A Review on the Mechanisms of Blood-Flow Restriction Resistance Training-Induced Muscle Hypertrophy

Abstract

It has traditionally been believed that resistance training can only induce muscle growth when the exercise intensity is greater than 65% of the 1-repetition maximum (RM). However, more recently, the use of low-intensity resistance exercise with blood-flow restriction (BFR) has challenged this theory and consistently shown that hypertrophic adaptations can be induced with much lower exercise intensities (<50% 1-RM). Despite the potent hypertrophic effects of BFR resistance training being demonstrated by numerous studies, the underlying mechanisms responsible for such effects are not well defined. Metabolic stress has been suggested to be a primary factor responsible, and this is theorised to activate numerous other mechanisms, all of which are thought to induce muscle growth via autocrine and/or paracrine actions. However, it is noteworthy that some of these mechanisms do not appear to be mediated to any great extent by metabolic stress but rather by mechanical tension (another primary factor of muscle hypertrophy). Given that the level of mechanical tension is typically low with BFR resistance exercise (<50% 1-RM), one may question the magnitude of involvement of these mechanisms aligned to the adaptations reported with BFR resistance training. However, despite the low level of mechanical tension, it is plausible that the effects induced by the primary factors (mechanical tension and metabolic stress) are, in fact, additive, which ultimately contributes to the adaptations seen with BFR resistance training. Exercise-induced mechanical tension and metabolic stress are theorised to signal a number of mechanisms for the induction of muscle growth, including increased fast-twitch fibre recruitment, mechanotransduction, muscle damage, systemic and localised hormone production, cell swelling, and the production of reactive oxygen species and its variants, including nitric oxide and heat shock proteins. However, the relative extent to which these specific mechanisms are induced by the primary factors with BFR resistance exercise, as well as their magnitude of involvement in BFR resistance training-induced muscle hypertrophy, requires further exploration.

Walking With Blood Flow Restriction Improves the Dynamic Strength of Women With Osteoporosis

“…Increased GH release, recruitment of type II fibers, increased mTOR levels, high nitric oxide synthesis, increased stimulation of growth factors, reduced myostatin levels and metabolite accumulation and creation of a metabolic environment similar to that of RT may explain the significant changes in MDS promoted by AT with BFR. 14,17,18 There is the need to highlight that, when comparing baseline measurements, the strength HI and CG groups showed significant smaller MDS levels than LIBFR and ABFR with elevated values of percentage variations (>40%). Lower strength levels sometimes are related with worst functional capacity and may indicate that those subjects were less trained than the other or, at least, practice less physical activities on their daily life 5,6 .…”

“…14,17,18 Few studies use training combined with BFR for rehabilitation, despite the evidence that it may be effective in the recovery of individuals with osteoporosis, 14,19-22 and were not found any studies that investigated both types of training (aerobic and resistance) combined with BFR in individuals diagnosed with osteoporosis.…”

The Benefits of Physical Activity on Climacteric Women

“…However, studies that investigated the BFR mechanisms airm that the explanation lies on a bigger metabolite concentration, stimulation of anaerobic growth factors, greater fast twitch ibers recruitment, increase on GH secretion, VGF1, fall on miostatine and rise on mTOR levels, greater nitric oxide synthesis, along with other factors that were not yet discovered [44][45][46].…”

Acute effect of aerobic exercise with blood flow restriction on blood pressure and heart rate in healthy young subjects

“…As pesquisas mostram sua eficácia sobre variáveis neuromusculares, como os ganhos de força e hipertrofia muscular (Pearson & Hussain, 2015), hormonais (Inagaki, Madarame, Neya, & Ishii, 2011), metabólicas (Burgomaster et al, 2003;Fujita et al, 2007), hemodinâmicas (Araújo et al, 2014;Brandner, Kidgell, & Warmington, 2014;Neto et al, 2015;Neto et al, 2016;Okuno, Pedro, Leicht, Ramos, & Nakamura, 2014;Rossow et al, 2011;Vieira, Chiappa, Umpierre, Stein, & Ribeiro, 2013) e complacência arterial (Iida et al, 2011;Iida et al, 2005).…”