Objective: The purpose of this article was to summarize the available evidence from systematic reviews on telerehabilitation in physical therapy. Methods: We searched Medline/PubMed, EMBASE, and Cochrane Library databases. In addition, the records in PROSPERO and Epistemonikos and PEDro were consulted. Systematic reviews of different conditions, populations, and contexts—where the intervention to be evaluated is telerehabilitation by physical therapy—were included. The outcomes were clinical effectiveness depending on specific condition, functionality, quality of life, satisfaction, adherence, and safety. Data extraction and risk of bias assessment were carried out by a reviewer with non-independent verification by a second reviewer. The findings are reported qualitatively in the tables and figures. Results: Fifty-three systematic reviews were included, of which 17 were assessed as having low risk of bias. Fifteen reviews were on cardiorespiratory rehabilitation, 14 on musculoskeletal conditions, and 13 on neurorehabilitation. The other 11 reviews addressed other types of conditions and rehabilitation. Thirteen reviews evaluated with low risk of bias showed results in favor of telerehabilitation versus in-person rehabilitation or no rehabilitation, while 17 reported no differences between the groups. Thirty-five reviews with unclear or high risk of bias showed mixed results. Conclusions: Despite the contradictory results, telerehabilitation in physical therapy could be comparable with in-person rehabilitation or better than no rehabilitation for conditions such as osteoarthritis, low-back pain, hip and knee replacement, and multiple sclerosis and also in the context of cardiac and pulmonary rehabilitation. It is imperative to conduct better quality clinical trials and systematic reviews. Impact: Providing the best available evidence on the effectiveness of telerehabilitation to professionals, mainly physical therapists, will impact the decision-making process and therefore yield better clinical outcomes for patients, both in these times of the COVID-19 pandemic and in the future. The identification of research gaps will also contribute to the generation of relevant and novel research questions.

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.

Habilidades motoras, cualidades físicas y períodos sensibles en el desarrollo escolar

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.