Training

Occlusion Training

Does it belong in the gym or should it be left in the clinic?

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Occlusion Training

About and he’ll tell you, “Go heavy or go home, bro.” I’ll admit I am one of the loudest preachers of the load-is-king approach to lifting. Hypertrophy-specific training (HST) is centered on the principle of progressive load. And why not? We’ve got years of research to back it up. The idea that heavy lifting builds real mass was first suggested by A. L. Goldberg more than 35 years ago. Working with rats, he observed rapid and predictable growth of the soleus muscle after a procedure called “synergistic ablation.” Synergistic ablation should be attempted only by the most committed lifters. (Totally kidding. Do not try this at home). Synergistic ablation involves surgically removing the gastrocnemius and allowing the soleus to remain intact, taking the brunt of the load that was previously shared by both muscles. Goldberg and his group observed that “increased tension development (either passive or active) is the critical event in initiating compensatory growth.” As I said at the beginning, load-is-king... or is it? 

WHAT IS IT?

Since Goldberg’s pioneering work in load-induced muscle hypertrophy, it has become widely accepted that metabolic factors also contribute to the hypertrophic effects of resistance exercise. Fatigue and metabolite accumulation have been shown to be important factors in the resistance exercise stimulus leading to increases in strength and muscle mass, respectively. These findings inspired some out-of-the-box thinking and exploration into methods involving tourniquet cuffs to partially or completely restrict muscle blood flow during training with very low resistance. The method was called “muscle occlusion training” and, sure enough, it led to increases in muscle strength and size. In these and in several subsequent studies, low-to moderate-intensity (20–50% of the one-rep max, or 1RM) resistance training with vascular occlusion has been shown to lead to gains in muscle strength and size comparable to those seen after conventional heavy resistance training and in a very short period of time. 

HOW DOES IT WORK?

The obvious question is, How can weight loads equaling 20% (without occlusion) of your 1RM lead to any real muscle growth? It’s a good question and one that I’m not sure has been answered adequately. One theory is that it’s just a matter of increasing motor unit recruitment. As you might know, motor unit recruitment can be estimated based on measures of electromyographic activity, or EMG. Yudai Takarada and his group showed that the EMG of the biceps using only 40% of a subject’s 1RM combined with partial occlusion of muscle blood flow was almost equal to that seen when using 80% of the subjects’ 1RM. I doubt that using a lighter weight with occlusion is the primary cause of the growth seen in these studies, however. Lifting a light weight as many times as you can without occlusion doesn’t cause the same level of growth. 

Another proposed mechanism that I reject outright is the hormonal response theory. Certain academics have gone on for years saying that the minuscule increases in anabolic hormones such as growth hormone (GH) and testosterone during resistance exercise are the cause of the muscle growth. Anyone who has any familiarity with the mechano-sensitive pathways involved in load-induced muscle growth could clearly see that tiny spikes in GH would have no discernible impact on localized growth. Later research has shown that this is precisely the case and other factors should be focused on to figure out just how lifting causes muscle to grow. 

The most reasonable explanation for the growth seen with occlusion training is elevated intracellular signaling molecules, cross activation of mechano-sensitive pathways, and suppression of anti-anabolic genes such as myostatin. Explaining how all of these signals and pathways work together to build muscle will have to wait for another day.

IS THIS PRACTICAL?

Although occlusion training can effectively stimulate growth in some situations, it is not very practical to use day to day. For one, cuffs appropriate for occlusion training are very expensive. In Japan, it is called Kaatsu training, and you can go to gyms where trainers will put cuffs on you and you perform exercises with light weights. Kaatsu cuffs are very expensive and difficult to find. I have heard of others trying to use belts and lifting straps. The problem here is that you have no idea how much pressure you are putting on the limb. In a research setting, pressure is held constant at 100–200 mmHg by a computer hooked up to the cuff. Too much pressure can cause damage to the underlying tissues as well as inhibit growth in those fibers running under the cuff. And you can hurt yourself with occlusion training. There have been reports of occlusion training inducing rhabdomyolysis (severe muscle damage with elevated creatine kinase levels) requiring nearly a month for full recovery. 

A fellow lifter and expert in the field of hypertrophy and occlusion training summed it up this way (see M. Wernbom, J. Augustsson, and T. Raastad), “...it seems reasonable to suggest that while the effects of blood flow–restricted training at low loads and traditional heavy-resistance training on muscle volume are similar, the effects of low-load ischemic training on tendons, and possibly also on neural adaptations, are less than with conventional strength training.” These sentiments are borne out in recent research showing inferior results compared with straightforward strength training. So for now, you are probably better off just getting your train- ing routine optimized and your diet and supplements in order, than trying to strangle your legs and hoping for the best.

 FLEX 

REFERENCES

[1] T. Abe, International Journal of Kaatsu Training Research, 2005: 1:6–12, 2005. [2] K.A. Burgomaster, Medicine & Science in Sports & Exercise, 35(7):1203–08, 2003; [3] S. Fujita, Journal of Applied Physiology, 103(3):903–10, 2007; [4] D.J. Glass, International Journal of Biochemistry & Cell Biology, 37(10):1974–84, 2005; [5] A.L. Goldberg, Medicine & Science in Sports & Exercise, 7(3):185–98, 1975; [6] E. Iversen and V. Røstad, Clinical Journal of Sports Medicine, 20(3):218–9, 2010; [7] K. Kubo et al., Journal of Ap- plied Biomechanics, 22(2):112–19, 2006; [8] G.C. Laurentino, Medicine & Science in Sports & Exercise, Sept. 3, 2011; [9] M.J. Rennie, British Journal of Sports Medicine, 37(2):100–105, 2003; [10] M.J. Rennie, Annual Review of Physiology, 66:799–828, 2004; [11] J. Schott, European Journal of Applied Physiology and Occupa- tional Physiology, 71(4):337–41, 1995; [12] M. Shinohara, European Journal of Applied Physiology and Occupational Physiology, 77(1- 2):189–91,1998; [13] Y. Takarada, Journal of Applied Physiology, 88(6):2097–2106, 2000; [14] J.G. Tidball, Journal of Applied Physiology, 98(5):1900–1908, 2005; [15] D.W. West et al., Journal of Physiology, 587(Pt 21):5239–47, 2009; [16] D.W. West, Journal of Applied Physiology, 108(1):60–7, 2010; [17] M. Wernbom, Scandinavian Journal of Medicine & Science in Sports, 18(4):401–16, 2008; [18] T. Yasuda, European Journal of Applied Physiology, 111(10):2525– 33, 2011. 

 

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