Prior exercise potentiates the thermic effect of a carbohydrate load

Metabolism ◽  
1986 ◽  
Vol 35 (11) ◽  
pp. 1048-1053 ◽  
Author(s):  
J.C. Young ◽  
J.L. Treadway ◽  
T.W. Balon ◽  
H.P. Gavras ◽  
N.B. Ruderman
1991 ◽  
Vol 70 (4) ◽  
pp. 1463-1468 ◽  
Author(s):  
T. W. Balon ◽  
G. J. Welk

It has been previously observed that the thermic effect of a glucose load is potentiated by prior exercise. To determine whether this phenomenon is observed when different carbohydrates are used and to ascertain the role of insulin, the thermic effects of fructose and glucose were compared during control (rest) and postexercise trials. Six male subjects ingested 100 g fructose or glucose at rest or after recovery from 45 min of treadmill exercise at 70% of maximal O2 consumption. Measurements of O2 consumption, respiratory exchange ratio, and plasma concentrations of glucose, insulin, glycerol, and lactate were measured for 3 h postingestion. Although glucose and fructose increased net energy expenditure by 44 and 51 kcal, respectively, over baseline during control trials, exercise increased the thermic effect of both carbohydrate challenges an additional 20-25 kcal (P less than 0.05). Glucose ingestion was associated with large (P less than 0.05) increases in plasma insulin concentration during control and exercise trials, in contrast to fructose ingestion. Because fructose, which is primarily metabolized by liver, and glucose elicited a similar postexercise potentiation of thermogenesis, the results indicate that the thermogenic phenomenon is not limited to skeletal muscle. These results also demonstrate that carbohydrate-induced postexercise thermogenesis is not related to an incremental increase in plasma insulin concentration.


Author(s):  
Penelope M. Warwick

The purpose of the study was to investigate thermic and glycemic responses to conventional meals with and without prior low-intensity exercise. Fourteen healthy volunteers (7 men, 7 women) undertook 4 treatments, 2 bread and 2 pasta meals, either with (E) or without (NE) prior exercise (a 45-min treadmill walk). Meals provided 58 g carbohydrate and 2360 kJ. Energy expenditure and blood-glucose concentrations were measured before and for 3 h after the meals. The thermic effect of food (TEF) was lower after pasta (121 ± 32 kJ/3 h) than after bread (154 ± 62 kJ/3 h), P = 0.009, but was not affected by exercise. Glycemic responses were lower after E (155 ± 113 mmol·L−1 ·3 h−1) than NE (199 ± 97 mmol·L−1 · 3 h−1) after pasta (P = 0.020) but not after bread. TEF was lower after pasta than bread but was not affected by prior low-intensity exercise. The effects of exercise on glycemic responses to meals were inconsistent.


1989 ◽  
Vol 67 (1) ◽  
pp. 10-16 ◽  
Author(s):  
Eric T. Poehlman ◽  
Pierre LaChance ◽  
Angelo Tremblay ◽  
André Nadeau ◽  
Jean Dussault ◽  
...  

The purposes of this study were to examine (a) the effects of acute exercise on metabolic rate 24 and 48 h postexercise and (b) the interaction of acute exercise and the thermic effect of caffeine on metabolic rate and hormonal changes during the late postexercise recovery period. In six young males, who were regular consumers of caffeine, resting energy expenditure was measured before and after caffeine (5 mg∙kg−1) and placebo ingestion under the following conditions: (i) control (e.g., no prior exercise), (ii) 24 h postexercise, and (iii) 48 h postexercise. Blood samples were drawn for plasma glucose, insulin, glycerol, free fatty acids, catecholamines, and thyroid hormones (triiodothyronine, thyroxine, and free thyroxine). Results showed that acute exercise did not exert a detectable effect on resting metabolic rate in the late postexercise recovery period, that is, resting metabolic rate was similar among the conditions of control (1.17 ± 0.12 kcal∙min−1), 24 h postexercise (1.16 ± 0.12), and 48 h postexercise (1.16 ± 0.11). Caffeine ingestion increased metabolic rate (~7%), but the thermic effect was not different among the experimental conditions. Plasma insulin and norepinephrine were lower after caffeine ingestion, whereas an increase in plasma free fatty acids was noted. Other hormones and substrates did not change significantly in response to caffeine ingestion. Furthermore, the hormonal and substrate milieu was not significantly different 24 and 48 h postexercise when compared with the control condition. Our results support the view that acute exercise does not alter the resting metabolic rate in the late postexercise recovery period. Moreover, acute exercise does not potentiate the thermic effect of caffeine in the late postexercise recovery in caffeine-tolerant males.Key words: caffeine, resting metabolic rate, acute exercise, hormones, substrates.


Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 751-P
Author(s):  
NICHOLE S. TYLER ◽  
RAVI REDDY ◽  
JOSEPH EL YOUSSEF ◽  
JESSICA R. CASTLE ◽  
PETER G. JACOBS

Peptides ◽  
2015 ◽  
Vol 71 ◽  
pp. 94-99 ◽  
Author(s):  
Lauryn M. Nyhoff ◽  
Timothy D. Heden ◽  
Heather J. Leidy ◽  
Nathan C. Winn ◽  
Young-Min Park ◽  
...  
Keyword(s):  

1989 ◽  
Vol 67 (4) ◽  
pp. 394-401 ◽  
Author(s):  
Jean Himms-Hagen

Obligatory thermogenesis is a necessary accompaniment of all metabolic processes involved in maintenance of the body in the living state, and occurs in ail organs. It includes energy expenditure involved in ingesting, digesting, and processing food (thermic effect of food (TEF)). At certain life stages extra energy expenditure for growth, pregnancy, or lactation would also be obligatory. Facultative thermogenesis is superimposed on obligatory thermogenesis and can be rapidly switched on and rapidly suppressed by the nervous system. Facultative thermogenesis is important in both thermal balance, in which control of thermoregulatory thermogenesis (shivering in muscle, nonshivering in brown adipose tissue (BAT)) balances neural control of heat loss mechanisms, and in energy balance, in which control of facultative thermogenesis (exercise-induced in muscle, diet-induced thermogenesis (DIT) in BAT) balances control of energy intake. Thermal balance (i.e., body temperature) is much more stringently controlled than energy balance (i.e., body energy stores). Reduced energy expenditure for thermogenesis is important in two types of obesity in laboratory animals. In the first type, deficient DIT in BAT is a prominent feature of altered energy balance. It may or may not be associated with hyperphagia. In a second type, reduced cold-induced thermogenesis in BAT as well as in other organs is a prominent feature of altered thermal balance. This in turn results in altered energy balance and obesity, exacerbated in some examples by hyperphagia. In some of the hyperphagic obese animals it is likely that the exaggerated obligatory thermic effect of food so alters thermal balance that BAT thermogenesis is suppressed. In all obese animals, deficient hypothalamic control of facultative thermogenesis and (or) food intake is implicated.Key words: thermogenesis, brown adipose tissue, energy balance, obesity, cold, thermoregulation, diet.


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