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Objective: To conduct a systematic review evaluating the impact of stretching on inflammation and its resolution using in vivo rodent models. Findings are evaluated for their potential to inform the design of clinical yoga studies to assess the impact of yogic stretching on inflammation and health. Methods: Studies were identified using four databases. Eligible publications included English original peer-reviewed articles between 1900–May 2020. Studies included those investigating the effect of different stretching techniques administered to a whole rodent model and evaluating at least one inflammatory outcome. Studies stretching the musculoskeletal and integumentary systems were considered. Two reviewers removed duplicates, screened abstracts, conducted full-text reviews, and assessed methodological quality. Results: Of 766 studies identified, 25 were included for synthesis. Seven (28%) studies had a high risk of bias in 3 out of 10 criteria. Experimental stretching protocols resulted in a continuum of inflammatory responses with therapeutic and injurious effects, which varied with a combination of three stretching parameters––duration, frequency, and intensity. Relative to injurious stretching, therapeutic stretching featured longer-term stretching protocols. Evidence of pro- and mixed-inflammatory effects of stretching was found in 16 muscle studies. Evidence of pro-, anti-, and mixed-inflammatory effects was found in nine longer-term stretching studies of the integumentary system. Conclusion: Despite the overall high quality of these summarized studies, evaluation of stretching protocols paralleling yogic stretching is limited. Both injurious and therapeutic stretching induce aspects of inflammatory responses that varied among the different stretching protocols. Inflammatory markers, such as cytokines, are potential outcomes to consider in clinical yoga studies. Future translational research evaluating therapeutic benefits should consider in vitro studies, active vs. passive stretching, shorter-term vs. longer-term interventions, systemic vs. local effects of stretching, animal models resembling human anatomy, control and estimation of non-specific stresses, development of in vivo self-stretching paradigms targeting myofascial tissues, and in vivo models accounting for gross musculoskeletal posture. [ABSTRACT FROM AUTHOR]

Aging is the major risk factor for neurodegenerative diseases such as Alzheimer's disease, but little is known about the processes that lead to age-related decline of brain structures and function. Here we use RNA-seq in combination with high resolution histological analyses to show that aging leads to a significant deterioration of neurovascular structures including basement membrane reduction, pericyte loss, and astrocyte dysfunction. Neurovascular decline was sufficient to cause vascular leakage and correlated strongly with an increase in neuroinflammation including up-regulation of complement component C1QA in microglia/monocytes. Importantly, long-term aerobic exercise from midlife to old age prevented this age-related neurovascular decline, reduced C1QA+ microglia/monocytes, and increased synaptic plasticity and overall behavioral capabilities of aged mice. Concomitant with age-related neurovascular decline and complement activation, astrocytic Apoe dramatically decreased in aged mice, a decrease that was prevented by exercise. Given the role of APOE in maintaining the neurovascular unit and as an anti-inflammatory molecule, this suggests a possible link between astrocytic Apoe, age-related neurovascular dysfunction and microglia/monocyte activation. To test this, Apoe-deficient mice were exercised from midlife to old age and in contrast to wild-type (Apoe-sufficient) mice, exercise had little to no effect on age-related neurovascular decline or microglia/monocyte activation in the absence of APOE. Collectively, our data shows that neurovascular structures decline with age, a process that we propose to be intimately linked to complement activation in microglia/monocytes. Exercise prevents these changes, but not in the absence of APOE, opening up new avenues for understanding the complex interactions between neurovascular and neuroinflammatory responses in aging and neurodegenerative diseases such as Alzheimer’s disease. [ABSTRACT FROM AUTHOR]