Few studies have directly compared the acute neuromuscular and perceptual responses to Blood flow restriction training (BFRT) at 60%, 70%, and 80% of arterial occlusion pressure (AOP) in healthy adults. This gap limits our understanding of how different AOP levels modulate training responses and tolerability. BFRT is a brief, low-intensity resistance training method that employs specialized compression devices (inflatable cuffs) applied to proximal limbs to partially occlude blood flow. This technique induces a hypoxic environment that enhances metabolic stress within targeted muscles, thereby promoting hypertrophy (Jessee et al., 2018; Pignanelli et al., 2021). Known as “KAATSU” in Japan, BFRT has gained traction across athletic performance enhancement and clinical rehabilitation (Bond et al., 2019; Hackney et al., 2018; Geng et al., 2021). Research indicates that while utilizing substantially lower intensities (20%–40% 1RM) than traditional resistance training, BFRT achieves comparable muscle hypertrophy with reduced muscle damage (Loenneke et al., 2012). This efficacy stems from high metabolic stress under appropriate blood flow restriction (Pearson and Hussain, 2015; Yuan et al., 2023), making pressure level selection a critical determinant of outcomes alongside exercise type and intensity (Mouser et al., 2017).

Theoretically, cuff pressure during BFRT must balance venous occlusion without arterial compromise (Loenneke et al., 2014). Therefore, to achieve this balance, pressure should be individualized based on cuff placement, limb circumference, subcutaneous fat thickness, and vascular health (Spranger et al., 2015). Excessively high pressures risk discomfort, pain, and vascular complications (Nascimento et al., 2022; Tabata et al., 2016), while insufficient pressures limit metabolic stimulus (Mouser et al., 2017).

Critically, individualized pressure settings are essential for BFRT efficacy and safety, as factors such as limb circumference, cuff width, and body position significantly influence the absolute pressure required to achieve consistent vascular occlusion. For example, larger limbs or narrower cuffs necessitate higher pressures to attain equivalent occlusion levels, meaning that arbitrary fixed pressures (e.g., a fixed absolute value 220 mmHg for all participants) may cause under-occlusion in individuals with larger limbs or over-occlusion in those with smaller limbs (Cook et al., 2014; Segal et al., 2015; Yasuda et al., 2014). This methodological limitation compromises both safety (e.g., vascular injury risk) and efficacy (inconsistent metabolic stimuli) (Patterson et al., 2019). Although some studies have attempted to use percentages of systolic blood pressure to set BFRT occlusion pressure (Abe et al., 2010; Hunt et al., 2016; Yasuda et al., 2006), it is an unreliable predictor of the occlusion pressure required in BFRT due to poor correlation with anthropometric determinants like limb circumference and subcutaneous fat thickness (Hunt et al., 2016; McEwen et al., 2019; de Queiros et al., 2024). Consequently, current guidelines advocate individualized pressures based on arterial occlusion pressure (AOP) to standardize the degree of blood flow restriction across diverse populations (Jessee et al., 2016; Patterson et al., 2019). AOP is a key factor in BFRT prescription, defined as the minimum cuff pressure required to completely occlude arterial blood flow to the limb. Determining each person’s AOP allows clinicians to set cuff inflation as a percentage of this value, ensuring a comparable degree of blood flow restriction across individuals. While AOP standardization improves reliability (Hughes et al., 2017; Masri et al., 2016), optimal percentages remain debated. Recent evidence highlights this balance: occlusion pressures below 50% AOP or near full occlusion (≥80% AOP) tend to produce suboptimal strength improvements, whereas mid-range pressures (50%–80% AOP) are more effective (Das and Paton, 2022; Roehl et al., 2023). These findings underscore the need to identify an optimal occlusion pressure that balances efficacy and tolerability in BFRT.

A recent review found that over 86% of studies of BFRT included no justification of the AOP chosen in their methodology (Clarkson et al., 2020). Given the centrality of AOP to the BFR stimulus, it is important to clarify how varying relative occlusion levels acutely affect performance and perceptual outcomes. To date, few studies have directly compared BFRT at different percentages of AOP in healthy adults. Therefore, this study employed Doppler ultrasound to directly measure AOP and investigated the acute effects of low-load resistance exercise performed with BFRT at various percentages of individually measured AOP in healthy young men. By examining neuromuscular and perceptual responses at each pressure level, this work aims to inform evidence-based guidelines for selecting BFR pressures that maximize training benefits while minimizing adverse responses. The null hypothesis (H₀) of this study is that there are no significant differences in muscle activation (%MVC), blood lactate concentration, or ratings of perceived exertion (RPE) across BFRT conditions set at 60%, 70%, and 80% AOP. The alternative hypothesis (H₁) is that BFRT at 70% and 80% AOP will elicit significantly greater muscle activation and blood lactate accumulation, along with higher RPE scores, compared to 60% AOP and the control condition.

Our findings clarify how acute physiological responses to low-load resistance exercise depend on the level of arterial occlusion. Both muscle activation (%MVC) and blood lactate were markedly elevated at 70% and 80% AOP compared to 60% AOP, whereas no significant differences emerged between 70% and 80%. In contrast, RPE was significantly higher at 80% than at 70% AOP, and several participants even requested cuff deflation at 80% due to discomfort (despite no formal pain scale being used). In short, pressures ≥70% AOP produced a strong physiological stimulus (higher muscle activation and lactate), but increasing pressure from 70% to 80% yielded no further increase in these markers while substantially increasing perceived effort.

In this study, the %MVC of lower limb muscles significantly increased through the BFRT protocol, which is consistent with previous findings (Fahs et al., 2015; Fatela et al., 2016; Loenneke et al., 2015a). This finding contributes to the existing body of knowledge by reinforcing the effectiveness of BFRT in enhancing muscle activation, which is crucial for muscle strength gains, and highlights the importance of individualized pressure settings to optimize training outcomes. From a metabolic perspective, BFRT induces a hypoxic environment within muscle tissue, leading to increased lactate accumulation and a concomitant decrease in pH levels (Kim et al., 2018; Pearson and Hussain, 2015). This shift toward anaerobic metabolism appears to be a central mechanism underlying the effects of BFRT. Hypoxia and decreased pH levels influence ATP rephosphorylation, stimulate the generation of reactive oxygen species (ROS) under hypoxic conditions, and alter cellular energy metabolism (Ferraro et al., 2014). As a result, hypoxia substantially impacts glycolysis and force production within muscle tissue (Horscroft and Murray, 2014). Furthermore, changes in myosin ATPase activity influence muscle recruitment patterns, resulting in varying degrees of muscle activation (Mijailovich et al., 2017). Notably, blood flow restriction affects capillary architecture and oxygen utilization, promoting muscle fiber adaptations and modulating motor neuron recruitment (Shimizu et al., 2016).

The enhanced muscle activation during BFRT can be attributed to metabolic “overload” within the muscle. During exercise, motor units are typically recruited according to the “size principle,” where smaller motor units are activated first, followed by larger ones. However, under conditions of restricted blood flow, the depletion of phosphocreatine stores and the decrease in intramuscular pH (Suga et al., 2010), coupled with insufficient oxygen supply to type I muscle fibers, lead to increased activation of type II muscle fibers, even at low intensities (Davies et al., 2016; Pearson and Hussain, 2015). Additionally, the reduction in oxygen supply and accumulation of metabolic byproducts due to restricted blood flow stimulate Type III and IV afferent nerves, further enhancing the recruitment of Type II fibers. This compensatory recruitment helps maintain muscle force and prevents motor neuron conduction failure during exercise (Wernbom and Aagaard, 2020).

In terms of muscle protein synthesis, key signaling proteins such as S6K1 are expressed at significantly higher levels in fast-twitch fibers compared to slow-twitch fibers (Qaisar et al., 2016; Tang et al., 2019). Low-intensity BFR training provides a novel mechanistic explanation for the activation of fast-twitch fibers, which were previously thought to be achievable only through intense physical stimuli, ultimately leading to the activation of muscle protein synthesis pathways. Moreover, lactate accumulation itself is increasingly recognized as a key metabolic signal for anabolic processes. Studies have shown that elevated lactate can stimulate the release of growth hormone and activate mTORC1 signaling pathways, which are essential for muscle protein synthesis (Deng et al., 2025; Kyun et al., 2024; Sumide et al., 2009). In this study, both 70% and 80% AOP produced significantly higher lactate concentrations than 60% AOP, suggesting that these levels may provide a sufficient metabolic stimulus for muscle adaptation. Mechanistically, lactate accumulation has long been proposed to enhance GH secretion and motor unit recruitment (Lim et al., 2022), and the current findings imply that only when occlusion is sufficient to build up lactate does GH/IGF-1 rise significantly (Dankel et al., 2017; Nalbandian and Takeda, 2016). Conversely, the lack of significant lactate response at 60% AOP may reflect insufficient metabolic stress, potentially limiting its efficacy in stimulating hypertrophic signaling. One explanation could be that partial venous occlusion at 60% AOP allowed sufficient oxygen delivery during low-load squatting, thereby blunting glycolytic flux and lactate production (Suga et al., 2010). Additionally, the lack of localized hypoxia may have reduced activation of fast-twitch muscle fibers, which are more reliant on anaerobic metabolism and therefore major contributors to lactate generation (Wernbom and Aagaard, 2020). These findings suggest that 60% AOP may fall below the “effective dose threshold” for BFR-induced metabolic signaling.

Notably, our results showed no significant differences in %MVC or lactate between 70% and 80% AOP, despite both being significantly higher than at 60% AOP. This pattern may indicate a physiological plateau effect, wherein pressures beyond 70% do not yield additional benefit in terms of muscle activation or metabolic stress. However, it is important to emphasize that this interpretation is speculative. The current findings only exhibit a plateau-like trend in the data; we do not claim to have definitively identified a plateau effect. More rigorous, targeted studies are needed to confirm whether such a threshold truly exists.

To further characterize the observed phenomenon, we conducted trend analyses examining the relationship between AOP level and acute physiological responses. The trend analysis for blood lactate concentration revealed a significant quadratic component across AOP levels, F (1, 45) = 4.22, p = 0.046, while the cubic component was not significant. This finding suggests that the dose–response relationship is not strictly linear, and instead may follow a curvilinear trajectory. Although we did not formally fit nonlinear regression models in the present study, the observed pattern implies that future research may benefit from modeling the pressure–response curve using polynomial or spline-based approaches to better define the optimal occlusion threshold. The observed lack of further increase in neuromuscular activation at pressures exceeding 70% AOP may be attributable to three interrelated physiological mechanisms: (1) Excessive compression at 80% AOP likely intensifies stimulation of group III/IV afferents by metabolites (H⁺, lactate, bradykinin) and mechanical stress. These nociceptive signals can reflexively inhibit ɑ-motoneuron output through spinal and supraspinal pathways, counteracting the drive for further muscle recruitment (Amann et al., 2013; Hug et al., 2015; Kennedy et al., 2015). Our observed RPE surge at 80% AOP supports this inhibitory feedback mechanism. (2) Near-complete arterial inflow restriction at ≥80% AOP critically compromises oxygen delivery and ATP resynthesis. While moderate hypoxia (70% AOP) potentiates type II fiber recruitment, severe hypoxia (80% AOP) may exceed the threshold where metabolic crisis impairs excitation-contraction coupling and force production (Gorgey et al., 2016; Scott et al., 2016). This aligns with Patterson et al.'s finding where pressures beyond “optimal occlusion” reduce metabolic stimulus efficiency (Patterson et al., 2019). (3) Cuff pressures approaching AOP (80%) may physically compress underlying neural structures and muscle spindles, potentially altering proprioceptive feedback and voluntary activation capacity (Wernbom et al., 2008). The discomfort reported by participants at 80% AOP likely reflects this mechanical stress.

The muscle cell swelling effect induced by BFRT is another key factor contributing to muscle hypertrophy (Loenneke et al., 2012). Muscle cell swelling increases intracellular pressure, which stimulates anabolic signaling pathways and promotes protein synthesis, thereby facilitating muscle growth. However, muscle cell swelling appears to reach a plateau beyond a certain level of blood flow restriction, indicating that further increases in pressure may not yield additional hypertrophic benefits. Indeed, elevated pressure levels exceeding 70% AOP may impair oxygen and nutrient delivery, leading to early muscle fatigue and an increased risk of injury (Ilett et al., 2019; Wernbom and Aagaard, 2020), which increases the risk of acute muscle fatigue and damage at 80% AOP, further suppressing muscle activation. Increased AOP levels may lead to reduced muscle oxygenation and accumulation of metabolic byproducts, ultimately worsening muscle fatigue and pain (Reis et al., 2019). Moreover, elevated pressure levels may activate sensory receptors in the nervous system, increasing perceived exertion and discomfort (Cockfield et al., 2024), potentially affecting exercise performance and adherence (Loenneke et al., 2015b; Mok et al., 2020). In the context of our study, the significantly elevated RPE observed at 80% AOP indicates a substantial increase in perceived effort and discomfort. Increasing the occlusion pressure beyond 70% AOP appears to yield diminishing physiological benefits while markedly increasing perceptual burden.

In this study, several participants reported excessive discomfort at 80% AOP, which hindered their ability to complete the required repetitions and led to requests for pressure reduction. However, it should be noted that RPE primarily reflects global exertion, not specific pain or discomfort. We did not employ a separate visual analog or pain scale for cuff discomfort, nor did we record any dedicated questionnaire on pressure-related pain. Our statement about greater discomfort at 80% was based on informal observation and participant comments.

While the present study provides valuable insight into the acute physiological responses to BFRT under varying occlusion pressures, several limitations must be acknowledged. First, all participants were healthy young males recruited from a single university cohort, which may limit the generalizability of the findings to females, older adults, clinical populations, or elite athletes. This gender homogeneity and potential volunteer bias should be addressed in future research through broader sampling strategies. Second, although individualized arterial occlusion pressures (AOP) were used, inter-individual variability in thigh circumference and tissue composition may influence actual occlusion levels, leading to discrepancies in physiological responses. Measuring AOP at rest may not fully reflect real-time occlusive effects during dynamic exercise due to acute changes in vascular tone and intramuscular pressure. Lastly, the modest sample size (n = 16) and non-randomized order of conditions may have introduced bias or limited statistical power to detect subtle effects, despite adequate power for primary outcomes.

Given these considerations, the findings of this study suggest that 70% AOP may provide a favorable balance between physiological efficacy and perceptual tolerability during low-load resistance training. However, caution is warranted in applying these pressures outside of athletic contexts. For clinical populations or novice trainees, higher AOP levels may pose discomfort or adherence challenges, and the safety profile of such protocols remains to be thoroughly assessed. Practitioners should therefore consider tailoring AOP intensity based on individual tolerance, training goals, and health status. Clear differentiation between athletic enhancement and clinical rehabilitation contexts is essential when prescribing BFRT.

Building on these implications, future research should pursue longitudinal intervention studies to evaluate the chronic adaptations to varying AOP levels, ideally employing mixed-effects modeling to account for inter- and intra-individual variability. Expanding the sample size (n > 20) and including diverse populations (e.g., females, older adults) would enhance external validity. Furthermore, integrating near-infrared spectroscopy (NIRS) could offer real-time insights into muscle oxygenation dynamics during BFRT, improving the physiological precision of occlusion monitoring. Such methodological enhancements will help refine BFRT protocols and identify optimal dosing strategies across populations and training conditions.

In conclusion, we propose that 70% AOP represents a potentially prudent trade-off in acute BFR exercise. It appears to elicit comparable metabolic and neuromuscular responses as 80% AOP, but with lower RPE and fewer subjective tolerance issues. However, this interpretation is tempered by the limitations of our discomfort assessment: we did not use a validated pain scale, and thus our observations of tolerability are qualitative. Future studies should include objective pain/discomfort measures (e.g., VAS pain scale) to confirm the relative tolerability of different pressures. For now, the evidence points toward 70% AOP as a practical choice that maximizes physiological stimulus while minimizing unnecessary discomfort. To strengthen these findings, future research should incorporate longitudinal designs with extended follow-up to evaluate chronic training adaptations, and employ mixed-effects modeling to account for inter-individual variability in pressure responses.