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Investigating the Role of Scheduled, Voluntary Exercise in Protecting Skeletal Muscle Core Clock and Health Against Alcohol-Induced Disruptions.

紀錄類型:	書目-語言資料,手稿 : Monograph/item
正題名/作者:	Investigating the Role of Scheduled, Voluntary Exercise in Protecting Skeletal Muscle Core Clock and Health Against Alcohol-Induced Disruptions./
作者:	Tice, Abigail L.
面頁冊數:	1 online resource (166 pages)
附註:	Source: Dissertations Abstracts International, Volume: 84-12, Section: B.
Contained By:	Dissertations Abstracts International84-12B.
標題:	Health sciences. -
電子資源:	click for full text (PQDT)
ISBN:	9798379743536

Investigating the Role of Scheduled, Voluntary Exercise in Protecting Skeletal Muscle Core Clock and Health Against Alcohol-Induced Disruptions.
Tice, Abigail L.

Investigating the Role of Scheduled, Voluntary Exercise in Protecting Skeletal Muscle Core Clock and Health Against Alcohol-Induced Disruptions. - 1 online resource (166 pages)

Source: Dissertations Abstracts International, Volume: 84-12, Section: B.

Thesis (Ph.D.)--The Florida State University, 2023.

Includes bibliographical references

The skeletal muscle clock contributes to the regulation of skeletal muscle health and function. Mutations to the muscle clock result in decreased muscle mass and strength, diminished mitochondrial health, and altered substrate metabolism in the muscle. Chronic alcohol (EtOH) ingestion disrupts components of the core molecular clock, alters mitochondrial function, and decreases muscle mass and strength. Exercise is a potent stimulator of the muscle clock, and exercise training promotes muscle and mitochondrial health. PURPOSE: In the current study, we examined the potential protective effects of scheduled, voluntary wheel running on alcohol-induced disruptions to the skeletal muscle clock and the effects of alcohol on exercise-induced muscle adaptations. METHODS: Female C57BL/6 mice were randomly assigned to one of 4 groups: CON SED (n=26), ETOH SED (n=27), CON EX (n=28), ETOH EX (n=25). Exercise (EX) mice had running wheel access from ZT13-15, while sedentary mice (SED) remained in their home cage. All mice were fed either a control (CON) or alcohol (ETOH)-containing liquid diet. Grip strength and body composition was measured before and after the interventions. After 6 weeks, muscle was collected every 4hrs and RT-PCR, Western blotting, and citrate synthase activity assays were performed in gastrocnemius muscle. Cross sectional area and percentage of fiber type were measured on the plantaris muscle. RESULTS: Transcription of Bmal1, Per1, and Per2 was disrupted in ETOH SED vs. CON SED, while core clock mRNA expression was unaltered in ETOH EX compared to ETOH SED. CON EX phase shifted Bmal1 and Per1 mRNA compared to CON SED. While ETOH SED phase delayed peak nuclear protein expression of MYOD1 and DBP compared to CON SED, CON EX phase advanced peak expression of both proteins and ETOH EX phase advanced peak DBP nuclear expression. While REVERBα and BMAL1 circadian nuclear expression was unaltered, However, overall BMAL1 nuclear expression was increased in ETOH EX compared to ETOH SED. Alcohol blunted the hypertrophic response to exercise in the gastrocnemius, plantaris, and soleus muscles, and overall lean mass and blunted the exercise induced increase in forelimb grip strength. Citrate synthase activity was increased with exercise training in control and EtOH mice, while Complex I-V mitochondrial protein content and Cytochrome C and COXIV protein expression was increased with exercise, regardless of diet. The exercise-induced increase in Pcg1α mRNA was impaired with alcohol, and mRNA expressions of Opa1, Mfn1, and Drp1 were significantly correlated with average daily running distance, regardless of diet. The mitophagy marker BECLIN was also increased with exercise. CONCLUSION: These data suggests that scheduled voluntary wheel running may not protect the muscle clock against alcohol-induced disruption and that alcohol partially blunts skeletal muscle adaptations to exercise training.

Electronic reproduction.
Ann Arbor, Mich. :
ProQuest,
2024

Mode of access: World Wide Web

ISBN: 9798379743536Subjects--Topical Terms:

1179212
Health sciences.
Subjects--Index Terms:

Aerobic exerciseIndex Terms--Genre/Form:

554714
Electronic books.

Investigating the Role of Scheduled, Voluntary Exercise in Protecting Skeletal Muscle Core Clock and Health Against Alcohol-Induced Disruptions.
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520 $a The skeletal muscle clock contributes to the regulation of skeletal muscle health and function. Mutations to the muscle clock result in decreased muscle mass and strength, diminished mitochondrial health, and altered substrate metabolism in the muscle. Chronic alcohol (EtOH) ingestion disrupts components of the core molecular clock, alters mitochondrial function, and decreases muscle mass and strength. Exercise is a potent stimulator of the muscle clock, and exercise training promotes muscle and mitochondrial health. PURPOSE: In the current study, we examined the potential protective effects of scheduled, voluntary wheel running on alcohol-induced disruptions to the skeletal muscle clock and the effects of alcohol on exercise-induced muscle adaptations. METHODS: Female C57BL/6 mice were randomly assigned to one of 4 groups: CON SED (n=26), ETOH SED (n=27), CON EX (n=28), ETOH EX (n=25). Exercise (EX) mice had running wheel access from ZT13-15, while sedentary mice (SED) remained in their home cage. All mice were fed either a control (CON) or alcohol (ETOH)-containing liquid diet. Grip strength and body composition was measured before and after the interventions. After 6 weeks, muscle was collected every 4hrs and RT-PCR, Western blotting, and citrate synthase activity assays were performed in gastrocnemius muscle. Cross sectional area and percentage of fiber type were measured on the plantaris muscle. RESULTS: Transcription of Bmal1, Per1, and Per2 was disrupted in ETOH SED vs. CON SED, while core clock mRNA expression was unaltered in ETOH EX compared to ETOH SED. CON EX phase shifted Bmal1 and Per1 mRNA compared to CON SED. While ETOH SED phase delayed peak nuclear protein expression of MYOD1 and DBP compared to CON SED, CON EX phase advanced peak expression of both proteins and ETOH EX phase advanced peak DBP nuclear expression. While REVERBα and BMAL1 circadian nuclear expression was unaltered, However, overall BMAL1 nuclear expression was increased in ETOH EX compared to ETOH SED. Alcohol blunted the hypertrophic response to exercise in the gastrocnemius, plantaris, and soleus muscles, and overall lean mass and blunted the exercise induced increase in forelimb grip strength. Citrate synthase activity was increased with exercise training in control and EtOH mice, while Complex I-V mitochondrial protein content and Cytochrome C and COXIV protein expression was increased with exercise, regardless of diet. The exercise-induced increase in Pcg1α mRNA was impaired with alcohol, and mRNA expressions of Opa1, Mfn1, and Drp1 were significantly correlated with average daily running distance, regardless of diet. The mitophagy marker BECLIN was also increased with exercise. CONCLUSION: These data suggests that scheduled voluntary wheel running may not protect the muscle clock against alcohol-induced disruption and that alcohol partially blunts skeletal muscle adaptations to exercise training.
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