To compare the acute effects of a cycling intervention on carotid arterial hemodynamics between basketball athletes and sedentary controls. Ten young long-term trained male basketball athletes (BA) and nine age-matched male sedentary controls (SC) successively underwent four bouts of exercise on a bicycle ergometer at the same workload. Hemodynamic variables at right common carotid artery were determined at rest and immediately following each bout of exercise. An ANCOVA was used to compare differences between the BA and SC groups at rest and immediately following the cycling intervention. The repeated ANOVA was used to assess differences between baseline and each bout of exercise within the BA or SC group. In both groups, carotid hemodynamic variables showed significant differences at rest and immediately after the cycling intervention. At rest, carotid arterial stiffness was significantly decreased and carotid arterial diameter was significantly increased in the BA group as compared to the SC group. Immediately following the cycling intervention, carotid arterial stiffness showed no obvious changes in the BA group but significantly increased in the SC group. It is worth noting that while arterial stiffness was lower in the BA group than in the SC group, the oscillatory shear index (OSI) was significantly higher in the BA group than in the SC group both at rest and immediately following the cycling intervention. Long-term basketball exercise had a significant impact on common carotid arterial hemodynamic variables not only at rest but also after a cycling intervention. The role of OSI in the remodeling of arterial structure and function in the BA group at rest and after cycling requires clarification.

Exercise has been found to either reduce or increase arterial stiffness. Land-based exercise modalities have been documented as effective physical therapies to decrease arterial stiffness. However, these land-based exercise modalities may not be suitable for overweight individuals, in terms of risks of joint injury. The purpose of this study was to determine the effects of 8-week swimming training and 4-week detraining on carotid arterial stiffness and hemodynamics in young overweight adults. Twenty young male adults who were overweight were recruited and engaged in 8-week of swimming training and 4-week detraining. Five individuals withdrew due to lack of interest and failure to follow the training protocol. Body Fat Percentage (BFP) and carotid hemodynamic variables were measured on a resting day at the following intervals: baseline, 4 weeks, 8 weeks after swimming training and 4 weeks after detraining. A repeated analysis of variance (ANOVA) was used to assess the differences between baseline and each measurement. When significant differences were detected, Tukey’s test for post hoc comparisons was used. Eight-week swimming training at moderate intensity decreased BFP, including the trunk and four extremities. Additionally, the BFP of the right and left lower extremities continued to decrease in these overweight adults 4 weeks after ceasing training. Carotid arterial stiffness decreased, while there were no significant changes in arterial diameters. Blood flow velocity, flow rate, maximal and mean wall shear stress increased, while systolic blood pressure and peripheral resistance decreased. No significant differences existed in minimal wall shear stress and oscillatory shear stress. Eight-week swimming training at moderate intensity exhibited beneficial effects on systolic blood pressure, arterial stiffness and blood supply to the brain in overweight adults. Moreover, maximal and mean wall shear stress increased after training. It is worth noting that these changes in hemodynamics did not last 4 weeks. Therefore, further studies are still warranted to clarify the underlying relationship between improvements in arterial stiffness and alterations in wall shear stress.

Background: Chronic musculoskeletal pain is a prevalent condition that causes substantial personal and societal burden, yet the effectiveness of non-pharmacological interventions remains debated. Cognitive behavioral therapy (CBT) and CBT-oriented cognitive-based interventions have been increasingly applied to pain management, but evidence has been fragmented across populations and treatment modalities. This study aimed to provide an updated synthesis of randomized controlled trials (RCTs) evaluating the efficacy of CBT for chronic musculoskeletal pain. Methods: We conducted a systematic search of PubMed, Web of Science, Scopus, Embase, PsycINFO, and the Cochrane Library. Eligible studies were screened according to predefined criteria, quality was assessed using the Cochrane Risk of Bias 2 tool (ROB 2.0) and statistical analyses were performed in Stata 15.1. Results: Fourteen high-quality RCTs involving 2,677 patients were included. Meta-analysis indicated that CBT significantly reduced pain catastrophizing (SMD = −0.77, 95% CI: −1.10 to −0.43, p < 0.05), pain intensity (SMD = −0.41, 95% CI: −0.62 to −0.20, p < 0.05), and functional disability (SMD = −0.20, 95% CI: −0.36 to −0.03, p < 0.05). Subgroup analyses of pain intensity further identified a cluster of six studies showing consistent intervention effects (SMD = −0.22, p < 0.001), although the specific factors underlying this consistency remain unclear. Functional disability outcomes varied by measurement tool, with significant and homogeneous effects in the RMDQ subgroup (SMD = −0.21, p < 0.05) but nonsignificant, heterogeneous results in the ODI subgroup. For catastrophizing, both CBT and pain-coping skills training (PCST) significantly reduced scores (SMD = −0.74 and −0.89, respectively). Conclusion: These findings suggest that CBT exerts consistent therapeutic benefits for chronic musculoskeletal pain, supporting its role as a reliable clinical non-pharmacological treatment option. Systematic review registration: This study protocol has been registered with the International Prospective Register of Systematic Reviews (PROSPERO) (registration number: CRD420251073898).