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Interaction of genetic background and exercise training intensity on endothelial function in mouse aorta.

ABSTRACT: The purpose of this study was to characterize the genetic contribution to endothelial adaptation to exercise training. Vasoreactivity was assessed in aortas from four inbred mouse strains (129S1, B6, NON, and SJL) after 4 weeks of moderate intensity continuous exercise training (MOD), high intensity interval training (HIT) or in sedentary controls (SED). Intrinsic variations in endothelium-dependent vasorelaxation (EDR) to acetylcholine (ACh) as well as vasocontractile responses were observed across SED groups. For responses to exercise training, there was a significant interaction between mouse strain and training intensity on EDR. Exercise training had no effect on EDR in aortas from 129S1 and B6 mice. In NON, EDR was improved in aortas from MOD and HIT compared with respective SED, accompanied by diminished responses to PE in those groups. Interestingly, EDR was impaired in aorta from SJL HIT compared with SED. The transcriptional activation of endothelial genes was also influenced by the interaction between mouse strain and training intensity. The number of genes altered by HIT was greater than MOD, and there was little overlap between genes altered by HIT and MOD. HIT was associated with gene pathways for inflammatory responses. NON MOD genes showed enrichment for vessel growth pathways. These findings indicate that exercise training has non-uniform effects on endothelial function and transcriptional activation of endothelial genes depending on the interaction between genetic background and training intensity.

SUBMITTER: Kim SK

PROVIDER: S-EPMC6940500 | biostudies-literature | 2020 Jan

REPOSITORIES: biostudies-literature

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Interaction of genetic background and exercise training intensity on endothelial function in mouse aorta.

Kim Seung Kyum SK Avila Joshua J JJ Massett Michael P MP

The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology 20200101 1

The purpose of this study was to characterize the genetic contribution to endothelial adaptation to exercise training. Vasoreactivity was assessed in aortas from four inbred mouse strains (129S1, B6, NON, and SJL) after 4 weeks of moderate intensity continuous exercise training (MOD), high intensity interval training (HIT) or in sedentary controls (SED). Intrinsic variations in endothelium-dependent vasorelaxation (EDR) to acetylcholine (ACh) as well as vasocontractile responses were observed ac ...[more]

PMID: 31908575

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Project description:BACKGROUND:The understanding of obsesity-related vascular dysfunction remains controversial mainly because of the diseases associated with vascular injury. Exercise training is known to prevent vascular dysfunction. Using an obesity model without comorbidities, we aimed at investigating the underlying mechanism of vascular dysfunction and how exercise interferes with this process. METHODS:High-sugar diet was used to induce obesity in mice. Exercise training was performed 5 days/week. Body weight, energy intake, and adipose tissues were assessed; blood metabolic and hormonal parameters were determined; and serum TNF? was measured. Blood pressure and heart rate were assessed by plethysmography. Changes in aortic isometric tension were recorded on myograph. Western blot was used to analyze protein expression. Nitric oxide (NO) was evaluated using fluorescence microscopy. Antisense oligodeoxynucleotides were used for inducible nitric oxide synthase isoform (iNOS) knockdown. RESULTS:Body weight, fat mass, total cholesterol, low-density lipoprotein cholesterol fraction, insulin, and leptin were higher in the sedentary obese group (SD) than in the sedentary control animals (SS). Exercise training prevented these changes. No difference in glucose tolerance, insulin sensitivity, blood pressure, and heart rate was found. Decreased vascular relaxation and reduced endothelial nitric oxide synthase (eNOS) functioning in the SD group were prevented by exercise. Contractile response to phenylephrine was decreased in the aortas of the wild SD mice, compared with that of the SS group; however, no alteration was noted in the SD iNOS(-/-) animals. The decreased contractility was endothelium-dependent, and was reverted by iNOS inhibition or iNOS silencing. The aortas from the SD group showed increased basal NO production, serum TNF?, TNF receptor-1, and phospho-I?B. Exercise training attenuated iNOS-dependent reduction in contractile response in high-sugar diet-fed animals, decreased iNOS expression, and increased eNOS expression. CONCLUSION:Obesity caused endothelium dysfunction, TNF?, and iNOS pathway up-regulation, decreasing vascular contractility in the obese animals. Exercise training was an effective therapy to control iNOS-dependent NO production and to preserve endothelial function in obese individuals.

Project description:Aging is associated with testicular morphological and functional alterations, but the underlying molecular mechanisms and the impact of physical exercise are poorly understood. In this study, we examined the effects of age and lifelong moderate-intensity exercise on rat testis. Mature adults (35 weeks) and middle-aged (61 weeks) Wistar Unilever male rats were maintained as sedentary or subjected to a lifelong moderate-intensity treadmill training protocol. Testis weight and histology, mitochondrial biogenesis and function, and proteins involved in protein synthesis and stress response were evaluated. Our results illustrate an age-induced testicular atrophy that was associated with alterations in stress response, and mitochondrial biogenesis and function. Aging was associated with increased testicular levels of heat shock protein beta-1 (HSP27) and antioxidant enzymes. Aging was also associated with decreased mRNA abundance of the nuclear respiratory factor 1 (Nrf1), a key transcription factor for mitochondrial biogenesis, which was accompanied by decreased protein levels of the oxidative phosphorylation system (OXPHOS) complexes subunits in the testes of older animals. On the other hand, exercise did not protect against age-induced testicular atrophy and led to deleterious effects on sperm morphology. Exercise led to an even more pronounced decrease in the Nrf1 mRNA levels in testes of both age groups and was associated with decreased mRNA abundance of other mitochondrial biogenesis markers and decreased protein levels of OXPHOS complexes subunits. Lifelong moderate-intensity exercise training was also associated with an increase in testicular oxidative stress markers and possibly with reduced translation. Together, our results indicate that exercise did not protect against age-induced testicular atrophy and was not associated with beneficial changes in mitochondria and stress response, further activating mechanisms of protein synthesis inhibition.

Project description:IntroductionExercise training is strongly recommended as a therapeutic approach to treat individuals with heart failure. High-intensity exercise training modalities still controversial in this population. The study aims to preliminary assess the consequences of high-intensity exercise training modalities, aerobic interval training (HIIT) and progressive high circuit-resistance training (CRT), on primarily endothelial function and cardiorespiratory fitness, and secondly on muscle strength and physical performance in heart failure patients.MethodsThis preliminary multicentric randomized controlled trial comprised 23 heart failure patients, aged 56 ± 10 years old, mainly New York Heart Association classification I and II (%), hemodynamically stable, who compromise at least 36 exercise sessions of a randomly assigned intervention (HIIT, CRT or control group). Endothelial function, cardiopulmonary exercise testing, muscle strength and physical performance were completed at baseline and post-intervention.ResultsAlthough no effects on endothelial function; both HIIT and CRT modalities were able to produce a positive effect on [Formula: see text] peak (HIIT = +2.1±6.5, CRT = +3.0±4.2 and control group = -0.1± 5.3 mL/kg/min, time*group p-value<0,05) and METs (HIIT = +0.6±1.8, CRT = +0.9±1.2 and control group = 0±1.6, time*group p-value<0,05). Only HIIT increased isokinetic torque peak (HIIT = +8.8±55.8, CRT = 0.0±60.7 and control group = 1.6±57.6 Nm) matched p-value<0,05. Regarding the physical performance, the CRT modality reduced chair stand test completion time (HIIT = -0.7±3.1, CRT = -3.3±3.2 and control group = -0.3±2.5 s, matched p-value<0,05 and HIIT improved global physical performance(time*group p<0,05).ConclusionThis preliminary study trends to indicate for the first time that high-intensity interval training promotes a jointly superior effect compared to progressive high intensity circuit-resistance training by improving cardiorespiratory fitness, muscular strength, and physical performance. Further research with larger cohort is necessary.Clinical trial registration numberReBEC RBR-668c8v.

Dataset Information

Interaction of genetic background and exercise training intensity on endothelial function in mouse aorta.

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Interaction of genetic background and exercise training intensity on endothelial function in mouse aorta.

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