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How to Maximize Weight Loss | Diet vs. Workout Deficit- Thomas DeLauer…
Study – The American Journal of Clinical Nutrition:
The objectives were to examine how the modality of an acute 3-day isocaloric 25% energy depletion by dieting alone or by aerobic exercise alone differently affects appetite and appetite-related hormones, ad libitum feeding, food reward (snack points), and olfaction in 10 male subjects.
2 experimental conditions:
25% daily needs energy deficits induced by diet only (DIET) and by exercise only (EX) and tested before [day 1 of DIET (DIET1) and day 1 of EX (EX1)] and after 3 d [day 4 of DIET (DIET4) and day 4 of EX (EX4)] of the intervention.
DIET represented a greater acute challenge to appetite regulation than EX, as demonstrated by greater appetite and ad libitum EI. Results confirmed that compared with depletions by exercise alone, acute caloric restriction results in rapid changes in appetite that result in compensatory eating. Note that in this study no changes in leptin or ghrelin were seen.
Exercise & Appetite:
Another study looking at the effects of exercise on the brain may explain why a solely exercise-induced deficit may stave off hunger more than diet alone. Body heat goes up during exercise, which has now been found to play a role in signaling to the brain that appetite needs to go down. When we eat foods that contain hot chili peppers, our body temperature seems to go up, and our appetite decreases. That is because chili peppers contain a compound called “capsaicin,” which interacts with sensory receptors (TRPV1 receptors) in the body, bringing about the sensation of being hot and flushed. Capsaicin has been shown to create a decrease in appetite
Study – PLOS:
Researchers focused on a set of neurons that coordinate appetite suppression, called “proopiomelanocortin” (POMC) neurons. These cells are found in a region of the hypothalamus known as the “arcuate nucleus and some are not screened by the brain-blood barrier. This is a membrane that prevents most of the cells in the brain from being exposed to serious fluctuations in blood plasma composition, thus protecting neural function. But, since some POMC brain cells have more direct communication with the rest of the system and interact with hormones released into the blood, it was thought they may also be able to respond to fluctuations in body temperature. In order to test this hypothesis, the researchers first experimented with mouse hypothalamus tissue that contained POMC brain cells. They exposed this tissue first to capsaicin, and then to heat, to see whether these cells would be able to respond to both stimuli. Both the presence of heat and that of the chili pepper compound activated POMC neurons, meaning that they had TRPV1 receptors. Researchers then conducted various tests using mice in order to understand how POMC neurons reduced appetite after their TRPV1 receptors were activated. When they exposed the arcuate nuclei of mice to capsaicin, the animals tended to eat less food over the following 12 hours. The researchers, however, were able to block the loss of appetite associated with capsaicin exposure either by blocking the TRPV1 receptors of POMC neurons before administering the compound, or by turning off the gene that encodes such receptors in mice. They then put some mice on treadmills, leaving them to run for a period for 40 minutes – in this way, they created the conditions that are typical of a regular workout session. As a result of this exercise, the animals’ body temperatures initially shot up, and then they reached a plateau after 20 minutes – body heat remained high for over an hour, and the mice’s appetite visibly decreased. The exercising mice had an approximately 50% lower food intake after the treadmill session than their counterparts that had not taken part in the exercise. Finally, exposure to treadmill exercise had no effect on the appetite of the mice whose TRPV1 receptors had been suppressed. This shows that heightened body heat due to physical activity stimulates relevant receptors in the brain to decrease the desire for food.
(POMC) neurons promote satiety as it’s believed that POMC neurons suppress appetite by releasing a neuropeptide called α-melanocyte stimulating hormone (α-MSH), which is an agonist at the anorectic melanocortin-4 receptors (MC4Rs)
MC4Rs are act on receptors in the hypothalamus in the brain to reduce appetite
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