We read the study by S. Afrasyabi et al. which looked at the effect of high intensity interval training (HIIT) on appetite with great interest. The article specifically measured the levels of ghrelin, PYY and GLP before and after exercise, with the hypothesis that HIIT training would suppress appetite and therefore lead to a decrease in ghrelin and a rise in PYY and GLP [1], suggesting that HIIT could help to treat obesity and controlling blood glucose levels in type 2 diabetic patients. The study concluded that HIIT had significantly decreased energy intake in the training groups compared to the control groups, attributing these findings to training ‘reducing TNF-α, PYY and ghrelin, also enhancing GLP-1 hormones’ [1].
Focusing on the findings of the study, the conclusion that a decrease in PYY levels contributed to a lower energy intake proves to be contradictory to current literature and is contrary to the results of the study. The results of the study show an increase in PYY levels in all training groups, with the highest increase in PYY levels shown in obese-diabetic-training groups (170 pg.ml- 210 pg.ml). Peptide YY is an anorexigenic peptide that is synthesised in the L-cells in the gut and is released in response to food entering the gastrointestinal tract. A study conducted C.W. le Roux et al. identified the importance of PYY on satiety, indicating that participants with an attenuated PYY response required a greater caloric intake to reach the same fullness as those with regular response to PYY [2]. Furthermore, the study also observed that administering exogenous PYY decreased food intake, a finding corroborated in the study by N.M. Neary, which showed a statistically significant 15% decrease of energy intake with subjects infused with PYY compared to the control group [3]. Looking at the current literature, and the results of the study itself, we must question the conclusion that the decrease in PYY contributed to the reduced appetite and offer an alternative conclusion that would suggest that a rise in PYY would lead to decreased food intake.
Another finding that needs to be explored further is the role of GLP on hunger and satiety. The study suggests that a rise in GLP was a factor involved in reduced food intake, with each of the training groups having a higher level of GLP in the blood 12 weeks after starting HIIT. The study by N.M Neary suggests that at lower concentrations of exogenous infusion in rats and humans, GLP does not significantly decrease food intake, however when co-administered with PYY, there is a 27% reduction of food intake in humans [3]. In contrast to this, the study by M. Shah states that GLP agonist enhances satiation and promotes weight loss [4], which is further supported by a meta-analysis conducted by V. Tisboll et al. that concluded that GLP agonist groups lost 2.9 kg more weight compared to control groups [5]. As a result, we can accept the conclusion that a rise from the study that a rise in GLP can be a cause of the reduced energy intake. Furthermore, the combination of a rise of PYY and GLP in obese diabetic training groups, alongside the data observed in the N.M Neary study strengthens the conclusions drawn by the author.
A limitation of the study was its short time span. The study by V. Ionut et al. reviewed the long-term impact of bariatric surgery on PYY and GLP levels. The review reported data from a range of studies which concluded that the levels of GLP and PYY were progressively increasing 2 years after surgery and were positively correlated to ‘reduction of hunger and increases in satiety, but no aversion to food’ [6]. Furthermore, the study by F. L Greenway observed significant decreases in PYY and GLP 1 year after lifestyle induced weight loss as opposed to progressively raised levels of PYY and GLP following a gastric bypass [7]. These compensatory physiological adaptations following lifestyle-induced weight loss leads to an increase in appetite, cravings and ultimately, weight regain. Therefore, we must question the efficacy of HIIT on long-term reduction of appetite and increased satiety and suggest that bariatric surgery may be the best method of treating these patients.
Declarations
Conflicts of interest
The author declared that they have no conflicts of interest.
Footnotes
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References
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