Abstract
BackgroundThe inverse relationship between exercise capacity and its variation over time and both cardiovascular and all-cause mortality suggests the existence of an etiological nexus between cardiometabolic diseases and the molecular regulators of exercise capacity. Coordinated adaptive responses elicited by physical training enhance exercise performance and metabolic efficiency and possibly mediate the health benefits of physical exercise. In contrast, impaired expression of genes involved in mitochondrial biogenesis or protein turnover in skeletal muscle—key biological processes involved in adaptation to physical training—leads to insulin resistance and obesity. Ingestion of fructose has been shown to suppress the exercise-induced GLUT4 response in rat skeletal muscle. To evaluate in greater detail how fructose ingestion might blunt the benefits of physical training, we investigated the effects of fructose ingestion on exercise induction of genes that participate in regulation of mitochondrial biogenesis and protein turnover in rat’s skeletal muscle.MethodsEight-week-old Wistar rats were randomly assigned to sedentary (C), exercise (treadmill running)-only (E), fructose-only (F), and fructose + exercise (FE) groups and treated accordingly for 8 weeks. Blood and quadriceps femoris were collected for biochemistry, serum insulin, and gene expression analysis. Expression of genes involved in regulation of mitochondrial biogenesis and autophagy, GLUT4, and ubiquitin E3 ligases MuRF-1, and MAFbx/Atrogin-1 were assayed with quantitative real-time polymerase chain reaction.ResultsAerobic training improved exercise capacity in both E and FE groups. A main effect of fructose ingestion on body weight and fasting serum triglyceride concentration was detected. Fructose ingestion impaired the expression of PGC-1α, FNDC5, NR4A3, GLUT4, Atg9, Lamp2, Ctsl, Murf-1, and MAFBx/Atrogin-1 in skeletal muscle of both sedentary and exercised animals while expression of Errα and Pparδ was impaired only in exercised rats.ConclusionsOur results show that fructose ingestion impairs the expression of genes involved in biological processes relevant to exercise-induced remodeling of skeletal muscle. This might provide novel insight on how a dietary factor contributes to the genesis of disorders of glucose metabolism.
Highlights
The inverse relationship between exercise capacity and its variation over time and both cardiovascular and all-cause mortality suggests the existence of an etiological nexus between cardiometabolic diseases and the molecular regulators of exercise capacity
Skeletal muscle myotubes from severely obese individuals are shown to have altered proteasome and autophagic proteolytic flux [21]. These findings suggest that Metabolic syndrome (MetS) is associated with morphological and functional abnormalities of skeletal muscle which might be a consequence of MetS per se or caused, at least in part, by altered proteolytic pathways or other cellular processes due to dietary habits or physical inactivity
The secondary aim of this study is to assess the effects of fructose ingestion and physical training on expression of selected genes involved in protein degradation in skeletal muscle
Summary
The inverse relationship between exercise capacity and its variation over time and both cardiovascular and all-cause mortality suggests the existence of an etiological nexus between cardiometabolic diseases and the molecular regulators of exercise capacity. Rats selectively bred for low exercise capacity exhibited defects characteristic of metabolic syndrome such as elevated blood pressure, impaired glucose tolerance, visceral adiposity, and elevated circulating levels of triglycerides [5]. These observations suggest that cardiometabolic diseases and the molecular determinants of exercise capacity are etiologically connected. Metabolic, nutritional, and oxidative stresses in engaged skeletal muscles These stimuli trigger a set of coordinated adaptive responses which result in modification of volume, protein content, mechanical properties, and metabolic capacities [6]. Mitochondrial biogenesis is a complex process that requires co-expression of genes from two distinct genomes (nuclear and mitochondrial) and is regulated by transcription factors and transcription co-activators [8]
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