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.

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.

Background:This article describes a new bone transport technique for femoral and tibial bone defects using lengthening nails combined with locking plates. We term it plate-assisted bone segment transport (PABST).Methods:Nine patients with five femoral and four tibial bone defects from open fractures or malignancies were treated between 2016 and 2018. Mean femoral defect length was 9.3 cm (range 7 to 11.5). Mean tibial defect was 8.9 cm (range 4.8 to 15). The patients were evaluated for time to weight bearing, consolidation index, mechanical axis deviation, and limb length discrepancy.Results:Seven of nine patients have fully consolidated. The mean consolidation time was 6.6 months. The consolidation index was 0.9 (femur) and 1.26 (tibia) mo/cm. Two patients required supplementary lengthening. One patient had mild varus, one mild valgus; the remainder had a normal mechanical axis. Limb length discrepancy remained acceptable in all patients. The main complications were heterotopic ossification, delayed healing, and reduced knee motion.Conclusion:Bone transport with lengthening nails and locking plates is an effective and patient-friendly way of treating bone defects, eliminating the adverse effects of external fixation and reducing treatment time. The plate provides stability during transport and docking; it can address concomitant fractures and facilitates acute shortenings.