Inactivity induces increases in abdominal fat

Abstract

Previously, inducing inactivity for 53 h after 21 days of voluntary running resulted in a 25 and 48% increase in epididymal and omental fat pad weights, respectively, while rats continued to eat more than a group that never had access to a running wheel (J Physiol 565: 911-925, 2005). We wanted to test the hypothesis that inactivity, independent of excessive caloric intake, could induce an increase in fat pad mass. Twenty-one-day-old rats were given access to voluntary running wheels for 42-43 days so that they were running ϳ9 km/day in the last week of running, after which wheels were locked for 5, 53, or 173 h (WL5, WL53, WL173) before the rats were killed. During the 53 and 173 h of inactivity, one group of animals was pair fed (PF) to match sedentary controls, whereas the other continued to eat ad libitum (AL). Epididymal and retroperitoneal fat masses were significantly increased in the WL173-PF vs. the WL5 group, whereas epididymal, perirenal, and retroperitoneal fat masses were all significantly increased in the WL173-AL group compared with the WL5 group. Additionally, hyperplasia, and not hypertrophy, of the epididymal fat mass was responsible for the increase at WL173-AL as demonstrated by a significant increase in cell number vs. WL5, with no change in cell diameter or volume. Thus two important findings have been elucidated: 1) increases in measured abdominal fat masses occur in both AL and PF groups at WL173, and 2) adipocyte expansion via hyperplasia occurred with an ad libitum diet following cessation of voluntary running. exercise; obesity; food; hyperplasia THE CENTERS FOR DISEASE CONTROL (CDC) has classified tobacco, poor diet, and physical inactivity as "actual causes" of premature death, distinguishing them from heart disease and malignant neoplasm as "leading causes" of death (20). The CDC defines physical inactivity as, "not engaging in any regular pattern of physical activity beyond daily functioning" (6); the model of inactivity employed here ceases voluntary running of rats with only regular cage activity remaining. Of the three major actual causes of death, physical inactivity has received the least attention. Having previously studied physical inactivity in rodents as a further reduction in activity from sedentary or caged conditions by physical restraint (4, 26), we have altered our approach by developing a model that would more closely approximate comparison between innate and voluntary physical activity with more sedentary but ambulatory conditions. It is known that the provision of running wheels to "caged" rats and mice results in their running 2-15 km per night, depending on the strain (9, 25); thus animals provided access to running wheels are naturally more physically active than caged animals. In conjunction with the CDC classification of physical inactivity as an actual cause of premature death, we speculated that allowing rats to have access to running wheels and then systematically locking the wheels would provide insight into processes important during the transition from ...

Voluntary wheel running initially increases adrenal sensitivity to adrenocorticotrophic hormone, which is attenuated with long-term training

“…It may be that rats of this age have a reduction in basal GC levels as a result of sexual maturation, as has been reported previously (31). It is also important to note that, as an alternative, S rats could have been exposed to the identical cage condition as the exercising rats but with the addition of a locked wheel, as has recently been used to study the metabolic effects of exercise cessation in rodents (20). Finally, it is important to note that the "short-term" training measurements, which included diurnal GC profiling, restraint stress, and ACTH challenge, were made over a span of 6 days to allow for a recovery from the restraint (see Fig.…”

Exercise-induced attenuation of obesity, hyperinsulinemia, and skeletal muscle lipid peroxidation in the OLETF rat

“…Possible explanations for the differences between the present findings and our previous report are differences in rat strain and voluntary running durations. In Fischer 344 ϫ Brown Norway rats, epididymal fat increased 1 wk after cessation of 3 or 6 wk of voluntary running (32,34); in OLETF rats, however, there was no change in epididymal fat 1 wk after cessation of 16 wk of voluntary running. Furthermore, 4-HNE in the epitrochlearis muscle was unchanged for the first 173 h after cessation of running.…”

“…The rationale for determining GST␣-4 mRNA is that it would be a marker for an enzyme that reduces electrophilic compounds, such as 4-HNE. Furthermore, our recent observations would suggest that these parameters would begin to return to preactivity levels upon a 7-day cessation of physical activity (31,32,34).…”

“…The literature suggests that increased physical activity in normal, healthy rats would facilitate the following adaptations: 1) lower levels of intra-abdominal fat (34) and of skeletal muscle lipid peroxidation via increases in SOD-1 (Cu/Zn SOD), SOD-2 (Mn SOD), and glutathione S-transferase (GST␣-4) (46,48), inasmuch as a sedentary lifestyle in mice has been associated with enhanced vascular oxidative stress, which in turn was shown to be associated with vascular dysfunction (33), and 2) higher values for skeletal muscle lipid oxidative capacity (24) and skeletal muscle mitochondrial markers [citrate synthase activity (24) and mRNAs for peroxisome proliferator-activated receptor (PPAR)-␦ and PPAR-␥ coactivator (PGC)-1␣ (5,38)]. Since several studies suggest a link between lipotoxicity, oxidative stress, and insulin resistance (15,25), lipid peroxidation was determined as an index of oxidative stress.…”

Efecto de la administración subcrónica de glucosamina oral en la regulación del peso corporal, glucemia y dislipidemias provocada por una dieta hipercalórica en rata Wistar

“…En este estudio, se ha descrito que, cuando el porcentaje de grasa en la dieta es elevado, se produce un desequilibrio entre la ingesta y la oxidación de la grasa que conduce a un aumento en el tamaño del tejido adiposo, hasta que los adipocitos se vuelven hipertróficos e hiperplásicos. Esto hace que la lipólisis en el tejido adiposo aumente y se liberen ácidos grasos libres 27,28 , con niveles de AGL también altos en este estudio (Figura 2B) y una correlación positiva de este aumento en los niveles de AGL y grasa Tabla 2. Correlaciones entre el contenido de grasa abdominal y las variables de perfil lipídico: c-HDL, ColT, AGL y TG y glucemia de ratas machos sometidas a una dieta comercial (GC) e hipercalórica (GH); con administración de 500 mg/kg de glucosamina respectivamente (GGlcN y GH+GlcN) en el agua de beber, al final del tratamiento de 20 semanas.…”