Bringing Light into the Dark: Effects of Compression Clothing on Performance and Recovery

Short-duration sprints, interspersed with brief recoveries, are common during most team sports. The ability to produce the best possible average sprint performance over a series of sprints (≤10 seconds), separated by short (≤60 seconds) recovery periods has been termed repeated-sprint ability (RSA). RSA is therefore an important fitness requirement of team-sport athletes, and it is important to better understand training strategies that can improve this fitness component. Surprisingly, however, there has been little research about the best training methods to improve RSA. In the absence of strong scientific evidence, two principal training theories have emerged. One is based on the concept of training specificity and maintains that the best way to train RSA is to perform repeated sprints. The second proposes that training interventions that target the main factors limiting RSA may be a more effective approach. The aim of this review (Part II) is to critically analyse training strategies to improve both RSA and the underlying factors responsible for fatigue during repeated sprints (see Part I of the preceding companion article). This review has highlighted that there is not one type of training that can be recommended to best improve RSA and all of the factors believed to be responsible for performance decrements during repeated-sprint tasks. This is not surprising, as RSA is a complex fitness component that depends on both metabolic (e.g. oxidative capacity, phosphocreatine recovery and H+ buffering) and neural factors (e.g. muscle activation and recruitment strategies) among others. While different training strategies can be used in order to improve each of these potential limiting factors, and in turn RSA, two key recommendations emerge from this review; it is important to include (i) some training to improve single-sprint performance (e.g. 'traditional' sprint training and strength/power training); and (ii) some high-intensity (80-90% maximal oxygen consumption) interval training to best improve the ability to recover between sprints. Further research is required to establish whether it is best to develop these qualities separately, or whether they can be developed concurrently (without interference effects). While research has identified a correlation between RSA and total sprint distance during soccer, future studies need to address whether training-induced changes in RSA also produce changes in match physical performance.

Arthrogenic muscle inhibition is an important underlying factor in persistent quadriceps muscle weakness after knee injury or surgery. To determine the magnitude and prevalence of volitional quadriceps activation deficits after knee injury. Web of Science database. Eligible studies involved human participants and measured quadriceps activation using either twitch interpolation or burst superimposition on patients with knee injuries or surgeries such as anterior cruciate ligament deficiency (ACLd), anterior cruciate ligament reconstruction (ACLr), and anterior knee pain (AKP). Means, measures of variability, and prevalence of quadriceps activation (QA) failure (<95%) were recorded for experiments involving ACLd (10), ACLr (5), and AKP (3). A total of 21 data sets from 18 studies were initially identified. Data from 3 studies (1 paper reporting data for both ACLd and ACLr, 1 on AKP, and the postarthroscopy paper) were excluded from the primary analyses because only graphical data were reported. Of the remaining 17 data sets (from 15 studies), weighted mean QA in 352 ACLd patients was 87.3% on the involved side, 89.1% on the uninvolved side, and 91% in control participants. The QA failure prevalence ranged from 0% to 100%. Weighted mean QA in 99 total ACLr patients was 89.2% on the involved side, 84% on the uninvolved side, and 98.5% for the control group, with prevalence ranging from 0% to 71%. Thirty-eight patients with AKP averaged 78.6% on the involved side and 77.7% on the contralateral side. Bilateral QA failure was commonly reported in patients. Quadriceps activation failure is common in patients with ACLd, ACLr, and AKP and is often observed bilaterally.

Exercise involving lengthening of an activated muscle can cause injury. Recent reports documented the mechanics of exercise-induced muscle injury as well as physiological and cellular events and manifestations of injury. Loss of the cytoskeletal protein desmin and loss of cellular integrity as evidenced by sarcolemmal damage occur early during heavy eccentric exercise. These studies indicate that the earliest events in muscle injury are mechanical in nature, while later events indicate that it may be more appropriate to conclude that intense exercise initiates a muscle remodeling process. We conclude that muscle injury after eccentric exercise is differently severe in muscles with different architecture, is fibre type-specific, primarily because of fibre strain in the acute phase, and is exacerbated by inflammation after the initial injury.