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The purpose of the present study was to investigate muscle hypertrophy, strength, and myonuclear and satellite cell (SC) responses to high-frequency blood flow-restricted resistance exercise (BFRRE). Thirteen individuals [24 ± 2 yr (mean ± SD), 9 men] completed two 5-day blocks of 7 BFRRE sessions, separated by a 10-day rest period. Four sets of unilateral knee extensions to voluntary failure at 20% of one repetition maximum (1RM) were conducted with partial blood flow restriction (90-100 mmHg). Muscle samples obtained before, during, 3 days, and 10 days after training were analyzed for muscle fiber area (MFA), myonuclei, SC, and mRNA and miRNA expression. Muscle size was measured by ultrasonography and magnetic resonance imaging and strength with 1RM knee extension. With the first block of BFRRE, SC number increased in both fiber types (70%-80%, P < 0.05), whereas type I and II MFA decreased by 6 ± 7% and 15 ± 11% (P < 0.05), respectively. With the second block of training, muscle size increased by 6%-8%, whereas the number of SCs (type I: 80 ± 63%, type II: 147 ± 95%), myonuclei (type I: 30 ± 24%, type II: 31 ± 28%), and MFA (type I: 19 ± 19%, type II: 11 ± 19%) peaked 10 days after the second block of BFRRE, whereas strength peaked after 20 days of detraining (6 ± 6%, P < 0.05). Pax7- and p21 mRNA expression were elevated during the intervention, whereas myostatin, IGF1R, MyoD, myogenin, cyclinD1 and -D2 mRNA did not change until 3-10 days postintervention. High-frequency lowload BFRRE induced robust increases in SC, myonuclei, and muscle size but modest strength gains. Intriguingly, the responses were delayed and peaked 10-20 days after the training intervention, indicating overreaching. [ABSTRACT FROM AUTHOR]

Purpose: Arterial occlusion pressure (AOP) measured in a supine position is often used to set cuff pressures for blood flow restricted exercise (BFRE). However, supine AOP may not reflect seated or standing AOP, thus potentially influencing the degree of occlusion. The primary aim of the study was to investigate the effect of body position on AOP. A secondary aim was to investigate predictors of AOP using wide and narrow cuffs. Methods: Twenty-four subjects underwent measurements of thigh circumference, skinfold and blood pressure, followed by assessments of thigh AOP in supine and seated positions with a wide and a narrow cuff, respectively, using Doppler ultrasound. Results: In the supine position, AOP was 148 ± 19 and 348 ± 94 mmHg with the wide and narrow cuff, respectively. This increased to 177 ± 20 and 409 ± 101 mmHg in the seated position, with correlations between supine and seated AOP of R = 0.81 and R = 0.50 for the wide and narrow cuff, respectively. For both cuff widths, thigh circumference constituted the strongest predictor of AOP, with diastolic blood pressure explaining additional variance with the wide cuff. The predictive strength of these variables did not differ between body positions. Conclusion: Our results indicate that body position strongly influences lower limb AOP, especially with narrow cuffs, yielding very high AOP (≥ 500-600 mmHg) in some subjects. This should be taken into account in the standardization of cuff pressures used during BFRE to better control the physiological effects of BFRE. [ABSTRACT FROM AUTHOR]

Purpose: To investigate hypertrophic signalling after a single bout of low-load resistance exercise with and without blood flow restriction (BFR). Methods: Seven subjects performed unilateral knee extensions at 30 % of their one repetition maximum. The subjects performed five sets to failure with BFR on one leg, and then repeated the same amount of work with the other leg without BFR. Biopsies were obtained from m. vastus lateralis before and 1, 24 and 48 h after exercise. Results: At 1-h post-exercise, phosphorylation of p70S6K Thr389 and p38MAPK Thr180/Tyr182 was elevated in the BFR leg, but not in the free-flow leg. Phospho-p70S6K Thr389 was elevated three- to fourfold in both legs at 24-h post-exercise, but back to baseline at 48 h. The number of visible satellite cells (SCs) per muscle fibre was increased for all post-exercise time points and in both legs (33–53 %). The proportion of SCs with cytoplasmic extensions was elevated at 1-h post in the BFR leg and the number of SCs positive for myogenin and/or MyoD was increased at 1- and 24-h post-exercise for both legs combined. Conclusion: Acute low-load resistance exercise with BFR resulted in early (1 h) and late (24 h) enhancement of phospho-p70S6K Thr389, an early response of p38MAPK, and an increased number of SCs per muscle fibre. Enhanced phospho-p70S6K Thr389 at 24-h post-exercise and increases in SC numbers were seen also in the free-flow leg. Implications of these findings for the hypertrophic effects of fatiguing low-load resistance exercise with and without BFR are discussed. [ABSTRACT FROM AUTHOR]

Key points In the last decade muscle training performed using a combination of low external loads and partial restriction of blood flow to the exercising limb has gained increasing interest, since it leads to significant gains in muscle strength and muscle mass., The cellular mechanisms responsible for the muscular adaptations induced by this training paradigm are not fully understood., This study shows that 3 weeks of high-frequency, low-intensity muscle exercise with partial blood flow restriction induces increases in maximal muscle strength accompanied by highly marked gains in muscle fibre size., Furthermore, the results indicate that these muscular adaptations rely on a considerable upregulation in myogenic satellite cells number, resulting in nuclear addition to the exercised myofibres., The results contribute to a better understanding of the physiological mechanisms underlying the gain in muscle strength and muscle mass observed with blood flow restricted low-intensity resistance exercise., Abstract Low-load resistance training with blood flow restriction has been shown to elicit substantial increases in muscle mass and muscle strength; however, the effect on myogenic stem cells (MSCs) and myonuclei number remains unexplored. Ten male subjects (22.8 ± 2.3 years) performed four sets of knee extensor exercise (20% 1RM) to concentric failure during blood flow restriction (BFR) of the proximal thigh (100 mmHg), while eight work-matched controls (21.9 ± 3.0 years) trained without BFR (control, CON). Twenty-three training sessions were performed within 19 days. Maximal isometric knee extensor strength (MVC) was examined pre- and post-training, while muscle biopsies were obtained at baseline (Pre), after 8 days intervention (Mid8) and 3 (Post3) and 10 days (Post10) post training to examine changes in myofibre area (MFA), MSC and myonuclei number. MVC increased by 7.1% (Post5) and 10.6% (Post12) ( P < 0.001) with BFR training, while type I and II MFA increased by 38% (Mid8), 35-37% (Post3) and 31-32% (Post10) ( P < 0.001). MSCs per myofibre increased with BFR training from 0.10 ± 0.01 (Pre) to 0.38 ± 0.02 (Mid8), 0.36 ± 0.04 (Post3) and 0.25 ± 0.02 (Post10) ( P < 0.001). Likewise, myonuclei per myofibre increased from 2.49 ± 0.07 (Pre) to 3.30 ± 0.22 (Mid8), 3.20 ± 0.16 (Post3) and 3.11 ± 0.11 (Post10), ( P < 0.01). Although MFA increased in CON at Mid8, it returned to baseline at Post3. No changes in MSC or myonuclei number were observed in CON. This study is the first to show that short-term low-load resistance exercise performed with partial blood flow restriction leads to marked proliferation of myogenic stem cells and resulting myonuclei addition in human skeletal muscle, which is accompanied by substantial myofibre hypertrophy. [ABSTRACT FROM AUTHOR]

Conflicting findings have been reported regarding muscle damage with low-intensity resistance exercise with blood flow restriction (BFR) by pressure cuffs. This study investigated muscle function and muscle fibre morphology after a single bout of low-intensity resistance exercise with and without BFR. Twelve physically active subjects performed unilateral knee extensions at 30% of their one repetition maximum (1RM), with partial BFR on one leg and the other leg without occlusion. With the BFR leg, five sets were performed to concentric torque failure, and the free-flow leg repeated the exact same number of repetitions and sets. Biopsies were obtained from vastus lateralis before and 1, 24 and 48 h after exercise. Maximum isometric torque (MVC) and resting tension were measured before and after exercise and at 4, 24, 48, 72, 96 and 168 h post-exercise. The results demonstrated significant decrements in MVC (lasting ≥48 h) and delayed onset muscle soreness in both legs, and increased resting tension for the occluded leg both acutely and at 24 h post-exercise. The percentage of muscle fibres showing elevated intracellular staining of the plasma protein tetranectin, a marker for sarcolemmal permeability, was significantly increased from 9% before exercise to 27-38% at 1, 24 and 48 h post-exercise for the BFR leg. The changes in the free-flow leg were significant only at 24 h (19%). We conclude that an acute bout of low-load resistance exercise with BFR resulted in changes suggesting muscle damage, which may have implications both for safety aspects and for the training stimulus with BFR exercise. [ABSTRACT FROM AUTHOR]

A reply to the letter to the editor in response to an article that suggests sarcolemmal permeability and muscle damage as factor in blood flow restricted resistance exercise is presented.

Blood flow‐restricted resistance exercise (BFRRE) has been shown to induce increases in muscle size and strength, and continues to generate interest from both clinical and basic research points of view. The low loads employed, typically 20%‐50% of the one repetition maximum, make BFRRE an attractive training modality for individuals who may not tolerate high musculoskeletal forces (eg, selected clinical patient groups such as frail old adults and patients recovering from sports injury) and/or for highly trained athletes who have reached a plateau in muscle mass and strength. It has been proposed that achieving a high degree of muscle fibre recruitment is important for inducing muscle hypertrophy with BFRRE, and the available evidence suggest that fatiguing low‐load exercise during ischemic conditions can recruit both slow (type I) and fast (type II) muscle fibres. Nevertheless, closer scrutiny reveals that type II fibre activation in BFRRE has to date largely been inferred using indirect methods such as electromyography and magnetic resonance spectroscopy, while only rarely addressed using more direct methods such as measurements of glycogen stores and phosphocreatine levels in muscle fibres. Hence, considerable uncertainity exists about the specific pattern of muscle fibre activation during BFRRE. Therefore, the purpose of this narrative review was (1) to summarize the evidence on muscle fibre recruitment during BFRRE as revealed by various methods employed for determining muscle fibre usage during exercise, and (2) to discuss reported findings in light of the specific advantages and limitations associated with these methods. [ABSTRACT FROM AUTHOR]