Attila Oláh, Alex A Sayour, Mihály Ruppert, Bálint A Barta, Béla Merkely, Attila Kovács, Tamás Radovits
{"title":"Dynamics of exercise training and detraining induced cardiac adaptations","authors":"Attila Oláh, Alex A Sayour, Mihály Ruppert, Bálint A Barta, Béla Merkely, Attila Kovács, Tamás Radovits","doi":"10.1016/j.cophys.2023.100657","DOIUrl":"https://doi.org/10.1016/j.cophys.2023.100657","url":null,"abstract":"<div><p>The effect of regular physical activity has been provided by numerous investigations in cardiology: both its role in primary and secondary cardiovascular prevention, as well as exercise-induced cardiac hypertrophy in athletes have already been well characterized. In this short review, we would summarize the rate of development and regression of the cardiac adaptations induced by long-term, regular training and its cessation. While most of the cross-sectional studies in sports cardiology compared athletes to healthy controls, we investigated longitudinal follow-up studies, those also have baseline data before regular exercise and/or detraining period. Intense exercise training induces significant improvement in functional characteristics after approximately two weeks, while the first marked alterations in sinus bradycardia<span> and left ventricular (LV) hypertrophy have been observed after two months of regular physical activity. Similar tendency with some earlier reports of morphological alterations has been observed in small animal studies. Both human and experimental data imply rapid morphological, functional, and electrical regression after cessation of exercise stimulus. These information suggest that exercise-associated cardiac functional improvements (early diastolic filling, maximal oxygen uptake) of the heart manifests earlier than the morphological and electrical alterations. The increased functional properties might be the primer alteration while the morphological and electrical adaptation might be a secondary consequence of the regular hemodynamic overload of the heart and systemic circulation. The regression of exercise-induced alterations seems to be an accelerated process compared to its development.</span></p></div>","PeriodicalId":52156,"journal":{"name":"Current Opinion in Physiology","volume":"33 ","pages":"Article 100657"},"PeriodicalIF":2.5,"publicationDate":"2023-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49817091","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Sex differences in healthspan and lifespan responses to geroprotective dietary interventions in preclinical models","authors":"Michael R MacArthur , Sarah J Mitchell","doi":"10.1016/j.cophys.2023.100651","DOIUrl":"https://doi.org/10.1016/j.cophys.2023.100651","url":null,"abstract":"<div><p><span>Dietary restriction (DR) remains the most consistent preclinical intervention to improve health and lifespan across multiple species. Various DR paradigms have gained interest in recent years and many show overlapping phenotypes with calorie restriction (CR), the oldest and most established form of DR. Until recently, the impact of sex as a biological variable on DR outcomes has been understudied. Here, we review studies that have advanced our understanding of sexual dimorphism in the healthspan and lifespan responses to DR over the past five years. We particularly focus on CR, ketogenic diet, amino acid restriction, </span>methionine restriction, and protein restriction in mice, flies, and worms.</p></div>","PeriodicalId":52156,"journal":{"name":"Current Opinion in Physiology","volume":"33 ","pages":"Article 100651"},"PeriodicalIF":2.5,"publicationDate":"2023-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49816855","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Kirsten T Nijholt , Suzanne N Voorrips , Pablo I Sánchez-Aguilera, Berend Daan Westenbrink
{"title":"Exercising heart failure patients: cardiac protection through preservation of mitochondrial function and substrate utilization?","authors":"Kirsten T Nijholt , Suzanne N Voorrips , Pablo I Sánchez-Aguilera, Berend Daan Westenbrink","doi":"10.1016/j.cophys.2023.100656","DOIUrl":"https://doi.org/10.1016/j.cophys.2023.100656","url":null,"abstract":"<div><p>Current heart failure (HF) therapy remains unable to substantially improve exercise capacity. Studies have shown that exercise training has beneficial effects on the heart in both health and disease. How mitochondria respond to exercise in this setting has, however, received less attention in literature. These beneficial effects may include protective changes in mitochondrial function and adaptations in substrate utilization. This review describes exercise-induced changes in cardiac metabolism, including changes in mitochondrial function and substrate utilization and their effects on cardiac function. We conclude that exercising HF patients can improve mitochondrial function and optimize substrate utilization, eventually improving or restoring cardiac function. This suggests that exercise itself should be incorporated in the HF treatment plan, to improve cardiac function and in term exercise capacity. Extending knowledge on mechanisms by which exercise exerts protective effects could potentially lead to development of therapies directed at improving mitochondrial function and substrate utilization in HF.</p></div>","PeriodicalId":52156,"journal":{"name":"Current Opinion in Physiology","volume":"33 ","pages":"Article 100656"},"PeriodicalIF":2.5,"publicationDate":"2023-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49816850","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The genetic basis of exercise and cardiorespiratory fitness – relation to cardiovascular disease","authors":"Marie Klevjer , Ada N Nordeidet , Anja Bye","doi":"10.1016/j.cophys.2023.100649","DOIUrl":"https://doi.org/10.1016/j.cophys.2023.100649","url":null,"abstract":"<div><p>Endurance training is associated with increased cardiorespiratory fitness (CRF) and decreased risk of cardiovascular disease (CVD). However, a causal relationship between exercise, CRF, and CVD has not been confirmed. Exercise and CRF have a strong genetic component, estimated to be ∼50%. However, few genetic studies have been performed, as the gold-standard method for quantifying CRF is expensive, time-consuming, and requires advanced equipment. Conversely, self-reported information on physical activity (PA) is more easily available, but the uncertainty related to these data can introduce bias. Improved knowledge of genetic variants associated with exercise and CRF could provide causal links between exercise and CVD and contribute to new prevention and treatment strategies for CVD. This review presents the current knowledge of the genetics of exercise and CRF, and potential relationship with CVD, by highlighting the most comprehensive genetic and epigenetic studies on CRF, PA, and exercise response, as well as studies of gene–environment interactions.</p></div>","PeriodicalId":52156,"journal":{"name":"Current Opinion in Physiology","volume":"33 ","pages":"Article 100649"},"PeriodicalIF":2.5,"publicationDate":"2023-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49816852","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Anja Angelov , Paul J Connelly , Christian Delles , Georgios Kararigas
{"title":"Sex-biased and sex hormone-dependent regulation of apolipoprotein A1","authors":"Anja Angelov , Paul J Connelly , Christian Delles , Georgios Kararigas","doi":"10.1016/j.cophys.2023.100654","DOIUrl":"https://doi.org/10.1016/j.cophys.2023.100654","url":null,"abstract":"<div><p><span><span>Pronounced sex differences in the development and outcome of cardiovascular diseases (CVD) exist. Apolipoprotein A1 (APOA1), the basic </span>structural protein of high-density lipoprotein (HDL), is involved in key metabolic processes. However, its role in the pathogenesis of CVD is incompletely understood. The effects of biological sex on factors influencing the APOA1-lipid balance and the underlying mechanisms are also poorly understood. Here, we summarize evidence supporting sex-biased and sex hormone-dependent regulation of APOA1. In particular, we discuss sex-biased </span><em>APOA1</em> genetic variation, sex differences in APOA1 regulation and cardiovascular physiology, and sex hormone-dependent regulation of APOA1 in cis- and transgender individuals. We put forward that studying the effects of biological sex will contribute to a better understanding of the role of APOA1 in cardiovascular physiology and its sex-biased association with CVD. Importantly, in situations of sex hormone therapy or inhibition, more sex-stratified data are required to inform clinical management of APOA1-related cardiovascular risk in a sex-dependent manner.</p></div>","PeriodicalId":52156,"journal":{"name":"Current Opinion in Physiology","volume":"33 ","pages":"Article 100654"},"PeriodicalIF":2.5,"publicationDate":"2023-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49816854","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Xi Wang , Corbin A Shields , Ubong Ekperikpe , Lorena M Amaral , Jan M Williams , Denise C Cornelius
{"title":"Vascular and renal mechanisms of preeclampsia","authors":"Xi Wang , Corbin A Shields , Ubong Ekperikpe , Lorena M Amaral , Jan M Williams , Denise C Cornelius","doi":"10.1016/j.cophys.2023.100655","DOIUrl":"10.1016/j.cophys.2023.100655","url":null,"abstract":"<div><p>Preeclampsia (PE) is a multisystem obstetric disorder that affects 2–10% of pregnancies worldwide and a leading cause of maternal and fetal morbidity and mortality. The etiology of PE development is not clearly delineated, but since delivery of the fetus and placenta often leads to symptom resolution in the most cases of PE, it is hypothesized that the placenta is the inciting factor of the disease. Current management strategies for PE focus on treating the maternal symptoms to stabilize the mother in an attempt to prolong the pregnancy. However, the efficacy of this management strategy is limited. Therefore, identification of novel therapeutic targets and strategies is needed. Here, we provide a comprehensive overview of the current state of knowledge regarding mechanisms of vascular and renal pathophysiology during PE and discuss potential therapeutic targets directed at improving maternal vascular and renal function.</p></div>","PeriodicalId":52156,"journal":{"name":"Current Opinion in Physiology","volume":"33 ","pages":"Article 100655"},"PeriodicalIF":2.5,"publicationDate":"2023-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10062189/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9282932","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Michael G Leahy , Shalaya Kipp, Andrew William Sheel
{"title":"The respiratory physiology of exercise: age and sex considerations","authors":"Michael G Leahy , Shalaya Kipp, Andrew William Sheel","doi":"10.1016/j.cophys.2023.100652","DOIUrl":"https://doi.org/10.1016/j.cophys.2023.100652","url":null,"abstract":"<div><p>The respiratory system is the first step in the transport of oxygen during dynamic exercise. This review outlines the anatomical and functional changes that occur to the respiratory system with healthy aging. Furthermore, we emphasize how age-related changes to the respiratory system may differ on the basis of sex. We outline investigations, both classic and recent, that have made key contributions to our understanding the integrated structure–function relationship of the pulmonary system. We add, what we believe, are considerable gaps and next steps in the field of respiratory exercise physiology.</p></div>","PeriodicalId":52156,"journal":{"name":"Current Opinion in Physiology","volume":"33 ","pages":"Article 100652"},"PeriodicalIF":2.5,"publicationDate":"2023-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49816853","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Autophagy at the synapse, an early site of dysfunction in neurodegeneration","authors":"Hilary Grosso Jasutkar , Ai Yamamoto","doi":"10.1016/j.cophys.2023.100631","DOIUrl":"10.1016/j.cophys.2023.100631","url":null,"abstract":"<div><p>Macroautophagy, herein referred to as autophagy, has long been implicated in the pathophysiology of neurodegenerative diseases. However, an incomplete understanding of how autophagy contributes to disease pathogenesis has limited progress in acting on this potential target for the development of disease-modifying therapeutics. Research in the past few decades has revealed that autophagy plays a specialized role in the synapse, a site of early dysfunction in multiple neurodegenerative diseases. In this review, we discuss the evidence suggesting that inadequate autophagy at the synapse may contribute to neurodegeneration, and why the functions of autophagy may be particularly relevant for synaptic function.</p></div>","PeriodicalId":52156,"journal":{"name":"Current Opinion in Physiology","volume":"32 ","pages":"Article 100631"},"PeriodicalIF":2.5,"publicationDate":"2023-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10035630/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9197631","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Jordan H Mallette, Breland F Crudup, Barbara T Alexander
{"title":"Growth restriction in preeclampsia: lessons from animal models","authors":"Jordan H Mallette, Breland F Crudup, Barbara T Alexander","doi":"10.1016/j.cophys.2023.100647","DOIUrl":"10.1016/j.cophys.2023.100647","url":null,"abstract":"<div><p>Preeclampsia remains a major health concern for mother and child. Yet, treatment options remain limited to early delivery. Placental dysfunction in preeclampsia occurs in response to an increase in oxidative stress<span><span> and inflammatory cytokines with vasoactive and antiangiogenic factors contributing to impaired maternal and fetal health. Moreover, recent studies indicate a potential role for epigenetic mediators in the pathophysiology of placental ischemia. Numerous </span>animal models<span><span> are utilized to explore the pathogenesis of preeclampsia and fetal growth restriction. This review provides a brief overview of recent progress in </span>preclinical studies regarding potential therapeutic targets for the treatment and prevention of preeclampsia with an emphasis on fetal growth restriction and the fetal programming of increased cardiovascular risk.</span></span></p></div>","PeriodicalId":52156,"journal":{"name":"Current Opinion in Physiology","volume":"32 ","pages":"Article 100647"},"PeriodicalIF":2.5,"publicationDate":"2023-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10035651/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9197630","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}