% 10 days after training! Kadi 2000, 2004; Olsen 2006 typical gains after high-load at 30-50% 30-40% increase in muscle fiber area in BFR
group Typical gains 15-20% after 12-16 weeks of heavy resistance in untrained men With increased CSA, increase in strength! IGF-1 and Satellite Cells Credit: Owens Recovery Science Metabolite Theory We now know that IGF-1 and satellite cells
help encourage hypertrophy, but what actually stimulates protein synthesis? Net Protein Balance = Muscle Protein Synthesis Muscle Protein Breakdown (remember this?) MTORC1 Mammalian Target of Rapamycin Protein that stimulates cell growth How do we activate it? Aforementioned growth factors, energy state of
the cell, exercise, and supply of amino acids Rapamycin immunosuppressant used to stop protein synthesis and cell growth in tumors MTORC1 Fujita 2007 Low-load with BFR vs low-load S6K1 expression and protein synthesis (S6K1 downstream marker of MTORC1) Low-load with BFR had significant rise in S6K1
after exercise Low-load with BFR had 46% increase in protein synthesis 3 hours after exercise MTORC1 Credit: Owens Recovery Science MTORC1 Does MTORC1 really increase MPS? Gunderman 2014 Two groups performed 20% 1-RM with BFR Experimental group took Rapamycin to block MTORC1
Group without Rapamycin 41.5% increase in protein synthesis 3 hours out; 69.4% 24hr out Group taking Rapamycin No significant changes Previously believed only high-load exercise would stimulate MTORC1 and thus MPS, but now shift in thinking with addition of BFR
Protein Synthesis NPB = MPS MPB With low-load exercise, do not have muscle fiber damage so there is not much mm protein breakdown after BFR plus exercise Avoidance of DOMS, very little muscle soreness several hours after; MVC of mm returned to normal few hours after BFR Stimulated MPS so high drive to create hypertrophy MUST have protein intake after BFR sessions to
maximize MPS Leucine AA key with MTORC1 Whey protein Younger: 20g/4 hours (for 24 hours) Older (60+): 40g/4 hours Myostatin Evil step child to MTORC1 Down-regulation of protein synthesis Lifting heavy typically results in decreased myostatin
Roth 2003, Forbes 2006, Hill 2003, Saremi 2010 Can BFR down-regulate myostatin? YES Laurentino 2012 20% 1-RM, 20% 1-RM with BFR, 80% 1-RM over 8 weeks Also looked at muscle strength and CSA Myostatin Credit: Owens Recovery Science
Myostatin Myostatin also linked to fibrosis/scarring via TFG-Beta family If we can down-regulate myostatin after an acute injury, we can minimize the risk of muscular scarring! In an acute injury, would NOT recommend lifting of 80% 1-RM, therefore low-load with BFR viable! Cell Swelling Hypothesis
Increase in cell size from fluid build-up Linked to MTORC1 (Schliess 2006) Ogawa 2012, Yasuda 2012, Fry 2010, Thiebaud 2013, Wilson 2013, and Yasuda 2008 All demonstrate increase in limb/cell swelling after application of BFR Even with just application of tourniquet (5 min bouts for 5 times with 3 min rest), disuse atrophy mitigated compared to isometrics and control
groups (Takarada 2000; Kubota 2008, 2011) Kubota 2008 no increase in GH with just tourniquet, so gives weight to cell-swelling hypothesis Bone Healing More studies needed, but several potential mechanisms for improving fracture healing with BFR Growth hormone given collagen synthesis, studies have shown quicker fx healing times with use of GH
vs controls Interstitial Fluid Flow pressure gradient resulting in fluid sheer stress on osteocytes Animal models show venous occlusion encourages new bone formation and increased bone density VEGF vascular endothelial growth factor Acute hypoxic states lead to increased VEGF expression and angiogenesis into bone fractures (Schipani 2009) How Do We Use BFR? Many occlusion options out there (ORS, B
Strong, Occlusion cuff, etc) Our training was through Owens Recovery Science Use of Delphi unit only FDA approved BFR device on market Doppler system determines individualized limb occlusion Set desired limb occlusion pressure LE 80% LOP UE 50% LOP
How Do We Use BFR? Goals of treatment: Cell swelling (acute injury or NWB) Minimal to no load, increased frequency 4-5x/week Follows 5min for 5 bouts in mentioned studies Occlusion stays on for 5 minutes while performing exercise such as SLR, LAQ, etc; 30s rest break in between each set 30/15/15/15 reps/sets model Helps mitigate any disuse atrophy, not necessarily hypertrophic gains
How Do We Use BFR? Goals of treatment: Metabolite Theory Hypertrophy and Strength 15-30% 1-RM loading 2-3x/week Still 30/15/15/15 repetition/set model 30s rest break in between sets, 1 min rest in between exercise (cuff deflated between exercise) Examples Examples
Paul Silvestri MS, LAT, ATC: Associate Director of Sports Health and head AT at UF football First athlete to use BFR at UF for football had high-grade biceps femoris strain Anticipated 4-6 week recovery Able to return in 3 weeks with use of BFR http://floridagators.com/news/ 2015/8/27/31116.aspx
Key Takeaways BFR is not a substitute for HIT If progressing athlete back to RTP, must transition to HIT for demands of sport Main risk is for superficial nn damage: mitigated with use of limb protection sleeves, wider cuffs, less pressure Use of BFR stimulates lactate production which leads to GH, IGF-1, MTORC, VEGF, IFF and muscle hypertophy/strength gains down the road Down-regulation of myostatin leading to protein synthesis
and decreased scarring! This is a very introductory explanation of BFR. If interested in more, would highly recommend Owens Recovery Science! References 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: 14601466, 2006
Abe T, Yasuda T, Midorikawa T, et al. Skeletal muscle size and circulating IGF-1 are increased after two weeks of twice daily KAATSU resistance training. Int J Kaatsu Train Res. 2005;1: 612 Cook SB, Murphy BG, Labarbera KE. Neuromuscular function following a bout of Low-load blood flow restricted exercise. Med Sci Sports Exerc 2013; 45:6774. Doessing S, Heinemeier KM, Holm L, et al. Growth hormone stimulates the collagen synthesis in human tendon and skeletal muscle without affecting myofibrillar protein synthesis. J Physiol. 2010;588(Pt 2):34151.
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Giles L, Webster KE, McClelland J, et al. Quadriceps strengthening with and without blood flow restriction in the treatment of patellofemoral pain: a double-blind randomised trial. Br J Sports MedPublished Online First: 12 May 2017. doi: 10.1136/bjsports-2016-096329 Goto, K., Ishii, N., Kizuka, T., & Takamatsu, K. (2005). The impact of metabolic stress on hormonal responses and muscular adaptations. Med Sci Sports Exerc, 37(6) 955-963 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
Hughes L, Paton B, Rosenblatt B, et al. Blood flow restriction training in clinical musculoskeletal rehabilitation: a systematic review and metaanalysis. Br J Sports Med 2017;51:1003-1011. Inagaki, Y., Madarame, H., Neya, M., & Ishii, N. (2011). Increase in serum growth hormone induced by electrical stimulation of muscle combined with blood flow restriction. Eur J Appl Physiol, 111(11), 2715-2721 Kadi F, Schjerling P, Andersen LL, Charifi N, Madsen JL, Christensen LR & Andersen JL (2004). The effects of heavy resistance training and
detraining on satellite cells in human skeletal muscles. J Physiol 558, 10051012 Kraemer WJ, Adams K, Cafarelli E, et al. American College of Sports Medicine position stand:progression models in resistance training for healthy adults. Med Sci Sports Exerc. 2002;34(2): 36480. Kraemer, W. J., Marchitelli, L., Gordon, S. E., Harman, E., Dziados, J. E., Mello, R., Fleck, S. J. (1990). Hormonal and growth factor responses to heavy resistance exercise protocols. J Appl Physiol (1985), 69(4), 1442-1450.
Kraemer, W. J., S. E. Gordon, S. J. Fleck, L. J. Marchitelli, R. Mello, J. E. Dziados, K. Friedl, E. Harman, C. Maresh, and A. C. Fry. Endogenous anabolic hormonal and growth factor responses to heavy resistance exercise in males and females. Int. J. Sports Med. 12: 228235, 1991 Kubota, Atsushi, et al. "Blood flow restriction by low compressive force prevents disuse muscular weakness." Journal of Science and Medicine in Sport 14.2 (2011): 95-99. References Kubota, Atsushi, et al. "Prevention of disuse muscular weakness by restriction of blood flow." Medicine and science in sports and exercise 40.3 (2008): 529-534
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Laurentino, G. C., Ugrinowitsch, C., Roschel, H., Aoki, M. S., Soares, A. G., Neves, M., Jr., Tricoli, V. (2012). Strength training with blood flow restriction diminishes myostatin gene expression. Med Sci Sports Exerc, 44(3), 406-412 Loenneke JP, Fahs CA, Thiebaud RS, et al. The acute muscle swelling effects of blood flow restriction. Acta Physiol Hung 2012;99:40010. Loenneke, J. P., Thiebaud, R. S., & Abe, T. (2014). Does blood flow restriction result in skeletal muscle damage? A critical review of available evidence. Scand J Med Sci Sports, 24(6), e415-422 Loenneke, J. P., Wilson, J. M., Marin, P. J., Zourdos, M. C., & Bemben, M. G. (2012). Low intensity blood flow restriction training: a meta- analysis. Eur J Appl Physiol, 112(5), 1849-1859. doi: 10.1007/s00421-011-2167-x Loenneke, J. P., Young, K. C., Fahs, C. A., Rossow, L. M., Bemben, D. A., & Bemben, M. G. (2012). Blood flow restriction: rationale for improving bone. Med Hypotheses, 78(4), 523-527. doi: 10.1016/j.mehy.2012.01.024
Manini TM, Vincent KR, Leeuwenburgh CL, et al. Myogenic and proteolytic mRNA expression following blood flow restricted exercise. Acta Physiol (Oxf) 2011;201:25563. Meyer, R. A. (2006). Does blood flow restriction enhance hypertrophic signaling in skeletal muscle? J Appl Physiol (1985), 100(5), 1443-1444 Moritani, T., W. Michael-Sherman, M. Shibata, T. Matsumoto, and M. Shinohara. Oxygen availability and motor unit activity in humans. Eur. J. Appl. Physiol. 64: 552556, 1992. 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 Pierce, J. R., Clark, B. C., Ploutz-Snyder, L. L., & Kanaley, J. A. (2006). Growth hormone and muscle function responses to skeletal muscle ischemia. J Appl Physiol (1985), 101(6), 1588-1595. doi: 10.1152/japplphysiol.00585.2006
Poton, R., & Polito, M. D. (2014). Hemodynamic response to resistance exercise with and without blood flow restriction in healthy subjects. Clin Physiol Funct Imaging. doi: 10.1111/cpf.12218 Scott, B. R., Loenneke, J. P., Slattery, K. M., & Dascombe, B. J. (2014). Exercise with Blood Flow Restriction: An Updated Evidence-Based Approach for Enhanced Muscular Development. Sports Med. doi: 10.1007/s40279-014-0288-1 Takarada Y, Nakamura Y, Aruga S, Onda T, Miyazaki S, Ishii N. Rapid increase in plasma growth hormone after low-intensity resistance exercise with vascular occlusion. J Appl Physiol (1985). 2000;88:61-65. Takarada, Y., Takazawa, H., Sato, Y., Takebayashi, S., Tanaka, Y., & Ishii, N. (2000). Effects of resistance exercise combined with moderate vascular occlusion on muscular function in humans. J Appl Physiol (1985), 88(6), 2097-2106.
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contraction. J Sport Rehabil 2004;13:28799. Yasuda T, Brechue WF, Fujita T, Sato Y, Abe T. Muscle activation during low intensity muscle contractions with varying levels of external limb compression. J Sports Sci Med 2008;7:46774. Yasuda T, Loenneke JP, Thiebaud RS, Abe T. Effects of blood flow restricted low intensity concentric or eccentric training on muscle size and strength. PLoS One 2012;7:e52843. Yasuda, T., Brechue, W. F., Fujita, T., Shirakawa, J., Sato, Y., & Abe, T. (2009). Muscle activation during low-intensity muscle contractions with restricted blood flow. J Sports Sci, 27(5), 479-489. doi: 10.1080/02640410802626567 Yasuda, T., Fukumura, K., Fukuda, T., Iida, H., Imuta, H., Sato, Y. Nakajima, T. (2014). Effects of lowintensity, elastic band resistance exercise combined with blood flow restriction on muscle activation. Scand J Med Sci Sports, 24(1), 55-61.
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