High-intensity interval exercise in the cold regulates acute and postprandial metabolism.

High-intensity interval exercise (HIIE) has been shown to be more effective than moderate-intensity exercise for increasing acute lipid oxidation and lowering blood lipids during exercise and postprandially. Exercise in cold environments is also known to enhance lipid oxidation; however, the immediate and long-term effects of HIIE exercise in cold are unknown. The purpose of this study was to examine the effects cold stress during HIIE on acute exercise metabolism and postprandial metabolism. Eleven recreationally active individuals (age: 23 ± 3 yr, weight: 80 ± 9.7 kg, V̇O2peak: 39.2 ± 5.73 mL·kg-1·min-1) performed evening HIIE sessions (10 × 60 s cycling, 90% V̇O2peak interspersed with 90 s active recovery, 30% V̇O2peak) in thermoneutral (HIIE-TN, control; 21°C) and cold environment (HIIE-CO; 0°C), following a balanced crossover design. The following morning, participants consumed a high-fat meal. Indirect calorimetry was used to assess substrate oxidation, and venous blood samples were obtained to assess changes in noncellular metabolites. During acute exercise, lipid oxidation was higher in HIIE-CO (P = 0.002) without differences in V̇O2 and energy expenditure (P ≥ 0.162) between conditions. Postprandial V̇O2, lipid and CHO oxidation, plasma insulin, and triglyceride concentrations were not different between conditions (P > 0.05). Postprandial blood LDL-C levels were higher in HIIE-CO 2 h after the meal (P = 0.003). Postprandial glucose area under curve was 49% higher in HIIE-CO versus HIIE-TN (P = 0.034). Under matched energy expenditure conditions, HIIE demonstrated higher lipid oxidation rates during exercise in the cold; but only marginally influenced postprandial lipid metabolism the following morning. In conclusion, HIIE in the cold seemed to be less favorable for postprandial lipid and glycemic responses.NEW & NOTEWORTHY This is the first known study to investigate the effects of cold ambient temperatures on acute metabolism during high-intensity interval exercise, as well as postprandial metabolism the next day. We observed that high-intensity interval exercise in a cold environment does change acute metabolism compared to a thermoneutral environment; however, the addition of a cold stimulus was less favorable for postprandial metabolic responses the following day.

The Protective Role of Hydrogen Sulfide Against Obesity-Associated Cellular Stress in Blood Glucose Regulation.

Circulating palmitic acid (PA) is increased in obesity and causes metabolic stress, leading to diabetes. This includes the impairment of the glucoregulatory hormone glucagon-like peptide-1 (GLP-1) secreted from intestinal L-cells. Recently, the anti-inflammatory gasotransmitter hydrogen sulfide (H2S) has been implicated in the enhancement of GLP-1 secretion. We hypothesized that H2S can reduce the oxidative stress caused by palmitate and play a protective role in L-cell function. This study was conducted on both human and mouse L-cells and a mouse model of Western diet (WD)-induced obesity. PA-induced L-cell stress was assessed using DCF-DA. H2S was delivered using the donor GYY4137. C57BL/6 mice were fed either chow diet or PA-enriched WD for 20 weeks with ongoing measurements of glycemia and GLP-1 secretion. In both L-cell models, we demonstrated that PA caused an increase in reactive oxygen species (ROS). This ROS induction was partially blocked by the H2S administration. In mice, the WD elevated body weight in both sexes and elevated fasting blood glucose and lipid peroxidation in males. Additionally, a single GYY4137 injection improved oral glucose tolerance in WD-fed male mice and also enhanced glucose-stimulated GLP-1 release. To conclude, H2S reduces oxidative stress in GLP-1 cells and can improve glucose clearance in mice.

A role for methanogens and methane in the regulation of GLP-1.

INTRODUCTION: The gastrointestinal (GI) microbiome has emerged as a potential regulator of metabolism. However, the precise mechanisms of how microorganisms may influence physiology remain largely unknown. Interestingly, GI microorganisms, including methanogens, are localized within the same regions as the glucagon-like peptide-1 (GLP-1) secreting L cells. GLP-1 plays key roles appetite and glucose regulation. Furthermore, both methane and GLP-1 levels are altered in obese humans with metabolic disease. We predict that high-fat diet-induced obesity alters the abundance of GI methanogens and that methane may play a role in the GLP-1 secretory response from the L cell. METHODS: To demonstrate this, GLP-1 secretion response and faecal methanogens were examined in mice given a high-fat diet for 14 weeks. In addition, the direct effect of methane on GLP-1 secretion was assessed in two L-cell models (NCI-H716 and GLUTag). RESULTS: High-fat diet caused a significant increase in both GLP-1 secretion and faecal methanogen content. There was a direct correlation between GLP-1 secretion response and faecal methanogen levels. In L cells, methane stimulated GLP-1 secretion and enhanced intracellular cAMP content. CONCLUSION: These results indicate that alterations in the methanogen communities occurring in obesity may play a vital role in directly enhancing GLP-1 secretion, and that methane can directly stimulate the secretion of GLP-1.