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Short-Term Adaptations in Skeletal Muscle Mitochondrial Oxidative Capacity and Metabolic pathways to Breaking Up Sedentary Behaviors with Short-Frequent Bouts of Physical Activity Compared to a Matched Daily Single-Continuous Bout in Obese Adults

ABSTRACT: Short-Term Adaptations in Skeletal Muscle Mitochondrial Oxidative Capacity and Metabolic pathways to Breaking Up Sedentary Behaviors with Short-Frequent Bouts of Physical Activity Compared to a Matched Daily Single-Continuous Bout in Obese Adults

PROVIDER: PRJNA775635 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16599600_1.fastq.gz	Fastqsanger.gz
	SRR16599600_2.fastq.gz	Fastqsanger.gz
	SRR16599601_1.fastq.gz	Fastqsanger.gz
	SRR16599601_2.fastq.gz	Fastqsanger.gz
	SRR16599602_1.fastq.gz	Fastqsanger.gz

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Project description:BackgroundTime awake with advancing age is increasingly spent sedentary and has several negative health consequences. We examined associations between the frequency of daily sedentary and active bouts with all-cause mortality.MethodsData are from 2816 men in the Osteoporotic Fractures in Men (MrOS) Study (mean age ± SD: 79.1 ± 5.2 years) with free-living activity monitor (SenseWear® Pro3 Armband) data (5.1 ± 0.3 days worn >90%) at the Year 7 visit (2007-2009). Sedentary bout frequency was defined as the number of sedentary bouts per day lasting 5+ min to activity of any intensity. Active bout frequency was defined as the number of active bouts per day lasting 5+ min to sedentary behavior. Sleep time was excluded from the analysis. Deaths were centrally adjudicated using death certificates. Cox proportional hazard models were used to separately examine associations between quartiles of sedentary (Q1 referent, <13.6 bouts/day) or active (Q1 referent, <5 bouts/day) bout frequency with mortality.ResultsAfter 9.3 ± 3.8 years of follow-up, 1487 (52.8%) men died. Men averaged 16.8 ± 5.1 and 8.2 ± 4.2 sedentary and active bouts/day, respectively. After full covariate adjustment, each quartile reflecting more frequent sedentary bouts (Q4 vs. Q1 HR: 0.69, 95%CI: 0.58, 0.81, p-trend <0.001) was associated with lower mortality risk. Likewise, each quartile reflecting more frequent active bouts (Q4 vs. Q1 HR: 0.58, 95%CI: 0.49, 0.70, p-trend <0.001) was associated with lower mortality risk. Results for the sedentary bouts model remained significant after adjusting for total minutes per day in sedentary behavior (Q4 vs. Q1 HR: 0.63, 95%CI: 0.61, 0.86, p-trend = 0.001). The association between active bout frequency with mortality was attenuated after adjusting for total minutes per day active.ConclusionsRegardless of total time spent sedentary, reducing duration of sedentary bouts with more frequent and shorter bouts may be a simple and feasible method to delay mortality risk among community-dwelling older men.

Project description:Exercise has multi-systemic benefits and attenuates the physiological impairments associated with aging. Emerging evidence suggests that circulating exosomes mediate some of the beneficial effects of exercise via the transfer of microRNAs between tissues. However, the impact of regular exercise and acute exercise on circulating exosomal microRNAs (exomiRs) in older populations remains unknown. In the present study, we analyzed circulating exomiR expression in endurance-trained elderly men and age-matched sedentary males at baseline (Pre), immediately after a forty minute bout of aerobic exercise on a cycle ergometer (Post), and three hours after this acute exercise (3hPost). Plasma exosomes were isolated, characterized, and exomiR levels were determined by sequencing. The effect of regular exercise on circulating exomiRs was assessed using paired t-tests of baseline expression levels in the trained and sedentary groups. The effect of acute exercise was determined by comparing baseline and post-training expression levels in each group. Regular exercise resulted in significantly increased baseline expression of three exomiRs (miR-486-5p, miR-215-5p, miR-941) and decreased expression of one exomiR (miR-151b). Acute exercise altered circulating exomiR expression in both groups. However, exomiRs regulated by acute exercise in the trained group (7 miRNAs at Post and 8 at 3hPost) were distinct from those in the sedentary group (9 at Post and 4 at 3hPost). Pathway analysis prediction and reported target validation experiments revealed that the majority of exercise-regulated exomiRs are targeting genes that are related to IGF-1 signaling, a pathway involved in exercise-induced muscle and cardiac hypertrophy. The immediately post-acute exercise exomiR signature in the trained group correlates with activation of IGF-1 signaling, whereas in the sedentary group it is associated with inhibition of IGF-1 signaling. These results suggest that training status may counteract age-related anabolic resistance by modulating circulating exomiR profiles both at baseline and in response to acute exercise.

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Short-Term Adaptations in Skeletal Muscle Mitochondrial Oxidative Capacity and Metabolic pathways to Breaking Up Sedentary Behaviors with Short-Frequent Bouts of Physical Activity Compared to a Matched Daily Single-Continuous Bout in Obese Adults

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