Physiology international最新文献

Anxiety is a common issue among university students, many of them experience anxiety, depression, and stress during their school life. This study aimed to compare the acute physiological stress responses of students divided into two groups according to their perceived anxiety levels (positive test anxiety, PTA+, and negative test anxiety, PTA-). Heart rate variability (HRV) and electrodermal activity (EDA) were used to assess stress.Thirty-one healthy volunteers participated in the study. Participants completed anxiety assessments, including the Westside Test Anxiety Scale (WTAS), the State-Trait Anxiety Inventory (STAI), and the Test State Anxiety Inventory (TSAI). Based on their scores, participants were categorized into PTA+ and PTA- groups. All participants underwent 24-h continuous recordings of pulse and electrodermal activity (EDA) on two separate occasions: one day prior to a written exam and during a designated exam-free day serving as a baseline control.We compared the HRV and EDA data obtained on a regular day and on an exam day between the two groups. Results showed that the PTA+ group had significantly higher heart rate, stress index, low frequency, and short-term detrended fluctuation analysis (DFAα1) on the exam day. The tonic EDA component was also higher in the PTA+ group. Stress-related HRV and EDA parameters were negatively correlated with exam scores.In conclusion, the study found that physiological stress indicators obtained from HRV and EDA are associated with perceived exam anxiety in students.

Background: Whole-body vibration (WBV) is used to enhance physical performance in sports and rehabilitation. The present study analyzed the effects of remobilization with WBV on the soleus muscle of Wistar rats.

Methods: Twenty-eight animals were separated into four experimental groups (n = 7): CON (control); IM (immobilized); FR (immobilization and free remobilization); and WBV (immobilization and remobilization with WBV). The immobilization of the pelvic limb was carried out according to the standard protocol using a plaster cast for 15 days. For remobilization with WBV, a Frequency of 60 Hz was applied for 10 min, five days a week, for two weeks. After the remobilization period, the animals were euthanized, and the right soleus muscle was dissected followed by processing for histomorphometric analysis and immunolocalization of Aquaporin 1 (AQP1).

Results: We observed a reduced larger diameter in IM compared to CON, with restored values in WBV. For the estimation of connective tissue, a significant increase was observed in the immobilized groups, while a reduction was noted in the remobilized groups. AQP1 expression decreased significantly in IM and increased in WBV.

Conclusion: Immobilization caused morphofunctional damage to the soleus muscle, and remobilization with WBV is efficient and offers advantages over free remobilization.

This study explored the effects of fructose-induced obesity and metabolic disorders on peripheral inflammatory hyperalgesia, employing quantitative sensory testing with the von Frey test and measuring paw edema to assess inflammatory responses. Wistar rats were administered water or 10% fructose solution ad libitum over a period of 5 weeks. After intraplantar administration of inflammatory agents such as carrageenan (1 mg/paw), lipopolysaccharide (LPS; 100 µg/paw), or prostaglandin E2 (PGE2, 100 ng/paw), we conducted mechanical hyperalgesia tests and paw edema evaluations. The fructose diet resulted in dyslipidemia, elevated insulin and leptin plasma levels, insulin resistance, and increased epididymal and retroperitoneal adiposity compared to control animals. In response to inflammatory agents, the fructose group displayed significantly enhanced peripheral hyperalgesia and more pronounced paw edema. Our results demonstrate that fructose not only contributes to the development of obesity and metabolic disorder but also exacerbates peripheral inflammatory pain responses by enhancing prostaglandin sensitivity.

Background: While the acute effects of high-load resistance training on the force generating capacity of muscles have been widely examined, limited data exist on the relationship with the force-velocity profile (FV). Evidence suggests high sensitivity of the vertical FV profile to monitor changes in the muscle's mechanical properties according to the type of the exercise protocol. However, the interpretation of the findings seems not as straightforward. Therefore, the purpose of this study was to examine the effects of a high-load resistance training protocol on the muscle's mechanical properties during loaded jumps and on the vertical force-velocity profile (FV) in relation to maximal strength.

Methods: 29 resistance-trained male (mean age±SD: 35.4 ± 7.8 years) and 29 female athletes (mean age±SD: 32.5 ± 7.0 years) participated in the study. Five-repetition maximum (5RM) in back squat, unloaded countermovement jump (CMJ) and FV profile were assessed. Loaded jumps were performed against 25, 50, 75, and 100 percent of body mass. Participants performed exercise protocols corresponding to their 5RM. Immediately after, unloaded CMJ and FV profile measurements were repeated.

Results: A significant decrease in CMJ height (∼5-6%) and in average power (∼4%) was recorded for both men and women. The FV profile did not change after the exercise protocol; however, there was a significant decrease in theoretical maximal power (from 4 to 5%) and in theoretical maximal velocity (∼3%). Maximal strength was not associated with the changes in FV profile.

Conclusions: Findings suggest that an acute high-load exercise decreased vertical jump performance and maximal power output, but without a concomitant change in FV profile. The large interindividual variability in FV measures indicates a less straightforward connection of the applied exercise with the acute response in the FV profile, highlighting the complexity of the FV profile to monitor changes in response to an acute training load.

The global temperature rise will have extensive consequences on our organ systems, but hypohydration caused by reduced water intake or increased water loss through sweating plays the most relevant role. Many studies have already demonstrated the association between hypohydration and impaired exercise performance, but data related to the cardiac burden of hypohydration are scarce. This study is a sub-investigation of our large, prospective, self-controlled trial on the effects of hypohydration on cardiopulmonary exercise capacity with previously published results. In the current sub-study, we analyzed the impact of hypohydration on cardiac burden in this cohort of fifty healthy, recreational athletes during cardiopulmonary exercise test.Therefore, each participant underwent cardiopulmonary exercise test with a standardized ramp protocol twice, once in hypohydrated state and once in euhydrated state as control, and the cardiac markers Troponin T, NT-pro-BNP and Chromogranin A were measured before and after the exercise test at each state. Mean age was 29.7 years and 34% of probands were female. Hypohydration led to a reduced body water, a significant decrease in oxygen uptake and lower levels of power output. Yet, Troponin T, NT-proBNP, Chromogranin A and lactate levels did not significantly differ between the two conditions.In this study cohort, decreased exercise capacity during hypohydration was more likely due to impaired cardiac output with diminished plasma volume rather than measurable cardiac stress from fluid deprivation. However, whether these data are generalizable to a diseased cohort is left unanswered and should be addressed in future randomized controlled trials.

Previous observational studies have investigated the association between urinary albumin excretion and the risk of colorectal cancer (CRC), but the results have been inconsistent. This study aimed to explore the causal association between urine albumin-to-creatinine ratio (ACR) and CRC risk through a two-sample Mendelian randomization (MR) analysis. The genome-wide association study (GWAS) data of ACR (n = 382,500) and CRC (CRC: 6,509 cases and 287,137 controls) were obtained from the IEU OpenGWAS project website and the FinnGen database, respectively. The TwoSampleMR and MR-PRESSO R packages were used to search for and analyze genetic variations that served as instrumental variables for ACR. The odds ratios (ORs) and 95% confidence intervals (95% CIs) were calculated using the inverse-variance weighted method, MR-Egger, and weighted median. Genetically predicted ACR was not associated with CRC risk (all P > 0.05). Further analysis based on the site of onset (colon or rectum) also did not show a significant association (all P > 0.05). MR-PRESSO, MR-Egger regression and leave-one-out sensitivity analysis all indicated that the current results were robust and reliable. These findings suggest that ACR does not affect CRC risk and may not be used as a marker of CRC risk in clinical practice. However, relevant studies especially in ethnically diverse populations are still needed to confirm the current findings.

The aim of this study is to show the relationship between the change in the strengthening of synaptic plasticity and tau phosphorylation and tau-kinases and phosphatase. The averages of the field excitatory-postsynaptic potential (fEPSP) and population spike (PS) in the last 5 min were used as a measure of LTP, LTD and MP. Total and phosphorylated levels of tau, kinases and phosphatases were evaluated by western blot and mRNA levels were evaluated by RT-qPCR. The stimulation of synapses by HFS and LFS+HFS increased the phosphorylation of total-tau and phospho-tau at the Thr181, Ser202/Thr205, Ser396 and Ser416 residues, and these were accompanied by increased enzymatic activity of Akt, ERK1/2. The increased phosphorylation of tau may mediate maintenance of LTP. If the increase in phosphorylation of tau cannot be prevented, together with inhibition of the subsequent LTP, this may indicate that the physiological role of hyperphosphorylated tau in synaptic plasticity may extend to pathological processes.

Liver cirrhosis is the consequence of chronicisation and of the evolution of untreated liver diseases. The complexity of the disease and the complications it can cause have been and are still intensively researched, aiming to discover new therapies or improve existing ones for the effective management of liver cirrhosis. Currently, the treatment used is directed against the cause that caused the disease, if it is known; in advanced cases, liver transplantation is the only valid therapeutic option. Hepatoprotectors that are currently on the market are numerous, having as common properties the antioxidant, anti-inflammatory, stabilizing properties of the hepatocytic membrane; A few examples: the ethanolic extract of Curcuma longa, the extract from the plant called Sophora flavescens, the extract of Glycyrrhiza glabra, silymarin (extracted from Sylibum marianum), the extract of Ganoderma lucidum, etc. Liver cirrhosis is accompanied by generalized hypovitaminosis, so supplementing the diet with hydro- and liposoluble vitamins is mandatory. Protein-caloric malnutrition can be prevented by a hyperprotein diet, especially beneficial being the supplementation with branched-chain amino acids, which are also applicable in the prophylaxis and treatment of hepatic encephalopathy. Nanoparticles are a state-of-the-art therapeutic option, proving increased bioavailability, for example polydopamine nanoparticles loaded with l-arginine have been tested as therapy in liver cirrhosis. Among the innovative treatment directions in liver cirrhosis are hybrid products (e.g. hybrid polymer nanoparticles loaded with caffeic acid), cell cultures and artificial or bioartificial liver support.

Poor sleep increases pain, at least in part, by disrupting endogenous pain modulation. However, the efficacy of endogenous analgesia in sleep-deprived subjects has never been tested. To assess this issue, we chose three different ways of triggering endogenous analgesia: (1) acupuncture, (2) acute stress, and (3) noxious stimulation, and compared their ability to decrease the pronociceptive effect induced by REM-SD (Rapid Eye Movement Sleep Deprivation) with that to decrease inflammatory hyperalgesia in the classical carrageenan model. First, we tested the ability of REM-SD to worsen carrageenan-induced hyperalgesia: A low dose of carrageenan (30 µg) in sleep-deprived Wistar rats resulted in a potentiated hyperalgesic effect that was more intense and longer-lasting than that induced by a higher standard dose of carrageenan (100 µg) or by REM-SD alone. Then, we found that (1) acupuncture, performed at ST36, completely reversed the pronociceptive effect induced by REM-SD or by carrageenan; (2) immobilization stress completely reversed the pronociceptive effect of REM-SD, while transiently inhibited carrageenan-induced hyperalgesia; (3) noxious stimulation of the forepaw by capsaicin also reversed the pronociceptive effect of REM-SD and persistently increased the nociceptive threshold above the baseline in carrageenan-treated animals. Therefore, acupuncture, stress, or noxious stimulation reversed the pronociceptive effect of REM-SD, while each intervention affected carrageenan-induced hyperalgesia differently. This study has shown that while sleep loss may disrupt endogenous pain modulation mechanisms, it does not prevent the activation of these mechanisms to induce analgesia in sleep-deprived individuals.