A Higher Kick Frequency Swimming Training Program Optimizes Swim-to-Cycle Transition in Triathlon.

ABSTRACT: Ambrosini, L, Presta, V, Vitale, M, Menegatti, E, Guarnieri, A, Bianchi, V, De Munari, I, Condello, G, and Gobbi, G. A higher kick frequency swimming training program optimizes swim-to-cycle transition in triathlon. J Strength Cond Res 38(5): 976-984, 2024-The purpose of this study was to evaluate the effect of an 8-week swimming training program on biomechanical and physiological responses during a swim-to-cycle simulation. Fifteen triathletes were randomly allocated to 3 groups: a 6-beat-kick group (K6), a 4-beat-kick group (K4), and a control group (CG). Biomechanical and physiological parameters were evaluated during a 400-m swim and a 10-minute cycle segment before (Pretraining) and after (Posttraining) the program. A lower stroke frequency ( p = 0.004) and a higher stroke length ( p = 0.002) was found in K6 compared with CG at Posttraining. A reduction in the K6 emerged between Pretraining and Posttraining during cycling for heart rate ( p = 0.005), V̇O 2 ( p = 0.014), and energy expenditure ( p = 0.008). A positive association emerged between swim kick index and cycling cadence in the K6 group. The improvement in stroke frequency and length observed in the K6 group could be explained as an improvement in swimming technique. Similarly, the reduction in energy expenditure during cycling at Posttraining for the K6 group suggests an improvement in the working economy. Triathlon coaches and athletes should consider the inclusion of high swim kick into their training programs to enhance swim and cycling performance, which can ultimately lead to an improvement in the swim-to-cycle transition and the overall triathlon performance.

Sodium-glucose cotransporter 2 inhibitors antagonize lipotoxicity in human myeloid angiogenic cells and ADP-dependent activation in human platelets: potential relevance to prevention of cardiovascular events.

BACKGROUND: The clear evidence of cardiovascular benefits in cardiovascular outcome trials of sodium-glucose cotransporter 2 inhibitors (SGLT2i) in type 2 diabetes might suggest an effect on atherosclerotic plaque vulnerability and/or thrombosis, in which myeloid angiogenic cells (MAC) and platelets (PLT) are implicated. We tested the effects of SGLT2i on inflammation and oxidant stress in a model of stearic acid (SA)-induced lipotoxicity in MAC and on PLT activation. The possible involvement of the Na+/H+ exchanger (NHE) was also explored. METHOD: MAC and PLT were isolated from peripheral blood of healthy subjects and incubated with/without SGLT2i [empagliflozin (EMPA) and dapagliflozin (DAPA) 1-100 µM] to assess their effects on SA (100 µM)-induced readouts of inflammation, oxidant stress and apoptosis in MAC and on expression of PLT activation markers by flow-cytometry after ADP-stimulation. Potential NHE involvement was tested with amiloride (aspecific NHE inhibitor) or cariporide (NHE1 inhibitor). Differences among culture conditions were identified using one-way ANOVA or Friedman test. RESULTS: NHE isoforms (1,5-9), but not SGLT2 expression, were expressed in MAC and PLT. EMPA and DAPA (100 µM) significantly reduced SA-induced inflammation (IL1ß, TNFα, MCP1), oxidant stress (SOD2, TXN, HO1), but not apoptosis in MAC. EMPA and DAPA (both 1 µM) reduced PLT activation (CD62p and PAC1 expression). SGLT2i effects were mimicked by amiloride, and only partially by cariporide, in MAC, and by both inhibitors in PLT. CONCLUSIONS: EMPA and DAPA ameliorated lipotoxic damage in stearate-treated MAC, and reduced ADP-stimulated PLT activation, potentially via NHE-inhibition, thereby pointing to plaque stabilization and/or thrombosis inhibition as potential mechanism(s) involved in SGLT2i-mediated cardiovascular protection.

ROS in Platelet Biology: Functional Aspects and Methodological Insights.

Reactive oxygen species (ROS) and mitochondria play a pivotal role in regulating platelet functions. Platelet activation determines a drastic change in redox balance and in platelet metabolism. Indeed, several signaling pathways have been demonstrated to induce ROS production by NAPDH oxidase (NOX) and mitochondria, upon platelet activation. Platelet-derived ROS, in turn, boost further ROS production and consequent platelet activation, adhesion and recruitment in an auto-amplifying loop. This vicious circle results in a platelet procoagulant phenotype and apoptosis, both accounting for the high thrombotic risk in oxidative stress-related diseases. This review sought to elucidate molecular mechanisms underlying ROS production upon platelet activation and the effects of an altered redox balance on platelet function, focusing on the main advances that have been made in platelet redox biology. Furthermore, given the increasing interest in this field, we also describe the up-to-date methods for detecting platelets, ROS and the platelet bioenergetic profile, which have been proposed as potential disease biomarkers.

PKCε promotes human Th17 differentiation: Implications in the pathophysiology of psoriasis.

PKCε is implicated in T cell activation and proliferation and is overexpressed in CD4+ -T cells from patients with autoimmune Hashimoto's thyroiditis. Although this might induce the suspicion that PKCε takes part in autoimmunity, its role in the molecular pathophysiology of immune-mediated disorders is still largely unknown. We studied PKCε expression in circulating CD4+ -T cells from patients with psoriasis, a skin disorder characterized by an increased amount of Th17 cells, a CD4+ subset that is critical in the development of autoimmunity. Although the mechanisms that underlie Th17 differentiation in humans are still unclear, we here show that: (i) PKCε is overexpressed in CD4+ -T cells from psoriatic patients, and its expression positively correlates with the severity of the disease, being reduced by effective phototherapy; (ii) PKCε interacts with Stat3 during Th17 differentiation and its overexpression results in an enhanced expression of Stat3 and pStat3(Ser727); iii) conversely, when PKCε is forcibly downregulated, CD4+ -T cells show lower levels of pStat3(Ser727) expression and defective in vitro expansion into the Th17-lineage. These data provide a novel insight into the molecular mechanisms of Th17 cell polarization that is known to play a crucial role in autoimmunity, pinpointing PKCε as a potential target in Th17-mediated diseases.

Human thrombopoiesis depends on Protein kinase Cδ/protein kinase Cε functional couple.

A deeper understanding of the molecular events driving megakaryocytopoiesis and thrombopoiesis is essential to regulate in vitro and in vivo platelet production for clinical applications. We previously documented the crucial role of PKCε in the regulation of human and mouse megakaryocyte maturation and platelet release. However, since several data show that different PKC isoforms fulfill complementary functions, we targeted PKCε and PKCδ, which show functional and phenotypical reciprocity, at the same time as boosting platelet production in vitro. Results show that PKCδ, contrary to PKCε, is persistently expressed during megakaryocytic differentiation, and a forced PKCδ down-modulation impairs megakaryocyte maturation and platelet production. PKCδ and PKCε work as a functional couple with opposite roles on thrombopoiesis, and the modulation of their balance strongly impacts platelet production. Indeed, we show an imbalance of PKCδ/PKCε ratio both in primary myelofibrosis and essential thrombocythemia, featured by impaired megakaryocyte differentiation and increased platelet production, respectively. Finally, we demonstrate that concurrent molecular targeting of both PKCδ and PKCε represents a strategy for in vitro platelet factories.

Proplatelet generation in the mouse requires PKCε-dependent RhoA inhibition.

During thrombopoiesis, megakaroycytes undergo extensive cytoskeletal remodeling to form proplatelet extensions that eventually produce mature platelets. Proplatelet formation is a tightly orchestrated process that depends on dynamic regulation of both tubulin reorganization and Rho-associated, coiled-coil containing protein kinase/RhoA activity. A disruption in tubulin dynamics or RhoA activity impairs proplatelet formation and alters platelet morphology. We previously observed that protein kinase Cepsilon (PKCε), a member of the protein kinase C family of serine/threonine-kinases, expression varies during human megakaryocyte differentiation and modulates megakaryocyte maturation and platelet release. Here we used an in vitro model of murine platelet production to investigate a potential role for PKCε in proplatelet formation. By immunofluorescence we observed that PKCε colocalizes with α/ß-tubulin in specific areas of the marginal tubular-coil in proplatelets. Moreover, we found that PKCε expression escalates during megakarocyte differentiation and remains elevated in proplatelets, whereas the active form of RhoA is substantially downregulated in proplatelets. PKCε inhibition resulted in lower proplatelet numbers and larger diameter platelets in culture as well as persistent RhoA activation. Finally, we demonstrate that pharmacological inhibition of RhoA is capable of reversing the proplatelet defects mediated by PKCε inhibition. Collectively, these data indicate that by regulating RhoA activity, PKCε is a critical mediator of mouse proplatelet formation in vitro.

Cytofluorimetric platelet analysis.

Blood platelets are highly specialized cells that drive hemostatic events and tissue repair mechanisms at the site of vascular injury. Their peculiar morphology and certain functional characteristics can be analyzed by flow cytometry (FCM). Specifically, platelet activation, a hallmark of prothrombotic states and inflammatory conditions, is associated with changes in expression of both surface and intracellular antigens that are recognized by specific monoclonal antibodies. Assessment of platelet activation status as ex vivo or in vitro reactivity to specific agonists has become relevant in particular conditions (namely, cardiovascular diseases, hematological malignancies, monitoring of pharmacological antiaggregation). In addition, aberrant surface marker expression that characterizes inherited and acquired platelet function disorders is also detected by FCM. This review discusses the main applications of FCM in platelet analyses, which are relevant for both research and clinical settings.

Laboratory diagnostics of inherited platelet disorders.

Abstract Inherited platelet disorders (IPDs) are the general and common denomination of a broad number of different rare and congenital pathologies affecting platelets. Even if these disorders are characterized by widely heterogeneous clinical presentations, all of them are commonly present as defects in hemostasis. Platelet number and/or function are affected by a wide spectrum of severity. IPDs might be associated with defects in bone marrow megakaryocytopoiesis and, rarely, with somatic defects. Although in the last few years new insights in the genetic bases and pathophysiology of IPDs have greatly improved our knowledge of these disorders, much effort still needs to be made in the field of laboratory diagnosis. This review discusses the laboratory approach for the differential diagnosis of the most common IPDs, suggesting a common multistep flowchart model which starts from the simpler test (platelet count) ending with the more selective and sophisticated analyses.

Protein kinase C ε in hematopoiesis: conductor or selector?

Mainly known for its cardioprotective properties, protein kinase C isoform ε (PKCε) is also progressively coming of age in terms of its role in hematopoiesis regulation, particularly that is related to erythropoiesis, megakaryocytopoiesis, and platelet production. Data available to date show that PKCε is differentially regulated in erythrocyte and megakaryocyte progenitors, strongly suggesting an addressing role toward maturation of either lineage. This function appears to be played by either selecting progenitors or conducting maturation toward a specific fate. Inappropriate expression of PKCε in human mature platelets is discussed as a recently described example of functional modification that may acquire pathophysiologic relevance in major thrombotic diseases. Preliminary evidence suggests that PKCε expression may be used as a surrogate marker for thrombotic risk stratification and as a possible target for antiplatelet therapy in patients with thrombotic disorders.

Protein kinase Cε regulates proliferation and cell sensitivity to TGF-1ß of CD4+ T lymphocytes: implications for Hashimoto thyroiditis.

We have studied the functional role of protein kinase Cε (PKCε) in the control of human CD4(+) T cell proliferation and in their response to TGF-1ß. We demonstrate that PKCε sustains CD4(+) T cell proliferation triggered in vitro by CD3 stimulation. Transient knockdown of PKCε expression decreases IL-2R chain transcription, and consequently cell surface expression levels of CD25. PKCε silencing in CD4 T cells potentiates the inhibitory effects of TGF-1ß, whereas in contrast, the forced expression of PKCε virtually abrogates the inhibitory effects of TGF-1ß. Being that PKCε is therefore implicated in the response of CD4 T cells to both CD3-mediated proliferative stimuli and TGF-1ß antiproliferative signals, we studied it in Hashimoto thyroiditis (HT), a pathology characterized by abnormal lymphocyte proliferation and activation. When we analyzed CD4 T cells from HT patients, we found a significant increase of PKCε expression, accounting for their enhanced survival, proliferation, and decreased sensitivity to TGF-1ß. The increased expression of PKCε in CD4(+) T cells of HT patients, which is described for the first time, to our knowledge, in this article, viewed in the perspective of the physiological role of PKCε in normal Th lymphocytes, adds knowledge to the molecular pathophysiology of HT and creates potentially new pharmacological targets for the therapy of this disease.

Notational Analysis of Wheelchair Paralympic Table Tennis Matches.

Paralympic table tennis is the third largest paralympic sport for the number of players. Performance analysis was conducted for the rally duration and interval and impact of serve, whilst none investigated the shots distribution among classes of physical impairment. Therefore, the purpose of this study was to conduct a notational analysis of international competitions in relation to the wheelchair classes. Five matches for each wheelchair class (C1-to-C5) were evaluated from 20 elite male right-handed players. Both players for each match were analyzed for the following performance indicators: strokes type, the area of ball bouncing, and the shots outcome. Backhand shots were the most used technique for all classes. The most used strokes for C1 players were backhand and forehand drive and backhand lob, while for C5 players they were backhand and forehand push and backhand topspin. Similar shots distribution was registered for C2-to-C5 players. The central and far-from-the-net zone was mainly reached by the serve for all classes. Errors shots were similar in all classes, whilst winning shots were more frequent in C1. The current notational analysis provided a meaningful performance modelling of indicators for coaches and athletes that can be used to design training programs for each class.

Interplay between Protein Kinase C Epsilon and Reactive Oxygen Species during Myogenic Differentiation.

Reactive oxygen species (ROS) are currently recognized as a key driver of several physiological processes. Increasing evidence indicates that ROS levels can affect myogenic differentiation, but the molecular mechanisms still need to be elucidated. Protein kinase C (PKC) epsilon (PKCe) promotes muscle stem cell differentiation and regeneration of skeletal muscle after injury. PKCs play a tissue-specific role in redox biology, with specific isoforms being both a target of ROS and an up-stream regulator of ROS production. Therefore, we hypothesized that PKCe represents a molecular link between redox homeostasis and myogenic differentiation. We used an in vitro model of a mouse myoblast cell line (C2C12) to study the PKC-redox axis. We demonstrated that the transition from a myoblast to myotube is typified by increased PKCe protein content and decreased ROS. Intriguingly, the expression of the antioxidant enzyme superoxide dismutase 2 (SOD2) is significantly higher in the late phases of myogenic differentiation, mimicking PKCe protein content. Furthermore, we demonstrated that PKCe inhibition increases ROS and reduces SOD2 protein content while SOD2 silencing did not affect PKCe protein content, suggesting that the kinase could be an up-stream regulator of SOD2. To support this hypothesis, we found that in C2C12 cells, PKCe interacts with Nrf2, whose activation induces SOD2 transcription. Overall, our results indicate that PKCe is capable of activating the antioxidant signaling preventing ROS accumulation in a myotube, eventually promoting myogenic differentiation.

Posture, gait and self-disorders: An empirical study in individuals with schizophrenia.

AIM: In schizophrenia, subjectively perceived disruptions of the sense of the Self (also referred to as "self-disorders") seem to be intimately associated with a perturbation of the implicit awareness of one's own body. Indeed, an early impairment of the motor system, including posture and gait, is now considered a marker of schizophrenia neurodevelopmental substrate and appears more pronounced in early-onset schizophrenia. Therefore, the present study was aimed at: (1) investigating a possible relationship between self-disorders, symptom dimensions and postural and gait profile in schizophrenia; (2) identifying a specific motor profile in early-onset conditions. METHODS: A total of 43 schizophrenia outpatients and 38 healthy controls underwent an exhaustive investigation of posture and gait pattern. The positive and negative syndrome scale (PANSS), the examination of anomalous self experience scale (EASE) and the abnormal involuntary movement scale (AIMS) were administered to the schizophrenia group. Subsequently, schizophrenia patients were divided into early and adult-onset subgroups and compared with respect to their motor profile. RESULTS: We found an association between specific postural patterns (impaired sway area), a general disruption of the gait cycle and subjective bodily experiences (concerning the loss of bodily integrity, cohesion and demarcation). Only motor parameters (increased sway area and gait cadence reduction) differentiated between early and adult-onset patients. CONCLUSION: The results of the present study hint at a link between motor impairment and self-disturbances in schizophrenia and candidate a specific motor profile as a possible marker of early-onset forms.

TRAIL up-regulation must be accompanied by a reciprocal PKCε down-regulation during differentiation of colonic epithelial cell: implications for colorectal cancer cell differentiation.

PKC isoenzymes play central roles in various cellular signalling pathways, participating in a variety of protein phosphorylation cascades that regulate/modulate cellular structure and gene expression. It has been firmly established that several isoforms of PKC have a role in the regulation of tumor necrosis factor-related apoptosis inducing ligand (TRAIL) activity. Our interest in probing the role of the epsilon isoform of PKC in the colonic cell differentiation stems from the discovery that PKCε and TRAIL are involved in the differentiation of other cell types like hematopoietic stem cells. Although the role of PKCε and TRAIL in the gastrointestinal system is unclear, it has been observed that PKCε has oncogenic activity in colon epithelial cells (CEC), while TRAIL increases the death of intestinal epithelial cells during inflammation. Here we demonstrate a reciprocal expression of PKCε and TRAIL in human colon mucosa: CECs at the bottom of the colonic crypts show high levels of PKCε, being negative for TRAIL expression. On the contrary, luminal CECs are positive for TRAIL, while negative for PKCε. Indeed, TRAIL- and butyrate-induced differentiation of the human colorectal cancer cell line HT29 requires the decrease of PKCε expression, whose absence in turn increases cell sensitivity to TRAIL-induced apoptosis. Moreover, TRAIL preferentially promotes HT29 differentiation into goblet cells. Taken together, this data demonstrate that TRAIL and PKCε must be reciprocally regulated to ensure physiological CEC differentiation starting from the stem cell pool, and that the down-regulation of PKCε is however critical for the differentiation and apoptosis of cancer cells.

Abnormal VWF modifies megakaryocytopoiesis: studies of platelets and megakaryocyte cultures from patients with von Willebrand disease type 2B.

von Willebrand factor (VWF) is an essential mediator of platelet adhesion to the vessel wall, but little is known about its role in megakaryocytopoiesis. VWF and its platelet receptor, glycoprotein Ibalpha (GPIbalpha), are both expressed during megakaryocyte (MK) maturation. This study was designed to evaluate whether the enhanced VWF-GPIbalpha interactions typical of patients with von Willebrand disease type 2B (VWD2B) modify platelet production. Platelets from 9 patients with VWD2B with 7 different gain-of-function mutations were examined by electron microscopy (EM) and immunofluorescence labeling. For the patients with VWD2B, EM characteristically showed variable numbers of structurally abnormal giant platelets, sometimes in agglutinates. Cultures of MKs from controls performed with or without purified VWF confirmed a positive influence of VWF on platelet production with specific inhibition by an antibody blocking VWF binding to GPIbalpha. VWD2B MK cultures examined by EM showed a disorganized demarcation membrane system and abnormal granule distribution. They produced platelets with structural abnormalities typical of VWD2B. Confocal examination of MK revealed limited extension of pseudopods with few large proplatelets. These results confirm that megakaryocytopoiesis is modified by the enhanced VWF-GPIbalpha interactions. These data obtained for controls and patients with VWD2B suggest a novel regulatory role of VWF-GPIbalpha interactions in platelet production.

Buffering Adaptive Immunity by Hydrogen Sulfide.

T cell-mediated adaptive immunity is designed to respond to non-self antigens and pathogens through the activation and proliferation of various T cell populations. T helper 1 (Th1), Th2, Th17 and Treg cells finely orchestrate cellular responses through a plethora of paracrine and autocrine stimuli that include cytokines, autacoids, and hormones. Hydrogen sulfide (H2S) is one of these mediators able to induce/inhibit immunological responses, playing a role in inflammatory and autoimmune diseases, neurological disorders, asthma, acute pancreatitis, and sepsis. Both endogenous and exogenous H2S modulate numerous important cell signaling pathways. In monocytes, polymorphonuclear, and T cells H2S impacts on activation, survival, proliferation, polarization, adhesion pathways, and modulates cytokine production and sensitivity to chemokines. Here, we offer a comprehensive review on the role of H2S as a natural buffer able to maintain over time a functional balance between Th1, Th2, Th17 and Treg immunological responses.

Evolution led humans to bipedalism, but we live in a sedentary society: Will "Sunday running" protect us from NCDs at no cost?

Evolution led humans to bipedal stance and movement. However, we live in a sedentary society that strongly challenges our willingness to be physically active. We (mis)understand that being at least a Sunday runner could protect us from sedentary-related diseases, but what if this compromises the healthier life expectancy anyway? Citing Paul Gauguin, we know where we come from and what we are, the question arises about where we are going. And also, how.

Interlink Between Physiological and Biomechanical Changes in the Swim-to-Cycle Transition in Triathlon Events: A Narrative Review.

Triathlon is a multisport composed of swim, cycle, and run segments and two transition periods. The swim-to-cycle transition is considered a critical period for the change in body position and the modifications in physiological (heart rate, VO2, lactate) and biomechanical parameters (cycling power and cadence, swimming stroke rate). Therefore, the aim of this review was to summarize the current evidence regarding the physiological and biomechanical changes and their interlink during the swim-to-cycle transition hinting at practical recommendations for coaches and athletes. The influence of the swim segment on cycle one is more evident for short-distance events. Greater modifications occur in athletes of lower level. The modulation of intensity during the swim segment affects the changes in the physiological parameters (heart rate, blood lactate, core temperature), with a concomitant influence on cycling gross efficiency. However, gross efficiency could be preserved by wearing a wetsuit or by swimming in a drafting position. A higher swim leg frequency during the last meters of the segment induces a higher cadence during the cycle segment. Training should be directed to the maintenance of a swimming intensity around 80-90% of a previous maximal swim test and with the use of a positive pacing strategy. When athletes are intended to train consecutively only swim and cycle segments, for an optimal muscle activation during cycling, triathletes could adopt a lower cadence (about 60-70% of their typical cadence), although an optimal pedaling cadence depends on the level and type of athlete. Future research should be focused on the combined measurements of physiological and biomechanical parameters using an intervention study design to evaluate training adaptations on swim kick rate and their effects on cycling performance. Coaches and athletes could benefit from the understanding of the physiological and biomechanical changes occurring during the swim-to-cycle transition to optimize the overall triathlon performance.

Tracking fibrosis in myeloproliferative neoplasms by CCR2 expression on CD34+ cells.

In myeloproliferative neoplasm (MPNs), bone marrow fibrosis - mainly driven by the neoplastic megakaryocytic clone - dictates a more severe disease stage with dismal prognosis and higher risk of leukemic evolution. Therefore, accurate patient allocation into different disease categories and timely identification of fibrotic transformation are mandatory for adequate treatment planning. Diagnostic strategy still mainly relies on clinical/laboratory assessment and bone marrow histopathology, which, however, requires an invasive procedure and frequently poses challenges also to expert hemopathologists. Here we tested the diagnostic accuracy of the detection, by flow cytometry, of CCR2+CD34+ cells to discriminate among MPN subtypes with different degrees of bone marrow fibrosis. We found that the detection of CCR2 on MPN CD34+ cells has a very good diagnostic accuracy for the differential diagnosis between "true" ET and prePMF (AUC 0.892, P<0.0001), and a good diagnostic accuracy for the differential diagnosis between prePMF and overtPMF (AUC 0.817, P=0.0089). Remarkably, in MPN population, the percentage of CCR2-expressing cells parallels the degree of bone marrow fibrosis. In ET/PV patients with a clinical picture suggestive for transition into spent phase, we demonstrated that only patients with confirmed secondary MF showed significantly higher levels of CCR2+CD34+ cells. Overall, flow cytometric CCR2+CD34+ cell detection can be envisioned in support of conventional bone marrow histopathology in compelling clinical scenarios, with the great advantage of being extremely rapid. For patients in follow-up, its role can be conceived as an initial patient screening for subsequent bone marrow biopsy when disease evolution is suspected.

Branched-Chain Amino Acids Supplementation Does Not Accelerate Recovery after a Change of Direction Sprinting Exercise Protocol.

BCAAs supplementation has been widely used for post-exercise recovery. However, no evidence is currently available to answer the question of whether BCAAs supplementation can attenuate muscle damage and ameliorate recovery after a bout of change of direction (COD) sprinting, which is an exercise motion frequently used during team sport actions. This study aimed to assess the effect of BCAAs supplementation on muscle damage markers, subjective muscle soreness, neuromuscular performance, and the vascular health of collegiate basketball players during a 72 h recovery period after a standardized COD protocol. Participants orally received either BCAAs (0.17 g/kg BCAAs + 0.17 g/kg glucose) or placebo (0.34 g/kg glucose) supplementation before and immediately after a COD exercise protocol in a randomized, crossover, double-blind, and placebo-controlled manner. Creatine kinase increased immediately after exercise and peaked at 24 h, muscle soreness remained elevated until 72 h, whilst arterial stiffness decreased after exercise for both supplemented conditions. A negligibly lower level of interleukin-6 was found in the BCAAs supplemented condition. In conclusion, the results of this study do not support the benefits of BCAAs supplementation on mitigating muscle damage and soreness, neuromuscular performance, and arterial stiffness after COD for basketball players.