Does blood flow restricted exercise result in prolonged torque decrements and muscle damage?

Abstract

We are writing in regard to the recent paper from Wernbom et al. (2011) titled ‘‘Contractile function and sarcolemmal permeability after acute low-load resistance exercise with blood flow restriction.’’ The authors sought to investigate neuromuscular fatigue and recovery, as well as fiber morphology, following an acute bout of low-load resistance exercise with blood flow restriction (BFR). The authors should be commended on investigating the effects of BFR at the muscle fiber level, as this is an area that is presently poorly considered in the current literature. The authors hypothesized that exercise with BFR would result in signs of muscle damage. However, we have some concerns with the interpretation of the data presented in this study. Several of the authors’ main findings, highlighted in the discussion, may not necessarily be attributed to muscle damage. The authors’ first main finding was that there were markedly larger acute reductions (1 and 2 min postexercise) in maximum voluntary contraction (MVC) in the BFR leg compared to the free-flow leg. It should be emphasized that these greater acute reductions observed in the BFR leg were obtained with a MVC completed under BFR. Following the release of the cuff, there were no longer differences between groups. Furthermore, we question the reasoning behind having subjects’ complete repetitions to muscular failure under BFR, followed by two MVC’s which were also completed under BFR. If the purpose was to investigate the effects of low-load BFR on muscle damage, it seems more appropriate to release the cuff following the completion of the exercise bout for at least one of the immediate post MVC’s. This marked decrease in MVC can be questioned, because previous research has shown that decreases observed in MVC with BFR are almost returned to baseline within a minute following the release of the cuff (Yasuda et al. 2009). The authors second main finding was that part of the decline in MVC was longer lasting (at least 48 h), especially in the BFR leg. Again, the MVC’s which were different between conditions, were only observed when the MVC was completed under BFR. The authors’ suggestion that the decline in MVC was longer lasting is not supported by the data presented in the paper, which showed that there were no differences between groups at 4, 24, or 48 h postexercise. The authors’ third main finding was that there was an increased occurrence of fibers with elevated tetranectin staining in the BFR leg. The authors suggest this elevated tetranectin staining is indicative of muscle damage, because unpublished data from their laboratory suggest that severe eccentric exercise caused marked increases with intracellular tetranectin staining. While this is interesting, it should be noted that the exercise completed in this study was submaximal and not severe eccentric exercise. Furthermore, elevations in tetranectin staining were also observed in the free-flow leg which was not taken to muscular failure (work matched with BFR leg), indicating that the elevation in tetranectin may not have been reflective of muscle damage. The authors did state that tetranectin elevations are not necessarily only associated with muscle damage, but may also contribute to mechanotransduction processes, which may be of mechanistic importance for the explanation of the muscle hypertrophy Communicated by Susan A. Ward.