Effect of intermittent hypoxia on pro- and antioxidant balance in rat heart during high-intensity chronic exercise

The purpose of the study was to determine whether exercise would activate JNK in the heart and whether chronic exercise training would alter the response. Untrained rats were familiarized with the treadmill and assigned to one of four groups: low intensity (LI), 10 min, 0%, 15 m/min; medium intensity (MI), 10 min, 0%, 33 m/min; high intensity (HI), 10 min, 25%, 33 m/min; long duration (LD), 30 min, 0%, 15 m/min. Another cohort of rats was subjected to a progressive 6 wk high-intensity training protocol that produced a 12% increase in heart mass. In untrained rats, JNK activity was LI: 1.5 (fold nonrun control), MI: 2.0, HI: 2.5, LD: 1.25 immediately after a single bout of exercise. In trained rats, no activation of JNK above baseline was detected after either a 10-min or 1-h bout of exercise. We concluded that treadmill exercise activates JNK in the rat heart in an intensity-dependent manner and that chronic training abrogates the myocardial JNK response to a bout of exercise.

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The Effects of Acute and Chronic Aerobic Activity on the Signaling Pathway of the Inflammasome NLRP3 Complex in Young Men

Medicina ◽

10.3390/medicina55040105 ◽

2019 ◽

Vol 55 (4) ◽

pp. 105 ◽

Cited By ~ 6

Author(s):

Iman Khakroo Abkenar ◽

Farhad Rahmani-nia ◽

Giovanni Lombardi

Keyword(s):

Heart Rate ◽

Aerobic Exercise ◽

Signaling Pathway ◽

High Intensity ◽

Serum Levels ◽

Moderate Intensity ◽

Chronic Exercise ◽

Maximum Heart Rate ◽

High Group ◽

Nlrp3 Gene

Background and Objectives: The results of the studies show that the intensity and volume of aerobic exercise activity produce different responses of the immune system. This study aims to show how the signaling pathway of the inflammatory NLRP3 complex is influenced by the acute and chronic effects of moderate and high-intensity aerobic exercises in young men. Materials and Methods: Accordingly, 60 healthy (BMI = 23.56 ± 2.67) young (24.4 ± 0.4) students volunteered to participate in the study that was randomly divided into two experimental (n = 20) groups and one control (n = 20) group. The training protocol started with two intensity levels of 50% for a moderate group and 70% of maximum heart rate for high group for 30 min and then continued until reaching 70% (moderate group) and 90% (high group) of the maximum heart rate, respectively. Using Real Time-PCR method, the expression of NLRP3 gene and ELISA- were measured by IL-1β, IL-18. Results: The results showed that acute aerobic exercise with moderate intensity had no significant effect on the expression of NLRP3 gene and serum levels of IL-1β and IL-18 cytokines (p > 0.05) when acute exercise, with high intensity, begins an initiation of the activity of the inflammatory complex with elevated serum levels of IL-1β, IL-18, and NLRP3 gene expression (p < 0.05). In addition, chronic exercise with moderate intensity significantly reduced the expression of NLRP3 gene and serum levels of IL-1β, IL-18 cytokines (p < 0.05). In the case of chronic exercise with high intensity, a significant increase in expression of gene, NLRP3 and serum levels of IL-1β, IL-18 cytokines were observed (p < 0.05). Conclusions: Generally, it can be concluded that chronic exercise with moderate intensity is effective in decreasing the expression of the inflammasome and inflammation.

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Proteomic adaptation to chronic high intensity swimming training in the rat heart

Comparative Biochemistry and Physiology Part D Genomics and Proteomics ◽

10.1016/j.cbd.2007.11.001 ◽

2008 ◽

Vol 3 (1) ◽

pp. 108-117 ◽

Cited By ~ 17

Author(s):

Biao Sun ◽

Jun hong Wang ◽

Yuan yuan Lv ◽

Shu shu Zhu ◽

Jin Yang ◽

...

Keyword(s):

High Intensity ◽

Rat Heart ◽

Swimming Training

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Effect of chronic exercise on glucose uptake and activities of glycolytic enzymes measured regionally in rat heart

Basic Research in Cardiology ◽

10.1007/bf01907927 ◽

1989 ◽

Vol 84 (2) ◽

pp. 174-190 ◽

Cited By ~ 16

Author(s):

H. Kainulainen ◽

J. Komulainen ◽

T. Takala ◽

V. Vihko

Keyword(s):

Glucose Uptake ◽

Rat Heart ◽

Glycolytic Enzymes ◽

Chronic Exercise

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F012 Infarction aggravation induced by intermittent hypoxia is abolished by the antioxidant drug tempol in the rat heart

Archives of Cardiovascular Diseases ◽

10.1016/s1875-2136(09)72265-x ◽

2009 ◽

Vol 102 ◽

pp. S57

Author(s):

A. Ramond ◽

J. Tonini ◽

J.-L. Samuel ◽

D. Godin-ribuot ◽

P. Levy ◽

...

Keyword(s):

Rat Heart ◽

Intermittent Hypoxia

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The effect of intermittent hypoxia on RNA synthesis in the isolated rat heart

Journal of Molecular and Cellular Cardiology ◽

10.1016/0022-2828(76)90017-1 ◽

1976 ◽

Vol 8 (6) ◽

pp. 419-429 ◽

Cited By ~ 7

Author(s):

L Gibb

Keyword(s):

Rat Heart ◽

Intermittent Hypoxia ◽

Rna Synthesis ◽

Isolated Rat Heart ◽

Isolated Rat

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Effects Of Intermittent Hypoxia On The Expression Levels Of Fatty Acid-Binding Protein In Rat Heart

10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a3869 ◽

2012 ◽

Author(s):

Judith C. Mak ◽

Qian Han ◽

Sze C. Yeung ◽

Mary S. Ip

Keyword(s):

Fatty Acid ◽

Rat Heart ◽

Intermittent Hypoxia ◽

Fatty Acid Binding Protein ◽

Binding Protein ◽

Fatty Acid Binding ◽

Expression Levels ◽

Acid Binding Protein

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High-intensity training reduces intermittent hypoxia-induced ER stress and myocardial infarct size

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.00448.2015 ◽

2016 ◽

Vol 310 (2) ◽

pp. H279-H289 ◽

Cited By ~ 24

Author(s):

Guillaume Bourdier ◽

Patrice Flore ◽

Hervé Sanchez ◽

Jean-Louis Pepin ◽

Elise Belaidi ◽

...

Keyword(s):

Protein Kinase ◽

Infarct Size ◽

Er Stress ◽

High Intensity ◽

Intermittent Hypoxia ◽

Myocardial Infarct ◽

Ischemia Reperfusion ◽

Myocardial Infarct Size ◽

High Intensity Training ◽

Intensity Training

Chronic intermittent hypoxia (IH) is described as the major detrimental factor leading to cardiovascular morbimortality in obstructive sleep apnea (OSA) patients. OSA patients exhibit increased infarct size after a myocardial event, and previous animal studies have shown that chronic IH could be the main mechanism. Endoplasmic reticulum (ER) stress plays a major role in the pathophysiology of cardiovascular disease. High-intensity training (HIT) exerts beneficial effects on the cardiovascular system. Thus, we hypothesized that HIT could prevent IH-induced ER stress and the increase in infarct size. Male Wistar rats were exposed to 21 days of IH (21-5% fraction of inspired O2, 60-s cycle, 8 h/day) or normoxia. After 1 wk of IH alone, rats were submitted daily to both IH and HIT (2 × 24 min, 15-30m/min). Rat hearts were either rapidly frozen to evaluate ER stress by Western blot analysis or submitted to an ischemia-reperfusion protocol ex vivo (30 min of global ischemia/120 min of reperfusion). IH induced cardiac proapoptotic ER stress, characterized by increased expression of glucose-regulated protein kinase 78, phosphorylated protein kinase-like ER kinase, activating transcription factor 4, and C/EBP homologous protein. IH-induced myocardial apoptosis was confirmed by increased expression of cleaved caspase-3. These IH-associated proapoptotic alterations were associated with a significant increase in infarct size (35.4 ± 3.2% vs. 22.7 ± 1.7% of ventricles in IH + sedenary and normoxia + sedentary groups, respectively, P < 0.05). HIT prevented both the IH-induced proapoptotic ER stress and increased myocardial infarct size (28.8 ± 3.9% and 21.0 ± 5.1% in IH + HIT and normoxia + HIT groups, respectively, P = 0.28). In conclusion, these findings suggest that HIT could represent a preventive strategy to limit IH-induced myocardial ischemia-reperfusion damages in OSA patients.

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