Effects of acute exercise on food intake and plasma free fatty acid levels

Phystology& Behavtor, Vol 39, pp 413--415.Copyright©PergamonJournals Ltd, 1987 Pnntedm the U.S A.

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Effects of Acute Exercise on Food Intake and Plasma Free Fatty Acid Levels CHRISTIANE LARUE-ACHAGIOTIS

AND JEANINE LOUIS-SYLVESTRE

Laboratoire de Neurobiologie de la Nutrition ( C . N . R . S , E.P.H.E), CollOge de France 11 place Marcelin Berthelot, 75231 Parts Cedex 05 R e c e i v e d 7 July 1986 LARUE-ACHAGIOTIS, C. AND J. LOUIS-SYLVESTRE. Effects oJ acute exerctse on food retake and plasma free fatty actd levels. PHYSIOL BEHAV 39(3) 413-415, 1987.--The effects of acute exercise (swimming) on food intake (FI) and plasma free fatty acids (PFFA) were examined m male adult rats. FI decreased dunng the first hour after swimming; it was unchanged during the second hour; it decreased again during the third hour. Body weight decreased over the 24 hours following exercise (-1.7--_ I g) while the animals gamed weight during no exerctse periods (+3.2-+ I g). At the end of exercise, plasma glucose augmented as well as PFFA levels. An increase m sympathoadrenal actlvlty per se and its inhibitory effect on msuhn release can both be responsible for fatty acid moblhzat~on from adipose t~ssue. Llpolysls could be a cause of hypophagm. Food retake

PFFA

Glucose level

Exerose

Swimming

EXERCISE has been reported to increase, decrease or have no effect on food intake (FI). These discrepancies may reflect differences in exercise type: treadmill versus swimming [24], as well as basic biological characteristics: sex [2-17], age [1] and species. It is also necessary to make a distinction between acute exercise and training for several weeks or months [3]. It was shown in 1957 by Mayer et al. [16] that when adult female rats, accustomed to a sedentary life, were exercised on a treadmill for daily periods of increasing duration (20 min to 1 hr), there was no corresponding increase m FI. On the contrary FI decreased slightly but significantly. The same finding was reported by Stevenson et al. [24] who showed a depression of FI for up to 18 hours following isolated bouts of exercise. The physiological mechanisms responsible for exercise induced hypophagia have not been elucidated. It has been suggested that suppression of feeding is caused by elevated blood levels of lactic acid [3] and/or catecholamines associated with the metabolic emotional stress of forced exercise [6,9]. But Chin et al. [5] however, measuring catecholamine and corticosteroid levels immediately after exercise, failed to show any significant change. Both acute and chronic exercise induces lipolysis, and therefore weight loss and depletion of fat stores. In the present study we examined the effects of acute exercise on FI and on the variations of plasma free fatty acid

(PFFA). The type of exerose was forced swimming, which was chosen because it constitutes a low level of physiological stress smce the heat produced during exercise is more readily dissipated in water than in air [23].

METHOD Male adult Wistar rats (300 g on the average) were used. Individually housed in Plexiglas cages, they ~vere placed in a quiet room in which a 12 hour hght-dark cycle was maintained (6 a.m.-6 p.m. light). Food (stock powdered diet) and water were presented ad lib unless when otherwise indicated. Feeding patterns were continuously recorded by means of a strain-gauge electric microbalance. The exercise program consisted of forced swimming in water mamtained at 36°C. There were four 15 min swimming bouts in a training session, with a 5 min pause between bouts. During the last 3 bouts, rats were loaded with a l0 g weight. This load was secured around the thoracic cage. The swimming "pools" consisted of round plastic dustbins, 48 cm height, 50 cm diameter (2 rats in each).

Experiment 1 In a first step, 15 rats (307.8_+5.8 g) were trained for 10 rain on 2 consecutive days in the early afternoon in order to

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LARUE-ACHAGIOTIS AND LOUIS-SYLVESTRE

familiarize them with the swimming procedure. Three to 5 days later, rats were randomly ascribed to 2 groups. One group was submitted to the previously described swimming schedule at about 4 30 p.m. The rats of the other group were put in a waiting cage near the swimming pools. They swam for 5 mm during the last pause of the swimming group. Three to 4 days later, the exercise conditions were reversed. For both groups food was removed during the exercise period. After swimming rats were dried with paper towels before they were returned to their lndwldual cage where food was available (at the beginning of the nocturnal phase).

FOOD

[~]

Another group of 7 rats (302.8_+4 g) were used. Rats were Implanted with a chronic cardiac catheter through the jugular vein under pentobarbital anesthesm. One week later, after rats had recovered from surgical trauma, they were submitted to the experimental schedule previously described: familiarization, no exercise control test, forced swimming test. Blood Samphng

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1

1

2

2

3

3

6

6

9

9

12

12

24

b

FIG 1 Cumulatwe food retake followmg swlmmmg or control tests Data are means_+SE, *p<0.05

PLASMA rn

Blood samples were drawn into heparmized syringes from the cardiac catheter, 5 rain before, a few mm after, and 1,2, 3, and 6 hours after swimming or control tests. Sample size was 0.2 e l . Samples were centrifuged immediately and the plasma obtained was stored at -20°C for PFFA and glucose assays. PFFA levels were determined in duplicate from 25/zl plasma samples with a colonmetric test (NEFA C. test WAKO-Blolyn). Plasma glucose was determined with a Glucose Analyzer (YSI Model 23 A), using an oxidase enzyme hydrogen peroxide sensor which is highly spemfic for glucose

f ontrol exercise

0

Expermtent 2

INTAKE

GLUCOSE

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FIG 2 Plasma glucose values before and after swlmmmg or control tests Data are means_+SE, ~rp<0.05

Statt,~tt~ al Method Student's paired titest was used. RESULTS FI and b wt. Ad lib intake after control or exercise tests was analyzed in terms of cumulaUve 12 hr intake during the dark and the light periods (Fig. 1). At night, intake decreased significantly on the first hour after exercise (1.6_+0.2 vs. 3_+0.4 g). The second hour was unchanged; during the 3rd hour intake significantly decreased (1 9+0.3 vs 3.1_+0.4 g). Later on FI was not significantly affected. However the 12 hour night intake was significantly diminished (17,6_+0.5 vs. 21_+0.7 g). Diurnal intake was not modified. A compensatory increase in FI was observed for 1 or 2 days after exercise. Body weight decreased durmg the 24 hours following exercise ( - 1.7_+ 1 g) while non exercised rats gained weight (+3.2_+ 1 g). Pla,~ma Glucose Levels (Ftg 2) At the end of exercise, PG augmented significantly as compared to plasma glucose of control period (155.7_+7 vs. 131.4_+ 3.4 mg/dl) This difference disappeared progressively over time. PFFA (Ftg. 3) After exercise, the mcrease in PFFA level was significantly higher than that observed m control rats (685.6_+87 vs.

PLASMA }JEq 7 0 0 _-

FREE

FATTY

ACIDS

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FIG 3 Plasma flee fatty acids levels after swtmmlng or control tests Data are means_+SE, ¢tp<0.05 401.2_+83/xEq/I). One hour later, a small but not significant difference was still present. Two hours later, PFFA level was identical in exercise and control ammals. DISCUSSION The present study confirms that acute exercise can depress FI and b.wt. gam in male rats on the day of exercise [17,25]. However as observed previously with treadmill exercise, this reduction only affects intake during the first hours after exercise [12]. Davis et al. [7] reported that FI

EXERCISE AND FOOD INTAKE

415

i n c r e a s e d d u r i n g t h e first 2 h o u r s a f t e r s w i m m i n g . T h i s disc r e p a n c y c o u l d p e r h a p s b e d u e to t h e t i m e o f e x e r c i s e : in b o t h e x p e r i m e n t s e x e r c i s e o c c u r r e d b y t h e e n d o f the d i u r n a l p h a s e , b u t in the D a v i s et al. e x p e r i m e n t , it s t a r t e d 3 h r b e f o r e t h e e n d o f t h e d a y , a n d 11/2 in t h e p r e s e n t study. D a v i s et al. o b s e r v e d significant h y p o p h a g i a for t h e first 3 h o u r s o f the d a r k p e r i o d o n l y ; m o r e o v e r , while t h e i r rats c o m p e n s a t e d for this r e d u c t m n o n t h e s a m e d a y , c o m p e n s a t i o n in o u r rats w a s d e l a y e d for 24 hr. T h e slight fall in P G o b s e r v e d m n o n - e x e r c i s e d rats w a s d u e to the s h o r t f o o d d e p r i v a t i o n w h i c h is k n o w n to affect P G at t h e e n d o f t h e diurnal p e r i o d [14]. T h e i n c r e a s e in P G a f t e r e x e r c i s e c o u l d b e due to a s t r e s s i n d u c e d h y p e r glycemm. T h e i n c r e a s e in P F F A a f t e r e x e r c i s e is c o n s i s t e n t with o t h e r r e p o r t s [11, 13, 19]. W h e n u n t r a i n e d rats w e r e exercised, P F F A levels w e r e e l e v a t e d . F F A are the m a j o r s o u r c e o f fuel d e l i v e r e d to w o r k i n g m u s c l e f r o m the blood. In rats, it h a s b e e n s h o w n t h a t noct u r n a l h p o g e n e s i s a n d d a y t i m e lipolysts e x e r t a p r i m a r y effect o n t h e c o n c o m i t a n t F I [15]. T h e effect o f hpid i n f u s m n s is n o t e a s y to d e m o n s t r a t e . In o n e s t u d y [18] i n t r a v e n o u s infusion of 50-100 k c a l / d a y m a d e m o s t o f the rats sick ~mm e d m t e l y ; n o effect o f t h e i n f u s m n s w a s n o t e d m the o t h e r a n i m a l s . In a n o t h e r s t u d y [4] i n f u s m n s o f a palmitlc acid/alb u m i n c o m p l e x p r o d u c e d a small d e c r e a s e m oral F I at n o n toxic d o s e s .

O n t h e o t h e r h a n d , in e x e r c i s i n g s u b j e c t s , a c t i v a t i o n mc r e a s e d in t h e s y m p a t h o a d r e n a l s y s t e m a n d t h e m o s t import a n t h o r m o n a l effect o f this a c t i v a t i o n is inhibition o f insulin release [9,22]. B o t h t h e i n c r e a s e in s y m p a t h o a d r e n a l activity a n d t h e e n s u i n g d e p r e s s i o n in insulin level e n h a n c e h e p a t i c glucose p r o d u c t i o n a n d fatty acids m o b i l i z a t i o n f r o m a d i p o s e tissue. T h e idea t h a t t h e s u p p l y o f utilizable m e t a b o l i c fuels is a c n t l c a l f a c t o r m t h e c o n t r o l o f F I is a t t r a c t i v e a n d the t w o major metabolic consequences of exercise can be proposed as p o s s i b l e h y p o p h a g l c factors. In fact, it is well k n o w n t h a t h e p a t i c p o r t a l i n f u s i o n s o f g l u c o s e s u p p r e s s feeding [21] a n d t h e g l u c a g o n - i n d u c e d i n h i b i t i o n o f feeding is e x p l a i n e d b y its effects o n h e p a t i c g l u c o s e p r o d u c t i o n . L l p o l y s i s also c o u l d b e a c a u s e o f h y p o p h a g i a ; this is s u p p o r t e d b y t h e o b s e r v a t i o n t h a t at t h e t e r m i n a t i o n o f a n insulin t r e a t m e n t , a t r a n s i e n t i n c r e a s e m fat m o b i l i z a t i o n appears t o g e t h e r w i t h a t r a n s i e n t h y p o p h a g i a [10,20]. H o w e v e r , a r e c e n t s t u d y [8] suggests t h a t i n c r e a s e d availability o f lipid s u b s t r a t e s is less i m p o r t a n t for h y p o p h a g i a t h a n h o w t h e s e s u b s t r a t e s are utilized. In this regard, t h e k e t o g e n l c pathway seems important. ACKNOWLEDGEMENT J Le Magnen is thanked for his helpful comments during the progression of this work.

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