We conclude that unaccustomed single-bout BFRE performed to failure induces significant muscle damage. Additionally, both ECC and BFRE can precondition against muscle damage induced by a subsequent bout of BFRE.

Purpose: It is well established that high-load resistance exercise (HLRE) can stimulate myofibrillar accretion. Additionally, recent studies suggest that HLRE can also stimulate mitochondrial biogenesis and respiratory function. However, in several clinical situations, the use of resistance exercise with high loading may not constitute a viable approach. Low-load blood flow restricted resistance exercise (BFRRE) has emerged as a time-effective low-load alternative to stimulate myofibrillar accretion. It is unknown if BFRRE can also stimulate mitochondrial biogenesis and respiratory function. If so, BFRRE could provide a feasible strategy to stimulate muscle metabolic health.Methods: To study this, 34 healthy previously untrained individuals (24 ± 3 years) participated in BFRRE, HLRE, or non-exercise control intervention (CON) 3 times per week for 6 weeks. Skeletal muscle biopsies were collected; (1) before and after the 6-week intervention period to assess mitochondrial biogenesis and respiratory function and; (2) during recovery from single-bout exercise to assess myocellular signaling events involved in transcriptional regulation of mitochondrial biogenesis. During the 6-week intervention period, deuterium oxide (D2O) was continuously administered to the participants to label newly synthesized skeletal muscle mitochondrial proteins. Mitochondrial respiratory function was assessed in permeabilized muscle fibers with high-resolution respirometry. Mitochondrial content was assessed with a citrate synthase activity assay. Myocellular signaling was assessed with immunoblotting.Results: Mitochondrial protein synthesis rate was higher with BFRRE (1.19%/day) and HLRE (1.15%/day) compared to CON (0.92%/day) (P < 0.05) but similar between exercise groups. Mitochondrial respiratory function increased to similar degree with both exercise regimens and did not change with CON. For instance, coupled respiration supported by convergent electron flow from complex I and II increased 38% with BFRRE and 24% with HLRE (P < 0.01). Training did not alter citrate synthase activity compared to CON. BFRRE and HLRE elicited similar myocellular signaling responses.Conclusion: These results support recent findings that resistance exercise can stimulate mitochondrial biogenesis and respiratory function to support healthy skeletal muscle and whole-body metabolism. Intriquingly, BFRRE produces similar mitochondrial adaptations at a markedly lower load, which entail great clinical perspective for populations in whom exercise with high loading is untenable.

1) insulin sensitivity is not improved after ESA treatment despite improved exercise capacity, 2) the calorigenic effects of ESA may be related to increased UCP2 gene expression in skeletal muscle, and 3) training and ESA exert opposite effects on lipolysis under basal conditions, increased FFA levels and liver fat fraction was observed after ESA treatment.

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.

Low‐load blood flow restricted resistance exercise (BFRE) performed to volitional failure is suggested to constitute an effective method for producing increases in muscle size and function. However, BFRE to failure may entail high levels of perceived exertion, discomfort, and/or delayed onset of muscle soreness (DOMS). The aim of the study was to compare BFRE performed to volitional failure (F‐BFRE) vs non‐failure BFRE (NF‐BFRE) on changes in muscle size, function and perceptual responses. Fourteen young untrained males had one leg randomized to knee extension F‐BFRE while the contralateral leg performed NF‐BFRE. The training consisted of 22 exercise bouts over an 8‐week period. Whole‐muscle cross‐sectional area (CSA) of quadriceps components, muscle function, and DOMS were assessed before and after the training period. Perceived exertion and discomfort were registered during each exercise bout. Both F‐BFRE and NF‐BFRE produced regional increases in muscle CSA in the range of: quadriceps (2.5%‐3.8%), vastus lateralis (8.1%‐8.5%), and rectus femoris (7.9%‐25.0%). All without differences between leg. Muscle strength (6.8%‐11.5%) and strength‐endurance capacity (13.9%‐18.6%) also increased to a similar degree in both legs. Less perceived exertion, discomfort, and DOMS were reported with NF‐BFRE compared to F‐BFRE. In conclusion, non‐failure BFRE enables increases in muscle size and muscle function, while involving reduced perceptions of exertion, discomfort, and DOMS. Non‐failure BFRE may be a more feasible approach in clinical settings.