Endurance Exercise-Induced Cardiac Remodeling: Not All Sports Are Created Equal

2015 ◽  
Vol 28 (12) ◽  
pp. 1434-1440 ◽  
Author(s):  
Meagan M. Wasfy ◽  
Rory B. Weiner ◽  
Francis Wang ◽  
Brant Berkstresser ◽  
Gregory D. Lewis ◽  
...  
Keyword(s):  
Endurance Exercise ◽  
Cardiac Remodeling ◽  
Exercise Induced

scholarly journals ENDURANCE EXERCISE-INDUCED CARDIAC REMODELING: NOT ALL SPORTS ARE CREATED EQUAL

2014 ◽  
Vol 63 (12) ◽  
pp. A1649
Author(s):  
Meagan Murphy Wasfy ◽  
Rory Weiner ◽  
James Deluca ◽  
Francis Wang ◽  
Brant Berkstresser ◽  
...  
Keyword(s):  
Endurance Exercise ◽  
Cardiac Remodeling ◽  
Exercise Induced

scholarly journals Endurance exercise training attenuates natriuretic peptide release during maximal effort exercise: biochemical correlates of the “athlete’s heart”

2018 ◽  
Vol 125 (6) ◽  
pp. 1702-1709 ◽  
Author(s):  
Ankit B. Shah ◽  
Jodi Zilinski ◽  
Marcel Brown ◽  
Jennifer H. Neary ◽  
Rory B. Weiner ◽  
...  
Keyword(s):  
Exercise Training ◽  
Natriuretic Peptide ◽  
Endurance Exercise ◽  
Cardiac Remodeling ◽  
Left Ventricular ◽  
Wall Thickening ◽  
Cardiac Wall ◽  
Endurance Exercise Training ◽  
Exercise Induced ◽  
Maximal Effort

Endurance exercise training (ET) stimulates eccentric left ventricular hypertrophy (LVH) with left atrial dilation. To date, the biochemical correlates of exercise-induced cardiac remodeling (EICR) remain incompletely understood. Collegiate male rowers ( n = 9) were studied with echocardiography and maximal-effort cardiopulmonary exercise testing (MECPET) before and after 90 days of ET intensification. Midregional proatrial natriuretic peptide (MR-proANP), NH2-terminal pro B-type natriuretic peptide (NT-proBNP), and high-sensitivity troponin T were measured at rest, peak MECPET, and 60 min post-MECPET at both study time points. Endurance exercise training resulted in eccentric LVH (LV mass = 102 ± 8 vs. 110 ± 11 g/m2, P = 0.001; relative wall thickness = 0.36 ± 0.04 vs. 0.37 ± 0.04, P = 0.103), left atrial dilation (74 ± 18 vs. 84 ± 15 ml, P < 0.001), and increased exercise capacity (peak V̇o2 = 53.0 ± 5.9 vs. 67.3 ± 8.2 ml·kg−1·min−1, P < 0.001). Left ventricular remodeling was characterized by an ~7% increase in LV wall thickness but only a 3% increase in LV chamber radius. The magnitude of natriuretic peptide release, examined as percent change from rest to peak exercise, was significantly lower for both MR-proANP (115 [95,127]% vs. 78 [59,87]%, P = 0.04) and NT-proBNP (46 [31,70]% vs. 27 [25,37]%, P = 0.02) after ET. Rowing-based ET and corollary EICR appear to result in an attenuated natriuretic peptide response to maximal effort exercise. This may occur as a function of decreased cardiac wall stress after ET as seen by disproportionally higher ventricular wall thickening compared with chamber dilation. NEW & NOTEWORTHY Using longitudinal pre- and postendurance training natriuretic peptide measurements, we demonstrate that the development of exercise-induced cardiac remodeling results in an attenuated natriuretic peptide response to acute bouts of maximal intensity exercise. Exercise-induced cardiac remodeling was associated with a disproportionally higher ventricular wall thickening compared with chamber dilation, a pattern that reduces cardiac wall stress. These observations advance our understanding of both the structural and biochemical adaptations that underlie the cardiovascular response to endurance training.

51 C/EBPβ CONTROLS EXERCISE-INDUCED CARDIAC GROWTH AND PROTECTS AGAINST PATHOLOGICAL CARDIAC REMODELING

2011 ◽  
Vol 12 (1) ◽  
pp. 11
Author(s):  
P. Bostrom ◽  
N. Mann ◽  
J. Wu ◽  
P.A. Quintero ◽  
E.R. Plovie ◽  
...  
Keyword(s):  
Cardiac Remodeling ◽  
Cardiac Growth ◽  
Exercise Induced

scholarly journals Exercise: Teaching myocytes new tricks

2017 ◽  
Vol 123 (2) ◽  
pp. 460-472 ◽  
Author(s):  
Scott K. Powers
Keyword(s):  
Skeletal Muscle ◽  
Exercise Training ◽  
Cardiac Myocytes ◽  
Endurance Exercise ◽  
Ischemia Reperfusion ◽  
Muscle Fibers ◽  
Cardiac Phenotype ◽  
Endurance Exercise Training ◽  
Skeletal Muscle Fibers ◽  
Exercise Induced

Endurance exercise training promotes numerous cellular adaptations in both cardiac myocytes and skeletal muscle fibers. For example, exercise training fosters changes in mitochondrial function due to increased mitochondrial protein expression and accelerated mitochondrial turnover. Additionally, endurance exercise training alters the abundance of numerous cytosolic and mitochondrial proteins in both cardiac and skeletal muscle myocytes, resulting in a protective phenotype in the active fibers; this exercise-induced protection of cardiac and skeletal muscle fibers is often referred to as “exercise preconditioning.” As few as 3–5 consecutive days of endurance exercise training result in a preconditioned cardiac phenotype that is sheltered against ischemia-reperfusion-induced injury. Similarly, endurance exercise training results in preconditioned skeletal muscle fibers that are resistant to a variety of stresses (e.g., heat stress, exercise-induced oxidative stress, and inactivity-induced atrophy). Many studies have probed the mechanisms responsible for exercise-induced preconditioning of cardiac and skeletal muscle fibers; these studies are important, because they provide an improved understanding of the biochemical mechanisms responsible for exercise-induced preconditioning, which has the potential to lead to innovative pharmacological therapies aimed at minimizing stress-induced injury to cardiac and skeletal muscle. This review summarizes the development of exercise-induced protection of cardiac myocytes and skeletal muscle fibers and highlights the putative mechanisms responsible for exercise-induced protection in the heart and skeletal muscles.

Exhaustive endurance exercise activates brain glycogen breakdown and lactate production more than insulin-induced hypoglycemia

2021 ◽  
Author(s):  
Takashi Matsui
Keyword(s):  
Endurance Exercise ◽  
Lactate Production ◽  
Severe Hypoglycemia ◽  
Exercise Group ◽  
Exhaustive Exercise ◽  
Endurance Capacity ◽  
Brain Glycogen ◽  
Insulin Group ◽  
Exercise Induced

Brain glycogen localized in astrocytes produces lactate via cAMP signaling, which regulates memory functions and endurance capacity. Exhaustive endurance exercise with hypoglycemia decreases brain glycogen, although the mechanism underlying this phenomenon remains unclear. Since insulin-induced hypoglycemia decreases brain glycogen, this study tested the hypothesis that hypoglycemia mediates exercise-induced brain glycogen decrease. To test the hypothesis, the effects of insulin- and exhaustive exercise-induced hypoglycemia on brain glycogen levels were compared using the microwave irradiation method in adult Wistar rats. The insulin challenge and exhaustive exercise induced similar levels of severe hypoglycemia. Glycogen in the hypothalamus and cerebellum decreased similarly with the insulin challenge and exhaustive exercise; however, glycogen in the cortex, hippocampus, and brainstem of the exercise group were lower compared to the insulin group. Blood glucose correlated positively with brain glycogen, but the slope of regression lines was greater in the exercise group compared to the insulin group in the cortex, hippocampus, and brainstem, but not the hypothalamus and cerebellum. Brain lactate and cAMP levels in the hypothalamus and cerebellum increased similarly with the insulin challenge and exhaustive exercise, but those in the cortex, hippocampus, and brainstem of the exercise group were higher compared to the insulin group. These findings support the hypothesis that hypoglycemia mediates the exercise-induced reduction in brain glycogen, at least in the hypothalamus and cerebellum. However, glycogen reduction during exhaustive endurance exercise in the cortex, hippocampus, and brainstem is not due to hypoglycemia alone, implicating the role of exercise-specific neuronal activity in brain glycogen decrease.

Endurance exercise‐induced and mental fatigue and the brain

2020 ◽  
Author(s):  
Romain Meeusen ◽  
Jeroen Van Cutsem ◽  
Bart Roelands
Keyword(s):  
Endurance Exercise ◽  
Mental Fatigue ◽  
Exercise Induced ◽  
The Brain

scholarly journals Potential signaling pathways of acute endurance exercise-induced cardiac autophagy and mitophagy and its possible role in cardioprotection

2017 ◽  
Vol 67 (6) ◽  
pp. 639-654 ◽  
Author(s):  
Youngil Lee ◽  
Insu Kwon ◽  
Yongchul Jang ◽  
Wankeun Song ◽  
Ludmila M. Cosio-Lima ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
Endurance Exercise ◽  
Exercise Induced

scholarly journals miR-222 Is Necessary for Exercise-Induced Cardiac Growth and Protects against Pathological Cardiac Remodeling

2015 ◽  
Vol 21 (4) ◽  
pp. 584-595 ◽  
Author(s):  
Xiaojun Liu ◽  
Junjie Xiao ◽  
Han Zhu ◽  
Xin Wei ◽  
Colin Platt ◽  
...  
Keyword(s):  
Cardiac Remodeling ◽  
Cardiac Growth ◽  
Exercise Induced

scholarly journals Identification of human exercise-induced myokines using secretome analysis

2014 ◽  
Vol 46 (7) ◽  
pp. 256-267 ◽  
Author(s):  
Milène Catoire ◽  
Marco Mensink ◽  
Eric Kalkhoven ◽  
Patrick Schrauwen ◽  
Sander Kersten
Keyword(s):  
Plasma Level ◽  
Exercise Training ◽  
Endurance Exercise ◽  
Acute Exercise ◽  
Exercise Intervention ◽  
Training Intervention ◽  
Secretome Analysis ◽  
Exercise Training Intervention ◽  
Exercise Induced ◽  
Male Subjects

Endurance exercise is associated with significant improvements in cardio-metabolic risk parameters. A role for myokines has been hypothesized, yet limited information is available about myokines induced by acute endurance exercise in humans. Therefore, the aim of the study was to identify novel exercise-induced myokines in humans. To this end, we carried out a 1 h one-legged acute endurance exercise intervention in 12 male subjects and a 12 wk exercise training intervention in 18 male subjects. Muscle biopsies were taken before and after acute exercise or exercise training and were subjected to microarray-based analysis of secreted proteins (secretome). For acute exercise, secretome analysis resulted in a list of 86 putative myokines, which was reduced to 29 by applying a fold-change cut-off of 1.5. Based on that shortlist, a selection of putative myokines was measured in the plasma by ELISA or multiplex assay. From that selection, CX3CL1 (fractalkine) and CCL2 (MCP-1) increased at both mRNA and plasma levels. From the known myokines, only IL-6 and FGF 21 changed at the mRNA level, whereas none of the known myokines changed at the plasma level. Secretome analysis of exercise training intervention resulted in a list of 69 putative myokines. Comparing putative myokines altered by acute exercise and exercise training revealed a limited overlap of only 13 genes. In conclusion, this study identified CX3CL1 and CCL2 as myokines that were induced by acute exercise at the gene expression and plasma level and that may be involved in communication between skeletal muscle and other organs.

scholarly journals Keto-Adaptation and Endurance Exercise Capacity, Fatigue Recovery, and Exercise-Induced Muscle and Organ Damage Prevention: A Narrative Review

Sports ◽  
2019 ◽  
Vol 7 (2) ◽  
pp. 40 ◽  
Author(s):  
Sihui Ma ◽  
Katsuhiko Suzuki
Keyword(s):  
Exercise Capacity ◽  
Endurance Exercise ◽  
Ketone Bodies ◽  
Organ Damage ◽  
The Body ◽  
Narrative Review ◽  
Endurance Capacity ◽  
Muscle Health ◽  
Improve Exercise Capacity ◽  
Exercise Induced

A ketogenic diet (KD) could induce nutritional ketosis. Over time, the body will acclimate to use ketone bodies as a primary fuel to achieve keto-adaptation. Keto-adaptation may provide a consistent and fast energy supply, thus improving exercise performance and capacity. With its anti-inflammatory and anti-oxidative properties, a KD may contribute to muscle health, thus preventing exercise-induced fatigue and damage. Given the solid basis of its potential to improve exercise capacity, numerous investigations into KD and exercise have been carried out in recent years. This narrative review aims to summarize recent research about the potential of a KD as a nutritional approach during endurance exercise, focusing on endurance capacity, recovery from fatigue, and the prevention of exhaustive exercise-induced muscle and organ damage.

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