Exercise or food restriction: effect on adipose tissue cellularity

Lb, Oscai; Babirak, SP; Dubach, FB; McGarr, JA; Spirakis, CN

doi:10.1152/ajplegacy.1974.227.4.901

Cited by 45 publications

(41 citation statements)

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“…Sedentary rats, either pair weighted to the exercising group or ad libitum fed, had 28 or 54%, respectively, more adipocytes per epididymal fat pad than a group of rats participating in a 14-to 16-wk swim training program (22). Craig et al (7) showed that sedentary rats had 108% more epididymal adipocytes than rats that had voluntarily ran in wheel from 6 to 12 mo of age (and subjected to an ϳ8% food restriction for approximately the last 2 mo).…”

Section: Discussionmentioning

confidence: 97%

Inactivity induces increases in abdominal fat

Laye¹,

Thyfault²,

Stump³

et al. 2007

Journal of Applied Physiology

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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 ...

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Section: Discussionmentioning

confidence: 97%

Inactivity induces increases in abdominal fat

Laye¹,

Thyfault²,

Stump³

et al. 2007

Journal of Applied Physiology

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“…As a consequence, male rats that exercise regularly are similar to foodrestricted rats in that they show growth retardation and have a decreased body fat content and reduced availability of calories for cellular proliferation (4,6,8,9,12). It has been variously hypothesized that the life-prolonging effect of food restriction is due to growth retardation with maintenance of growth potential (11), prevention of excess body fat accumulation (2), and/or a shift in biological state from cell proliferation and reproduction to maintenance/repair pathways (14,15).…”

Section: Discussionmentioning

confidence: 99%

Mortality rate and longevity of food-restricted exercising male rats: a reevaluation

Holloszy

1997

Journal of Applied Physiology

135

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Holloszy, John O. Mortality rate and longevity of foodrestricted exercising male rats: a reevaluation. J. Appl. Physiol. 82(2): 399-403, 1997.-Food restriction increases the maximal longevity of rats. Male rats do not increase their food intake to compensate for the increase in energy expenditure in response to exercise. However, a decrease in the availability of energy for growth and cell proliferation that induces an increase in maximal longevity in sedentary rats only results in an improvement in average survival, with no extension of maximal life span, when caused by exercise. In a previous study (J. O. Holloszy and K. B. Schechtman. J. Appl. Physiol. 70: 1529-1535, 1991, to test the possibility that exercise prevents the extension of life span by food restriction, wheel running and food restriction were combined. The food-restricted runners showed the same increase in maximal life span as food-restricted sedentary rats but had an increased mortality rate during the first one-half of their mortality curve. The purpose of the present study was to determine the pathological cause of this increased early mortality. However, in contrast to our previous results, the food-restricted wheel-running rats in this study showed no increase in early mortality, and their survival curves were virtually identical to those of sedentary animals that were food restricted so as to keep their body weights the same as those of the runners. Thus it is possible that the rats in the previous study had a health problem that had no effect on longevity except when both food restriction and exercise were superimposed on it. Possibly of interest in this regard, the rats in this study did considerably more voluntary running than those in the previous study. It is concluded that 1) moderate caloric restriction combined with exercise does not normally increase the early mortality rate in male rats, 2) exercise does not interfere with the extension of maximal life span by food restriction, and 3) the beneficial effects of food restriction and exercise on survival are not additive or synergistic.aging; caloric intake; life extension; survival curves; voluntary wheel running FOOD RESTRICTION has been shown to increase maximal longevity in a number of species, including rats (see Ref. 15 for review). It has been hypothesized that the life-prolonging effect of food restriction is mediated by a shift in biological state from cellular proliferation and reproduction to one in which cellular maintenance and repair mechanisms are maximized (14,15). In contrast to food restriction, exercise appears to improve average survival time in rats without increasing their maximal longevity (7-9). Male rats are unusual in their response to exercise in that they do not increase their food intake to compensate for the increase in energy expenditure (8, 9). As a consequence, like food restriction, exercise results in a reduced availability of energy for cell proliferation and growth in male rats; it does not, however, increase their maximal life span (7, 9). It ...

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“…It has been found that the number of adipocytes produced in young rats depends on diet and exercise regime and that, in adult humans, increased cell number plays a more important role in the development of the grossly overweight condition than does cell size [11] . One can therefore see how a family environmental effect of diet at an early age could continue to manifest itself as an E2 effect in adult life when twins are no longer living together.…”

Section: Discussionmentioning

confidence: 99%

Sex Differences in the Inheritance of Some Anthropometric Characters in Twins

Clarke

Jardine

Martin

et al. 1980

Acta genet. med. gemellol.: twin res.

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Biometrical genetical techniques have been applied to the analysis of certain anthropometric characters measured in 134 pairs of adult twins. After allowing for assortative mating it appears that there is a family environment (E2 ) component for variation in height larger than previously reported. "Fatness" traits -weight, ponderal index, and skinfold thickness -all show higher heritabilities in males and substantial Ez components in females, and reasons for this are discussed. The same is true for cephalic index and forearm length but the reason for these differences is not so obvious. Head length shows a much higher heritability than head breadth. A larger sample of DZ opposite-sex pairs would allow more powerful discrimination, but the variety of patterns of variation revealed by the modelfitting approach used here justify its use over more traditional techniques.

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Exercise or food restriction: effect on adipose tissue cellularity

Cited by 45 publications

References 0 publications

Inactivity induces increases in abdominal fat

Inactivity induces increases in abdominal fat

Mortality rate and longevity of food-restricted exercising male rats: a reevaluation

Sex Differences in the Inheritance of Some Anthropometric Characters in Twins

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