Effects of exercise training on nitric oxide, blood pressure and antioxidant enzymes

Tsukiyama, Yorika; Itö, Tatsuo; Nagaoka, Kenjiro; Eguchi, Eri; Oginö, Kazuhíde

doi:10.3164/jcbn.16-108

Cited by 73 publications

(59 citation statements)

References 50 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…(35) nitric oxide (NO) involved in vascular endothelial function increases after aerobic exercise training. (36) MBP is determined by cardiac output and peripheral vascular resistance (e.g., peripheral endothelial function). We found that ankle MBP increased from baseline after the 75-g OGTT after the intervention in the CON group, whereas ankle MBP did not change after the intervention in the PAI group.…”

Section: Discussionmentioning

confidence: 99%

Effects of a short-term increase in physical activity on arterial stiffness during hyperglycemia

Kobayashi

Sato

Takahashi³

et al. 2020

J. Clin. Biochem. Nutr.

View full text Add to dashboard Cite

We examined the effects of increasing physical activity on arterial stiffness during hyperglycemia. Nineteen glucose intolerant elderly participated in the study. We randomly assigned 10 participants to increase their daily activity in everyday life, regardless of the time or intensity, for 1 month (PAI group) (age, 74.6 ± 1.3 years; mean ± SE) and nine participants to maintain their level of activity (CON group) (age, 79.2 ± 2.1 years; mean ± SE). The 75 g oral glucose tolerance test was conducted in each participant in both groups before and after the start of the intervention to confirm glucose intolerance. Brachial-ankle pulse wave velocity and cardio ankle vascular index significantly increased from baseline at 30, 60, and 90 min after the 75 g glucose ingestion after the intervention in the CON group (p<0.05), but not in the PAI group. Heart-brachial pulse wave velocity did not change compared to baseline after the 75 g glucose ingestion in either group and did not change from baseline at 30, 60, and 90 min after the 75 g glucose ingestion before and after the intervention in both groups. The present findings indicate that a short term increase in physical activity suppresses the increase in arterial stiffness after glucose intake.

show abstract

Section: Discussionmentioning

confidence: 99%

Effects of a short-term increase in physical activity on arterial stiffness during hyperglycemia

Kobayashi

Sato

Takahashi³

et al. 2020

J. Clin. Biochem. Nutr.

View full text Add to dashboard Cite

show abstract

“…Further research is needed in order to clarify these mechanisms. The increase in circulating Klotho following exercise training may be the result of an increase in the transcription factor peroxisome proliferator‐activated receptor γ, a decline in angiotensin II type I receptor signalling and reduction of oxidative stress, endothelin 1, TGFβ and inflammation that follow exercise training (Faul et al., 2011; Kawamura et al., 2004; Saetre et al., 2011; Tsukiyama, Ito, Nagaoka, Eguchi, & Ogino, 2017; Wilund, 2007) and lead to an increase in the expression of Klotho mRNA and protein (Lim et al., 2012; Mitobe et al., 2005; Saito, Ishizaka, Mitani, Ohno, & Nagai, 2003; Zhang et al., 2008). Also, the increase in shear stress, hypoxia, endothelial biomarker changes, stimulation of peroxisome proliferator‐activated receptor γ coactivator 1α, and increase in antioxidant capacity may be the stimulus to increase Klotho following HIIT, but clarification of these mechanisms is needed and more research is needed to understand the mechanisms that are effective in exercise training‐induced changes in plasma and myocardial levels of Klotho.…”

Section: Discussionmentioning

confidence: 99%

High‐intensity interval training increases myocardial levels of Klotho and protects the heart against ischaemia–reperfusion injury

Ramez

Ramezani

Nasirinezhad

et al. 2020

Experimental Physiology

View full text Add to dashboard Cite

Cardiovascular disease, especially coronary artery disease, remains a major cause of morbidity and mortality in the world, and ischaemia-reperfusion (IR) insult is the main pathological cause leading to death. Exercise training is associated with a reduced risk of cardiovascular disease and the development of cardioprotection against IR injury. Therefore, the purpose of this study was to investigate the effect of preconditioning with high-intensity interval training (HIIT) on myocardial and plasma levels of Klotho and its related axes as novel mechanisms of exercise-induced cardioprotection against IR injury. Seventy male Wistar rats were randomly divided into five groups of control, HIIT, sham, IR and HIIT group that underwent IR injury (H-IR). The training group performed five sessions of HIIT on the treadmill. The cardiac IR injury was induced by ligation of the left anterior descending coronary artery for 30 min followed by 24 h reperfusion. Infarct size and histopathological assessment of cardiac tissues were determined through Evans Bluetriphenyltetrazolium chloride and haematoxylin-eosin staining, respectively. We investigated lipid peroxidation and markers of cardiac injury, antioxidant enzymes and the plasma levels of Klotho using enzyme-linked immunosorbent assays. Also, myocardial levels of Klotho and TRPC6 expression were determined by western blot assays. The results demonstrated a significant increase in myocardial and plasma levels of Klotho following HIIT and a significant decrease during IR injury. Myocardial TRPC6 channel expression increased following IR. HIIT also prevented a significant reduction of Klotho during IR and consequently reduced the expression of the TRPC6 channel in the H-IR group compared with the IR group. Furthermore, HIIT decreased the infarct size, cardiac injury, lipid peroxidation, lactate dehydrogenase, creatine kinase myocardial band and cardiac troponin-I, and improved total antioxidant capacity and catalase, superoxide dismutase and glutathione peroxidase activities following IR injury. The findings of the present study suggest that HIIT improves cardioprotection against IR injury and reduces cardiac damages through an increase in myocardial and plasma levels of Klotho and its related axes (TRPC6 and antioxidant defence). These findings can help to develop preventive and therapeutic approaches. K E Y W O R D SAntioxidant defence, cardioprotection, high-intensity interval training, Klotho, TRPC6 channels wileyonlinelibrary.com/journal/eph Experimental Physiology. 2020;105:652-665.

show abstract

“…Interestingly, blocking NO actually reduced exercise performance in both of these groups below that observed in the untrained WT group, supporting the major role of the NO pathway in mediating the enhanced exercise performance found in both these groups. Although NO is known to be a mediator of exercise performance [17, 21], and is involved in exercise training [28, 30], this is the first demonstration that the increased exercise performance induced by exercise training can not only be completely eliminated by NO blockade, but can be reduced below levels observed in untrained animals. One reason for this novelty is that NO blockade did not reduce exercise performance in untrained WT mice, the model that has been examined most extensively in prior studies.…”

Section: Discussionmentioning

confidence: 99%

Disruption of adenylyl cyclase type 5 mimics exercise training

et al. 2017

View full text Add to dashboard Cite

Exercise training is key to healthful longevity. Since exercise training compliance is difficult, it would be useful to have a therapeutic substitute that mimicked exercise training. We compared the effects of exercise training in wild type (WT) littermates with adenylyl cyclase type 5 knock out (AC5 KO) mice, a model of enhanced exercise performance. Exercise performance, measured by maximal distance and work to exhaustion, was increased in exercise trained WT to levels already attained in untrained AC5 KO. Exercise training in AC5 KO further enhanced their exercise performance. The key difference in untrained AC5 KO and exercise trained WT was the β-adrenergic receptor signaling, which was decreased in untrained AC5 KO compared to untrained WT but was increased in WT with exercise training. Despite this key difference, untrained AC5 KO and exercise trained WT mice shared similar gene expression, determined by deep sequencing, in their gastrocnemius muscle with 183 genes commonly up or down-regulated, mainly involving muscle contraction, metabolism and mitochondrial function. The SIRT1/PGC-1α pathway partially mediated the enhanced exercise in both AC5 KO and exercise trained WT mice, as reflected in the reduced exercise responses after administering a SIRT1 inhibitor, but did not abolish the enhanced exercise performance in the AC5 KO compared to untrained WT. Increasing oxidative stress with paraquat attenuated exercise performance more in untrained WT than untrained AC5 KO, reflecting the augmented oxidative stress protection in AC5 KO. Blocking nitric oxide actually reduced the enhanced exercise performance in untrained AC5 KO and trained WT to levels below untrained WT, demonstrating the importance of this mechanism. These results suggest that AC5 KO mice, without exercise training, share similar mechanisms responsible for enhanced exercise capacity with chronic exercise training, most importantly increased nitric oxide, and demonstrate more reserve with the addition of exercise training. A novel feature of the enhanced exercise performance in untrained AC5 KO mice is their decreased sympathetic tone, which is also beneficial to patients with cardiovascular disease.

show abstract

Effects of exercise training on nitric oxide, blood pressure and antioxidant enzymes

Cited by 73 publications

References 50 publications

Effects of a short-term increase in physical activity on arterial stiffness during hyperglycemia

Effects of a short-term increase in physical activity on arterial stiffness during hyperglycemia

High‐intensity interval training increases myocardial levels of Klotho and protects the heart against ischaemia–reperfusion injury

Disruption of adenylyl cyclase type 5 mimics exercise training

Contact Info

Product

Resources

About