Change in PGC-1α Expression in Rat Skeletal Muscle after Low-intensity Prolonged Swimming Exercise

Fujimoto, Eri; Yamaguchi, Wataru; Terada, Shin; Higuchi, Mitsuru; Tabata, Izumi

doi:10.2114/jpa2.30.23

Cited by 6 publications

(8 citation statements)

References 19 publications

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“…Thus, according to the literature a single bout of exercise can activate calcium/calmodulin-dependent protein kinase (CaMK), p38 mitogen-activated protein kinase (p38 MAPK), cyclic adenosine monophosphate (cAMP), and phosphorylate AMP activated protein kinase (AMPK), which are the molecular signals responsible for the increase in PGC-1 α expression ( Bonen, 2009 ; Lira et al, 2010 ; Perry and Hawley, 2018 ; Memme et al, 2021 ). Our results are in accordance with the literature and demonstrate that a single bout of exercise increases the expression and/or content of PGC-1 α ( Wright et al, 2007 ; Ikeda et al, 2008 ; Seebacher and Glanville, 2010 ; Fujimoto et al, 2011 ; Shute et al, 2018 ) and NRF-1 ( Murakami et al, 1998 ; Seebacher and Glanville, 2010 ; Daussin et al, 2012 ). More importantly, our main finding is that melatonin potentiates the up-regulation of PGC-1 α expression.…”

Section: Discussionsupporting

confidence: 93%

“…However, in an opposite scenario of high PGC-1 α , there are evidences showing a lower endurance performance in skeletal muscle-specific PGC-1 α knockout (PGC-1 α MKO) ( Handschin et al, 2007 ) and whole-body PGC-1 α knockout animals (PGC-1 α KO) ( Leone et al, 2005 ). Although it is well established that a single bout of exercise is able to increase content and/or expression of PGC-1 α ( Wright et al, 2007 ; Ikeda et al, 2008 ; Seebacher and Glanville, 2010 ; Fujimoto et al, 2011 ; Shute et al, 2018 ) and NRF-1 ( Murakami et al, 1998 ; Seebacher and Glanville, 2010 ; Daussin et al, 2012 ), reports on these proteins after exercise until exhaustion are lacking for animals treated with melatonin.…”

Section: Introductionmentioning

confidence: 99%

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Melatonin Potentiates Exercise-Induced Increases in Skeletal Muscle PGC-1α and Optimizes Glycogen Replenishment

et al. 2022

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Compelling evidence has demonstrated the effect of melatonin on exhaustive exercise tolerance and its modulatory role in muscle energy substrates at the end of exercise. In line with this, PGC-1α and NRF-1 also seem to act on physical exercise tolerance and metabolic recovery after exercise. However, the literature still lacks reports on these proteins after exercise until exhaustion for animals treated with melatonin. Thus, the aim of the current study was to determine the effects of acute melatonin administration on muscle PGC-1α and NRF-1, and its modulatory role in glycogen and triglyceride contents in rats subjected to exhaustive swimming exercise at an intensity corresponding to the anaerobic lactacidemic threshold (iLAn). In a randomized controlled trial design, thirty-nine Wistar rats were allocated into four groups: control (CG = 10), rats treated with melatonin (MG = 9), rats submitted to exercise (EXG = 10), and rats treated with melatonin and submitted to exercise (MEXG = 10). Forty-eight hours after the graded exercise test, the animals received melatonin (10 mg/kg) or vehicles 30 min prior to time to exhaustion test in the iLAn (tlim). Three hours after tlim the animals were euthanized, followed by muscle collection for specific analyses: soleus muscles for immunofluorescence, gluteus maximus, red and white gastrocnemius for the assessment of glycogen and triglyceride contents, and liver for the measurement of glycogen content. Student t-test for independent samples, two-way ANOVA, and Newman keuls post hoc test were used. MEXG swam 120.3% more than animals treated with vehicle (EXG; p < 0.01). PGC-1α and NRF-1 were higher in MEXG with respect to the CG (p < 0.05); however, only PGC-1α was higher for MEXG when compared to EXG. Melatonin reduced the triglyceride content in gluteus maximus, red and white gastrocnemius (F = 6.66, F = 4.51, and F = 6.02, p < 0.05). The glycogen content in red gastrocnemius was higher in MEXG than in CG (p = 0.01), but not in EXG (p > 0.05). In conclusion, melatonin was found to enhance exercise tolerance, potentiate exercise-mediated increases in PGC-1α, decrease muscle triglyceride content and increase muscle glycogen 3 h after exhaustive exercise, rapidly providing a better cellular metabolic environment for future efforts.

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Section: Discussionsupporting

confidence: 93%

Section: Introductionmentioning

confidence: 99%

Melatonin Potentiates Exercise-Induced Increases in Skeletal Muscle PGC-1α and Optimizes Glycogen Replenishment

et al. 2022

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“…In addition, a mouse study conducted by Pang et al has reported that PGC-1α expression increased during 30 min of treadmill exercise but decreased during 1 h of treadmill exercise, suggesting that the regulation of gene and protein expression may differ according to the duration of exercise [11]. A few studies suggested 6-h prolonged acute bout of swimming exercise-induced an elevated mRNA expression of PGC-1 immediately after [21]and elevation of PGC-1α protein was maintained 18 and 24 h after the exercise in rat epitrochlearis muscle [22]. Given these previous findings, the expression of PGC-1α is considered to occur when some time has passed after exercise.…”

Section: Discussionmentioning

confidence: 99%

The Acute Effects of Swimming Exercise on PGC-1α-FNDC5/Irisin-UCP1 Expression in Male C57BL/6J Mice

et al. 2021

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Irisin is a myokine primarily secreted by skeletal muscles and is known as an exercise-induced hormone. The purpose of this study was to determine whether the PGC-1α -FNDC5 /Irisin-UCP1 expression which is an irisin-related signaling pathway, is activated by an acute swimming exercise. Fourteen to sixteen weeks old male C57BL/6J mice (n = 20) were divided into control (CON, n = 10) and swimming exercise groups (SEG, n = 10). The SEG mice performed 90 min of acute swimming exercise, while control (non-exercised) mice were exposed to shallow water (2 cm of depth) for 90 min. The mRNA and protein expression of PGC-1α, FNDC5 and browning markers including UCP1 were evaluated by quantitative real-time PCR and western blotting. Serum irisin concentration was measured by enzyme-linked immunosorbent assay. An acute swimming exercise did not lead to alterations in the mRNA and protein expression of PGC-1α in both soleus and gastrocnemius muscles, the mRNA and protein expression of UCP1 in brown adipose tissue, mRNA browning markers in visceral adipose tissue and circulating irisin when compared with the control group. On the other hand, an acute swimming exercise led to increases in the mRNA and protein expressions of FNDC5 in the soleus muscle, the protein expression of FNDC5 in the gastrocnemius muscles and the protein expression of UCP1 in subcutaneous adipose tissue.

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“…On the other hand, it has been suggested in animal studies that low intensity exercise can activate PGC-1α [ 62 , 63 ] independently of 5′ adenosine monophosphate-activated protein kinase (AMPK) activation, which might only occur with exercise of higher intensity [ 64 ].…”

Section: Discussionmentioning

confidence: 99%

Effects of non-supervised low intensity aerobic excise training on the microvascular endothelial function of patients with type 1 diabetes: a non-pharmacological interventional study

Moraes

Bavel

Gomes

et al. 2016

BMC Cardiovasc Disord

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BackgroundThe aim of the present study was to evaluate changes in microvascular density and reactivity in patients with type 1 diabetes (T1D) resulting from low intensity chronic exercise training.MethodsThis study included 22 (34 ± 7 years) consecutive outpatients with T1D and disease duration > 6 years. We used intravital video-microscopy to measure basal skin capillary density and capillary recruitment using post-occlusive reactive hyperemia (PORH) in the dorsum of the fingers. Endothelium-dependent and -independent vasodilation of the skin microcirculation was evaluated in the forearm with a laser Doppler flow monitoring (LDF) system in combination with acetylcholine and sodium nitroprusside iontophoresis, PORH and local thermal hyperemia.ResultsThe basal mean capillary density (MCD) after exercise training was significantly higher than before exercise (134 ± 25 vs. 119 ± 19 capillaries/mm2, respectively; P = 0.0013). MCD during PORH was also higher after exercise (140 ± 26 vs. 121 ± 24 capillaries/mm2, respectively; P < 0.0001). Endothelium-dependent capillary recruitment during PORH was also significantly higher after exercise (140 ± 26 vs. 134 ± 25 capillaries/mm2, respectively; P < 0.0012). There were no significant changes in skin microvascular reactivity after exercise as investigated using LDF.ConclusionsOur results showed that low intensity aerobic exercise, performed four times per week for 12 weeks by patients with T1D, induces significant increases in microvascular density and endothelial-dependent capillary reactivity.Trial registrationClinicalTrials.gov NCT02441504. Registered 7 May 2015.Electronic supplementary materialThe online version of this article (doi:10.1186/s12872-016-0191-9) contains supplementary material, which is available to authorized users.

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Change in PGC-1α Expression in Rat Skeletal Muscle after Low-intensity Prolonged Swimming Exercise

Cited by 6 publications

References 19 publications

Melatonin Potentiates Exercise-Induced Increases in Skeletal Muscle PGC-1α and Optimizes Glycogen Replenishment

Melatonin Potentiates Exercise-Induced Increases in Skeletal Muscle PGC-1α and Optimizes Glycogen Replenishment

The Acute Effects of Swimming Exercise on PGC-1α-FNDC5/Irisin-UCP1 Expression in Male C57BL/6J Mice

Effects of non-supervised low intensity aerobic excise training on the microvascular endothelial function of patients with type 1 diabetes: a non-pharmacological interventional study

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