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OBJECTIVE: Myofascial release (MFR) comprises a set of manual therapeutic techniques applied to many conditions, but specific evidence concerning its effects on body posture, muscle tension and voice has been lacking. Thus, the aim of this study was to verify the effects of MFR in teachers' posture, muscular tension and voice quality. STUDY DESIGN: Randomized controlled trial - crossover. METHODS: Twenty-four teachers, after completing a Sociodemographic and Clinical Questionnaire and providing written informed consent, were randomly distributed into two groups designated Group 1 (G1; n = 12; received MFR first) and Group 2 (G2; n = 12; belong to control group first). All participants received treatment and were into control group, since, after a 14 day period, procedures were switched between groups. Photogrammetry, muscle tension assessed through palpation, algometry, aerodynamic assessment of voice, acoustic and auditory-perceptual analysis of voice were performed before and after interventions. RESULTS: Regarding voice, statistically significant differences were found when intervention was applied to both groups for maximum phonation time (MPT) (G1 P = 0.019; G2 P = 0.004). The acoustic variables did not differ. Concerning the auditory-perceptual analysis of voice statistically significant differences were found when intervention was applied in both groups for Grade in G2 (P = 0.046) and for Roughness in G1 (P = 0.025). Regarding the photogrammetry assessment statistically significant differences were found when intervention was applied to both groups in many parameters while as control group they did not. Concerning the algometry and muscle tension assessed through palpation statistically significant differences were found when intervention was applied in all muscles. CONCLUSIONS: Findings indicated that MFR seems to be an effective therapy in improving MPT, two subscales (Grade and Roughness) of the GRABASH scale, muscle tension assessed through palpation and algometry. Regarding photogrammetry, MFR had an immediately effect in improvement of the posture, especially related with head.

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OBJECTIVE: This investigation aimed to verify if there were any differences in autonomic nervous system function and voice parameters of teachers with and without voice complaints. STUDY DESIGN: Cross-sectional study. METHODS: The Questionnaire of Autonomic Dysfunction was answered by 24 teachers, 6 males, and 18 females, whose heart rate variability was also assessed. Aerodynamic assessment of voice, acoustic and auditory-perceptual analysis of voice were done. Participants were divided into two groups: without voice complaints (WVCG; n = 11) and with voice complaints (VCG; n = 13) based on the completion of the Sociodemographic and Clinical Questionnaire. RESULTS: For auditory-perceptual analysis, VCG showed significantly higher values on GRBASH subscales Grade (P < 0.001) and Roughness (P = 0.011). Regarding the heart rate variability, it was found that in the VCG, the square root of the mean squared difference of successive RR intervals (RMSSD) and the percentage of adjacent NN intervals differing by more than 50 milliseconds (pNN50) were significantly lower than in the WVCG (P = 0.023 and P = 0.032, respectively). The VCG presented a higher occurrence of neurovegetative symptoms directly related to voice, namely in fluctuating nose obstruction (P = 0.011), neck pain (while or after speaking) (P = 0.017) and in fatigability when speaking (P = 0.004). Concerning the aerodynamic assessment of voice, acoustic analysis of voice and neurovegetative symptoms not directly related to voice, no statistically significant differences between groups were found. CONCLUSIONS: Findings indicated significantly lower values in RMSSD and pNN50 of teachers VCG when compared with teachers WVCG and that the teachers VCG presented a higher occurrence of neurovegetative symptoms directly related to voice than the ones WVCG.

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OBJECTIVE: The interaction between muscle tension, posture, and vocal use is very complex as clinical research suggests that abnormal laryngeal posture can be associated with muscle adaptive changes, although specific evidence concerning body posture and voice disorders has been lacking. Thus, the aim of this study was to verify if there were differences in posture, muscle tension and voice between teachers with and without voice complaints. STUDY DESIGN: Cross-sectional study. METHODS: Twenty-four teachers, 6 males and 18 females, were submitted to photogrammetry, muscle tension assessed trough palpation and algometry assessment. Aerodynamic assessment of voice, acoustic and auditory-perceptual analysis of voice were done. Participants were divided into without voice complaints group (WVCG; n = 11) and voice complaints group (VCG; n = 13) based on Sociodemographic and Clinical Questionnaire completion. RESULTS: For auditory-perceptual analysis, VCG showed a significant higher values on GRBASH subscales Grade (p < 0.001) and Roughness (p = 0.011). The VCG showed statistically significant higher values on muscle tension of suprahyoids (p = 0.001), thyrohyoids (P = 0009) and cricothyroids muscles (p = 0.040) and statistically significant lower values on algometry of the cricothyroid (p = 0.023 left and p = 0.026 right), suprahyoids (p = 0.017 left & p = 0.018 right), thyrohyoids (p = 0.006 left and p = 0.007 right) and pharyngolaryngeal (p = 0.016 left and p = 0.021 right) muscles of both sides. Concerning the aerodynamic assessment of voice and acoustic analysis of voice, no statistically significant differences between the groups were found. CONCLUSIONS: Findings indicated statistically significant differences in muscle tension in laryngeal intrinsic muscles and auditory-perceptual analysis between teachers with and without voice complaints.

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OBJECTIVE: The study aimed to verify the relation between autonomic nervous system (ANS) dysfunctions, voice, and dysphonia. STUDY DESIGN: The study is a systematic review. METHODS: According to the PRISMA flowchart, a search on Pubmed/Medline, SciELO, RCAAP, LILACS, Cochrane Library, PEDro, and Isi Web of Knowledge was performed up to April 2019 using the following key words: autonomic nervous system and voice or dysphonia. Inclusion criteria were full-text articles published in French, English, Portuguese, or Spanish, exploring the relationship between ANS and voice or dysphonia, in human adults. Exclusion criteria were additional treatments for voice disorders, literature reviews and meta-analysis, case studies, and opinion articles. All studies were analyzed using a modified version of the Newcastle-Ottawa scale. RESULTS: Nine papers met the inclusion criteria, all with high methodological quality. The review shows that ANS is related to voice and dysphonia. Individuals with dysphonia tend to show more symptoms of ANS dysfunction concurrent with laryngeal muscles activation and that heartbeat modulates the F0 of human voice. CONCLUSION: Changes in ANS function are associated with voice as well as with dysphonia.

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INTRODUCTION: Strenuous physical exercise may cause acute muscle soreness (AMS), which occurs directly after exercise, as well as delayed onset muscle soreness (DOMS), which occurs about 24 h after exercise. Studies of acupuncture's effect on DOMS have had contradictory results, whereas its effect on AMS has not been extensively studied. The main goal of this study was to evaluate acupuncture's effects on AMS and DOMS and on the prevention of DOMS. METHOD: 45 volunteers were randomised into a verum acupuncture group, a sham acupuncture group and a control group. After exercise-induced muscle damage was elicited, muscle soreness and pressure pain threshold were assessed at different time points. The outcome assessments were performed before (T1) and 20 min after the first acupuncture treatment (T2); then, 24 h later, they were performed before (T3) and 20 min after the second acupuncture treatment (T4). In the verum and sham acupuncture groups, acupuncture was performed for 2 min, immediately after T1 and T3 assessments, whereas subjects in the control group simply rested for 2 min without treatment. Verum acupuncture was given at ST34, ST36 and LR3, whereas sham acupuncture was given at three nontraditional points. RESULTS: We found that verum acupuncture can reduce the occurrence of AMS by one-half and DOMS by one-third. We also found specific and nonspecific acupuncture effects in AMS and DOMS. CONCLUSION: The uneven induction of muscle damage identified by our study, as shown by heterogeneity in pressure pain threshold values, may have led to the contradictory results in published studies on DOMS.

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OBJECTIVE: The study aimed to systematize the associations between posture, voice, and dysphonia in order to support future research directions and possible clinical interventions. STUDY DESIGN: The study is a systematic review. METHODS: According to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses flowchart, a search on PubMed/Medline, SciELO, RCAAP, LILACS, Cochrane Library, PEDro, and Isi Web of Knowledge was performed from their inception through January of 2017 using the key words "posture" and ("voice" or "dysphonia"). The inclusion criteria were full-text journal articles in French, English, Portuguese, or Spanish, exploring the relationship between posture and voice or dysphonia, in adult human beings. The exclusion criteria coupled treatments for voice disorders, literature reviews and meta-analyses, case studies, opinion articles, and studies linking breathing with posture without assessing voice. Studies were analyzed using a modified version of the Newcastle-Ottawa Scale (NOS). RESULTS: Twelve papers met the inclusion criteria with high methodological quality through the NOS. The review shows that a correct posture is necessary for an efficient voice production; however, the relation between dysphonia and posture seems to be contradictory. CONCLUSION: An effective posture allows a subject in a static posture or while moving to more easily shift the tension between muscles, allowing for a free movement of the larynx without blockages and with benefits to voice production.

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The treatment of voice disorders includes physiotherapy and complementary therapies. However, research to support these treatments is scarce. OBJECTIVE: to verify the effectiveness of physiotherapy and complementary therapies on voice disorders. Research on electronic databases PubMed/Medline, SciELO, and LILACS was performed using the combination: voice AND (treatment OR intervention) according to PRISMA guidelines. Only randomized controlled trials (RCTs) were included in the review. Studies were analyzed using the physiotherapy evidence database (PEDro) scale and the Center for Evidence-Based Medicine's Levels of Evidence scale. Eight papers met the inclusion criteria. From the RCTs included in this review, six assessed massage, one transcutaneous electrical nerve stimulation (TENS), one refer to spinal manipulative therapy, and one to acupuncture. The literature regarding the effectiveness of physiotherapy and complementary therapies was good in both quality and results, indicating that massage, TENS, and acupuncture seem to be effective treatments to reduce voice complaints and improve voice quality, supporting the inclusion of complementary therapies but mostly physiotherapy interventions in the treatment of patients with voice disorders.

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Eccentric exercise (EE) is known to induce damage and dysfunction in skeletal muscle. However, the possible role of mitochondrial (dys)function, including the vulnerability to mitochondrial permeability transition pore (MPTP) opening, is unclear. Therefore, this study aimed to analyze the impact of a single acute bout of downhill running on skeletal muscle mitochondrial function. Thirty 12-week-old Charles River CD1 male mice were randomly assigned into control (C) or exercised groups. EE consisted of 120 min of downhill treadmill running at a -16° gradient. Exercised animals were sacrificed immediately (Ecc0h) and 48 h (Ecc48h) after the end of the running bout. Plasma and skeletal muscles were then obtained. Muscle mitochondrial function, including oxygen consumption prior to and after anoxia and reoxygenation, membrane potential, and MPTP opening, were evaluated. Respiratory chain complexI, II, and V activities were determined. EE significantly increased plasma creatine kinase activity (119.4 ± 5.6 vs. 1061.3 ± 46.3 vs. 256.8 ± 15.3 U·L(-1), C, Ecc0h and Ecc48h, respectively) and myoglobin and interleukin-6 content. Impaired state 3 and respiratory control ratio (8.4 ± 0.4 vs. 5.6 ± 0.9 vs. 8.4 ± 0.5, C, Ecc0h and Ecc48h, respectively), as well as increased susceptibility to MPTP opening, seen by cyclosporin A-sensitive high swelling amplitude, lower time to maximal swelling velocity (313.8 ± 17.7 vs. 244.5 ± 19.4 vs. 298.5 ± 8.7 s, C, Ecc0h and Ecc48h, respectively), and calcium release immediately after the end of exercise (C vs. Ecc0h) were observed. EE induced a transient impairment in the activity of complex V (C vs. Ecc0h). No significant changes from the C group were observed 48 h after the end of EE (C vs. Ecc48h) in any analyzed parameters. In conclusion, prolonged EE transiently impaired mice skeletal muscle mitochondrial function and increased susceptibility to calcium-induced MPTP opening.

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Cardiac damage is a major contributor to the morbidity and mortality particularly associated with coronary artery disease. Moreover, it is also related to some metabolic diseases such as diabetes and to some side effects of drug treatments. Regular exercise has been confirmed as a pragmatic countermeasure to protect against cardiac injury. Specifically, life-long physical activity and endurance exercise training have been proven to provide cardioprotection against cardiac insults in both young and old animals. It is suggested that the beneficial effects resulting from increased physical activity levels occur at different levels of cellular organization, being mitochondria preferential target organelles. At present, it remains unclear what the protective mechanisms that are essential for exercise-induced cardioprotection are. Proposed mechanisms to explain the cardioprotective effects of exercise are mediated, at least partially, by redox changes and include the up-regulation of mitochondrial chaperones, improved antioxidant capacity, and/or elevation of other protective molecules against cellular death. It is possible that under some conditions, exercise also diminishes the increased susceptibility of cardiac mitochondria to undergo permeability transition pore opening through the modulation of pore components or sensitizers. The role of physical exercise against the impairment of heart mitochondrial function that accompany ageing, diabetes, administration of the anti-cancer agent Doxorubicin and ischemia-reperfusion is analysed in the present review, which provides biochemical, functional and morphological data illustrating the cross tolerance effect of exercise in these conditions predisposing to cardiac "mitotoxicity". However, further work should be addressed in order to clarify the precise regulatory mechanisms by which physical exercise augments heart mitochondrial tolerance against many conditions predisposing to dysfunction.

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The use of DOX (doxorubicin), an antibiotic used in oncological treatments, is limited by a dose-related cardiotoxicity against which acute exercise is protective. However, the mitochondrial-related mechanisms of this protection remain unknown. Therefore the present study aimed to determine the effects of an acute endurance exercise bout performed 24 h before DOX treatment on heart and liver mitochondrial function. A total of 20 adult male Wistar rats were divided into groups as follows: non-exercised with saline (NE + SAL), non-exercised DOX-treated (NE + DOX), exercised with saline (EX + SAL) and exercised DOX-treated (EX + DOX). The animals performed a 60 min exercise bout on a treadmill or remained sedentary 24 h before receiving either a DOX bolus (20 mg/kg of body weight) or saline. Heart and liver mitochondrial function [oxygen consumption, membrane potential (DeltaPsi) and cyclosporin-A-sensitive calcium-induced MPTP (mitochondrial permeability transition pore) opening] were evaluated. The activities of the respiratory complex, Mn-SOD (superoxide dismutase), caspases 3 and 9, as well as the levels of ANT (adenine nucleotide translocase), VDAC (voltage-dependent anion channel), CypD (cyclophilin D), Bax and Bcl-2, were measured. Acute exercise prevented the decreased cardiac mitochondrial function (state 3, phosphorylative lagphase; maximal DeltaPsi generated both with complex I- and II-linked substrates and calcium-induced MPTP opening) induced by DOX treatment. Exercise also prevented the DOX-induced decreased activity of cardiac mitochondrial chain complexes I and V, and increased caspase 3 and 9 activities. DOX administration and exercise caused increased cardiac mitochondrial SOD activity. Exercise ameliorated liver mitochondrial complex activities. No alterations were observed in the measured MPTP and apoptosis-related proteins in heart and liver mitochondria. The results demonstrate that acute exercise protects against cardiac mitochondrial dysfunction, preserving mitochondrial phosphorylation capacity and attenuating DOX-induced decreased tolerance to MPTP opening.

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The present study analyzed the effects of endurance training against cardiac mitochondrial dysfunction, particularly on the susceptibility to mitochondrial permeability transition pore (MPTP) induction in streptozotocin (STZ)-induced hyperglycemia. Twenty-four young male Wistar rats were randomly assigned into sedentary citrate (SED+CIT), sedentary type I diabetes (SED+STZ; 50mg/kg), T+CIT (14-week treadmill running, 60min/day) and T+STZ (injected 4weeks before training). After 18weeks, isolated heart mitochondria were used for in vitro oxygen consumption and transmembrane potential (∆Ψ) assessment. Cyclosporin-A (CyclA)-sensitive osmotic swelling and Ca(2+) fluxes were measured to study MPTP susceptibility. Voltage-dependent anion channel (VDAC), adenine nucleotide translocator (ANT), cyclophilin D (CypD), transcription factor A (Tfam), Bax, Bcl-2 contents, caspase-3 and -9 activities were determined. In the sedentary group, long-term severe hyperglycemia decreased state 3, CCCP-induced uncoupling and increased oligomycin-inhibited respiration, state 4 and lag phase with glutamate-malate. A decreased state 3 and state 4 with succinate were observed. Moreover, hyperglycemia decreased Ca(2+) uptake and increased CyclA-sensitive Ca(2+) release and Ca(2+)-induced mitochondrial swelling. The oxygen consumption and ∆Ψ parameters impaired by long-term severe hyperglycemia were reverted by endurance training (SED+STZ vs. T+STZ). Training increased mitochondrial Ca(2+) uptake and decreased Ca(2+) release in hyperglycemic groups. Additionally, endurance training reverted the hyperglycemia-induced CypD elevation, attenuating decrease of ANT, VDAC and Tfam. Moreover, training prevented the STZ-induced elevation in Bax, Bax-to-Bcl-2 ratio, caspase-3 and -9 and the increased Bcl-2. Endurance training reestablished heart mitochondrial respiratory dysfunction caused by long-term severe hyperglycemia and reduced the increased susceptibility to MPTP induction probably by modulation of MPTP regulatory proteins.

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BACKGROUND: Hyperglycaemia-resulting in mitochondrial bioenergetics' complications is associated with skeletal muscle dysfunction. The aim of this work was to analyse the effect of long-term severe hyperglycaemia on gastrocnemius mitochondrial bioenergetics, with special relevance on the susceptibility to mitochondrial permeability transition pore (MPTP) opening. METHODS: Sixteen adult (6- to 8-week-old) male Wistar rats were randomly divided into two groups (n = 8/group): control and diabetic. A single dose (50 mg kg(-1)) of streptozotocin (STZ) was administrated i.p. to induce hyperglycaemia. In vitro mitochondrial oxygen consumption rates, membrane potential (Delta psi) fluctuations, MPTP induction as followed by osmotic swelling and extramitochondrial calcium movements and caspase 9-like activity were evaluated 18 weeks after STZ treatment. RESULTS: STZ treatment induced an increase in state 4 and a decrease in the respiratory control ratio with complex I substrates (P < 0.05), whereas no differences were observed using complex II substrates. In both conditions, no significant differences were observed when measuring maximal Delta psi, although STZ treatment increased Delta psi during ADP-induced depolarization when succinate was used. The most critical result was that muscle mitochondria isolated from STZ-treated rats showed a decrease susceptibility to MPTP induction by calcium, as followed by two different experimental protocols. Interestingly, the protection was accompanied by a decrease in muscle caspase 9-like activity. CONCLUSIONS: These data demonstrate that 18 weeks of STZ treatment lead to a decrease in gastrocnemius mitochondrial respiratory control ratio and to decreased calcium-dependent mitochondrial MPTP. Results from this and other works suggest that mitochondrial effects of hyperglycaemia are time and organ specific.

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The aim of the present work was to test the hypothesis that moderate endurance treadmill training ameliorates gastrocnemius mitochondrial bioenergetics and increases the tolerance to the calcium-induced mitochondrial permeability transition pore (MPTP) opening. Twelve adult (6-8 week old) male Wistar rats were randomly divided into two groups (n=6per group): sedentary and trained (14 week of endurance treadmill running, 60min/day). Several end-points for invitro gastrocnemius mitochondrial function including oxygen consumption, transmembrane electric potential and susceptibility to calcium-induced MPTP opening were evaluated. Caspase-9 activity was measured in the intact tissue. Endurance training induced significant increases in state 3 and in respiratory control ratio both with complex I and II-linked substrates (malate+pyruvate and succinate, respectively). Increased CCCP-induced uncoupled respiration with succinate as substrate was also observed (p<0.05). No differences were found regarding state 4 and ADP/O ratio with both substrates. In addition, training significantly decreased the phosphorylative lag phase, whereas no changes were observed on maximal transmembrane electric potential, ADP-induced depolarization and repolarization potential (p<0.05). Interestingly and as opposed to our hypothesis, muscle mitochondria isolated from trained rats were more susceptible to MPTP induction by calcium, although in an initial phase muscle mitochondria isolated from trained rats had an increased calcium uptake. Interestingly, we also verified that endurance training increased the activity of caspase 9. The data obtained confirms that endurance training results in a general improvement in the gastrocnemius mitochondrial respiratory function, although mitochondrial and cellular alterations during training also result in increased calcium-induced MPTP opening.

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