Artificial intelligence (AI)-enabled wearable sensors are increasingly studied in sport rehabilitation, but the literature spans multiple disciplines and application settings. This study aimed to map publication patterns, major contributors, research themes, and temporal trends within the focused intersection of AI, wearable sensing, and sport rehabilitation. English-language articles and reviews were retrieved from the Web of Science Core Collection (SCIE and ESCI) from December 15, 2005 to December 15, 2024. After applying date, document-type, language, and manual title/abstract relevance screening, bibliometric and visualization analyses were conducted with CiteSpace. Analyses covered publication trends, authors, institutions, countries/regions, Web of Science categories, keywords, citation bursts, and co-citation patterns. A total of 81 publications were included. Within this Web of Science corpus, the USA and China contributed the largest numbers of publications (36 and 12, respectively), and the Pennsylvania Commonwealth System of Higher Education had the highest institutional output. Keyword and temporal patterns were dominated by machine learning, wearable sensors, gait analysis, musculoskeletal disorders, rehabilitation, activity recognition, and risk prediction. These patterns are consistent with increasing research attention to AI-supported and personalized rehabilitation applications, but they should be interpreted descriptively given the small corpus. This study provides a focused bibliometric map of AI and wearable sensors in sport rehabilitation rather than a comprehensive evidence synthesis. The observed publication, keyword, and co-citation patterns suggest growing research attention to AI-supported rehabilitation applications, but bibliometric mapping cannot establish clinical effectiveness or demonstrate technological transformation. Interpretation is limited by the single-database, English-language search, manual relevance screening, small corpus, and citation- and keyword-related biases. Future studies should use multi-database searches, independent screening, sensitivity analyses, and clinical evidence synthesis.
Angiotensin II (Ang II) is a main cause of cardiac remodeling from hypertension, will lead to inflammation, impaired autophagy, and ferroptosis. It is well established that exercise has cardioprotective benefits. However, it is not clear whether exercise alters ferroptosis and autophagy in Ang II-induced cardiac injury. Twenty-four male C57BL/6 mice were randomly divided into four groups: control, Ang II, Ang II+low-intensity exercise (LIE), and Ang II+high-intensity exercise (HIE). Ang II was administered for 4 weeks, while the exercise groups performed treadmill exercise 5 days/week. Cardiac tissue was analyzed using hematoxylin–eosin staining, Western blotting, reverse transcription quantitative PCR, and correlation analysis. After 4 weeks of intervention, Ang II injection increased TNF-α and p62 protein levels (p < 0.05). Ang II+HIE significantly reduced TNF-α and IL-6 expression and restored autophagy markers (p < 0.05). Regarding ferroptosis, exercise did not change the NRF2 and GPX4 protein levels, but Gpx4 mRNA was elevated in the Ang II+LIE group. Pearson correlation analysis revealed that TNF-α was negatively correlated with NRF2/GPX4 and autophagy proteins, while NRF2 was positively correlated with ATG3/ATG7 and negatively correlated with p62. The findings indicate that HIE had a greater influence on Ang II-induced cardiac inflammatory responses and autophagy-related markers. In contrast, LIE showed partial effects, including decreased p62 expression and increased Gpx4 mRNA expression. The changes in exercise-induced ferroptosis-related factors were mainly at the transcription level, not protein level. The results suggest that exercise intensity differentially modulates inflammation, autophagy-related markers, and ferroptosis-related responses in Ang II-induced cardiac stress.
Tobacco control in low- and middle-income countries (LMICs) predominantly emphasises smoking cessation, with limited integration of physical activity despite its potential complementary benefits. This study examines the dual physiological effects—mitigating and risk-revealing—of structured aerobic exercise on active smokers in a Nigerian setting. A quasi-experimental 12-week intervention was conducted with 26 male participants (13 active smokers, 13 non-smokers) aged 20–55 years in Gusau, Zamfara State, Nigeria. Participants completed supervised, progressive treadmill sessions (40 min, three times weekly: 5-min warm-up, 30-min continuous aerobic exercise at 60–80
This study investigated physical and psychological attributes associated with sprint-event specialization among athletes competing in the 100 m, 200 m, and 400 m events. It examined differences in body composition, explosive power, sprint-protocol time, strength, endurance, estimated maximal aerobic capacity, and mental toughness. A cross-sectional study included 75 competitive male sprinters, with 25 athletes in each of the 100 m, 200 m, and 400 m groups. Body composition, including BIA-estimated skeletal muscle mass (SMM; kg), was assessed using multi-frequency bioelectrical impedance analysis, lower-limb explosive power using the standing broad jump, total sprint-protocol time using a 30 m sprint test comprising acceleration and flying phases, and upper-body power using underhand forward and overhead backward medicine-ball throws. Agility, aerobic endurance, anaerobic speed endurance, and estimated maximal aerobic capacity were evaluated using standardized field tests. The Sport Mental Toughness Questionnaire (SMTQ) assessed confidence, constancy, and control. Differences among the three sprint-event groups were examined using one-way analysis of variance followed by Tukey-adjusted or Games–Howell post hoc comparisons, as appropriate. Mean bias-reduced multinomial logistic regression was used to examine associations of standardized body-composition, physical-performance, and mental-toughness variables with sprint-event specialization, with the 100 m group specified as the reference category. Significant between-group differences were observed across several physical and psychological outcomes. The 100 m sprinters demonstrated the greatest standing broad jump distance (2.52 ± 0.13 m), whereas the 400 m sprinters achieved the lowest (2.07 ± 0.16 m, p < 0.001). Total 30 m sprint-protocol time was lowest in the 100 m group (7.92 ± 0.88 s), followed by the 400 m group (9.44 ± 1.21 s), and was highest in the 200 m group (10.66 ± 1.94 s, p < 0.001). The 400 m group demonstrated the highest shuttle-run-derived estimated VO2max (61.48 ± 1.88 mL.kg−1.min−1, p < 0.001) and total mental toughness score (37.04 ± 2.54, p < 0.001), whereas the 200 m sprinters recorded the lowest mean times in the 150 m flying-sprint (14.77 ± 2.48 s) and 300 m standing-start sprint tests (36.11 ± 1.39 s) (p < 0.001). In the exploratory mean bias-reduced multinomial logistic regression, a one-standard-deviation increase in BIA-estimated skeletal muscle mass was associated with lower relative odds of membership in the 200 m group versus the 100 m group (OR = 0.17, 95
Although increasing physical activity (PA) can substantially curb the metabolic syndrome, the causal effect of specific PA modification on the incidence of type 2 diabetes mellitus (T2DM) remains unclear. In this Mendelian randomization (MR) study, we evaluated the causal role of eight PA traits on T2DM, and investigated potential mediators linking PA to T2DM. Genetic instruments for PA and potential mediators were obtained from UK Biobank. Summary statistics for the association of these traits with T2DM were obtained from FinnGen. Potential mediators were identified via performing phenome-wide association study and searching for literature. Inverse-variance weighted model was used to estimate the causal effect. Mediating role of traits linking PA and T2DM were evaluated using multi-variable MR. Rigorous sensitivity analyses were conducted to assess the robustness of results. Accelerometer-measured vigorous physical activity (VPA) (OR = 0.402, 95
