The current manuscript sets out a series of guidelines for blood flow restriction exercise, focusing on the methodology, application and safety of this mode of training. With the emergence of this technique and the wide variety of applications within the literature, the aim of this review is to set out a current research informed guide to blood flow restriction training to practitioners. This covers the use of blood flow restriction to enhance muscular strength and hypertrophy via training with resistance and aerobic exercise and preventing muscle atrophy using the technique passively. The authorship team for this article was selected from the researchers focused in blood flow restriction training research with expertise in exercise science, strength and conditioning and sports medicine.

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) (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.

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We show that the spectral dimension d s of two-dimensional quantum gravity coupled to Gaussian fields is two for all values of the central charge c ≤ 1.The same arguments provide a simple proof of the known result d s = 4/3 for branched polymers.

Previous studies indicate that low-load muscle contractions performed under local blood flow restriction (BFR) may initially induce muscle damage and stress. However, whether these factors are evoked with longitudinal BFR training remains unexplored at the myocellular level. Two distinct study protocols were conducted, covering 3 weeks (3 wk) or one week (1 wk). Subjects performed BFR exercise (100 mmHg, 20% 1RM) to concentric failure (BFRE) (3 wk/1 wk), while controls performed work-matched (LLE) (3 wk) or high-load (HLE; 70% 1RM) (1 wk) free-flow exercise. Muscle biopsies (3 wk) were obtained at baseline (Pre), 8 days into the intervention (Mid8), and 3 and 10 days after training cessation (Post3, Post10) to examine macrophage (M1/M2) content as well as heat shock protein (HSP27/70) and tenascin-C expression. Blood samples (1 wk) were collected before and after (0.1-24 h) the first and last training session to examine markers of muscle damage (creatine kinase), oxidative stress (total antibody capacity, glutathione) and inflammation (monocyte chemotactic protein-1, interleukin-6, tumour necrosis factor α). M1-macrophage content increased 108-165% with BFRE and LLE at Post3 (P < 0.05), while M2-macrophages increased (163%) with BFRE only (P < 0.01). Membrane and intracellular HSP27 expression increased 60-132% at Mid8 with BFRE (P < 0.05-0.01). No or only minor changes were observed in circulating markers of muscle damage, oxidative stress and inflammation. The amplitude, timing and localization of the above changes indicate that only limited muscle damage was evoked with BFRE. This study is the first to show that a period of high-frequency, low-load BFR training does not appear to induce general myocellular damage. However, signs of tissue inflammation and focal myocellular membrane stress and/or reorganization were observed that may be involved in the adaptation processes evoked by BFR muscle exercise.

Purpose The present study investigated muscle metabolism and fatigue during simulated elite male ice hockey match-play. Methods Thirty U20 male national team players completed an experimental game comprising three periods of 8 × 1-min shifts separated by 2-min recovery intervals. Two vastus lateralis biopsies were obtained either during the game (n = 7) or pregame and postgame (n = 6). Venous blood samples were drawn pregame and at the end of the first and last periods (n = 14). Activity pattern and physiological responses were continuously monitored using local positioning system and heart rate recordings. Further, repeated-sprint ability was tested pregame and after each period. Results Total distance covered was 5980 ± 199 m with almost half the distance covered at high skating speeds (>17 km·h−1). Average and peak on-ice heart rate was 84% ± 2% and 97% ± 2% of maximum heart rate, respectively. Muscle lactate increased (P ≤ 0.05) more than fivefold and threefold, whereas muscle pH decreased (P ≤ 0.05) from 7.31 ± 0.04 pregame to 6.99 ± 0.07 and 7.13 ± 0.11 during the first and last periods, respectively. Muscle glycogen decreased by 53% postgame (P ≤ 0.05) with ~65% of fast- and slow-twitch fibers depleted of glycogen. Blood lactate increased sixfold (P ≤ 0.05), whereas plasma free fatty acid levels increased 1.5-fold and threefold (P ≤ 0.05) after the first and last periods. Repeated-sprint ability was impaired (~3%; P ≤ 0.05) postgame concomitant with a ~10% decrease in the number of accelerations and decelerations during the second and last periods (P ≤ 0.05). Conclusions Our findings demonstrate that a simulated ice hockey match-play scenario encompasses a high on-ice heart rate response and glycolytic loading resulting in a marked degradation of muscle glycogen, particularly in specific sub-groups of fibers. This may be of importance both for fatigue in the final stages of a game and for subsequent recovery.

Introduction Heavy‐load strength training (HLT) is generally considered the Gold Standard exercise modality for inducing gains in skeletal muscle strength. However, use of heavy external exercise loads may be contraindicative in frail individuals. Low‐load resistance exercise combined with partial blood‐flow restriction (LL‐BFR exercise) may offer an effective alternative for increasing mechanical muscle strength and size. The aim of this study was to compare the effect of LL‐BFR training to HLT on maximal muscle strength gains. Prospero registration‐id (CRD42014013382). Materials and methods A systematic search in six healthcare science databases and reference lists was conducted. Data selected for primary analysis consisted of post‐intervention changes in maximal muscle strength. A random‐effects meta‐analysis with standardized mean differences (SMD) was used. Results Of 1413 papers identified through systematic search routines, sixteen papers fulfilled the inclusion criteria, totalling 153 participants completing HLT and 157 completing LL‐BFR training. The magnitude of training‐induced gains in maximal muscle strength did not differ between LL‐BFR training and HLT (SMD of −0.17 (95% CI: −0.40; 0.05)). Low between‐study heterogeneity was noted (I2 = 0.0%, Chi2 P = 9.65). Conclusion Low‐load blood‐flow‐restricted training appears equally effective of producing gains in maximal voluntary muscle strength compared to HLT in 20‐ to 80‐year‐old healthy and habitually active adults.

IMPORTANCE Previous trials have suggested that vasopressin and methylprednisolone administered during in-hospital cardiac arrest might improve outcomes.OBJECTIVE To determine whether the combination of vasopressin and methylprednisolone administered during in-hospital cardiac arrest improves return of spontaneous circulation. DESIGN, SETTING, AND PARTICIPANTS Multicenter, randomized, double-blind, placebo-controlled trial conducted at 10 hospitals in Denmark. A total of 512 adult patients with in-hospital cardiac arrest were included between October 15, 2018, and January 21, 2021. The last 90-day follow-up was on April 21, 2021.INTERVENTION Patients were randomized to receive a combination of vasopressin and methylprednisolone (n = 245) or placebo (n = 267). The first dose of vasopressin (20 IU) and methylprednisolone (40 mg), or corresponding placebo, was administered after the first dose of epinephrine. Additional doses of vasopressin or corresponding placebo were administered after each additional dose of epinephrine for a maximum of 4 doses. MAIN OUTCOMES AND MEASURESThe primary outcome was return of spontaneous circulation. Secondary outcomes included survival and favorable neurologic outcome at 30 days (Cerebral Performance Category score of 1 or 2). RESULTS Among 512 patients who were randomized, 501 met all inclusion and no exclusion criteria and were included in the analysis (mean [SD] age, 71 [13] years; 322 men [64%]). One hundred of 237 patients (42%) in the vasopressin and methylprednisolone group and 86 of 264 patients (33%) in the placebo group achieved return of spontaneous circulation (risk ratio, 1.30 [95% CI, 1.03-1.63]; risk difference, 9.6% [95% CI, 1.1%-18.0%]; P = .03). At 30 days, 23 patients (9.7%) in the intervention group and 31 patients (12%) in the placebo group were alive (risk ratio, 0.83 [95% CI, 0.50-1.37]; risk difference: −2.0% [95% CI, −7.5% to 3.5%]; P = .48). A favorable neurologic outcome was observed in 18 patients (7.6%) in the intervention group and 20 patients (7.6%) in the placebo group at 30 days (risk ratio, 1.00 [95% CI, 0.55-1.83]; risk difference, 0.0% [95% CI, −4.7% to 4.9%]; P > .99). In patients with return of spontaneous circulation, hyperglycemia occurred in 77 (77%) in the intervention group and 63 (73%) in the placebo group. Hypernatremia occurred in 28 (28%) and 27 (31%), in the intervention and placebo groups, respectively.CONCLUSIONS AND RELEVANCE Among patients with in-hospital cardiac arrest, administration of vasopressin and methylprednisolone, compared with placebo, significantly increased the likelihood of return of spontaneous circulation. However, there is uncertainty whether this treatment results in benefit or harm for long-term survival.