Optimization of different intensities of exercise preconditioning in protecting exhausted exercise induced heart injury in rats

Interleukin-6 (IL-6) is a pleiotropic cytokine that protects against cardiac ischemia-reperfusion (I/R) injury following pharmacological and ischemic preconditioning (IPC), but the affiliated role in exercise preconditioning is unknown. Our study purpose was to characterize exercise-induced IL-6 cardiac signaling ( aim 1) and evaluate myocardial preconditioning ( aim 2). In aim 1, C57 and IL-6−/− mice underwent 3 days of treadmill exercise for 60 min/day at 18 m/min. Serum, gastrocnemius, and heart were collected preexercise, immediately postxercise, and 30 and 60 min following the final exercise session and analyzed for indexes of IL-6 signaling. For aim 2, a separate cohort of exercise-preconditioned (C57 EX and IL-6−/− EX) and sedentary (C57 SED and IL-6−/− SED) mice received surgical I/R injury (30 min I, 120 min R) or a time-matched sham operation. Ischemic and perfused tissues were examined for necrosis, apoptosis, and autophagy. In aim 1, serum IL-6 and IL-6 receptor (IL-6R), gastrocnemius, and myocardial IL-6R were increased following exercise in C57 mice only. Phosphorylated (p) signal transducer and activator of transcription 3 was increased in gastrocnemius and heart in C57 and IL-6−/− mice postexercise, whereas myocardial iNOS and cyclooxygenase-2 were unchanged in the exercised myocardium. Exercise protected C57 EX mice against I/R-induced arrhythmias and necrosis, whereas arrhythmia score and infarct outcomes were higher in C57 SED, IL-6−/− SED, and IL-6−/− EX mice compared with SH. C57 EX mice expressed increased p-p44/42 MAPK (Thr202/Tyr204) and p-p38 MAPK (Thr180/Tyr182) compared with IL-6−/− EX mice, suggesting pathway involvement in exercise preconditioning. Findings indicate exercise exerts cardioprotection via IL-6 and strongly implicates protective signaling originating from the exercised skeletal muscle.

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Exercise-induced cardiac preconditioning: how exercise protects your achy-breaky heart

Journal of Applied Physiology ◽

10.1152/japplphysiol.00004.2011 ◽

2011 ◽

Vol 111 (3) ◽

pp. 905-915 ◽

Cited By ~ 66

Author(s):

Chad R. Frasier ◽

Russell L. Moore ◽

David A. Brown

Keyword(s):

Ischemia Reperfusion ◽

Epidemiological Studies ◽

Review Article ◽

Buffering Capacity ◽

Future Research ◽

Cardiac Mitochondria ◽

Exercise Preconditioning ◽

Cardiac Preconditioning ◽

Exercise Induced ◽

Intensity Of Exercise

The ability of exercise to protect the heart against ischemia-reperfusion (I/R) injury is well known in both human epidemiological studies and experimental animal models. In this review article, we describe what is currently known about the ability of exercise to precondition the heart against infarction. Just 1 day of exercise can protect the heart against ischemia/reperfusion damage, and this protection is upheld with months of exercise, making exercise one of the few sustainable preconditioning stimuli. Exercise preconditioning depends on the model and intensity of exercise, and appears to involve heightened oxidant buffering capacity, upregulated subunits of sarcolemmal ATP-sensitive potassium channels, and adaptations to cardiac mitochondria. We review the putative mechanisms involved in exercise preconditioning and point out many areas where future research is necessary to advance our understanding of how this stimulus confers resistance against I/R damage.

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Exercise Preconditioning Alleviate LPS Induced Acute Heart Injury Through GCN2 Pathway

Medicine & Science in Sports & Exercise ◽

10.1249/01.mss.0000680396.30855.a3 ◽

2020 ◽

Vol 52 (7S) ◽

pp. 567-567

Author(s):

Xin Xu ◽

Zhongguang Sun ◽

Xiaoci Zheng ◽

Linlin Zhao ◽

Jing Jing ◽

...

Keyword(s):

Exercise Preconditioning ◽

Heart Injury

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Exercise-induced expression of VEGF and salvation of myocardium in the early stage of myocardial infarction

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.01393.2007 ◽

2009 ◽

Vol 296 (2) ◽

pp. H389-H395 ◽

Cited By ~ 30

Author(s):

Guifu Wu ◽

Jamal S. Rana ◽

Joanna Wykrzykowska ◽

Zhimin Du ◽

Qingen Ke ◽

...

Keyword(s):

Exercise Training ◽

Exercise Group ◽

Angiogenic Factors ◽

Vegf Expression ◽

Infarcted Myocardium ◽

Sedentary Group ◽

Exercise Preconditioning ◽

Exercise Induced ◽

Response To Exercise ◽

The Impact

The mechanism of exercise-induced benefit and angiogenesis in ischemic heart disease remains poorly defined. This study was designed to investigate the effects of exercise training on the expression of angiogenic factors and angiogenesis in the infarcted myocardium [myocarial infaction (MI)]. Sixty-three male FVB mice were used for study and were divided into subgroups to test the response to exercise: the time-dependent expression of angiogenic factors to exercise training in normal ( group 1; n = 12) and infarcted myocardium ( group 2; n = 15) and the exercise-induced angiogenic response in normal and infarcted myocardium ( group 3; n = 20) as well as the impact of exercise preconditioning on infarcted myocardium ( group 4; n = 26). Exercise training consisted of daily treadmill exercise for 1 h for 3 days. Expression of VEGF and its receptors Flt-1 and Flk-1 was upregulated by exercise training in mice with MI. Exercise-induced VEGF expression in the MI group was higher than that in the sham (control) group. Cell proliferation assessment showed a significantly higher ( P < 0.05) number of bromodeoxyuridine-positive cells in post-MI mice in the exercise group as opposed to post-MI mice in the sedentary group. 2,3,5-Triphenyltetrazolium chloride staining revealed a profound difference in the size of MI (18.25 ± 2.93%) in the exercise group versus the sedentary group (29.26 ± 7.64%, P = 0.02). Moreover, exercise preconditioning before MI promoted VEGF expression at both mRNA and protein levels. In conclusion, activation of VEGF and its receptors occurs in the infarcted mice heart in response to exercise, which results in decreased infarct size and improved angiogenesis.

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Comparison of myocardial ischemic/hypoxic staining techniques for evaluating the alleviation of exhaustive exercise-induced myocardial injury by exercise preconditioning

Journal of Molecular Histology ◽

10.1007/s10735-021-09958-0 ◽

2021 ◽

Author(s):

Yue Huang ◽

Shan- Shan Pan ◽

Yuan-Pan Guo ◽

Jia-Yin Wang ◽

Dong-Feng Wan ◽

...

Keyword(s):

Myocardial Injury ◽

Exhaustive Exercise ◽

Exercise Preconditioning ◽

Staining Techniques ◽

Exercise Induced

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Protective effects of acute exercise preconditioning on disuse-induced muscular atrophy in aged muscle: a narrative literature review

The Journal of Physiological Sciences ◽

10.1186/s12576-020-00783-w ◽

2020 ◽

Vol 70 (1) ◽

Author(s):

Toshinori Yoshihara ◽

Hisashi Naito

Keyword(s):

Skeletal Muscle ◽

Acute Exercise ◽

Muscular Atrophy ◽

Protective Effects ◽

Older Individuals ◽

Age Related ◽

Exercise Preconditioning ◽

Narrative Literature Review ◽

Exercise Induced ◽

Effects Of Aging

AbstractAging is associated with a progressive loss of skeletal muscle mass and strength, resulting in frailty and lower quality of life in older individuals. At present, a standard of clinical or pharmacological care to prevent the adverse effects of aging does not exist. Determining the mechanism(s) responsible for muscular atrophy in disused aged muscle is a required key step for the development of effective countermeasures. Studies suggest an age-related differential response of genes and signalings to muscle disuse in both rodents and humans, implying the possibility that effective countermeasures to prevent disuse muscle atrophy may be age-specific. Notably, exercise preconditioning can attenuate disuse-induced muscular atrophy in rodent and human skeletal muscles; however, information on age-specific mechanisms of this exercise-induced protection remains limited. This mini-review aimed to summarize the protective effects of acute exercise preconditioning on muscular atrophy in aged muscle and provide potential mechanisms for its preventive effect on skeletal muscle wasting.

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Late Exercise Preconditioning Promotes Autophagy against Exhaustive Exercise-Induced Myocardial Injury through the Activation of the AMPK-mTOR-ULK1 Pathway

BioMed Research International ◽

10.1155/2019/5697380 ◽

2019 ◽

Vol 2019 ◽

pp. 1-10

Author(s):

Hong-Tao Liu ◽

Shan-Shan Pan

Keyword(s):

Myocardial Protection ◽

Myocardial Injury ◽

Troponin I ◽

Picric Acid ◽

Exhaustive Exercise ◽

Class Iii ◽

Hypoxic Injury ◽

Exercise Preconditioning ◽

Exercise Induced ◽

The Relationship

Accumulating evidence shows that the AMPK-mTOR pathway modulates autophagy via coordinated phosphorylation of ULK1. The aim of the present study was to investigate the relationship between AMPK, mTOR, and ULK1 during late exercise preconditioning (LEP), and to explore whether LEP-induced myocardial protection is related to the autophagy. The exercise preconditioning (EP) protocol was as follows: rats were instructed to for run four repeated in duration of 10 minutes (including 10 minutes rest between each period) on a treadmill. Exhaustive exercise (EE) after LEP pretreatment and administration of wortmannin (an autophagy inhibitor that suppresses Class III PI3K-kinase (PI3KC3) activity) were added to test the protective effect. Cardiac troponin I (cTnI), and transmission electron microscopy (TEM), along with hematoxylin-basic fuchsin-picric acid (HBFP) staining, were used to evaluate the myocardial ischemic-hypoxic injury and protection. Western blot was used to analyze the relationship of autophagy-associated proteins. Exhaustive exercise caused severe myocardial ischemic-hypoxic injury, which led to an increase in cTnI levels, changes of ischemia–hypoxia, and cells ultrastructure. Compared with the EE group, LEP significantly suppressed exhaustive exercise-induced myocardial injury. However, wortmannin attenuated LEP-induced myocardial protection by inhibiting autophagy. Compared with the C group, AMPK was increased in the LEP, EE, and LEP+EE groups, but phosphorylation of AMPK at Thr172 was not significantly changed. Exercise did not have any effect on mTOR expression. Compared with the C group, ULK1 was increased and the ULK1ser757/ULK1 ratio was decreased in the LEP and LEP+EE groups. ULK1 was not significantly affected in the EE group, however, phosphorylation of ULK1 at Ser757 was remarkably decreased. To sum up, our results suggested that LEP promoted autophagy through the activation of AMPK-mTOR-ULK1 pathway, and that activated autophagy was partially involved in myocardial protection against EE-induced myocardial ischemic-hypoxic injury.

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