The effect of eccentric exercise with blood flow restriction on neuromuscular activation, microvascular oxygenation, and the repeated bout effect

Lauver, Jakob D.; Cayot, Trent E.; Rotarius, Timothy R.; Scheuermann, Barry W.

doi:10.1007/s00421-017-3589-x

Cited by 37 publications

(40 citation statements)

References 70 publications

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“…The results regarding the differences in muscle excitation between LL and LL-BFR training demonstrated a significant increase in surface muscle EMG in favor of LL-BFR. The longitudinal changes which are reviewed in this work, resemble findings from cross-sectional studies looking at the acute effects of training with partial vascular occlusion (Kinugasa et al, 2006;Lauver et al, 2017Lauver et al, , 2019Husmann et al, 2018;Ilett et al, 2019;Kjeldsen et al, 2019). In a frequently cited study by Moritani et al (1992) participants were instructed to complete a 4-min bout of repeated intermittent isometric hand grip contractions (20% MVC) with one group having the blood flow restricted during the second minute (cuff pressure 200 mmHg).…”

Section: Muscle Excitationmentioning

confidence: 85%

“…Although a small number of previous investigations have already examined the magnitude of neuromuscular responses following LL-BFR training, these findings are conflicting with some studies reporting no differences between HL and LL-BFR (Sousa et al, 2017;Cook et al, 2018) and another study showing higher neural activation when training with HL only (Kubo et al, 2006). Similar inconsistent findings have been observed when comparing LL training with LL-BFR training (Thiebaud et al, 2014;Lauver et al, 2017;Oranchuk et al, 2019). This second comparison (LL vs. LL-BFR) is not less important, considering the common implementation of low-load regimens in clinical settings especially during the early phases of rehabilitation (Bousquet et al, 2018).…”

Section: Introductionmentioning

confidence: 89%

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A Systematic Review and Meta-Analysis on Neural Adaptations Following Blood Flow Restriction Training: What We Know and What We Don't Know

Centner

Lauber

2020

Front. Physiol.

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Objective: To summarize the existing evidence on the long-term effects of low-load (LL) blood flow restricted (BFR) exercise on neural markers including both central and peripheral adaptations. Methods: A systematic review and meta-analysis was conducted according to the PRISMA guidelines. The literature search was performed independently by two reviewers in the following electronic databases: PubMed, Web of Science, Scopus and CENTRAL. The systematic review included long-term trials investigating the effects of LL-BFR training in healthy subjects and compared theses effects to either LL or high-load (HL) training without blood flow restriction. Results: From a total of N = 4499 studies, N = 10 studies were included in the qualitative synthesis and N = 4 studies in a meta-analysis. The findings indicated that LL-BFR resulted in enhanced levels of muscle excitation compared to LL training with pooled effect sizes of 0.87 (95% CI: 0.38-1.36). Compared to HL training, muscle excitation following LL-BFR was reported as either similar or slightly lower. Differences between central activation between LL-BFR and LL or HL are less clear. Conclusion: The summarized effects in this systematic review and meta-analysis highlight that BFR training facilitates neural adaptations following LL training, although differences to conventional HL training are less evident. Future research is urgently needed to identify neural alterations following long-term blood flow restricted exercise.

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Section: Muscle Excitationmentioning

confidence: 85%

Section: Introductionmentioning

confidence: 89%

A Systematic Review and Meta-Analysis on Neural Adaptations Following Blood Flow Restriction Training: What We Know and What We Don't Know

Centner

Lauber

2020

Front. Physiol.

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“…This is likely due to the hypoxic muscular environment generated during BFR and accelerated onset of fatigue [117]. Several studies have shown greater internal muscle activation with BFR exercise [119,120] relative to external load [121,122], which is greater than matched workload exercise without BFR [123,124]. Considering the importance of high threshold motor unit recruitment to the magnitude of EIH, early preferential recruitment of these motor units during low intensity BFR exercise may contribute to a hypoalgesia effect.…”

Section: Bfr Exercise and Hypoalgesiamentioning

confidence: 99%

Low intensity blood flow restriction exercise: Rationale for a hypoalgesia effect

Hughes¹,

Patterson²

2019

Medical Hypotheses

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Exercise-induced hypoalgesia is characterised by a reduction in pain sensitivity following exercise. Recently, low intensity exercise performed with blood flow restriction has been shown to induce hypoalgesia. The purpose of this manuscript is to discuss the mechanisms of exercise-induced hypoalgesia and provide rationale as to why low intensity exercise performed with blood flow restriction may induce hypoalgesia. Research into exercise-induced hypoalgesia has identified several potential mechanisms, including opioid and endocannabinoid-mediated pain inhibition, condition pain modulation, recruitment of high threshold motor units, exercise-induced metabolite production and an interaction between cardiovascular and pain regulatory systems. We hypothesise that several mechanisms consistent with prolonged high intensity exercise may drive the hypoalgesia effect observed with blood flow restriction exercise. These are likely triggered by the high level of intramuscular stress in the exercising muscle generated by blood flow restriction including hypoxia, accumulation of metabolites, accelerated fatigue onset and ischemic pain. Therefore, blood flow restriction exercise may induce hypoalgesia through similar mechanisms to prolonged higher intensity exercise, but at lower intensities, by changing local tissue physiology, highlighting the importance of the blood flow restriction stimulus. The potential to use blood flow restriction exercise as a pain modulation tool has important implications following acute injury and surgery, and for several load compromised populations with chronic pain.

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“…Fatiguing low-load and/or high-volume resistance exercise has been shown to produce greater ATP turnover compared to traditional high-load resistance exercise (Gorostiaga et al, 2012 ; Ahtiainen et al, 2015 ). Furthermore, fatiguing low-load resistance exercise conducted with slow and tonic contraction phase or application of external restriction of blood flow to the exercising muscle, has been shown to impose a more pronounced decrease in tissue oxygenation compared to traditionally performed high- and low-load resistance exercise (Tanimoto and Ishii, 2006 ; Karabulut et al, 2014 ; Lauver et al, 2017 ). It therefore seems plausible that fatiguing low-load resistance exercise entail greater metabolic stress, to potentially accentuate mitochondrial biogenesis.…”

Section: Considerations On the Utilization Of Low-load Resistance Exementioning

confidence: 99%

Impact of Resistance Training on Skeletal Muscle Mitochondrial Biogenesis, Content, and Function

2017

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Skeletal muscle metabolic and contractile properties are reliant on muscle mitochondrial and myofibrillar protein turnover. The turnover of these specific protein pools is compromised during disease, aging, and inactivity. Oppositely, exercise can accentuate muscle protein turnover, thereby counteracting decay in muscle function. According to a traditional consensus, endurance exercise is required to drive mitochondrial adaptations, while resistance exercise is required to drive myofibrillar adaptations. However, concurrent practice of traditional endurance exercise and resistance exercise regimens to achieve both types of muscle adaptations is time-consuming, motivationally demanding, and contended to entail practice at intensity levels, that may not comply with clinical settings. It is therefore of principle interest to identify effective, yet feasible, exercise strategies that may positively affect both mitochondrial and myofibrillar protein turnover. Recently, reports indicate that traditional high-load resistance exercise can stimulate muscle mitochondrial biogenesis and mitochondrial respiratory function. Moreover, fatiguing low-load resistance exercise has been shown capable of promoting muscle hypertrophy and expectedly entails greater metabolic stress to potentially enhance mitochondrial adaptations. Consequently, fatiguing low-load resistance exercise regimens may possess the ability to stimulate muscle mitochondrial adaptations without compromising muscle myofibrillar accretion. However, the exact ability of resistance exercise to drive mitochondrial adaptations is debatable, not least due to some methodological challenges. The current review therefore aims to address the evidence on the effects of resistance exercise on skeletal muscle mitochondrial biogenesis, content and function. In prolongation, a perspective is taken on the specific potential of low-load resistance exercise on promoting mitochondrial adaptations.

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The effect of eccentric exercise with blood flow restriction on neuromuscular activation, microvascular oxygenation, and the repeated bout effect

Abstract: This study suggests that the neuromuscular and deoxygenation (i.e., metabolic stress) responses were considerably different between LI and LI-BFR groups; however, these differences did not lead to improvements in the RBE inferred by performing LI and LI-BFR.

Cited by 37 publications

References 70 publications

A Systematic Review and Meta-Analysis on Neural Adaptations Following Blood Flow Restriction Training: What We Know and What We Don't Know

A Systematic Review and Meta-Analysis on Neural Adaptations Following Blood Flow Restriction Training: What We Know and What We Don't Know

Low intensity blood flow restriction exercise: Rationale for a hypoalgesia effect

Impact of Resistance Training on Skeletal Muscle Mitochondrial Biogenesis, Content, and Function

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