The effect of water-based plyometric training on vertical stiffness and athletic performance

© 2018 Sporri et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Since higher vertical stiffness is related to superior athletic performance, training has traditionally been aimed at augmenting this variable to enhance neuromuscular output. However, research has linked elevated stiffness with increased injury risk, therefore, this study examined the effect of a novel training intervention on vertical stiffness and athletic performance. Vertical stiffness, jump performance and athletic performance were assessed in two randomly allocated groups, prior to, and following, an eight-week period. One group was exposed to a training intervention involving aqua-based plyometrics (n = 11) over the 8 weeks while the other acted as a control group (n = 9). The training intervention involved hopping, jumping and bounding in water at a depth of 1.2m whilst control participants performed their normal training. There were no significant changes in vertical stiffness in either group. Countermovement jump height and peak power significantly increased within the aqua plyometric group (p < 0.05). Athletic performance markers improved in the aqua plyometric group as measured using an agility and a 5-bound test exhibiting superior values at the post-test (p < 0.05). The results suggest that an aqua plyometric training program can enhance athletic performance without elevating stiffness. The increase in athletic performance is likely due to a reduction in ground reaction forces created by the buoyancy of the water, causing a shorter amortization phase and a more rapid application of concentric force. The findings from this study can inform exercise professionals and medical staff regarding the ability to enhance neuromuscular performance without elevating vertical stiffness. This has implications for improving athletic performance while concurrently minimising injury risk

Biceps femoris long head morphology in youth competitive alpine skiers is associated with age, biological maturation and traumatic lower extremity injuries

Lower extremity injuries are common in competitive alpine skiers, and the knee and lower leg are often affected. The hamstring muscles, especially the biceps femoris long head (BFlh), can stabilize the knee and the hip and may counteract various adverse loading patterns during typical mechanisms leading to severe lower extremity injuries. The aim of the present study was to describe BFlh morphology in youth competitive alpine skiers in relation to sex, age and biological maturation and to investigate its association with the occurrence of traumatic lower extremity injuries in the upcoming season. 95 youth skiers underwent anthropometric measurements, maturity offset estimations and ultrasound assessment, followed by 12-months prospective injury surveillance. Unpaired t tests showed that the two sexes did not differ in BFlh morphology, including fascicle length (Lf), pennation angle (PA), muscle thickness (MT) and average anatomical cross-sectional area (ACSAavg). In contrast, U16 skiers had longer fascicles than U15 skiers (9.5 ± 1.3 cm vs 8.9 ± 1.3 cm, p < 0.05). Linear regression analyses revealed that maturity offset was associated with Lf (R2 = 0.129, p < 0.001), MT (R2 = 0.244, p < 0.001) and ACSAavg (R2 = 0.065, p = 0.007). No association was found between maturity offset and PA (p = 0.524). According to a binary logistic regression analysis, ACSAavg was significantly associated with the occurrence of traumatic lower extremity injuries (Chi-square = 4.627, p = 0.031, RNagelkerke2 = 0.064, Cohen f = 0.07). The present study showed that BFlh morphology is age- and biological maturation-dependent and that BFlh ACSAavg can be considered a relevant modifiable variable associated with lower extremity injuries in youth competitive alpine skiers

IL-18, but not IL-15, contributes to the IL-12-dependent induction of NK-cell effector functions by Leishmania infantum in vivo

Activation of NK cells is a hallmark of infections with intracellular pathogens. We previously showed that the protozoan parasite Leishmania infantum triggered a rapid NK-cell response in mice that required TLR9-positive myeloid DC and IL-12, but no IFN-α/β. Here, we investigated whether IL-15 or IL-18 mediate the activity of IL-12 or function as independent activators of NK cells. In contrast to earlier studies that described IL-15 as crucial for NK-cell priming in response to TLR ligands, the expression of IFN-γ, FasL, perforin and granzyme B by NK cells in L. infantum-infected mice was completely preserved in the absence of IL-15, whereas the proliferative capacity of NK cells was lower than in WT mice. IFN-γ secretion, cytotoxicity and FasL expression of NK cells from infected IL-18−/− mice were significantly reduced compared with controls, but, unlike IL-12, IL-18 was not essential for NK-cell effector functions. Part of the NK-cell-stimulatory effect of IL-12 was dependent on IL-18. We conclude that IL-15 is not functioning as a universal NK-cell priming signal and that IL-18 contributes to the NK-cell response in visceral leishmaniasis. The cytokine requirements for NK-cell activation appear to differ contingent upon the infectious pathogen

TLR-mediated stimulation of APC: Distinct cytokine responses of B cells and dendritic cells

In addition to their role in humoral immunity, B lymphocytes are important antigen-presenting cells (APC). In the same way as other APC, B cells make cytokines upon activation and have the potential to modulate T cell responses. In this study, we investigated which mouse B cell subsets are the most potent cytokine producers, and examined the role of Toll-like receptors (TLR) in the control of secretion of IL-6, IL-10, IL-12 and IFN-γ by B cells. Production of some cytokines was restricted to particular subsets. Marginal zone and B1 cells were the predominant source of B cell IL-10 in the spleen. Conversely, follicular B cells were found to express IFN-γ mRNA directly ex vivo. The nature of the activating stimulus dramatically influenced the cytokine made by B cells. Thus, in response to combined TLR stimulation, or via phorbol esters, IFN-γ was secreted. IL-10 was elicited by T-dependent activation or stimulation through TLR2, 4 or 9. This pattern of cytokine expression contrasts with that elicited from dendritic cells. QRT-PCR array data indicate that this may be due to differential expression of TLR signalling molecules, effectors and adaptors. Our data highlight the potentially unique nature of immune modulation when B cells act as APC

Modeling T Cell Antigen Discrimination Based on Feedback Control of Digital ERK Responses

T-lymphocyte activation displays a remarkable combination of speed, sensitivity, and discrimination in response to peptide–major histocompatibility complex (pMHC) ligand engagement of clonally distributed antigen receptors (T cell receptors or TCRs). Even a few foreign pMHCs on the surface of an antigen-presenting cell trigger effective signaling within seconds, whereas 1 × 10(5)–1 × 10(6) self-pMHC ligands that may differ from the foreign stimulus by only a single amino acid fail to elicit this response. No existing model accounts for this nearly absolute distinction between closely related TCR ligands while also preserving the other canonical features of T-cell responses. Here we document the unexpected highly amplified and digital nature of extracellular signal-regulated kinase (ERK) activation in T cells. Based on this observation and evidence that competing positive- and negative-feedback loops contribute to TCR ligand discrimination, we constructed a new mathematical model of proximal TCR-dependent signaling. The model made clear that competition between a digital positive feedback based on ERK activity and an analog negative feedback involving SH2 domain-containing tyrosine phosphatase (SHP-1) was critical for defining a sharp ligand-discrimination threshold while preserving a rapid and sensitive response. Several nontrivial predictions of this model, including the notion that this threshold is highly sensitive to small changes in SHP-1 expression levels during cellular differentiation, were confirmed by experiment. These results combining computation and experiment reveal that ligand discrimination by T cells is controlled by the dynamics of competing feedback loops that regulate a high-gain digital amplifier, which is itself modulated during differentiation by alterations in the intracellular concentrations of key enzymes. The organization of the signaling network that we model here may be a prototypic solution to the problem of achieving ligand selectivity, low noise, and high sensitivity in biological responses

Using distinct molecular signatures of human monocytes and dendritic cells to predict adjuvant activity and pyrogenicity of TLR agonists

We present a systematic study that defines molecular profiles of adjuvanticity and pyrogenicity induced by agonists of human Toll-like receptor molecules in vitro. Using P3CSK4, Lipid A and Poly I:C as model adjuvants we show that all three molecules enhance the expansion of IFNγ+/CD4+ T cells from their naïve precursors following priming with allogeneic DC in vitro. In contrast, co-culture of naive CD4+ T cells with allogeneic monocytes and TLR2/TLR4 agonists only resulted in enhanced T cell proliferation. Distinct APC molecular signatures in response to each TLR agonist underline the dual effect observed on T cell responses. Using protein and gene expression assays, we show that TNF-α and CXCL10 represent DC-restricted molecular signatures of TLR2/TLR4 and TLR3 activation, respectively, in sharp contrast to IL-6 produced by monocytes upon stimulation with P3CSK4 and Lipid A. Furthermore, although all TLR agonists are able to up-regulate proIL-1β specific gene in both cell types, only monocyte activation with Lipid A results in detectable IL-1β release. These molecular profiles, provide a simple screen to select new immune enhancers of human Th1 responses suitable for clinical application

Surface-Anchored Monomeric Agonist pMHCs Alone Trigger TCR with High Sensitivity

At the interface between T cell and antigen-presenting cell (APC), peptide antigen presented by MHC (pMHC) binds to the T cell receptor (TCR) and initiates signaling. The mechanism of TCR signal initiation, or triggering, remains unclear. An interesting aspect of this puzzle is that although soluble agonist pMHCs cannot trigger TCR even at high concentrations, the same ligands trigger TCR very efficiently on the surface of APCs. Here, using lipid bilayers or plastic-based artificial APCs with defined components, we identify the critical APC-associated factors that confer agonist pMHCs with such potency. We found that CD4+ T cells are triggered by very low numbers of monomeric agonist pMHCs anchored on fluid lipid bilayers or fixed plastic surfaces, in the absence of any other APC surface molecules. Importantly, on bilayers, plastic surfaces, or real APCs, endogenous pMHCs did not enhance TCR triggering. TCR triggering, however, critically depended upon the adhesiveness of the surface and an intact T cell actin cytoskeleton. Based on these observations, we propose the receptor deformation model of TCR triggering to explain the remarkable sensitivity and specificity of TCR triggering

Constitutively elevated levels of SOCS1 suppress innate responses in DF-1 immortalised chicken fibroblast cells.

The spontaneously immortalised DF-1 cell line is rapidly replacing its progenitor primary chicken embryo fibroblasts (CEFs) for studies on avian viruses such as avian influenza but no comprehensive study has as yet been reported comparing their innate immunity phenotypes. We conducted microarray analyses of DF-1 and CEFs, under both normal and stimulated conditions using chicken interferon-α (chIFN-α) and the attenuated infectious bursal disease virus vaccine strain PBG98. We found that DF-1 have an attenuated innate response compared to CEFs. Basal expression levels of Suppressor of Cytokine Signalling 1 (chSOCS1), a negative regulator of cytokine signalling in mammals, are 16-fold higher in DF-1 than in CEFs. The chSOCS1 “SOCS box” domain (which in mammals, interacts with an E3 ubiquitin ligase complex) is not essential for the inhibition of cytokine-induced JAK/STAT signalling activation in DF-1. Overexpression of SOCS1 in chIFN-α-stimulated DF-1 led to a relative decrease in expression of interferon-stimulated genes (ISGs; MX1 and IFIT5) and increased viral yield in response to PBG98 infection. Conversely, knockdown of SOCS1 enhanced induction of ISGs and reduced viral yield in chIFN-α-stimulated DF-1. Consequently, SOCS1 reduces induction of the IFN signalling pathway in chicken cells and can potentiate virus replication