Abstract
Exercise can prevent the sedentary lifestyle-related risk of metabolic and cognitive decline, but mechanisms and mediators of exercise effects on human brain are relatively unexplored. We measured acute exercise-induced changes in adiponectin, insulin and other bioactive molecules in cerebrospinal fluid (CSF) and serum from young lean individuals. Samples of serum and CSF were obtained before and 1-h after the 90-min run (75–80% HRmax; maximal heart rate), additional serum was taken at finish-line. Body composition, physical fitness, metabolic rate, cognitive functions, food preference, glucose, insulin and albumin were measured. The spectrum of 174 cytokines was assessed by protein arrays, adiponectin was also determined by ELISA and immunoblotting. CSF adiponectin decreased post-exercise by 21.3% (arrays) and 25.8% (ELISA) (p < 0.009). Immunoblotting revealed reduction in a low-molecular-weight-adiponectin (p < 0.005). CSF adiponectin positively correlated with CSF/serum albumin ratio (p < 0.022), an indicator of blood-brain-barrier permeability. CSF and serum adiponectin were positively associated with memory and running-induced changes in insulinemia and CSF insulin. Additionally, running modulated CSF levels of 16 other cytokines. Acute running reduced CSF adiponectin and modulated insulin and albumin in CSF and serum. Associations of adiponectin with memory and metabolism indicate the potential role of this bioactive molecule in mediating exercise-induced adaptive response in human brain.
Highlights
Regular exercise represents an effective prevention and treatment of metabolic and neurodegenerative diseases[1]
Neumeier et al used the relationship between cerebrospinal fluid (CSF)/serum ratios of albumin and adiponectin to indicate changes of blood-brain-barrier or blood-CSF-barrier permeability, which could be implicated in adiponectin transport[12]
Neuroprotective actions of adiponectin were observed in murine brain[18,19,20,21], while adiponectin deficiency in mice was associated with reduced dendritic lenght/branching/spine density of neurons and decreased neurogenesis, which could be reversed by intracerebroventricular infusion of adiponectin[21]
Summary
Regular exercise represents an effective prevention and treatment of metabolic and neurodegenerative diseases[1]. Mechanisms mediating exercise-induced health benefits in both periphery and the brain include changes in body composition[2] and energy metabolism[3], reduction of systemic inflammation[4] and secretion of bioactive molecules[5,6]. Aged adiponectin-deficient mice display spatial memory and learning impairments, fear-conditioned memory deficits as well as anxiety These mice even develop Alzheimer’s disease (AD) pathology, which is associated with hippocampal insulin resistance[20]. The aim of our study was to investigate effects of running on levels of CSF and/or serum cytokines, insulin and albumin in young healthy individuals in association with cognitive functions, metabolism, food preference and physical fitness, in order to identify putative molecular mediators of exercise-induced effects on the brain
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