Vitamin D has been widely studied for its implications on type 2 diabetes mellitus, a chronic condition characterized by insulin resistance, inflammation, and metabolic dysfunction. This review explores the molecular mechanisms underpinning vitamin D’s effects on glucose metabolism, inflammation, and adipogenesis, while assessing its potential clinical applications in type 2 diabetes. In its 1,25-dihydroxyvitamin D3 form, vitamin D modulates various metabolic processes, affecting proinflammatory cytokines and activating the AMPK pathway, inhibiting mTOR signaling, and promoting adipocyte differentiation. These effects enhance insulin sensitivity and reduce chronic inflammation, key contributors to metabolic dysfunction. In this context, the progression of prediabetes has been linked to vitamin D, which limits pathological progression and increases the likelihood of restoring a normal metabolic state, crucial in diabetes progression. Moreover, vitamin D has been reported to reduce the likelihood of developing diabetes by 15%, particularly in doses higher than the traditional recommendations for bone health. Despite promising evidence, discrepancies in study designs, serum vitamin D measurements, and population-specific factors highlight the need for standardized methodologies and personalized approaches. In conclusion, vitamin D has complementary therapeutic potential in treating type 2 diabetes, revealing gaps in research, such as optimal dosing and long-term effects across populations. Future studies should integrate molecular insights into clinical practice to optimize vitamin D’s impact on metabolic health.

Sarcopenia is a progressive age-related musculoskeletal disorder characterized by loss of muscle mass, strength, and physical performance, contributing to functional decline and increased risk of disability. Emerging evidence suggests that vitamin D (Vit D) plays a pivotal role in skeletal muscle physiology beyond its classical functions in bone metabolism. This review aims to critically analyze the relationship between serum Vit D levels and sarcopenia in older adults, focusing on pathophysiological mechanisms, diagnostic criteria, clinical evidence, and preventive strategies. An integrative narrative review of observational studies, randomized controlled trials, and meta-analyses published in the last decade was conducted. The analysis incorporated international diagnostic criteria for sarcopenia (EWGSOP2, AWGS, FNIH, IWGS), current guidelines for Vit D sufficiency, and molecular mechanisms related to Vit D receptor (VDR) signaling in muscle tissue. Low serum 25-hydroxyvitamin D levels are consistently associated with decreased muscle strength, reduced physical performance, and increased prevalence of sarcopenia. Although interventional trials using Vit D supplementation report variable results, benefits are more evident in individuals with baseline deficiency and when combined with protein intake and resistance training. Mechanistically, Vit D influences muscle health via genomic and non-genomic pathways, regulating calcium homeostasis, mitochondrial function, oxidative stress, and inflammatory signaling. Vit D deficiency represents a modifiable risk factor for sarcopenia and functional impairment in older adults. While current evidence supports its role in muscular health, future high-quality trials are needed to establish optimal serum thresholds and dosing strategies for prevention and treatment. An individualized, multimodal approach involving supplementation, exercise, and nutritional optimization appears most promising.

Type 2 Diabetes Mellitus (T2DM) is a complex metabolic disorder characterized by insulin resistance, chronic low-grade inflammation, and progressive metabolic dysfunction affecting multiple organs. This review explores the molecular and physiological mechanisms underlying T2DM, emphasizing the role of intracellular metabolic signaling pathways, mitochondrial function, and inter-organ communication in the development and progression of metabolic dysregulation. Particular attention is given to key regulatory pathways such as AMP-activated protein kinase (AMPK) and the mechanistic target of rapamycin (mTOR), which play central roles in cellular energy sensing, glucose metabolism, and lipid homeostasis. Dysregulation of these pathways contributes to impaired insulin signaling, mitochondrial dysfunction, oxidative stress, and altered adipogenesis, all of which are critical factors in the pathophysiology of T2DM. In addition, growing evidence highlights the importance of metabolic crosstalk between skeletal muscle, adipose tissue, liver, pancreas, and the gut microbiota through signaling molecules including adipokines, myokines, hepatokines, and gut-derived metabolites. These inter-organ networks influence systemic inflammation, metabolic flexibility, and glucose homeostasis. Lifestyle factors such as physical activity, nutritional patterns, and micronutrient status have also been shown to modulate these molecular pathways, improving mitochondrial function and insulin sensitivity while reducing inflammatory signaling. Despite significant advances in understanding the molecular basis of T2DM, important challenges remain, including heterogeneity in disease progression and variability in individual metabolic responses. In conclusion, T2DM should be understood as a multisystem metabolic disorder driven by complex interactions between molecular signaling pathways and systemic metabolic regulation. Future research integrating molecular mechanisms with clinical and lifestyle interventions may help develop more effective strategies for prevention and treatment.

Physical exercise is a potent non-pharmacological strategy for the prevention and management of chronic non-communicable diseases (NCDs), including type 2 diabetes, cardiovascular diseases, obesity, and certain cancers. Growing evidence demonstrates that the benefits of exercise extend beyond its physiological effects and are largely mediated by coordinated molecular and cellular adaptations. This review synthesizes current knowledge on the key mechanisms through which exercise modulates metabolic health, emphasizing intracellular signaling pathways, epigenetic regulation, and myokine-driven inter-organ communication. Exercise induces acute and chronic activation of pathways such as AMPK, PGC-1α, mTOR, MAPKs, and NF-κB, leading to enhanced mitochondrial biogenesis, improved oxidative capacity, refined energy sensing, and reduced inflammation. Additionally, repeated muscle contraction stimulates the release of myokines—including IL-6, irisin, BDNF, FGF21, apelin, and others—that act through endocrine and paracrine routes to regulate glucose and lipid metabolism, insulin secretion, adipose tissue remodeling, neuroplasticity, and systemic inflammatory tone. Epigenetic modifications and exercise-responsive microRNAs further contribute to long-term metabolic reprogramming. Collectively, these molecular adaptations establish exercise as a systemic biological stimulus capable of restoring metabolic homeostasis and counteracting the pathophysiological processes underlying NCDs. Understanding these mechanisms provides a foundation for developing targeted, personalized exercise-based interventions in preventive and therapeutic medicine.

This study aimed to associate morphological variables and physical fitness with health-related quality of life (HRQoL) in physically active older people. A cross-sectional study was carried out that evaluated 470 older people (89.57% female) with a mean age of 70.13 ± 6.57 years, residing in two regions of Chile. Morphological variables (body weight, bipedal height, waist circumference, body mass index, and waist to height ratio), physical fitness through the Senior Fitness Test protocol, and HRQoL using the SF-36 questionnaire were obtained. Logistic regression analysis was used to identify risk factors between morphological variables and physical fitness associated with HRQoL. The main results indicated that overweight (OR = 1.52; p = 0.034), a waist circumference with risk (OR = 1.56; p = 0.021), poor performance in the back scratch tests (OR = 1.02; p = 0.008) and timed up-and-go (OR = 1.19; p = 0.040) increased the probability of having a low general HRQoL. Also, the low performance of chair stand and arm curl tests was associated with poor physical and social dimensions of HRQoL (p < 0.05). In conclusion, a low HRQoL in physically active older people is associated with both morphological and physical fitness factors.

Introducción: El método de entrenamiento de fuerza isoinercial presenta beneficios tanto en el campo del deporte y la rehabilitación. La evidencia disponible sugiere que este tipo de entrenamiento aumenta la fuerza y velocidad de las respuestas musculares. El objetivo de este estudio fue analizar los efectos de seis semanas de entrenamiento isoinercial sobre la capacidad de salto, velocidad de carrera y equilibrio postural dinámico en adultos no entrenados. Método: El diseño de este estudio fue pre-experimental. La selección de los participantes fue realizada de manera no probabilística por conveniencia. La muestra fue compuesta por 8 adultos, 4 personas de sexo femenino y 4 de sexo masculino. Se realizaron evaluaciones de evaluación de la fuerza explosiva a través del countermovement jump (CMJ), la prueba de carrera de 20 metros y la prueba de equilibrio postural dinámico Star Excursion Balance Test modificada (SEBTm). Todas las evaluaciones fueron realizadas pre y post un entrenamiento isoinercial. Resultados: Posterior al programa de entrenamiento isoinercial, la capacidad de salto aumentó un 17% en hombres y un 15% en mujeres. El tiempo de carrera disminuyó un 22% tanto en hombres como mujeres. El equilibrio postural dinámico también mostró un mejor rendimiento en las tres direcciones evaluadas en hombres y mujeres sometidos al entrenamiento isoinercial. Conclusión: El entrenamiento de fuerza con el método isoinercial parece ser una herramienta eficaz para la mejora de la capacidad de salto CMJ, velocidad de carrera y equilibrio postural dinámico en adultos saludables no entrenados. Palabras clave: entrenamiento de fuerza; fuerza muscular; destreza motora; control postural; rendimiento físico funcional. Introduction: The isoinertial strength training method has benefits both in the field of sports and rehabilitation. The available evidence suggests that this type of training increases the strength and velocity of muscle responses. The aim of this study was to analyze the effects of six weeks of isoinertial training on jumping ability, running speed, and dynamic postural balance in untrained adults. Method: The design of this study was pre-experimental. The selection of the participants was carried out in a non-probabilistic way for convenience. The sample was composed of 8 adults, 4 females and 4 males. Explosive strength assessment tests were performed through the countermovement jump (CMJ), the 20-meter sprint test, and the modified Star Excursion Balance Test (SEBTm) for dynamic postural balance test. All evaluations were performed before and after isoinertial training. Results: After the isoinertial training program, jump ability increased by 17% in men and 15% in women. Race time decreased by 22% in both men and women. Dynamic postural balance also showed better performance in the three directions evaluated in men and women who underwent isoinertial training. Conclusion: Strength training with the isoinertial method seems to be an effective tool for improving CMJ jump ability, running velocity and dynamic postural balance in healthy untrained adults. Keywords: strength training; muscular strength; motor skills; Postural control; functional physical performance.