Getting the same results with half the effort, is it possible? Experts of blood flow restriction training say so!
By Pierre-Luc Dubé
What is vascular occlusion training?
Vascular occlusion training is a method using proximal blood restriction to the upper and/or lower limbs to create localized ischemia in the muscle regions in combination with resistance training.
This method was invented by Dr Yoshiaki Sato in 1966 and developed over 7 years to arrive at the data and methods that are used today in the world of training.
How to prescribe it?
Theoretically, the pressure used to apply vascular occlusion should be high enough to prevent venous return, while keeping the blood supply to the muscle active. The optimal pressure needed to beneficially induce maximum adaptation is still unknown by science. Despite everything, studies suggest that a moderate pressure corresponding to approximately 50% of the total vascular occlusion pressure, i.e. the pressure completely blocking blood flow at rest, would maximize the anabolic response of skeletal muscle by avoiding the potential negative effects linked to high blood pressure.
This pressure is found using a blood pressure monitor in the supine position after a period of calm. Values are then measured for the lower and upper limbs. The cuff should be placed a little above the elbow for the upper limb and at the level of the inguinal fold for the lower limb.
Nevertheless, it is very difficult to precisely select the pressure of the occlusion due to the high interindividual variability with respect to vascular compliance and the response to the increase in pressure. It is important to note that the width of the cuff influences the degree of occlusion. A larger cuff would increase blood restriction.
Effects of resistance training by vascular occlusion
Vascular occlusion training would maximize gains in strength and hypertrophy. Indeed, resistance training, even at low intensity with the use of occlusion, would increase muscle mass and strength. The study by Yasuda et al. (2011) compared the effect of vascular occlusion compared to training of different intensities. Three groups, one in high intensity resistance (75% of 1RM), one in low intensity (30% of 1RM) and a combination of low intensity training in vascular occlusion with high intensity training, were subjected to a training protocol of 3 days a week for 6 weeks. The occlusion group had similar gains to the high intensity group even with lower intensity training volume. Both of these groups saw greater improvements in strength, compared to groups using low intensity resistance training. Laurentino et al. (2012) arrived at similar results with the use of occlusion.
In summary, hypoxia training simulates training with a high load, using loads of 20% to 50% of the 1RM. This practice induces changes in the expression of genes linked to growth and muscular adaptations to exercise.
Does HIF-1 α explain adaptations to skeletal muscle?
Factor HIF-1 (hypoxia-induced factor) is a protein complex that stimulates and promotes the expression of specific genes in the presence of a low oxygen concentration. It is composed of 2 subunits, i.e. the α and β subunits. HIF-1α consists of 826 amino acids and represents 15 exons on chromosome 14q21-q24 of the human genotype. There are 3 types of HIF-α; HIF-1α, HIF-2α and HIF-3α. The factor is stabilized by the presence of reactive oxygen species, by nitric oxide and by certain products and wastes from the oxidative system.
Roles and influences of HIF-1α
Although the adaptations sought in the majority of people are gaining muscle mass and increasing strength, HIF-1α is implicated in several physiological processes such as growth of the vascular system, production of red blood cells, cell growth and aging, inflammatory reactions and energetic metabolism. So skeletal muscle is directly influenced by this protein.
In fact, HIF-1α plays an essential role in the regulation of anaerobic glycolysis. Mason et al. (2004) demonstrated that the absence of HIF-1α leads to a reduction in the concentration of lactate in hypoxic situations, for the same use of cellular adenosine triphosphate (ATP). This implies that the contribution of the aerobic system is increased, given the absence of lactate from the accumulation of pyruvate, the end product of glycolysis. This phenomenon could be explained by an increase in the activity of enzymes found in the mitochondria and by a greater contribution of fatty acids. These adaptations would be used to compensate for the drop in energy intake (ATP) normally coming from glycolysis. In this sense, physical activity mimics a situation of local hypoxia, which reduces the level of oxygen and causes the accumulation of cellular HIF-1α. With the reduced oxygen level, HIFs would promote the enzymatic activity found in anaerobic lactic metabolism. In addition, factor HIF-1α would stimulate the production of erythropoietin (EPO) and increase the concentration of red blood cells.
HIF-1α is said to be responsible for phagocytic invasion in order to remove cellular debris following trauma, in addition to accelerating the growth and regeneration of skeletal muscle. For example, a tissue break (physical activity, direct hit, etc.) would induce stress on the muscle promoting the accumulation of HIF-1α in the cell. Thus, the expression of specific genes responding to hypoxia would result in a higher level of macrophages at the site of the lesion. In addition, cell proliferation as well as a greater quantity of growth factors and proteins responsible for cell replication are noticed in the presence of trauma.
An increase in vascularization has been observed following an infarction with selective inhibition of PHD, the protein responsible for keeping HIFs inactive in normal situations. Bao et al. (2010) also note an increase in circulating hemoglobin (the cell responsible for transporting blood oxygen) and EPO. This same activation is observed in the skeletal muscles and the kidneys. De Theije et al. (2015) have also shown an increase in the number of capillaries for type I fibers of the soleus muscle in mice with hypoxia.
Pressing the cuff too much could cause venous thrombosis and cause chronic occlusion, even after the normal infusion is returned. This occlusion could cause necrosis of muscle cells, vessels and the nervous system. In addition, too high a pressure could reduce the effectiveness of training by decreasing the volume and the work capacity of the individual. Conversely, too low a pressure would not favor the changes and adaptations sought by the occlusion method.
Occlusion training is still a little-known science in Canada. However, it is beginning to resonate more and more in the world of bodybuilding. Indeed, this method really seems to have virtues allowing improvements on the muscular level. However, it should be used with caution and moderation given the risks associated with its misuse.
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