scholarly journals Acute Effects of Energy Deficit Induced by Moderate-Intensity Exercise or Energy-Intake Restriction on Postprandial Lipemia in Healthy Girls

2015 ◽  
Vol 27 (2) ◽  
pp. 192-202 ◽  
Author(s):  
Alice Emily Thackray ◽  
Laura Ann Barrett ◽  
Keith Tolfrey

Eleven healthy girls (mean ± SD: age 12.1 ± 0.6 years) completed three 2-day conditions in a counterbalanced, crossover design. On day 1, participants either walked at 60 (2)% peak oxygen uptake (energy deficit 1.55[0.20] MJ), restricted food energy intake (energy deficit 1.51[0.25] MJ) or rested. On day 2, capillary blood samples were taken at predetermined intervals throughout the 6.5 hr postprandial period before, and following, the ingestion of standardized breakfast and lunch meals. Fasting plasma triacylglycerol concentrations (TAG) was 29% and 13% lower than rest control in moderate-intensity exercise (effect size [ES] = 1.39, p = .01) and energy-intake restriction (ES = 0.57, p = .02) respectively; moderate-intensity exercise was 19% lower than energy-intake restriction (ES = 0.82, p = .06). The moderate-intensity exercise total area under the TAG versus time curve was 21% and 13% lower than rest control (ES = 0.71, p = .004) and energy-intake restriction (ES = 0.39, p = .06) respectively; energy-intake restriction was marginally lower than rest control (-10%; ES = 0.32, p = .12). An exercise-induced energy deficit elicited a greater reduction in fasting plasma TAG with a trend for a larger attenuation in postprandial plasma TAG than an isoenergetic diet-induced energy deficit in healthy girls.

2019 ◽  
Vol 123 (5) ◽  
pp. 592-600
Author(s):  
D. Thivel ◽  
J. Roche ◽  
M. Miguet ◽  
A. Fillon ◽  
M. Khammassi ◽  
...  

AbstractExercise modifies energy intake (EI) in adolescents with obesity, but whether this is mediated by the exercise-induced energy deficit remains unknown. The present study examined the effect of exercise with and without dietary replacement of the exercise energy expenditure on appetite, EI and food reward in adolescents with obesity. Fourteen 12–15-year-old adolescents with obesity (eight girls; Tanner 3–4; BMI 34·8 (sd 5·7) kg/m2; BMI z score 2·3 (sd 0·4)) randomly completed three experimental conditions: (i) rest control (CON); (ii) 30-min cycling (EX) and (iii) 30-min cycling with dietary energy replacement (EX + R). Ad libitum EI was assessed at lunch and dinner, and food reward (Leeds Food Preference Questionnaire) before and after lunch. Appetite was assessed at regular intervals. Lunch, evening and total EI (excluding the post-exercise snack in EX − R) were similar across conditions. Lunch and total EI including the post-exercise snack in EX + R were higher in EX − R than CON and EX; EX and CON were similar. Total relative EI was lower in EX (6284 (sd 2042) kJ) compared with CON (7167 (sd 2218) kJ; P < 0·05) and higher in EX + R (7736 (sd 2033) kJ) compared with CON (P < 0·001). Appetite and satiety quotients did not differ across conditions (P ≥ 0·10). Pre-meal explicit liking for fat was lower in EX compared with CON and EX + R (P = 0·05). There was time by condition interaction between EX and CON for explicit wanting and liking for fat (P = 0·01). Despite similar appetite and EI, adolescents with obesity do not adapt their post-exercise food intake to account for immediate dietary replacement of the exercise-induced energy deficit, favouring a short-term positive energy balance.


2008 ◽  
Vol 100 (5) ◽  
pp. 1109-1115 ◽  
Author(s):  
Stephen Whybrow ◽  
Darren A. Hughes ◽  
Patrick Ritz ◽  
Alexandra M. Johnstone ◽  
Graham W. Horgan ◽  
...  

The effects of incremental exercise on appetite, energy intake (EI), expenditure (EE) and balance (EB) in lean men and women were examined. Six men (age 29·7 (sd5·9) years, weight 75·2 (sd15·3) kg, height 1·75 (sd0·11) m) and six women (age 24·7 (sd5·9) years, weight 66·7 (sd9·10) kg, height 1·70 (sd0·09) m) were each studied three times during a 16 d protocol, corresponding to no additional exercise (Nex), moderate-intensity exercise (Mex; 1·5–2·0 MJ/d) and high-intensity exercise (Hex; 3·0–4·0 MJ/d) regimens. Subjects were fed to EB during days 1–2, and during days 3–16 they fedad libitumfrom a medium-fat diet of constant composition. Daily EE, assessed using the doubly labelled water method, was 9·2, 11·6 and 13·7 MJ/d (P < 0·001;sed0·45) for the women and 12·2, 14·0 and 16·7 MJ/d (P = 0·007;sed1·11) for the men on the Nex, Mex and Hex treatments, respectively. EI was 8·3, 8·6 and 9·9 MJ/d (P = 0·118;sed0·72) for the women and 10·6, 11·6 and 12·0 MJ/d (P = 0·031;sed0·47) for the men, respectively. On average, subjects compensated for about 30 % of the exercise-induced energy deficit. However, the degree of compensation varied considerably among individuals. The present study captured the initial compensation in EI for exercise-induced energy deficits. Total compensation would take a matter of weeks.


2015 ◽  
Vol 117 (4) ◽  
pp. 602-610 ◽  
Author(s):  
Joanna L. Varley-Campbell ◽  
Melanie S. Moore ◽  
Craig A. Williams

AbstractEnergy intake (EI) and energy expenditure (EE) should not be considered independent entities, but more an inter-connected system. With increased physical activity and reduced snacking initiatives as prevalent Public Health measures, any changes to subsequent EI from these recommendations should be monitored. The aim of this study was to investigate changes in acute EI and appetite over four conditions: (1) a control condition with no snack and no exercise (CON); (2) a snack condition (+1 MJ; SK); (3) a moderate-intensity cycling exercise condition (−1 MJ; EX); and finally (4) both snack and exercise condition (+1 MJ, −1 MJ; EXSK). Acute changes in appetite (visual analogue scale) and lunchtime EI (ad libitum pizza meal) were recorded in twenty boys and eighteen girls (12–13 years). Lunch EI was not significantly different between conditions or sexes (P>0·05). Relative EI was calculated, where the energy manipulation (+1 MJ from the snack or −1 MJ from the exercise) was added to lunchtime EI. Relative EI indicated no significant differences between the sexes (P>0·05); however, in the EX condition, relative EI was significantly lower (P<0·001) compared with all other conditions. Appetite increased significantly over time (P<0·001) and was significantly higher in the CON and EX conditions compared with the SK and EXSK conditions. No significant sex differences were found between conditions. When aiming to evoke an acute energy deficit, increasing EE created a significantly larger relative energy deficit than the removal of the mid-morning snack. Sex was not a confounder to influence EI or appetite between any of the conditions.


2019 ◽  
Vol 126 (2) ◽  
pp. 305-313
Author(s):  
Naoto Fujii ◽  
Miki Kashihara ◽  
Glen P. Kenny ◽  
Yasushi Honda ◽  
Tomomi Fujimoto ◽  
...  

Hyperthermia causes hyperventilation at rest and during exercise. We previously reported that carotid chemoreceptors partly contribute to the hyperthermia-induced hyperventilation at rest. However, given that a hyperthermia-induced hyperventilation markedly differs between rest and exercise, the results obtained at rest may not be representative of the response in exercise. Therefore, we evaluated whether carotid chemoreceptors contribute to hyperthermia-induced hyperventilation in exercising humans. Eleven healthy young men (23 ± 2 yr) cycled in the heat (37°C) at a fixed submaximal workload equal to ~55% of the individual’s predetermined peak oxygen uptake (moderate intensity). To suppress carotid chemoreceptor activity, 30-s hyperoxia breathing (100% O2) was performed at rest (before exercise) and during exercise at increasing levels of hyperthermia as defined by an increase in esophageal temperature of 0.5°C (low), 1.0°C (moderate), 1.5°C (high), and 2.0°C (severe) above resting levels. Ventilation during exercise gradually increased as esophageal temperature increased (all P ≤ 0.05), indicating that hyperthermia-induced hyperventilation occurred. Hyperoxia breathing suppressed ventilation in a greater manner during exercise (−9 to −13 l/min) than at rest (−2 ± 1 l/min); however, the magnitude of reduction during exercise did not differ at low (0.5°C) to severe (2.0°C) increases in esophageal temperature (all P > 0.05). Similarly, hyperoxia-induced changes in ventilation during exercise as assessed by percent change from prehyperoxic levels were not different at all levels of hyperthermia (~15–20%, all P > 0.05). We show that in young men carotid chemoreceptor contribution to hyperthermia-induced hyperventilation is relatively small at low-to-severe increases in body core temperature induced by moderate-intensity exercise in the heat. NEW & NOTEWORTHY Exercise-induced increases in hyperthermia cause a progressive increase in ventilation in humans. However, the mechanisms underpinning this response remain unresolved. We showed that in young men hyperventilation associated with exercise-induced hyperthermia is not predominantly mediated by carotid chemoreceptors. This study provides important new insights into the mechanism(s) underpinning the regulation of hyperthermia-induced hyperventilation in humans and suggests that factor(s) other than carotid chemoreceptors play a more important role in mediating this response.


1994 ◽  
Vol 266 (1) ◽  
pp. E136-E143 ◽  
Author(s):  
L. A. Mendenhall ◽  
S. C. Swanson ◽  
D. L. Habash ◽  
A. R. Coggan

We have previously shown that 12 wk of endurance training reduces the rate of glucose appearance (Ra) during submaximal exercise (Coggan, A. R., W. M. Kohrt, R. J. Spina, D. M. Bier, and J. O. Holloszy. J. Appl. Physiol. 68: 990-996, 1990). The purpose of the present study was to examine the time course of and relationship between training-induced alterations in glucose kinetics and endocrine responses during prolonged exercise. Accordingly, seven men were studied during 2 h of cycle ergometer exercise at approximately 60% of pretraining peak oxygen uptake on three occasions: before, after 10 days, and after 12 wk of endurance training. Ra was determined using a primed, continuous infusion of [6,6-2H]glucose. Ten days of training reduced mean Ra during exercise from 36.9 +/- 3.3 (SE) to 28.5 +/- 3.4 mumol.min-1.kg-1 (P < 0.001). Exercise-induced changes in insulin, C-peptide, glucagon, norepinephrine, and epinephrine were also significantly blunted. After 12 wk of training, Ra during exercise was further reduced to 21.5 +/- 3.1 mumol.min-1.kg-1 (P < 0.001 vs. 10 days), but hormone concentrations were not significantly different from 10-day values. The lower glucose Ra during exercise after short-term (10 days) training is accompanied by, and may be due to, altered plasma concentrations of the major glucoregulatory hormones. However, other adaptations must be responsible for the further reduction in Ra with more prolonged training.


2013 ◽  
Vol 2013 ◽  
pp. 1-6 ◽  
Author(s):  
Emilie Pérusse-Lachance ◽  
Patrice Brassard ◽  
Jean-Philippe Chaput ◽  
Vicky Drapeau ◽  
Normand Teasdale ◽  
...  

The aim of this study was to examine the acute effects of mental work and moderate-intensity physical activity on various components of energy balance in young and healthy adults. With the use of a randomized crossover design, 35 participants aged 24 ± 3 years completed three 45-min conditions, namely, (i) resting in a sitting position (control), (ii) reading and writing (mental work (MW)), and (iii) exercising on a treadmill at 40% of peak oxygen uptake (exercise), followed by an ad libitum lunch. The endpoints were spontaneous energy intake (EI), energy expenditure (EE), appetite sensations, and EI for the remainder of the day. We observed that the energy cost of the control and MW conditions was about the same whereas the exercise condition increased EE to a greater extent in men than women. Exercise induced a decrease in EI relative to EE compared to the control condition that was more pronounced in men than women. However, women tended to increase their energy intake after the MW condition compared to the control one whereas an opposite trend was observed in men. None of the appetite sensation markers differed significantly between both sexes. In conclusion, men and women have specific food intake patterns when submitted to cognitive and physical stimuli.


1999 ◽  
Vol 31 (Supplement) ◽  
pp. S69
Author(s):  
J. J. Ferris ◽  
D. J. Jacobsen ◽  
J. E. Donnelly

2019 ◽  
Vol 30 (2) ◽  
pp. 525-533 ◽  
Author(s):  
J J Steventon ◽  
C Foster ◽  
H Furby ◽  
D Helme ◽  
R G Wise ◽  
...  

Abstract Long-term exercise interventions have been shown to be a potent trigger for both neurogenesis and vascular plasticity. However, little is known about the underlying temporal dynamics and specifically when exercise-induced vascular adaptations first occur, which is vital for therapeutic applications. In this study, we investigated whether a single session of moderate-intensity exercise was sufficient to induce changes in the cerebral vasculature. We employed arterial spin labeling magnetic resonance imaging to measure global and regional cerebral blood flow (CBF) before and after 20 min of cycling. The blood vessels’ ability to dilate, measured by cerebrovascular reactivity (CVR) to CO2 inhalation, was measured at baseline and 25-min postexercise. Our data showed that CBF was selectively increased by 10–12% in the hippocampus 15, 40, and 60 min after exercise cessation, whereas CVR to CO2 was unchanged in all regions. The absence of a corresponding change in hippocampal CVR suggests that the immediate and transient hippocampal adaptations observed after exercise are not driven by a mechanical vascular change and more likely represents an adaptive metabolic change, providing a framework for exploring the therapeutic potential of exercise-induced plasticity (neural, vascular, or both) in clinical and aged populations.


2018 ◽  
Vol 43 (12) ◽  
pp. 1298-1306 ◽  
Author(s):  
Aaron Raman ◽  
Jeremiah J. Peiffer ◽  
Gerard F. Hoyne ◽  
Nathan G. Lawler ◽  
Andrew J. Currie ◽  
...  

This study examined the effect of 2 forms of exercise on glucose tolerance and the concurrent changes in markers associated with the interleukin (IL)-6 pathways. Fifteen sedentary, overweight males (29.0 ± 3.1 kg/m2) completed 2 separate, 3-day trials in randomised and counterbalanced order. An oral glucose tolerance test (OGTT; 75 g) was performed at the same time on each day of the trial. Day 2 of each trial consisted of a single 30-min workload-matched bout of either high-intensity intermittent exercise (HIIE; alternating 100% and 50% of peak oxygen uptake) or continuous moderate-intensity exercise (CME; 60 % of peak oxygen uptake) completed 1 h prior to the OGTT. Venous blood samples were collected before, immediately after, 1 h after, and 25 h after exercise for measurement of insulin, C-peptide, IL-6, and the soluble IL-6 receptors (sIL-6R; soluble glycoprotein 130 (sgp130)). Glucose area under the curve (AUC) was calculated from capillary blood samples collected throughout the OGTT. Exercise resulted in a modest (4.4%; p = 0.003) decrease in the glucose AUC when compared with the pre-exercise AUC; however, no differences were observed between exercise conditions (p = 0.65). IL-6 was elevated immediately after and 1 h after exercise, whilst sgp130 and sIL-6R concentrations were reduced immediately after exercise. In summary, exercise was effective in reducing glucose AUC, which was attributed to improvements that took place between 60 and 120 min into the OGTT, and was in parallel with an increased ratio of IL-6 to sIL-6R, which accords with an increased activation via the “classical” IL-6 signalling pathway. Our findings suggest that acute HIIE did not improve glycaemic response when compared with CME.


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