Short-term meditation training alters brain activity and sympathetic responses at rest, but not during meditation.

Although more people are engaging in meditation practices that require specialized training, few studies address the issues associated with nervous activity pattern changes brought about by such training. For beginners, it remains unclear how much practice is needed before objective physiological changes can be detected, whether or not they are similar across the novices and what are the optimal strategies to track these changes. To clarify these questions we recruited individuals with no prior meditation experience. The experimental group underwent an eight-week Taoist meditation course administered by a professional, while the control group listened to audiobooks. Both groups participated in audio-guided, 34-min long meditation sessions before and after the 8-week long intervention. Their EEG, photoplethysmogram, respiration, and skin conductance were recorded during the mediation and resting state periods. Compared to the control group, the experimental group exhibited band-specific topically organized changes of the resting state brain activity and heart rate variability associated with sympathetic system activation. Importantly, no significant changes were found during the meditation process prior and post the 8-week training in either of the groups. The absence of notable changes in CNS and ANS activity indicators during meditation sessions, for both the experimental and control groups, casts doubt on the effectiveness of wearable biofeedback devices in meditation practice. This finding redirects focus to the importance of monitoring resting state activity to evaluate progress in beginner meditators. Also, 16 h of training is not enough for forming individual objectively different strategies manifested during the meditation sessions. Our results contributed to the development of tools to objectively monitor the progress in novice meditators and the choice of the relevant monitoring strategies. According to our findings, in order to track early changes brought about by the meditation practice it is preferable to monitor brain activity outside the actual meditation sessions.

Postural control in emotional states: An effect of biofeedback.

BACKGROUND: Emotional states in the short term and affective impairments, such as anxiety and depression in the long run, can have a significant impact on postural control. Individuals with these conditions often struggle with maintaining balance during emotionally charged situations, which can increase their risk of falls and injuries. Biofeedback has been proposed as a potential intervention to improve postural control during emotional induction. RESEARCH QUESTION: How do emotional stimuli affect postural control performance in the presence of real-time postural feedback? METHODS: Forty-two participants took part in the study. The visual stimuli used in the experiment to induce emotions of various valence in the subjects were video clips, containing a series of pictures (24 positive, 24 neutral and 24 negative pictures). During the experiment, participants were required to maintain balance standing on a force platform while watching the videos on a computer screen. For each subject, three sessions of 480 s were generated, each of which included two conditions: with and without biofeedback (a target on the screen indicating the subject's position relative to the center of pressure (CoP). RESULTS: The No Feedback condition provoked a higher medial-lateral and anterior-posterior sway, but lower velocity of CoP than the Feedback condition. We did not find any effect of the valence of emotional videos on indicators of postural control in No Feedback condition. However, both negative and positive videos provoked a lower velocity of CoP in comparison to neutral videos in the Feedback condition. SIGNIFICANCE: Changes observed in postural control during the Feedback condition in the presence of emotional stimuli (both negative and positive) could be explained by the shift in attention from the task of maintaining posture to the emotional videos. The results of this study have important implications for clinicians involved in postural training and rehabilitation.

Cortical and autonomic responses during staged Taoist meditation: Two distinct meditation strategies.

Meditation is a consciousness state associated with specific physiological and neural correlates. Numerous investigations of these correlates reported controversial results which prevented a consistent depiction of the underlying neurophysiological processes. Here we investigated the dynamics of multiple neurophysiological indicators during a staged meditation session. We measured the physiological changes at rest and during the guided Taoist meditation in experienced meditators and naive subjects. We recorded EEG, respiration, galvanic skin response, and photoplethysmography. All subjects followed the same instructions split into 16 stages. In the experienced meditators group we identified two subgroups with different physiological markers dynamics. One subgroup showed several signs of general relaxation evident from the changes in heart rate variability, respiratory rate, and EEG rhythmic activity. The other subgroup exhibited mind concentration patterns primarily noticeable in the EEG recordings while no autonomic responses occurred. The duration and type of previous meditation experience or any baseline indicators we measured did not explain the segregation of the meditators into these two groups. These results suggest that two distinct meditation strategies could be used by experienced meditators, which partly explains the inconsistent results reported in the earlier studies evaluating meditation effects. Our findings are also relevant to the development of the high-end biofeedback systems.

Semax, synthetic ACTH(4-10) analogue, attenuates behavioural and neurochemical alterations following early-life fluvoxamine exposure in white rats.

Selective serotonin reuptake inhibitors (SSRI) are commonly used to treat depression during pregnancy. SSRIs cross the placenta and may influence the maturation of the foetal brain. Clinical and preclinical findings suggest long-term consequences of SSRI perinatal exposure for the offspring. The mechanisms of SSRI effects on developing brain remain largely unknown and there are no directional approaches for prevention of the consequences of maternal SSRI treatment during pregnancy. The heptapeptide Semax (MEHFPGP) is a synthetic analogue of ACTH(4-10) which exerts marked nootropic and neuroprotective activities. The aim of the present study was to investigate the long-term effects of neonatal exposure to the SSRI fluvoxamine (FA) in white rats. Additionally, the study examined the potential for Semax to prevent the negative consequences of neonatal FA exposure. Rat pups received FA or vehicle injections on postnatal days 1-14, a time period equivalent to 27-40 weeks of human foetal age. After FA treatment, rats were administered with Semax or vehicle on postnatal days 15-28. During the 2nd month of life, the rats underwent behavioural testing, and monoamine levels in brain structures were measured. It was shown that neonatal FA exposure leads to the impaired emotional response to stress and novelty and delayed acquisition of food-motivated maze task in adolescent and young adult rats. Furthermore, FA exposure induced alterations in the monoamine levels in brains of 1- and 2- month-old rats. Semax administration reduced the anxiety-like behaviour, improved learning abilities and normalized the levels of brain biogenic amines impaired by the FA exposure. The results demonstrate that early-life FA exposure in rat pups produces long-term disturbances in their anxiety-related behaviour, learning abilities, and brain monoamines content. Semax exerts a favourable effect on behaviour and biogenic amine system of rats exposed to the antidepressant. Thus, peptide Semax can prevent behavioural deficits caused by altered 5-HT levels during development.

Activation of Systemic Inflammation and Oxidative Stress in Adolescent Girls with Polycystic Ovary Syndrome in Combination with Metabolic Disorders and Excessive Body Weight.

RELEVANCE: Mitochondrial dysfunction and systemic inflammation are believed to play pivotal role in the pathogenesis of polycystic ovary syndrome (PCOS) and related complications of metabolic disorders in adult patients. Though such researches are limited or almost absent in adolescents. The aim of the study is to evaluate the impact of mitochondrial dysfunction and systemic inflammation on PCOS pathogenesis during adolescence with regard to body mass index and insulin resistance. DESIGN: a case-control study. METHODS: The study included 95 adolescent girls (15 to 17 years old inclusive) diagnosed with PCOS based on the Rotterdam criteria. The control group consisted of 30 healthy girls of the same age with a regular menstrual cycle. All participants were subjected to a full clinical and instrumental examination, as well as an assessment of the levels of leptin, C-reactive protein (CRP), and malondialdehyde (MDA) as oxidative stress marker. Serum levels of IL-6, IL-10, IL-18, TNF-α, and plasma concentrations of macrophage migration inhibitory factor (MIF), sFas, and sFasL were determined. Patients with PCOS were divided into groups according to the presence of metabolic disorders (MD) (impaired glucose tolerance and/or over insulin resistance) and normal weight or excessive weight (NW or OW). RESULTS: Patients with PCOS of NW in the absence of metabolic disorders (MD-/NW) had a lower concentration of MDA and a higher level of IL-10 compared to healthy girls (p < 0.05). The group (MD-/NW) was characterized with lower levels of CRP, leptin, MDA, and higher levels of sFasL, when compared to OW patients with PCOS in the absence of metabolic disorders (MD-/OW) (p < 0.05). Overweight adolescent girls with PCOS and metabolic disorders (MD+/OW) showed higher CRP, leptin, and a two-fold increase in IL-6 and IL-18 concentrations compared to the control group of healthy girls (p < 0.05 for all parameters). The group (MD+/OW) was also characterized with higher levels of CRP, leptin, MDA, IL-18, MIF (p < 0.05), when compared to overweight patients with PCOS in the absence of metabolic disorders (MD-/NW). In comparison with the MD-/OW group, the obese insulin resistant girls with PCOS (MD+/OW) had a highera level of IL-18 (p < 0.05). Moreover, the MD+/OW girls demonstrated a significant increase in CRP, MDA and IL-18 levels when compared to the MD+/NW group (p < 0.05). OW girls with PCOS without MD (MD-/OW) had lower concentrations of sFasL compared to healthy girls (p < 0.05), and higher levels of MDA compared to MD+/NW (p < 0.05). Adolescent girls of NW with PCOS and with MD (MD+/NW) had lower levels of MDA compared to the control group of healthy girls (p < 0.05). These data are confirmed by a correlation analysis and two-factor ANOVA test. CONCLUSIONS: Lean girls with PCOS demonstrate the protective mechanism of decrease in oxidative stress mediated by the activation of antioxidant defense, reduction of lipid peroxidation and systemic inflammation. Excessive weight and metabolic disorders in adolescents with PCOS are the most significant factors in reducing the capacity of antioxidant systems, activation of oxidative stress, mitochondrial dysfunction, and systemic inflammation.

Knockdown of the neuronal gene Lim3 at the early stages of development affects mitochondrial function and lifespan in Drosophila.

Understanding the molecular mechanisms underlying variation in lifespan is central to ensure long life. Lim3 encoding a homolog of the vertebrate Lhx3/4 transcription factors plays a key role in Drosophila neuron development. Here, we demonstrated that Lim3 knockdown early in life decreased survival of adult flies. To study the mechanisms underlying this effect, we identified embryonic Lim3 targets using combined RNA-seq and RT-qPCR analyses complemented by in silico analysis of Lim3 binding sites. Though genes with neuronal functions were revealed as Lim3 targets, the characteristics of neurons were not affected by Lim3 depletion. Many of the direct and indirect Lim3 target genes were associated with mitochondrial function, ATP-related activity, redox processes and antioxidant defense. Consistent with the observed changes in the embryonic transcription of these genes, ROS levels were increased in embryos, which could cause changes in the transcription of indirect Lim3 targets known to affect lifespan. We hypothesize that altered mitochondrial activity is crucial for the decrease of adult lifespan caused by Lim3 knockdown early in life. In adults that encountered Lim3 depletion early in life, the transcription of several genes remained altered, and mitochondrial membrane potential, ATP level and locomotion were increased, confirming the existence of carry-over effects.

Gestation age-associated dynamics of mitochondrial calcium uniporter subunits expression in feto-maternal complex at term and preterm delivery.

Calcium plays a role of universal cellular regulator in the living cell and one of the crucial regulators of proper fetal development during gestation. Mitochondria are important for intracellular calcium handling and signaling. Mitochondrial calcium uniporter (mtCU) is a multiprotein complex of the mitochondrial inner membrane responsible for the transport of calcium to the mitochondrial matrix. In the present study, we analyzed the expression level of mtCU components in two parts of the feto-maternal system - placenta and myometrium at full-term delivery and at preterm birth (PTB) on different stages: 22-27, 28-32, 33-36 weeks of gestation (n = 50). A gradual increase of mRNA expression and changes in protein content of MCU and MICU1 subunits were revealed in the placenta during gestation. We also observed slower depolarization rate of isolated placental mitochondria induced by Ca2+ titration at PTB. In myometrium at PTB relative gene expression level of MCU, MCUb and SMDT1 increased as compared to full-term pregnancy, but the tendency to gradual increase of MCU protein simultaneous with MCUb increase and MICU1 decline was shown in gestational dynamics. Changes observed in the present study might be considered both natural dynamics as well as possible pathological mechanisms underlying preterm birth.

Effect of aerobic training on baseline expression of signaling and respiratory proteins in human skeletal muscle.

Most studies examining the molecular mechanisms underlying adaptation of human skeletal muscles to aerobic exercise focused on the response to acute exercise. Here, we examined the effect of a 2-month aerobic training program on baseline parameters in human muscle. Ten untrained males performed a one-legged knee extension exercise for 1 h with the same relative intensity before and after a 2-month aerobic training program. Biopsy samples were taken from vastus lateralis muscle at rest before and after the 2 month training program (baseline samples). Additionally, biopsy samples were taken from the exercised leg 1 and 4 h after the one-legged continuous knee extension exercise. Aerobic training decreases baseline phosphorylation of FOXO1Ser256 , increases that of CaMKIIThr286 , CREB1Ser133 , increases baseline expression of mitochondrial proteins in respiratory complexes I-V, and some regulators of mitochondrial biogenesis (TFAM, NR4A3, and CRTC2). An increase in the baseline content of these proteins was not associated with a change in baseline expression of their genes. The increase in the baseline content of regulators of mitochondrial biogenesis (TFAM and NR4A3) was associated with a transient increase in transcription after acute exercise. Contrariwise, the increase in the baseline content of respiratory proteins does not seem to be regulated at the transcriptional level; rather, it is associated with other mechanisms. Adaptation of human skeletal muscle to regular aerobic exercise is associated not only with transient molecular responses to exercise, but also with changes in baseline phosphorylation and expression of regulatory proteins.

Alterations in antioxidant system, mitochondrial biogenesis and autophagy in preeclamptic myometrium.

Preeclampsia is a pregnancy complication which causes significant maternal and fetal morbidity and mortality worldwide. Although intensive research has been performed in the last 40 years, the pathology of preeclampsia is still poorly understood. The present work is a comparative study of the myometrium of women with normal pregnancy, and those with late- and early-onset preeclampsia (n = 10 for each group). We observed significant changes in the levels of antioxidant enzymes, markers of mitochondrial biogenesis and autophagy proteins in preeclamptic myometrium. Levels of superoxide dismutase 1 and catalase were lower in both preeclamptic groups than the control group. In late-onset preeclampsia, expression levels of essential mitochondria-related proteins VDAC1, TFAM, hexokinase 1, PGC-1α and PGC-1ß, and autophagy marker LC3A, were significantly elevated. In the myometrium of the early-onset preeclampsia group OPA1 and Bcl-2 were up-regulated compared to those of the control (p < 0.05). These findings suggest that crucial molecular changes in the maternal myometrium occur with the development of preeclampsia.

Cumulus cell mitochondrial activity in relation to body mass index in women undergoing assisted reproductive therapy.

Most studies have considered the negative influence of obesity on fertility in both genders. In the present study, we assessed mitochondrial activity expressed as the mitochondrial potential index (MPI) in cumulus cells from obese women and women with a normal body mass index (BMI) during assisted reproductive therapy. The results revealed a significant reduction of MPI with increased body mass. The lower MPI levels in cumulus cells from obese women may reflect mitochondrial dysfunction caused by oxidative stress, which can affect the cumulus-oocyte complex and have an impact on oocyte development.

Mitochondrial role in adaptive response to stress conditions in preeclampsia.

Preeclampsia (PE) is a pregnancy-specific syndrome, characterized in general by hypertension with proteinuria or other systemic disturbances. PE is the major cause of maternal and fetal morbidity and mortality worldwide. However, the etiology of PE still remains unclear. Our study involved 38 patients: 14 with uncomplicated pregnancy; 13 with early-onset PE (eoPE); and 11 with late-onset PE (loPE). We characterized the immunophenotype of cells isolated from the placenta and all biopsy samples were stained positive for Cytokeratin 7, SOX2, Nestin, Vimentin, and CD44. We obtained a significant increase in OPA1 mRNA and protein expression in the eoPE placentas. Moreover, TFAM expression was down-regulated in comparison to the control (p < 0.01). Mitochondrial DNA copy number in eoPE placentas was significantly higher than in samples from normal pregnancies. We observed an increase of maximum coupled state 3 respiration rate in mitochondria isolated from the placenta in the presence of complex I substrates in the eoPE group and an increase of P/O ratio, citrate synthase activity and decrease of Ca(2+)-induced depolarization rate in both PE groups. Our results suggest an essential role of mitochondrial activity changes in an adaptive response to the development of PE.