1. Personalized Blood Flow Restriction: The Athlete
Dewey Joern PT, DPT
Giancarlo Bonifazi PT, DPT

2. There are no conflicts of interest to announce during this presentation

3. 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

4. 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 subject’s one-repetition maximum. (Donnelly 2009)
Good rule of thumb is 70% of 1-RM for maximal hypertrophy gains per ACSM

5. 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!

6. Strength Training
Neural and muscular adaptations to strength training over time, according to Moritani and deVries (1979).

7. 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!

8. 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 post-operative restrictions, general weakness, and/or pain post-injury

9. 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

10. Muscle Physiology and Size Principle
If stuck performing low load exercises, will never be able to recruit large, fast-twitch mm fibers

11. Muscle Physiology and Size Principle

12. Cori Cycle (Anaerobic Metabolism)

13. Krebs Cycle (Aerobic)

14. 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 low-loading exercises?

15. The Answer:
Here’s Johnny!

16. 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

17. 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 high-intensity 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”

18. 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

19. 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?

20. 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 

21. Metabolite Theory Takarada 2000 – 20% 1-RM with and without BFR
Credit: Owens Recovery Science

22. Metabolite Theory
Takarada 2000 – as occlusion pressure increased, so did plasma lactate concentrations
Takarada 2000

23. Metabolite Theory
Takarada 2000 – need exercise to increase lactate, but too heavy resistance causes pumping effect
Takarada 2000

24. Metabolite Theory
Poton 2014 – 20% 1RM with BFR, 20% 1RM without BFR, 80% 1RM
Credit: Owens Recovery Science

25. Metabolite Theory Takeaways: Why the hype about lactate?
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?

26. 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

27. 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

28. Growth Hormone
Accumulation of lactate and H+ ions results in augmented GH release in response to exercise
Goto 2005, Takarada 2000
Sodium bicarbonate, McArdle’s Syndrome = decreased lactate production, less GH release following exsc
If lactate production = GH release, and BFR = lactate production, does BFR increase GH production?
YES!

29. Growth Hormone
Takarada 2000 – 290% greater GH release with BFR than matched-control!
Takarada 2000

30. 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

31. 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

32. Growth Hormone
So Human Growth Hormone will result in muscle anabolism and increased performance right?
Wrong
Liu no effect of exogenous HGH on athletic performance, muscle CSA, strength

33. Growth Hormone
If exercise is one of the most potent stimulators of GH, what is GH’s 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

34. Growth Hormone

35. 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

36. 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?

37. 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!

38. 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

39. IGF-1 and Satellite Cells
Nielsen 2012
Credit: Owens Recovery Science

40. 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 %
30-40% increase in muscle fiber area in BFR group
Typical gains 15-20% after weeks of heavy resistance in untrained men
With increased CSA, increase in strength!

41. IGF-1 and Satellite Cells
Nielsen 2012
Credit: Owens Recovery Science

42. 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?) 

43. MTORC1 Mammalian Target of Rapamycin How do we activate it?
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

44. 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

45. MTORC1
FSR – fractional synthetic rate
Credit: Owens Recovery Science

46. 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

47. 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

48. 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
Hunter-gatherer: muscle is metabolically expensive!

49. Myostatin
Even slightly higher myostatin reduction in BFR (45%) than HIT (41%)
Credit: Owens Recovery Science

50. 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!

51. 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

52. 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)

53. 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

55. 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

56. 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)

57. Examples

58. 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

59. 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!

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