Experimental Physiology最新文献

High-altitude exercise affects cardiac function. This study investigated how altitude and exercise intensity interacted to affect cardiac function of Sprague-Dawley rats. Four altitudes (410, 3600, 4600 and 5600 m) and three exercise intensities (non-exercise (N), low-intensity exercise (L) and high-intensity exercise (H)) were tested combinatorically. After 4 weeks of exercise, cardiac function and specific markers of myocardial injury were assessed. With regard to cardiac function, (a) at the same intensity, stroke volume and left ventricular end-diastolic volume were higher in the 3600 m group but lower in the 4600 and 5600 m groups; and (b) the heart rate increased with altitude and intensity. The biochemical results showed that the levels of creatine kinase, myoglobin and cardiac troponin I generally increased with increasing altitude and exercise intensity, significantly for creatine kinase and myoglobin at 4600 and 5600 m. For pathological results, (a) in the non-exercise group, pathological damage was observed only in the 5600 N group; and (b) in the exercised state, varying degrees of injury were noted, except for the 410 and 3600 L groups. There may be a turning point at 3600 m where the injury to the heart increases. Myocardial injury markers exhibited abnormalities before cardiac dysfunction. Detecting these markers is crucial to provide warnings for the individual from cardiac disease during high-altitude exercise.

Heart failure (HF) remains a significant global health concern with limited effective treatments available. C1q/TNF-related protein 6 (CTRP6) is a member of the CTRP family analogous to adiponectin and its role in HF pathogenesis remains unclear. Here, we investigated the impact of CTRP6 on HF progression. To mimic heart failure with reduced ejection fraction (HFrEF), we used isoproterenol injection in mice and administered adenovirus vectors expressing CTRP6 (Ad-CTRP6) via tail vein injection. We assessed cardiac function through echocardiography and histology. CTRP6's effects on hypertrophy, fibrosis, apoptosis, oxidative stress and mitochondrial function were analysed. Downstream pathways (phosphorylated AMP-activated protein kinase (p-AMPK), sirtuin 1 (SIRT1) and peroxisome proliferator-activated receptor γ coactivator 1-α (PGC-1α) were studied in heart tissues. In vitro, isoproterenol-stimulated H9c2 cardiomyocytes were treated with CTRP6 to examine viability, apoptosis, F-actin and signalling proteins. Compound C was used to assess AMPK involvement. CTRP6 expression was lower in the plasma of HF patients. In an isoproterenol-induced HFrEF mouse model, adenovirus-mediated overexpression of CTRP6 ameliorated cardiac dysfunction and reduced cardiomyocyte apoptosis, oxidative stress, inflammation and myocardial injury markers. Mechanistically, CTRP6 activation of the AMPK/SIRT1/PGC-1α signalling pathway restored mitochondrial homeostasis, evidenced by reduced mitochondrial reactive oxygen species levels, increased ATP content, and enhanced mitochondrial complex I/III activities in cardiac tissues. In vitro studies using isoproterenol-stimulated H9c2 cardiomyocytes corroborated these findings, demonstrating that CTRP6 upregulation attenuated hypertrophy, apoptosis, oxidative stress and mitochondrial dysfunction. Furthermore, these effects were partially reversed by the AMPK inhibitor Compound C, implicating the involvement of the AMPK pathway in CTRP6-mediated cardioprotection. CTRP6 alleviates HF progression through the AMPK/SIRT1/PGC-1α signalling pathway.

During unilateral static and rhythmic handgrip exercise, middle cerebral artery blood velocity (MCAv) increases in the contralateral side to the exercising limb. However, whether this neurovascular coupling-mediated increase in contralateral MCAv is apparent against a background of fluctuating perfusion pressure produced by dynamic resistance exercise (RE) is unclear. We examined the cerebral haemodynamic response to unilateral dynamic RE in 30 healthy individuals (female = 16, mean ± SD: age, 26 ± 6 years; height, 175 ± 10 cm; weight, 74 ± 15 kg; body mass index, 24 ± 5 kg m^-2). Participants completed four sets of 10 paced repetitions (15 repetitions min^-1) of unilateral bicep curl exercise at 60% of the predicted one-repetition maximum (7 ± 3 kg). Beat-to-beat blood pressure, bilateral MCAv and end-tidal carbon dioxide were measured throughout. One-way ANOVA was used to analyse cardiovascular variables and two-way ANOVA to analyse dependent cerebrovascular variables (side × sets, 2 × 5). A linear mixed model analysis was also performed to investigate the effects of end-tidal carbon dioxide and mean arterial blood pressure on MCAv. In comparison to baseline, within-exercise mean arterial blood pressure increased (P < 0.001) across the sets, whereas bilateral MCAv decreased (P < 0.001). However, no significant interaction effect was observed for any dependent variables (all P > 0.787). The linear mixed model revealed that end-tidal carbon dioxide had the greatest effect on MCAv (estimate = 1.019, t = 8.490, P < 0.001). No differences were seen in contralateral and ipsilateral MCAv during dynamic RE, suggesting that neurovascular coupling contributions during dynamic RE might be masked by other regulators, such as blood pressure.

Acute mountain sickness (AMS) causes serious illness for many individuals ascending to high altitude (HA), although preventable with appropriate acclimatisation. AMS is a clinical diagnosis, with symptom severity evaluated using the Lake Louise Score (LLS). Reliable methods of predicting which individuals will develop AMS have not been developed. This systematic review evaluates whether a predictive relationship exists between oxygen saturation and subsequent development of AMS. PubMed, PubMed Central, MEDLINE, Semantic Scholar, Cochrane Library, University of Birmingham Library and clinicaltrials.gov databases were systematically searched from inception to 15 June 2023. Human studies involving collection of peripheral blood oxygen saturation ( $S_{p{O}_2}$ ) from healthy lowlanders during ascent to HA that evaluated any relationship between $S_{p{O}_2}$ and AMS severity were considered for eligibility. Risk of bias was assessed using a modified Newcastle-Ottawa Tool for cohort studies (PROPSPERO CRD42023423542). Seven of 980 total identified studies were ultimately included for data extraction. These studies evaluated $S_{p{O}_2}$ and AMS (via LLS) in 1406 individuals during ascent to HA (3952-6300 m). Risk of bias was 'low' for six and 'moderate' for one of the included studies. Ascent profiles and $S_{p{O}_2}$ measurement methodology varied widely, as did the statistical methods for AMS prediction. Decreasing oxygen saturation measured with pulse oximetry during ascent shows a positive predictive relationship for individuals who develop AMS. Studies have high heterogeneity in ascent profile and oximetry measurement protocols. Further studies with homogeneous methodology are required to enable statistical analysis for more definitive evaluation of AMS predictability by pulse oximetry.

Retraction: J.-K. Yoo, D.-D. Sun, R. S. Parker, M. A. Urey, S. A. Romero, J. S. Lawley, S. Sarma, W. Vongpatanasin, C. G. Crandall, and Q. Fu. (2018). Augmented Venoarteriolar Response with Ageing is Associated with Morning Blood Pressure Surge. Experimental Physiology 103(11), 1448-1455. https://doi.org/10.1113/EP087166

The above article, published online on 20 August 2018 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the authors; the journal Editor in Chief, Damian Bailey; The Physiological Society; and John Wiley and Sons Ltd. The authors reported that hypertensive patients had been included by mistake in the database from which the data for this study were drawn. The retraction has been agreed to because the editors and authors agree that these errors substantially altered the results and conclusions of this article.

Respiratory function assessment is crucial in optimizing athletic performance, safeguarding respiratory health, and ensuring athletes can perform at their peak potential while minimizing the risk of respiratory-related issues. The S-Index Test is a dynamic evaluation of respiratory muscle strength. However, no comprehensive reference values regarding the S-Index Test have been reported yet. A total of 597 participants performed the S-Index Test. They were either well-trained athletes (WTA), or e-sports athletes (ESA), or age-matched controls (AMC) groups. The differences in S-Index Test results between sexes and for group-sex, and performance calibre tier-sex interactions were examined. The relationships between S-Index Test results and age, anthropometric indices and training experience were assessed. Reference values for all the groups were provided. Amongst athletes, the highest values were observed in swimmers and rowers, and the lowest in figure skaters and runners. The S-Index Test results were different for the group-sex interaction (P = 0.004, 151.6 ± 29.0 cmH₂O for WTA males and 109.8 ± 21.6 cmH₂O for WTA females, 136.7 ± 28.0 cmH₂O for ESA males and 101.8 ± 22.0 cmH₂O for ESA females, 128.7 ± 28.8 cmH₂O for AMC males and 70.3 ± 24.7 cmH₂O for AMC females) and higher in males than females (P < 0.001, 145.1 ± 30.5 cmH₂O for males and 100.8 ± 27.6 cmH₂O for females). The higher athletic level, presented as performance calibre tier, was not linked to higher respiratory muscle strength in the WTA group (P = 0.094). However, the Bonferroni correction revealed that except for the singular tier in females, there was a significant effect for all the other tiers and sexes (P < 0.001). The obtained results confirm that regardless of the level of physical activity, the anthropometric features are positively linked with respiratory muscle strength. Furthermore, age and training experience were positively correlated with the S-Index Test results in the WTA group.

Hyperglycaemia, hyperlipidaemia, hypertension and obesity are the main risk factors affecting the development and prognosis of ischaemic heart disease, which is still an important cause of death today. In our study, male Sprague–Dawley rats were fed either a standard diet (SD) or a high fat and high carbohydrate diet (HF-HCD) for 8 weeks and streptozotocin (STZ) was injected at the seventh week of the feeding period. In one set of rats, a mixture of a prebiotic and probiotics (synbiotic, SYN) was administered by gavage starting from the beginning of the feeding period. Experimental myocardial ischaemia–reperfusion (30 min/60 min) was induced at the end of 8 weeks. Hyperglycaemia, hypertension and increased serum low-density lipoprotein levels occurred in SD- and HF-HCD-fed and STZ-treated rats followed for 8 weeks. Increased density of the Proteobacteria phylum was observed in rats with increased blood glucose levels, indicating intestinal dysbiosis. The severity of cardiac damage was highest in the dysbiotic HF-HCD-fed hyperglycaemic rats, which was evident with increased serum creatine kinase-MB (CK-MB), cardiac troponin I (cTnI), tumour necrosis factor-α, and interleukin-6 levels, along with a decrease in ST-segment resolution index. SYN supplementation to either a normal or a high-fat high-carbohydrate diet improved gut dysbiosis, reduced anxiety, decreased CK-MB and cTnI levels, and alleviated myocardial ischaemia–reperfusion injury in hyperglycaemic rats.