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.

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Regular exercise ameliorates motor symptoms in Parkinson’s disease (PD). Here, we aimed to provide evidence that exercise brings additional benefits to the whole-body metabolism and skeletal muscle molecular and functional characteristics, which might help to explain exercise-induced improvements in the clinical state. 3-months supervised endurance/strength training was performed in early/mid-stage PD patients and age/gender-matched individuals (n = 11/11). The effects of exercise on resting energy expenditure (REE), glucose metabolism, adiposity, and muscle energy metabolism (31P-MRS) were evaluated and compared to non-exercising PD patients. Two muscle biopsies were taken to determine intervention-induced changes in fiber type, mitochondrial content, and expression of genes related to muscle energy metabolism, as well as proliferative and regenerative capacity. Exercise improved the clinical disability score (MDS-UPDRS), bradykinesia, balance, walking speed, REE, and glucose metabolism and increased muscle expression of energy sensors (AMPK). However, the exercise-induced increase in muscle mass/strength, mitochondrial content, type II fiber size, and postexercise phosphocreatine (PCr) recovery (31P-MRS) were found only in controls. Nevertheless, MDS-UPDRS was associated with muscle AMPK and mechano-growth factor (MGF) expression. Improvements in fasting glycemia were positively associated with muscle function and the expression of Sirt1 and Cox7a1, and the parameters of fitness/strength were positively associated with the expression of MyHC2, MyHC7, and MGF. Moreover, reduced bradykinesia was associated with better muscle metabolism (maximal oxidative capacity and postexercise PCr recovery; 31P-MRS). Exercise training improved the clinical state in early/mid-stage Parkinson’s disease patients, including motor functions and whole-body metabolism. Although the adaptive response to exercise in PD was different from that of controls, exercise-induced improvements in the PD clinical state were associated with specific adaptive changes in muscle functional, metabolic, and molecular characteristics.Clinical Trial Registration, identifier NCT02253732.

The study compared the effect of 12-week multimodal training programme performed twice a week at the regular exercise facility (REF) with the 12-week multimodal training programme performed three times per week as a part of the research programme (EX). Additionally, the study analysed how the experimental training programme affect the physical performance of cognitive healthy and mild cognitive impaired elderly (MCI). The REF training group included 19 elderly (65.00±3.62 years). The experimental training programme combined cognitively healthy (EXH: n=16; 66.3±6.42 years) and age-matched individuals with MCI (EXMCI: n=14; 66.00±4.79 years). 10m maximal walking speed (10mMWS), Five Times Sit-to-Stand Test (FTSS), maximal and relative voluntary contraction (MVC & rel. MVC) were analysed. The REF group improved in 10mMWS (t=2.431, p=.026), the MVC (t=-3.528, p=.002) and relative MVC (t=3.553, p=.002). The EXH group improved in FTSS (t=5.210, P=.000), MVC (t=2.771, p=.018) and relative MVC (t=-3.793, p=.004). EXMCI improved in FTSS (t=2.936, p=.012) and MVC (t=-2.276, p=.040). According to results, both training programmes sufficiently improved walking speed and muscle strength in cognitively healthy elderly. Moreover, the experimental training programme improved muscle strength in MCI elderly.

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Background Physical inactivity accelerates ageing‐associated cognitive decline while regular physical exercise improves neurocognitive health, in parallel with improvements of physical fitness and whole‐body metabolism. However, the knowledge on putative bioactive molecules, mediators of exercise benefits in human brain is still very limited. Our aim was to evaluate effects of the aerobic‐strength training intervention on the spectrum of chemokines/cytokines in the cerebrospinal fluid (CSF) of elderly individuals. Method The CSF from the subgroup of ten elderly individuals (1M/9F; controls/MCI patients 4/6; age = 65.7 ± 3.9yrs; BMI = 25.8 ± 3.5 kg/m2), who underwent 3‐month supervised aerobic‐strength training (3 × 1 h/week), was obtained by the atraumatic lumbar puncture technique before and after training intervention. Levels of 174 chemokines/cytokines were measured with the aid of the cytokine array (RayBiotech). Body weight and composition (Dual‐energy x‐ray absorptiometry/DEXA), BMI, physical fitness (VO2max, Rockport walk test) and cognitive functions (Addenbrooke's Cognitive Examination/ACE‐R, Trail making test A/TMT‐A, computerized cognitive test Cogstate) were assessed. Result Aerobic‐strength training improved aerobic fitness (VO2max, p = 0.03), cognitive functions (ACE‐R score, p = 0.0033; TMT‐A time score, p = 0.027; Learning/working memory, p = 0.016; Visual learning, p = 0.03) and reduced gynoid fat mass (p = 0.01). Three‐month supervised aerobic‐strength training intervention significantly modulated 5 out of 174 examined cytokines in CSF of the elderly individuals. Levels of 2 cytokines were increased by +11.7% and +11.3%, respectively (both p < 0.05), and another three cytokines displayed reduced levels >5% (p < 0.05 for all) in response to training. All distinctly regulated cytokines have previously been shown to be involved in the regulation of neuroinflammation, blood‐brain‐barrier integrity, and neuroprotection. Conclusion Supervised 3‐month aerobic‐strength training improved aerobic physical fitness and cognitive functions in the elderly. The distinct modulation of chemokines and cytokines in cerebrospinal fluid in response to training intervention could indicate a role of these bioactive molecules in the exercise‐induced adaptive response in human brain. Funding: APVV 15/0253, VEGA 2/0107/18, SAS‐MOST JRP 2018/10.