Impact of Strength Training Intensity on Brain-derived Neurotrophic Factor.

The present study employed a randomized crossover design to investigate the effect of strength-training exercise at varying intensities on acute changes in plasma brain-derived neurotrophic factor (BDNF) levels. Fourteen trained male subjects (41.0±5.8 years old) were enrolled in the current study. The strength-training protocol included bench press, leg press, and lat pull-down exercises. Participants performed four sets with repetition failure at 60% or 80% of their one-repetition maximum (1RM), with a two-minute rest period. The order of intensity was randomized among volunteers. Blood samples were collected before, immediately after, and one hour after each exercise protocol. A time-point comparison revealed that a single session of strength training at 60% of 1RM increased lactate plasma concentrations from 1.2 to 16 mmol/L (p<0.0001). However, no significant changes were observed in the plasma BDNF concentration. Conversely, the training session at 80% of 1RM increased lactate concentrations from 1.3 to 14 mmol/L (p<0.0001) and BDNF concentrations from 461 to 1730 pg/ml (p=0.035) one hour after the session's conclusion. These findings support the hypothesis that a single strength-training session at 80% 1RM can significantly enhance circulating levels of BDNF.

Acute and Chronic Effects of Strength Training on Plasma Levels of Adipokines in Man.

Adipose tissue is specialized cells that produce and release adipokines. Exercise may modulate adipokine production in adipocytes. The aim of this longitudinal study was to evaluate the acute and chronic effects of strength training (ST) on plasma levels of adiponectin, leptin, and resistin. Twelve untrained young male participants (23.42±2.67 years) were selected. The training protocol consisted of 3 exercises, with 3 sets of 65% of 1RM (one-repetition maximum) with pause of 90 s between sets with duration of 5 s/repetition (2 s conc/3 s ecc), 3 times a week for 10 weeks. Blood was collected at four time points: before and after the first ST session and before and after the last ST session. The comparisons between adipokine levels before and after the same training session showed acute changes, while the comparisons between levels before or after the first session versus before or after the last session revealed chronic alterations. ST increased adiponectin levels after the first exercise session in comparison to levels before this session [50 952 (46 568-51 894) pg/mL vs. 52 981 (49 901-54 467) pg/mL, p=0.019]. Similar differences were observed for resistin levels, which were higher after the last session compared to before [4 214.4 (±829) pg/mL vs. pre-S30 2 251.3 (±462.2) pg/mL, p=0.0008] and in the comparison between after the last and after the first ST sessions [4 214.4 (±829.0) pg/mL vs. 1 563.7 (±284.8) pg/mL, p=0.004]. Leptin levels acutely changed in the last training session. ST produced acute and chronic changes in plasma adipokines.

Telomere shortening in late-life depression: A potential marker of depression severity.

OBJECTIVES: Telomeres are structures at the extremity of chromosomes that prevents genomic instability, and its shortening seems to be a hallmark of cellular aging. Past studies have shown contradictory results of telomere length (TL) in major depression, and are a few studies in late-life depression (LLD). This explores the association between TL as a molecular marker of aging and diagnosis of LLD, the severity of depressive symptoms, and cognitive performance in older adults. METHODS/DESIGN: We included 78 older adults (45 with LLD and 33 nondepressed controls, according to DSM-V criteria), aged 60-90 years. TL was measured in leukocytes by a quantitative polymerase chain reaction, determining the relative ratio (T/S) between the telomere region copy number (T) and a single copy gene (S), using a relative standard curve. RESULTS: TL was significantly shorter in the LLD compared with control participants (p = .039). Comparing groups through the severity of depressive symptoms, we found a negative correlation with the severity of depressive symptoms (Hamilton Depression Rating Scale-21, r = -0.325, p = .004) and medical burden (r = -0.271, p = .038). There was no significant correlation between TL and cognitive performance (Mattis Dementia Rating Scale, r = 0.152, p = .21). CONCLUSIONS: We found that older adults with LLD have shorter telomere than healthy controls, especially those with a more severe depressive episode. Our findings suggest that shorter TL can be a marker of the severity of depressive episodes in older adults and indicate that these individuals may be at higher risk of age-associated adverse outcomes linked to depression.

Brain-enriched MicroRNA-184 is downregulated in older adults with major depressive disorder: A translational study.

Changes in microRNAs (miRNAs) expression have been described in major depressive disorder in young and middle-aged adults. However, no study has evaluated miRNA expression in older adults with major depression (or late-life depression [LLD]). Our primary aim was to evaluate the expression of miRNAs in subjects with LLD. We first evaluated the miRNA expression using next-generation sequencing (NGS) and then we validated the miRNAs found in NGS in an independent sample of LLD patients, using RT-qPCR. Drosophila melanogaster model was used to evaluate the impact of changes in miRNA expression on behavior. NGS analysis showed that hsa-miR-184 (log2foldchange = -4.21, p = 1.2 × 10-03) and hsa-miR-1-3p (log2foldchange = -3.45, p = 1.3 × 10-02) were significantly downregulated in LLD compared to the control group. RT-qPCR validated the downregulation of hsa-miR-184 (p < 0.001), but not for the hsa-miR-1-3p. The knockout flies of the ortholog of hsa-miR-184 showed significantly reduced locomotor activity at 21-24 d.p.e (p = 0.04) and worse memory retention at 21-24 d.p.e (24h post-stimulus, p = 0.02) compared to control flies. Our results demonstrated that subjects with LLD have significant downregulation of hsa-miR-184. Moreover, the knockout of hsa-miR-184 in flies lead to depressive-like behaviors, being more pronounce in older flies.