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Blood Flow Restriction (BFR) Training

What is Blood Flow Restriction Training?

Blood Flow Restriction Training or Therapy (BFR) is a relatively new treatment intervention with its own protocols amongst the many techniques within the ethos of healthcare. All-in-all, the big picture of what BFR is, is quite simple to understand. A blood pressure cuff, or torniquet, is placed around a limb in order to occlude (limit or “cut off”), partially or entirely, the blood flow to a desired limb for a specific amount of time and/or repetition of a movement. Benefits are noted within as little as 10 minutes of usage.

How Does Blood Flow Restriction Training Work?

This can be a nuanced question. At its core, BFR works by altering the chemistry happening within the body – specifically, the desired limb. At a cellular level, BFR follows very similar principles to that of strength training. However, there is a macro difference between the two. Strength training requires a person to utilize heavy load to produce certain positive growth chemicals within the body, while BFR can achieve the same chemical effect without requiring a heavy load. This can be a huge advantage for certain individuals.

Both heavy strength training (≥ 70% or higher of a 1 rep max (RM)) and BFR force the body into a “hypoxic state,” (without oxygen), which in turn activates certain chemical pathways to increase positive growth chemicals, by switching from an aerobic state (with oxygen) to an anerobic state (requiring more energy than what oxygen can solely provide). This lack of energy output via oxygen alone increases positive chemicals within the limb for increased growth such as Lactate, Growth Hormones (GH), IGF-1, Gene Expression, Myostatin, and much more still being investigated.

Blood Flow Restriction Training and Bone Healing

There appears to be positive effects noted with bone, as well as tendons and muscular structures noted earlier, via GH stimulation.29 Lack of GH results in osteopenia and reduced cortical bone.30 New bone production, in response to increased GH, have been noted in healthy individuals31 32 in post-menopausal osteoporosis33 and men with idiopathic osteoporosis.34

There are numerous studies now highlighting the positive effect of GH supplementation post hip35 36 and tibial fractures37 as well as hip replacement surgery.38 Regarding tibial (inside shin bone) fractures, individuals given GH had remarkably faster healing times – up to 26% faster.39 BFR can stimulate GH without the need for loading a broken bone. This will help not only improve healing time, as noted above, but allow an athlete to stay muscularly strong as noted further above. Additional chemicals, venous endothelial growth factor (VEGF), have also been noted to help heal injured bone faster,40 which become more activated via hypoxia and lactate.41 42 BFR significantly increases lactate and VEGA.43

Blood Flow Restriction Training and Weightlifting

For those of you who have landed on this page to read this section specifically, we highly recommend reading the entire page as it will better highlight how different chemicals produce positive net gains through BFR or weightlifting.

That said, research conducted on older and younger men compared GH levels after BFR or heavy load. Both age brackets accomplished higher levels of GH, which is not surprising to say stress to the tissue had a positive effect, and that the younger men had a higher GH increase after BFR than heavy training.44 We can always micro-dissect any lifting program; however, from a bird’s-eye view, this is fascinating. Researchers concluded that rest periods during traditional lifting may be the underlying culprit, which may surprise you. A rest period of 1-minute had a 100-fold increase in GH production compared to a 3-minute rest period and all other factors remaining constant – load and volume.45 46 With traditional strength programs, a 3-minute rest period is not uncommon to see when the load exceeds 80% 1RM. This research would indicate higher GH secretion is noted with shorter duration rest periods. This might be due to the nature of the Lactate Energy System maintaining higher levels of lactate within the area, therefore there is a lack of ability to clear Lactate from the area and the Krebs System (ATP-mg energy source) and its inability to produce ATP-mg fast enough in relation to lactate build up to help our muscles relax. Simply, lactate fatigues muscles and ATP-magnesium relaxes muscles. With BFR, rest periods are always relatively short – less than 90 seconds while the blood supply stays limited. This helps to keep lactate high and, in turn, GH high therefore increased collagen synthesis – AKA increased healing.

Blood Flow Restriction Training, Weightlifting, and Muscle Activation

Lactate production may also be a large contributor to increased muscle activation as seen via EMG readings. Buildup of lactate in our muscles, decreases or halts the activation of surrounding muscle fibers. As a result, other motor units need to be recruited to keep force production high for the movement/lift at hand.47 48 49 Through the increase of lactate via BFR, group III and IV afferent nerve fibers “fire” harder to complete the task at hand and in so doing recruit larger motor units (i.e. stronger muscle activation).

Blood Flow Restriction Training, Weightlifting, and Knee Wraps

Knee wraps used as tourniquets, while performing BFR protocols, did not produce an increase in lactate. It is assumed that the knee wraps do not provide enough occlusion to the target limb or are unable to trap metabolites to produce lactate build up.50 This may suggest that “proper pneumatic tourniquets” are required for metabolite accumulation. Further research may be needed due to the anecdotal positive results with non-pneumatic tourniquets being utilized within gym settings. There may be a placebo, “belief theory,” effect with these units.

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Blood Flow Restriction Training and Lactate Production

Lactate is a chemical byproduct which occurs in our body as the result of using fast twitch muscle fibers. Fast twitch muscle fibers are utilized through aggressive and/or explosive movements such as lifting heavy weights or sprinting. The energy source for fast twitch muscle fibers is different than for slow twitch muscle fibers.

To set the stage correctly, aerobic and anerobic systems are not with and without oxygen respectively. Aerobic means the body can produce enough energy, for the task at hand, via oxygen and food solely. Anerobic is the next phase in energy production when our cells demand more energy than what oxygen alone can produce. Anerobic training produces higher levels of lactate than aerobic training for an energy source. However, your body is still using oxygen in an anerobic state; simply, your body needs additional fuel to help achieve the task at hand.

Through the process of limiting the blood supply to a limb, the tissue(s) for the limb need more fuel for energy than what oxygen alone can provide. As a result, lactate is produced. Elevated lactate works as a signaling molecule, in some ways not yet fully understood, to help the brain-body understand that more energy is needed to help accommodate the desired task at hand.

It is important to note here there are different energy use systems with in one’s body. This is a beautiful design. For physical recovery and physical therapy/rehab, studies conclude loads as little as 15-30% of a person’s 1 rep max (RM) created the largest effect on muscular size and strength when utilizing a reliable BFR unit.1 Furthermore, it is important to note the use of bands, typically seen in a physical therapy setting, offers little to no muscular and chemical benefit to help the desired tissue growth.2

Blood Flow Restriction Training and Growth Hormone (GH)

Growth Hormone (GH) is a chemical released from the pituitary gland within the brain. The name growth hormone seems fairly self-explanatory in its function; however, it is very different than what almost all people understand it as. It is important to note that GH is released when specific nerves, group III – IV afferent nerves, are stimulated by lactate build up within the muscle(s).3 Without lactate production, GH in not released. This is noted in a condition called McArdle’s Syndrome.4

What is Growth Hormone’s Function?

Exogenous, or externally produced, GH does not increase muscular size (AKA hypertrophy) through protein synthesis (creation),5 strength or power.6 7 HGH (human growth hormone) does not have an effect on athletic performance.8 Now stating this, it is well understood that exercise does stimulate GH.9 10 The question at hand is – how? The answer lies within collagen synthesis.11 GH production in response to exercise creates a protective response for our tendons and other collagen rich tissue to recover faster and more efficiently. For recovery or physical therapy/rehab, incorporating training programs such as BFR which increase GH can help collagen rich tissue heal faster. This has been wonderfully highlighted with treatment for elderly and those experiencing tendinosis or tendonitis complications such as Achilles Tendonitis.12 Through the use of BFR, one can increase GH, up to 300 times from baseline, without having to breakdown the surrounding tissue, or adding heavy loads to a potentially injured joint or bone.

Blood Flow Restriction Training and IGF-1 and Satellite Cells

Insulin-like growth factor (IGF-1) is a muscle mass regulator growth protein found in humans13 14 which is stimulated by GH production. It is believed to be more correlated with strength gains15 instead of protein synthesis noted in muscle growth.16 At a quick glance, this does not make sense. How does it regulate muscle mass but not be involved in protein synthesis to create larger muscle(s)? This is where satellite cells come into play. Satellite cells are adult stem cells for skeletal muscles. When muscle become damaged through working out, GH stimulates IGF-1 which transports satellite cells into the damaged muscle fiber to then become new muscle cells within the muscle fiber.

Through research with the use of BFR in comparison to research without the use of BFR, one can conclude activation of these chemicals produced far greater benefit to an individual regarding recovery, tissue growth, and tissue remodel.17 Comparing BFR to non-BFR usage, satellite cells were 280% greater at mid-training, 250% 3 days after, and 140% at 10 days after. The control group had no satellite gain. Satellite gains typically noted after high load workouts are 30-50%.18 19 20 This benefit is not limited or specific to Type II (fast twitch) vs Type I (slow twitch) muscle fibers either.21 Hopefully, cumulation of this research helps to highlight the importance with incorporating Blood Flow Restriction training into your recovery care plan and how it can produce drastic effects in not only getting out of pain but also into long-term training benefits.

Blood Flow Restriction Training and Myostatin Production

Myostatin is the link between Satellite Cells and Hypertrophy. Myostatin is a chemical which blocks muscle cell growth. Simply, it’s the body’s switch to stop muscle development. The reason why our bodies do this is because muscle is a very energy costly tissue. By having this “switch” our bodies can help preserve energy better. During more physically and environmentally demanding days, being able to conserve energy was needed. Today, there is extensive research going into producing supplementations to achieve the goal of shutting this gene expression off.

Lucky for us, BFR can help facilitate turning this gene expression off for bouts of time. It is understood that heavy strength training can down-regulate myostatin which in turn correlated to increased muscle strength and hypertrophy.22 23 24 25 26 Improvements, due to this factor, have been seen within misunderstood conditions such as idiopathic myositis.27 28 This accumulation of research incorporating BFR helps to highlight a core principle we preach – the body longs for movement and incorporations of increased strain for positive health outcomes.

What Side Effects May I Feel with Blood Flow Restriction Therapy?

With high-quality, 3rd generation tourniquets, the risk of tourniquet complication ranges from 0.04% to 0.8%.51 52 Side effects during use with BFR may include:

  • Numbness
  • Nerve Injury
  • Skin Injury
  • Pain
  • Chemical Burns
  • Tingling
  • Respiratory, cardiovascular, cerebral circulatory, and hematological effects caused by prolonged ischemia
  • Temperature Changes
  • Arterial Injury
  • Prolonged postoperative swelling of the affected limb
  • Skin discoloration (purple)
  • Soreness

Blood Flow Restriction Therapy Risks

Circulation issues are of great concern. Indicators of poor circulation include shining or scaly skin, brittle or dry nails, and extremity hair loss. Varicose veins and capillary filling issues are also of note for risk. Obesity or loose limb tissue may be of challenge due to risk of shifting tourniquet.

Additional Patients Who May Be at Risk:

  • Arterial calcification
  • Abnormal clotting times
  • Diabetes
  • Sickle cell trait
  • Tumor
  • General infection
  • Hypertension
  • Cardiopulmonary conditions
  • Renal compromise
  • Clinically significant acid-base imbalance
  • Atherosclerotic vessels
  • Anti-hypertensive drug use
  • Creatine supplementation use

If you have any of these or have other concerns, please ask one of our doctors. These are not full contraindications in that we should not consider BFR as an option of care. However, it is beneficial for all parties to have a common understanding.

Blood Flow Restriction Therapy Contraindications

  • Venous Thromboembolism
  • Impaired circulation
  • Peripheral vascular compromise
  • Previous revascularization
  • Extremities with dialysis access
  • Elbow surgery (where there is concomitant excess swelling)
  • Secondary or delayed procedures after immobilization
  • Lymphectomies
  • Acidosis
  • Sickle cell anemia
  • Extremity infection
  • Tumor distal to tourniquet
  • Clotting risk medications
  • Skin grafts (in which all bleeding points must be readily distinguished)
  • Vascular grafting
  • Cancer
  • Open Fracture
  • Increased intracranial pressure
  • Open soft tissue injuries
  • Severe Hypertension
  • Severe crushing injuries
  • Secondary or delayed procedures after immobilization
  • Post-traumatic lengthy hand reconstructions
  • Deep Vein Thrombosis

Blood Flow Restriction Training and Tourniquet History

Tourniquets have been used since the 4th century BC. A French physician, Jean Louis Petit, coined “tourniquet” for its meaning to “turn.” In 1904, Harvey Cushing developed the first pneumatic tourniquet. This 1st generation was beneficial in reducing nerve-related damage from the compression. In the 1980’s, James McEwan PhD, invented the first electronic tourniquet. Via the electronic capabilities, precise pressure control, audio visual alarms, self-checks, calibrations, monitoring of time and inflation/deflation became possible. This is considered Gen. 2 tourniquet systems. Gen. 3 tourniquets can now automatically measure minimum pressure required for limb occlusion and personalize needed pressures. Sleeve design and usage improved alongside these features, and now, contours to the curvature of body shapes better, enabling better calculations.

Blood Flow Restriction Therapy, via the use of pneumatic tourniquets, came about through rehabilitation of military veterans. Shrapnel and other body damaging artifacts led to the need to help facilitate faster and more efficient healing. Through many trials, BFR helped to facilitate this healing for our injured soldiers.

Content Written by Dr. Keith Sparks, DC | Blood Flow Restriction Rehab - Owens Recovery Science, Smart Cuffs Level 1 Blood Flow Restriction Training
Content Reviewed by Dr. Sam Reals, DC | Blood Flow Restriction Rehab - Owens Recovery Science

View Citations and References

1 Loenneke JP, Wilson JM, Marín PJ, Zourdos MC, Bemben MG. Low intensity blood flow restriction training: a meta-analysis. Eur J Appl Physiol. 2012;112(5):1849-1859. doi:10.1007/s00421-011-2167-x.

2 Sundberg CJ. Exercise and training during graded leg ischaemia in healthy man with special reference to effects on skeletal muscle. Acta Physiol Scand Suppl. 1994;615:1-50.

3 Gosselink KL, Grindeland RE, Roy RR, et al. Skeletal muscle afferent regulation of bioassayable growth hormone in the rat pituitary. J Appl Physiol (1985). 1998;84(4):1425-1430. doi:10.1152/jappl.1998.84.4.1425.

4 Godfrey RJ, Whyte GP, Buckley J, Quinlivan R. The role of lactate in the exercise-induced human growth hormone response: evidence from McArdle disease. Br J Sports Med. 2009;43(7):521-525. doi:10.1136/bjsm.2007.041970.

5 Yarasheski KE, Campbell JA, Smith K, Rennie MJ, Holloszy JO, Bier DM. Effect of growth hormone and resistance exercise on muscle growth in young men. Am J Physiol. 1992;262(3 Pt 1):E261-E267. doi:10.1152/ajpendo.1992.262.3.E261.

6 Lange KH, Andersen JL, Beyer N, et al. GH administration changes myosin heavy chain isoforms in skeletal muscle but does not augment muscle strength or hypertrophy, either alone or combined with resistance exercise training in healthy elderly men. J Clin Endocrinol Metab. 2002;87(2):513-523. doi:10.1210/jcem.87.2.8206.

7 Rennie MJ. Claims for the anabolic effects of growth hormone: a case of the emperor's new clothes?. Br J Sports Med. 2003;37(2):100-105. doi:10.1136/bjsm.37.2.100.

8 Liu H, Bravata DM, Olkin I, et al. Systematic review: the effects of growth hormone on athletic performance. Ann Intern Med. 2008;148(10):747-758. doi:10.7326/0003-4819-148-10-200805200-00215.

9 Weltman A, Weltman JY, Schurrer R, Evans WS, Veldhuis JD, Rogol AD. Endurance training amplifies the pulsatile release of growth hormone: effects of training intensity. J Appl Physiol (1985). 1992;72(6):2188-2196. doi:10.1152/jappl.1992.72.6.2188.

10 Pritzlaff CJ, Wideman L, Weltman JY, et al. Impact of acute exercise intensity on pulsatile growth hormone release in men. J Appl Physiol (1985). 1999;87(2):498-504. doi:10.1152/jappl.1999.87.2.498.

11 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):341-351. doi:10.1113/jphysiol.2009.179325.

12 Boesen AP, Dideriksen K, Couppé C, et al. Effect of growth hormone on aging connective tissue in muscle and tendon: gene expression, morphology, and function following immobilization and rehabilitation. J Appl Physiol (1985). 2014;116(2):192-203. doi:10.1152/japplphysiol.01077.2013.

13 Haddad F, Adams GR. Inhibition of MAP/ERK kinase prevents IGF-I-induced hypertrophy in rat muscles. J Appl Physiol (1985). 2004;96(1):203-210. doi:10.1152/japplphysiol.00856.2003.

14 Stewart CE, Pell JM. Point:Counterpoint: IGF is/is not the major physiological regulator of muscle mass. Point: IGF is the major physiological regulator of muscle mass. J Appl Physiol (1985). 2010;108(6):1820-1832. doi:10.1152/japplphysiol.01246.2009.

15 Hameed M, Lange KH, Andersen JL, et al. The effect of recombinant human growth hormone and resistance training on IGF-I mRNA expression in the muscles of elderly men. J Physiol. 2004;555(Pt 1):231-240. doi:10.1113/jphysiol.2003.051722.

16 Velloso CP, Harridge SD. Insulin-like growth factor-I E peptides: implications for aging skeletal muscle. Scand J Med Sci Sports. 2010;20(1):20-27. doi:10.1111/j.1600-0838.2009.00997.x.

17 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: 6–12. doi:10.3806/ijktr.1.6.

18 Kadi F, Schjerling P, Andersen LL, et al. The effects of heavy resistance training and detraining on satellite cells in human skeletal muscles. J Physiol. 2004;558(Pt 3):1005-1012. doi:10.1113/jphysiol.2004.065904.

19 Kadi F, Thornell LE. Concomitant increases in myonuclear and satellite cell content in female trapezius muscle following strength training. Histochem Cell Biol. 2000;113(2):99-103. doi:10.1007/s004180050012.

20 Olsen S, Aagaard P, Kadi F, et al. Creatine supplementation augments the increase in satellite cell and myonuclei number in human skeletal muscle induced by strength training [published correction appears in J Physiol. 2006 Sep 15;575(Pt 3):971]. J Physiol. 2006;573(Pt 2):525-534. doi:10.1113/jphysiol.2006.107359.

21 Nielsen JL, Aagaard P, Bech RD, et al. Proliferation of myogenic stem cells in human skeletal muscle in response to low-load resistance training with blood flow restriction. J Physiol. 2012;590(17):4351-4361. doi:10.1113/jphysiol.2012.237008.

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23 Forbes D, Jackman M, Bishop A, Thomas M, Kambadur R, Sharma M. Myostatin auto-regulates its expression by feedback loop through Smad7 dependent mechanism. J Cell Physiol. 2006;206(1):264-272. doi:10.1002/jcp.20477.

24 Hill JJ, Qiu Y, Hewick RM, Wolfman NM. Regulation of myostatin in vivo by growth and differentiation factor-associated serum protein-1: a novel protein with protease inhibitor and follistatin domains. Mol Endocrinol. 2003;17(6):1144-1154. doi:10.1210/me.2002-0366.

25 Saremi A, Gharakhanloo R, Sharghi S, Gharaati MR, Larijani B, Omidfar K. Effects of oral creatine and resistance training on serum myostatin and GASP-1. Mol Cell Endocrinol. 2010;317(1-2):25-30. doi:10.1016/j.mce.2009.12.019.

26 Willoughby DS. Effects of heavy resistance training on myostatin mRNA and protein expression. Med Sci Sports Exerc. 2004;36(4):574-582. doi:10.1249/01.mss.0000121952.71533.ea.

27 Gualano B, Neves M Jr, Lima FR, et al. Resistance training with vascular occlusion in inclusion body myositis: a case study. Med Sci Sports Exerc. 2010;42(2):250-254. doi:10.1249/MSS.0b013e3181b18fb8.

28 Santos AR, Neves MT Jr, Gualano B, et al. Blood flow restricted resistance training attenuates myostatin gene expression in a patient with inclusion body myositis. Biol Sport. 2014;31(2):121-124. doi:10.5604/20831862.1097479.

29 Fielder PJ, Mortensen DL, Mallet P, Carlsson B, Baxter RC, Clark RG. Differential long-term effects of insulin-like growth factor-I (IGF-I) growth hormone (GH), and IGF-I plus GH on body growth and IGF binding proteins in hypophysectomized rats. Endocrinology. 1996;137(5):1913-1920. doi:10.1210/endo.137.5.8612531.

30 Sims NA, Clément-Lacroix P, Da Ponte F, et al. Bone homeostasis in growth hormone receptor-null mice is restored by IGF-I but independent of Stat5. J Clin Invest. 2000;106(9):1095-1103. doi:10.1172/JCI10753.

31 Brixen K, Nielsen HK, Mosekilde L, Flyvbjerg A. A short course of recombinant human growth hormone treatment stimulates osteoblasts and activates bone remodeling in normal human volunteers. Journal of Bone and Mineral Research. 1990;5(6):609–618. doi 10.1002/jbmr.5650050610.

32 Erdtsieck RJ, Pols HA, Valk NK, et al. Treatment of post-menopausal osteoporosis with a combination of growth hormone and pamidronate: a placebo controlled trial. Clin Endocrinol (Oxf). 1995;43(5):557-565. doi:10.1111/j.1365-2265.1995.tb02920.x.

33 Clemmesen B, Overgaard K, Riis B, Christiansen C. Human growth hormone and growth hormone releasing hormone: a double-masked, placebo-controlled study of their effects on bone metabolism in elderly women. Osteoporos Int. 1993;3(6):330-336. doi:10.1007/BF01637319.

34 Gillberg P, Mallmin H, Petrén-Mallmin M, Ljunghall S, Nilsson AG. Two years of treatment with recombinant human growth hormone increases bone mineral density in men with idiopathic osteoporosis. J Clin Endocrinol Metab. 2002;87(11):4900-4906. doi:10.1210/jc.2002-020231.

35 Van der Lely AJ, Lamberts SW, Jauch KW, et al. Use of human GH in elderly patients with accidental hip fracture. Eur J of Endocrinology. 2000;143(5):585–592.

36 Yeo AL, Levy D, Martin FC, et al. Frailty and the biochemical effects of recombinant human growth hormone in women after surgery for hip fracture. Growth Horm IGF Res. 2003;13(6):361-370. doi:10.1016/j.ghir.2003.08.001.

37 Krusenstjerna-Hafstrøm T, Rasmussen MH, Raschke M, Govender S, Madsen J, Christiansen JS. Biochemical markers of bone turnover in tibia fracture patients randomly assigned to growth hormone (GH) or placebo injections: Implications for detection of GH abuse. Growth Horm IGF Res. 2011;21(6):331-335. doi:10.1016/j.ghir.2011.08.003.

38 Weissberger AJ, Anastasiadis AD, Sturgess I, Martin FC, Smith MA, Sönksen PH. Recombinant human growth hormone treatment in elderly patients undergoing elective total hip replacement. Clin Endocrinol (Oxf). 2003;58(1):99-107. doi:10.1046/j.1365-2265.2003.01700.x.

39 Raschke M, Rasmussen MH, Govender S, Segal D, Suntum M, Christiansen JS. Effects of growth hormone in patients with tibial fracture: a randomised, double-blind, placebo-controlled clinical trial. Eur J Endocrinol. 2007;156(3):341-351. doi:10.1530/EJE-06-0598.

40 Schipani E, Maes C, Carmeliet G, Semenza GL. Regulation of osteogenesis-angiogenesis coupling by HIFs and VEGF. J Bone Miner Res. 2009;24(8):1347-1353. doi:10.1359/jbmr.090602.

41 Hunt TK, Aslam R, Hussain Z, Beckert S. Lactate, with oxygen, incites angiogenesis. Adv Exp Med Biol. 2008;614:73-80. doi:10.1007/978-0-387-74911-2_9.

42 Constant JS, Feng JJ, Zabel DD, et al. Lactate elicits vascular endothelial growth factor from macrophages: a possible alternative to hypoxia. Wound Repair Regen. 2000;8(5):353-360. doi:10.1111/j.1524-475x.2000.00353.x.

43 Takano H, Morita T, Iida H, et al. Hemodynamic and hormonal responses to a short-term low-intensity resistance exercise with the reduction of muscle blood flow. Eur J Appl Physiol. 2005;95(1):65-73. doi:10.1007/s00421-005-1389-1.

44 Manini TM, Yarrow JF, Buford TW, Clark BC, Conover CF, Borst SE. Growth hormone responses to acute resistance exercise with vascular restriction in young and old men. Growth Horm IGF Res. 2012;22(5):167-172. doi:10.1016/j.ghir.2012.05.002.

45 Kraemer WJ, Marchitelli L, Gordon SE, et al. Hormonal and growth factor responses to heavy resistance exercise protocols. J Appl Physiol (1985). 1990;69(4):1442-1450. doi:10.1152/jappl.1990.69.4.1442.

46 Kraemer WJ, Gordon SE, Fleck SJ, et al. Endogenous anabolic hormonal and growth factor responses to heavy resistance exercise in males and females. Int J Sports Med. 1991;12(2):228-235. doi:10.1055/s-2007-1024673.

47 Moritani T, Sherman WM, Shibata M, Matsumoto T, Shinohara M. Oxygen availability and motor unit activity in humans. Eur J Appl Physiol Occup Physiol. 1992;64(6):552-556. doi:10.1007/BF00843767.

48 Sundberg CJ. Exercise and training during graded leg ischaemia in healthy man with special reference to effects on skeletal muscle. Acta Physiol Scand Suppl. 1994;615:1-50.

49 Miller, KJ, Garland, SJ, Ivanova, T, Ohtsuki, T. Motor-unit behavior in humans during fatiguing arm movements. J. Neurophysiol. 1996;75(4): 1629–1636. Doi: 10.1152/jn.1996.75.4.1629.

50 Loenneke JP, Wilson JM, Marín PJ, Zourdos MC, Bemben MG. Low intensity blood flow restriction training: a meta-analysis. Eur J Appl Physiol. 2012;112(5):1849-1859. doi:10.1007/s00421-011-2167-x.

51 Odinsson A, Finsen V. Tourniquet use and its complications in Norway. The Journal of Bone and Joint surgery. British Volume. 2006 Aug;88(8):1090-1092. DOI: 10.1302/0301-620x.88b8.17668. PMID: 16877612

52 Kalla TP, Younger A, McEwen JA, Inkpen K. Survey of tourniquet use in podiatric surgery. J Foot Ankle Surg. 2003;42(2):68-76. doi:10.1016/s1067-2516(03)70004-0.

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