Purpose: The aims of this study were 1) to model the temporal profile of W′ recovery after exhaustion, 2) to estimate the contribution of changing V ˙O2 kinetics to this recovery, and 3) to examine associations with aerobic fitness and muscle fiber type (MFT) distribution. Methods: Twenty-one men (age = 25 ± 2 yr, V ˙O2peak = 54.4 ± 5.3 mL•min −1 •kg −1 ) performed several constant load tests to determine critical power and W′ followed by eight trials to quantify W′ recovery. Each test consisted of two identical exhaustive work bouts (WB1 and WB2), separated by a variable recovery interval of 30, 60, 120, 180, 240, 300, 600, or 900 s. Gas exchange was measured and muscle biopsies were collected to determine MFT distribution. W′ recovery was quantified as observed W′ recovery (W′ OBS ), model-predicted W′ recovery (W′ BAL ), and W′ recovery corrected for changing V ˙O2 kinetics (W′ ADJ ). W′ OBS and W′ ADJ were modeled using mono-and biexponential fitting. Root-mean-square error (RMSE) and Akaike information criterion (ΔAIC C ) were used to evaluate the models' accuracy. Results: The W′ BAL model (τ = 524 ± 41 s) was associated with an RMSE of 18.6% in fitting W′ OBS and underestimated W′ recovery for all durations below 5 min (P < 0.002). Monoexponential modeling of W′ OBS resulted in τ = 104 s with RMSE = 6.4%. Biexponential modeling of W′ OBS resulted in τ 1 = 11 s and τ 2 = 256 s with RMSE = 1.7%. W′ ADJ was 11% ± 1.5% lower than W′ OBS (P < 0.001). ΔAIC C scores favored the biexponential model for W′ OBS , but not for W′ ADJ . V ˙O2peak (P = 0.009) but not MFT distribution (P = 0.303) was associated with W′ OBS . Conclusion: We showed that W′ recovery from exhaustion follows a two-phase exponential time course that is dependent on aerobic fitness. The appearance of a fast initial recovery phase was attributed to an enhanced aerobic energy provision resulting from changes in V ˙O2 kinetics.

Purpose The goal is to evaluate the passive stability of a bicruciate retaining, cruciate retaining and bicruciate substituting TKA design in relation to the native knee stability in terms of the laxity envelope. A bicruciate retaining knee prosthesis was hypothesized to offer a closer to normal knee stability in vitro. Methods Fourteen cadaveric knee specimens have been tested under passive conditions with and without external loads, involving a varus/valgus and an external/internal rotational torque, distraction/compression force and an anteroposterior shear force. Subsequently, the native knee, bicruciate retaining, cruciate retaining and finally a bicruciate substituting total knee arthroplasty were tested. Results Through the range of motion, the width of the varus/valgus and internal/external laxity envelope for the native knee and the bicruciate retaining knee were almost equivalent, whereas the cruciate retaining and the bicruciate substituting knee displayed less laxity and more joint distraction. In all prosthetic knees, an equal anteroposterior laxity was seen for the lateral and medial side whereas in the native knee, a difference in laxity was seen between the stable medial side and the more mobile lateral side. Conclusion Bicruciate retaining knee prostheses can restore normal laxity and thus have the potential to offer more normal knee function. Restoration of natural peri‐articular soft‐tissue tension is clinically important because of its obvious effects on joint stability and range of motion. Furthermore, the results of this study could help to establish the ideal ligament tension and laxity in more conventional implants by approaching the normal values for passive knee evaluation as presented here.

Despite the high prevalence of tendon pathology in athletes, the underlying pathogenesis is still poorly understood. Various aetiological theories have been presented and rejected in the past, but the tendon cell response model still holds true. This model describes how the tendon cell is the key regulator of the extracellular matrix and how pathology is induced by a failed adaptation to a disturbance of tissue homeostasis. Such failure has been attributed to various kinds of stressors (eg, mechanical, thermal and ischaemic), but crucial elements seem to be missing to fully understand the pathogenesis. Importantly, a disturbance of tissue pressure homeostasis has not yet been considered a possible factor, despite it being associated with numerous pathologies. Therefore, we conducted an extensive narrative literature review on the possible role of intratendinous pressure in the pathogenesis of tendon pathology. This review explores the current understanding of pressure dynamics and the role of tissue pressure in the pathogenesis of other disorders with structural similarities to tendons. By bridging these insights with known structural changes that occur in tendon pathology, a conceptual model was constituted. This model provides an overview of the possible mechanism of how an increase in intratendinous pressure might be involved in the development and progression of tendon pathology and contribute to tendon pain. In addition, some therapies that could reduce intratendinous pressure and accelerate tendon healing are proposed. Further experimental research is encouraged to investigate our hypotheses and to initiate debate on the relevance of intratendinous pressure in tendon pathology.

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