Moving on to our third and final researcher, Burd et al looked at bigger weights might not mean bigger muscles as well as the second study where they looked at low-load high volume resistance training stimulating muscle protein synthesis. The first study stated the following: \u201cIt is often recommended that heavier training intensities (\u223c70%-80% of maximal strength) be lifted to maximize muscle growth. However, we have reported that intensities as low as 30% of maximum strength, when lifted to volitional fatigue, are equally effective at stimulating muscle protein synthesis rates during resistance exercise recovery. This paper discusses the idea that high-intensity contractions are not the exclusive driver of resistance exercise-induced changes in muscle protein synthesis rates\u201d (4.) Finishing off our literature was the second study that had fifteen men performed 4 sets of unilateral leg extension exercise at different exercise loads and\/or volumes: 90% of repetition maximum (1RM) until volitional failure (90FAIL), 30% 1RM work-matched to 90%FAIL, or 30% 1RM performed until volitional failure (30FAIL). Infusion of phenylalanine with biopsies was used to measure rates of mixed, myofibrillar, and sarcoplasmic protein synthesis at rest, and 4 h and 24 h after exercise. Exercise at 30WM induced a significant increase above rest in MIX (121%) and MYO (87%) protein synthesis at 4 h post-exercise and but at 24 h in the MIX only. The increase in the rate of protein synthesis in MIX and MYO at 4 h post-exercise with 90FAIL and 30FAIL was greater than 30WM, with no difference between these conditions; however, MYO remained elevated above rest at 24 h only in 30FAIL. There was a significant increase in Akt at 24h in all conditions and mTOR phosphorylation at 4 h post-exercise. Phosporylation of Erk1\/2, p70S6K, and 4E-BP1 increased significantly only in the 30FAIL condition at 4 h post-exercise, whereas, 4E-BP1 phosphorylation was greater 24 h after exercise than at rest in both 90FAIL and 30FAIL conditions. Pax7 mRNA expression increased at 24 h post-exercise regardless of condition. The mRNA expression of MyoD and myogenin were consistently elevated in the 30FAIL condition. These results suggest that low-load high volume resistance exercise is more effective in inducing acute muscle anabolism than high-load low volume or work matched resistance exercise modes (5.)<\/p>\n
Based on this literature we can now equate this to anecdotal evidence as well as some common sense. We know from the works of Brad Schoenfeld that the three main mechanisms for muscular hypertrophy are muscular damage, mechanical tension, and metabolic stress (6.) Beyond those three I have discussed cellular swelling and increased innervation\/tension as being 2 other mechanisms of hypertrophy that are often overlooked (7, 8.) With these 5 mechanisms of hypertrophy in mind, it needs to be understood they can be achieved through a variety of methods. Those methods include low load training, high load training, low volume\/high intensity training, high volume\/lower intensity training, high frequency training, blood flow restriction training, strength specific training, hypertrophy specific training, etc. The list literally goes on and on on HOW to activate those 5 mechanisms. So bringing the common sense into the equation, if we are doing the following, doesn’t it make sense that low load training is merely a tool we can utilize? If we are:<\/p>\n
\u2026then there is no way we cannot increase hypertrophy. Although this seems to make common sense now that we have broken down the literature and correlated the key points, I can understand why people often misunderstand studies stating that you can grow from low load training\u2026because it is simply 1 of 5 tools that you MUST be utilizing if your goal is to maximally stimulate skeletal muscle hypertrophy. This doesnt mean it needs to all be done within one session. This means you should be utilizing these mechanisms and methods throughout a couple days or even a week\u2019s worth of training (depending on your frequency.) The take away message is utilize every mechanism of hypertrophy at your disposal in a smart and methodical manner while always prioritizing the basic needs to be met first and foremost.<\/p>\n
Alex Kikel<\/p>\n
MS, PES, CPT, Speed and Explosion Specialist Level II<\/p>\n
Owner of \u201cThePrepCoach.com<\/a>\u201d<\/p>\n Reference List<\/p>\n 1. Mitchell CJ, Churchward-Venne TA, West DD, Burd NA, Breen L, Baker SK and Phillips SM. Resistance exercise load does not determine training-mediated hypertrophic gains in young men. J Appl Physiol 113: 71-77, 2012. (https:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC3404827\/<\/a>)<\/p>\n 2. Schoenfeld BJ, Peterson MD, Ogborn D, Contreras B and Sonmez GT. Effects of Low- vs. High-Load Resistance Training on Muscle Strength and Hypertrophy in Well-Trained Men. J Strength Cond Res 29: 2954-2963, 2015. (https:\/\/www.ncbi.nlm.nih.gov\/pubmed\/25853914<\/a>)<\/p>\n 3. Schoenfeld BJ, Wilson JM, Lowery RP and Krieger JW. Muscular adaptations in low- versus high-load resistance training: A meta-analysis. Eur J Sport Sci 1-10, 2014. (https:\/\/www.ncbi.nlm.nih.gov\/pubmed\/25530577<\/a>)<\/p>\n 4. Burd NA, Mitchell CJ, Churchward-Venne TA and Phillips SM. Bigger weights may not beget bigger muscles: evidence from acute muscle protein synthetic responses after resistance exercise. Appl Physiol Nutr Metab 37: 551-554, 2012. (https:\/\/www.ncbi.nlm.nih.gov\/pubmed\/22533517<\/a>)<\/p>\n 5. Burd NA, West DW, Staples AW, Atherton PJ, Baker JM, Moore DR, Holwerda AM, Parise G, Rennie MJ, Baker SK and Phillips SM. Low-Load High Volume Resistance Exercise Stimulates Muscle Protein Synthesis More Than High-Load Low Volume Resistance Exercise in Young Men. PLoS ONE 5: e12033, 2010. (http:\/\/journals.plos.org\/plosone\/article?id=10.1371\/journal.pone.0012033<\/a>)<\/p>\n 6. Brad J. Schoenfeld . The mechanisms of muscle hypertrophy and their application to resistance training. J Strength Cond Res. 2010. (https:\/\/www.ncbi.nlm.nih.gov\/pubmed\/20847704<\/a>)<\/p>\n