Discussion
The present study reveals that total physical activity energy expenditure is not detectably altered by either restricting free sugars to less than 5% of energy intake or restricting overall carbohydrate intake to less than 8% of energy intake in the initial 24 h (~ 19 h free-living), despite distinct physiological responses with ketogenic carbohydrate restriction. Manipulating the type and/or amount of dietary carbohydrate also did not alter energy intake across 24 h. Twenty-four hours of a low-carbohydrate ketogenic diet did, however, reduce serum glucose, insulin, triglyceride, leptin, and FGF21 concentrations, and increased βOHB, NEFA, and LDL-cholesterol concentrations.In the present study, no detectable effect of carbohydrate or sugar restriction on directly measured physical activity energy expenditure was observed in the initial 24-h of commencing the diets (of which ~ 19 h were free-living). Prior work has indicated that carbohydrate availability may alter physical activity as demonstrated by energy expenditure in response to genetically increased hepatic glycogen stores in mice [The absence of any meaningful differences in physical activity energy expenditure was observed in the presence of similar 24-h energy intake between conditions. In a manner designed to enhance external validity, ad libitum intake of lunch and dinner was permitted and, despite differences in nutrient composition and palatability, 24-h energy intake did not differ between conditions. Energy density was relatively closely matched between conditions. Room calorimetry studies have shown that large differences in energy density (from 1.15 to 1.68 kcal gThe similar energy intake and physical activity between conditions in the present study were observed in the presence of substantial changes in substrate metabolism and hormone availability linked to energy balance behaviours. Considerable decreases in FGF21 (85 pg mLIn the present study, carbohydrate (but not sugar) restriction lowered postprandial glucose and insulin concentrations alongside carbohydrate oxidation rates, whilst raising postprandial TAG, NEFA and glycerol concentrations alongside greater fat oxidation rates. The following morning, fasting serum TAG concentrations were markedly reduced with carbohydrate restriction. The higher immediate postprandial TAG concentrations and the lower fasting TAG concentrations the following morning are likely explained by the increased fat intake (thus greater chylomicron appearance), as well as less suppression of VLDL-TAG due to lower insulinaemia, as insulin suppresses VLDL secretion directly and indirectly [Serum lactate was the only metabolic effect measured, which responded specifically to sugar restriction, whereby postprandial lactate concentrations were lowered by sugar restriction, and lowered further still by total carbohydrate restriction. Whereas ingestion of any carbohydrates in sufficient amounts will stimulate carbohydrate utilization and thus can increase lactate concentrations, the higher lactate concentrations with sugar ingestion are likely to reflect hepatic fructose metabolism [To the best of the authors knowledge, this is the first evidence that a low-carbohydrate ketogenic diet can raise LDL-cholesterol concentrations over such a short timeframe (24 h), despite similar total energy intake between conditions. The reduced insulin concentrations and increased NEFA concentrations observed in the present study are likely to have increased VLDL production [In addition to sex-specific responses with LDL cholesterol, our data demonstrate that carbohydrate restriction causes a reduction in leptin concentrations in females but not in males. Leptin concentrations were considerably lower in male participants than females in the present study, which is consistent with previous literature and appears to be only partly explained by body fat mass [Whilst a strength of the study is providing real foods in their natural matrix, rather than meal replacements or supplements, it should be noted that the results presented are specific to the context of the foods provided, and not necessarily representative of different foods which fit the same macronutrient profile. This highlights the requirement for multiple studies to validate findings when investigating the effects of macronutrient manipulation per se. Furthermore, the laboratory confinement following the breakfast meal may have impacted the interpretation of 24-h physical activity energy expenditure by influencing a period where physical activity could have varied. Whilst this was deemed necessary for the present study, to provide context about the physiological stimuli of each diet, future studies should include measurement of physical activity in the immediate postprandial period following breakfast.In summary, these data demonstrate that, when energy density is controlled for, the amount of dietary carbohydrate has little impact on physical activity and energy intake in the initial 24 h (~ 19 h free-living). This is despite rapid, profound changes in circulating metabolites and appetite hormones with total carbohydrate restriction. These data also demonstrate that restricting sugar intake from 20 to 5% of energy intake does not acutely alter postprandial triglyceride or LDL-cholesterol concentrations nor fasting triglyceride or LDL-cholesterol concentrations the following morning. Conversely, carbohydrate restriction lowered triglyceride concentrations after 24 h but markedly increased LDL-cholesterol concentrations. Interestingly, the largest changes in leptin and LDL-cholesterol concentrations occurred in female participants. Together, these data suggest that specifically reducing dietary sugar intake does not acutely alter energy intake or metabolic health markers, at least within the context of a healthy body mass. Since many of the hormonal responses were more clearly observed after 24 h of dietary manipulation, the longer-term effects of these diets require further examination.