Search

Effective storage of excess energy in abdominal subcutaneous adipose tissue during periods of overeating may help attenuate weight-gain-related insulin resistance. The objective of this study was to assess changes in the expression of factors regulating abdominal subcutaneous adipose tissue storage capacity in response to a brief exposure to overeating in nonobese adults. Because exercise can alter the expression of genes involved in regulating adipose tissue storage capacity, we compared the responses to overeating in regular exercisers (EX, n = 11) and nonexercisers (nonEX, n = 11). Abdominal subcutaneous adipose tissue samples and oral glucose tolerance tests were performed before and after participants ate 30% above their estimated daily energy requirements for 1 week. Both EX and nonEX gained ∼1 kg ( P

Excessive adipose tissue mass underlies much of the metabolic health complications in obesity. Although exercise training is known to improve metabolic health in individuals with obesity, the effects of exercise training without weight loss on adipose tissue structure and metabolic function remain unclear. Thirty-six adults with obesity (body mass index = 33 ± 3 kg · m

New findings What is the central question of this study? Obesity is associated with complex perturbations to iron homeostasis: is plasma ferritin concentration (a biomarker of whole-body iron stores) related to the abundance of ferritin (the key tissue iron storage protein) in skeletal muscle in adults with obesity? What is the main finding and its importance? Plasma ferritin concentration was tightly correlated with the abundance of ferritin in skeletal muscle, and this relationship persisted when accounting for sex, age, body mass index and plasma C-reactive protein concentration. Our findings suggest that skeletal muscle may be an important iron store. Abstract Obesity is associated with complex perturbations to whole-body and tissue iron homeostasis. Recent evidence suggests a potentially important influence of iron storage in skeletal muscle on whole-body iron homeostasis, but this association is not clearly resolved. The primary aim of this study was to assess the relationship between whole-body and skeletal muscle iron stores by measuring the abundance of the key iron storage (ferritin) and import (transferrin receptor) proteins in skeletal muscle, as well as markers of whole-body iron homeostasis in men (n = 19) and women (n = 43) with obesity. Plasma ferritin concentration (a marker of whole-body iron stores) was highly correlated with muscle ferritin abundance (r = 0.77, P = 2 × 10-13 ) and negatively associated with muscle transferrin receptor abundance (r = -0.76, P = 1 × 10-12 ). These relationships persisted when accounting for sex, age, BMI and plasma C-reactive protein concentration. In parallel with higher whole-body iron stores in our male versus female participants, men had 2.2-fold higher muscle ferritin abundance (P = 1 × 10-4 ) compared with women. In accordance with lower muscle iron storage, women had 2.7-fold higher transferrin receptor abundance (P = 7 × 10-10 ) compared with men. We conclude that muscle iron storage and import proteins are tightly and independently related to plasma ferritin concentration in adults with obesity, suggesting that skeletal muscle may be an underappreciated iron store.

Although the health benefits of exercise in adults with obesity are well described, the direct effects of exercise on adipose tissue that may lead to improved metabolic health are poorly understood. The primary aims of this study were to perform an unbiased analysis of the subcutaneous abdominal adipose tissue transcriptomic response to acute exercise in adults with obesity, and to compare the effects of moderate-intensity continuous exercise versus high-intensity interval exercise on this response. Twenty-nine adults with obesity performed a session of either high-intensity interval exercise (HI; 10 × 1 min at 90%HRpeak, 1 min recovery between intervals; n = 14) or moderate-intensity continuous exercise (MI; 45 min at 70%HRpeak; n = 15). Groups were well matched for BMI (HI 33 ± 3 vs. MI 33 ± 4 kg/m(2)), sex (HI: 9 women vs. MI: 10 women), and age (HI: 32 ± 6 vs. MI: 29 ± 5). Subcutaneous adipose tissue was collected before and 1 h after the session of HI or MI, and samples were processed for RNA sequencing. Gene set enrichment analysis revealed 7 of 21 gene sets enriched postexercise overlapped between HI and MI. Interestingly, both HI and MI upregulated gene sets involved in inflammation (IL6-JAK-STAT3 signaling, allograft rejection, TNFα signaling via NFκB, and inflammatory response; FDR q value < 0.25). Exercise also downregulated adipogenic and oxidative metabolism gene sets in both groups. Overall, these data suggest genes involved in subcutaneous adipose tissue metabolism and inflammation may be an important part of the initial response after a session of exercise. NEW & NOTEWORTHY This study compared the effects of a single session of high-intensity interval exercise versus moderate-intensity continuous exercise on transcriptional changes in subcutaneous abdominal adipose tissue collected from adults with obesity. Our novel findings indicate exercise upregulated inflammation-related gene sets, while it downregulated metabolism-related gene sets – after both high-intensity and moderate-intensity exercise. These data suggest exercise can alter the adipose tissue transcriptome 1 h after exercise in ways that may impact inflammation and metabolism.

Calorie restriction (CR) and the resultant weight-loss are known to improve metabolic health, but the effects of CR on factors regulating white adipose tissue (WAT) metabolic function and remodeling remain unclear. The purpose of this study was to examine the effects of 8 weeks of CR on markers of lipid storage/release, endoplasmic reticulum (ER) stress, and apoptosis in inguinal and epididymal WAT collected from aged rats. We harvested inguinal and epididymal adipose tissue from 24-month-old male Fischer-344 x Brown Norway rats that were either fed an ad libitum chow diet (AL, n=6) or subjected to CR (consuming 35% below AL intake) of the same diet (n=6) for 8 weeks. Using standard immunoblotting methods, inguinal WAT from CR had a greater abundance of phosphorylated hormone sensitive lipase (pHSL) than AL (11.1±6.6 vs. 4.5±3.3 arbitrary units (AU); P=0.05) indicative of elevated lipase activity in CR, and a lower protein abundance of the esterification marker, diacylglycerol acyltransferase (DGAT; 1.0±0.2 vs. 2.4±0.6 AU; P In summary, CR-mediated responses in WAT of aged rats appeared to be depot-specific and CR may contribute to important metabolic modifications and may impact cellular remodeling of inguinal adipose tissue. Disclosure P. Varshney: None. M. W. Schleh: None. C. Ahn: None. A. Zheng: None. E. B. Arias: None. G. D. Cartee: None. J. F. Horowitz: None. Funding National Institutes of Health (R01DK077966, P30DK089503, R01AG010026)

Low sensitivity to the antilipolytic effects of insulin in adipose tissue has been linked with impaired insulin-mediated glucose uptake in skeletal muscle. The aims of this study were: 1) to compare adipose tissue morphology in obese adults with high- (HIGH) vs. low-sensitivity (LOW) to the antilipolytic effects of insulin, and 2) compare the effects of exercise training on adipose tissue from HIGH vs. LOW subjects. Using isotopic dilution methods before and during a hyperinsulinemic-euglycemic clamp, we measured the antilipolytic response to insulin in a total of 36 obese adults - and we identified sub-cohorts of 13 LOW (64±7% lipolytic suppression by insulin; BMI: 34±4kg/m2) and 13 HIGH (82±3% lipolytic suppression by insulin; BMI:33±3kg/m2). Abdominal subcutaneous adipose tissue (aSAT) samples were collected before the clamp (non-insulin stimulated). Measurements were made before and after a 12-week endurance exercise training program (4 days/week). Before training, capillary density (# of capillaries/mm2) in aSAT samples for LOW was significantly lower than HIGH (p=0.004). Collagen abundance in aSAT extracellular matrix (ECM) was lower in LOW (p=0.013). In response to training, the antilipolytic response to insulin was significantly improved in LOW (72±5% lipolytic suppression by insulin; p In summary, aSAT from obese adults with low antilipolytic sensitivity to insulin displayed lower capillarization and ECM collagen abundance compared with obese adults with high sensitivity to the antilipolytic effects of insulin. Importantly, morphological adaptations to exercise training accompanied an increased antilipolytic sensitivity to insulin in subjects with low antilipolytic sensitivity before training. Disclosure C. Ahn: None. M. W. Schleh: None. B. J. Ryan: None. A. Ludzki: None. P. Varshney: None. J. B. Gillen: None. S. Chen: None. J. F. Horowitz: None. Funding National Institutes of Health (R01DK077966, P30DK089503, T32DK007245, F32DK117522); Canadian Institutes of Health Research (DFS146190, 338735)

Heat acclimation lowers physiological strain when exercising in the heat, and may be enhanced by promoting dehydration during acclimation. The purpose was to compare fluid intake during heat acclimation by promoting dehydration (DEH=0.5 mL kg−1 15 min−1, ~2.4% dehydration per acclimation session) compared to euhydration (EUH=2.0 mL kg−1 15 min−1, ~1.4% dehydration per acclimation session) following four heat acclimation bouts on thermal strain, and exercise performance. Thirteen males completed 90 min heat stress tests (HST) at 50% VO2max (40 °C, 30%RH) before and after three 90 min heat acclimation trials, involving consecutive bouts with 4-fold less fluid (DEH) or EUH. DEH and EUH trials were separated by 48 h and assigned in a random crossover design separated by a 5 week washout. Wildland firefighter (WLFF) Nomex: shirt, pants, and a cotton T-shirt baselayer were worn. Peak core temperature (Tc) from the HST significantly decreased following both DEH (39.5 ± 0.1–39.0 ± 0.1 °C: P In conclusion, short-term heat acclimation (~360 min) attenuates heat stress, and improves exercise capacity in the heat, and was not impaired nor improved by promoting DEH during acclimation.

New findings What is the central question of this study? Does exercise training modify tissue iron storage in adults with obesity? What is the main finding and its importance? Twelve weeks of moderate-intensity exercise or high-intensity interval training lowered whole-body iron stores, decreased the abundance of the key iron storage protein in skeletal muscle (ferritin) and tended to lower hepatic iron content. These findings show that exercise training can reduce tissue iron storage in adults with obesity and might have important implications for obese individuals with dysregulated iron homeostasis. Abstract The regulation of iron storage is crucial to human health, because both excess and deficient iron storage have adverse consequences. Recent studies suggest altered iron storage in adults with obesity, with increased iron accumulation in their liver and skeletal muscle. Exercise training increases iron use for processes such as red blood cell production and can lower whole-body iron stores in humans. However, the effects of exercise training on liver and muscle iron stores in adults with obesity have not been assessed. The aim of this study was to determine the effects of 12 weeks of exercise training on whole-body iron stores, liver iron content and the abundance of ferritin (the key iron storage protein) in skeletal muscle in adults with obesity. Twenty-two inactive adults (11 women and 11 men; age, 31 ± 6 years; body mass index, 33 ± 3 kg/m2 ) completed 12 weeks (four sessions/week) of either moderate-intensity continuous training (MICT; 45 min at 70% of maximal heart rate; n = 11) or high-intensity interval training (HIIT; 10 × 1 min at 90% of maximal heart rate, interspersed with 1 min active recovery; n = 11). Whole-body iron stores were lower after training, as indicated by decreased plasma concentrations of ferritin (P = 3 × 10-5 ) and hepcidin (P = 0.02), without any change in C-reactive protein. Hepatic R2*, an index of liver iron content, was 6% lower after training (P = 0.06). Training reduced the skeletal muscle abundance of ferritin by 10% (P = 0.03), suggesting lower muscle iron storage. Interestingly, these adaptations were similar in MICT and HIIT groups. Our findings indicate that exercise training decreased iron storage in adults with obesity, which might have important implications for obese individuals with dysregulated iron homeostasis.

The primary aim of this study was to determine the impact of high-intensity interval training [HIIT] and moderate-intensity continuous training [MICT] on skeletal muscle lipidomic profile in obese adults. 17 obese adults (BMI = 34±3 kg·m-2; age = 31±6 years) completed 12 weeks of either HIIT (10 x 1 min @ 90%HRmax + 1 min recovery between intervals; n=8) or MICT (45 min steady-state exercise at 70% HRmax; n=9). Subjects exercised 4d/week and body weight was strictly maintained to assess the direct effects of exercise, independent of changes in body weight or fat mass. Skeletal muscle samples were collected from the vastus lateralis after an overnight fast both before training and 4 days after the last exercise session (to wash out the acute effects of exercise). Using shotgun lipidomics (LC MS/MS) we detected 734 lipid species from 26 different classes. Neither MICT nor HIIT significantly altered abundance of the primary muscle acylglycerides (tri- and di-acylglyceride) or ceramide abundance. Muscle acylcarnitine abundance increased after both MICT and HIIT (main effect, P = 0.04), specifically polyunsaturated acylcarnitines (P = 0.03). We also found phosphatidylcholine (PC) increased after training in both groups (main effect, P = 0.03), while the increase in phosphatidylethanolamine (PE) was greater after HIIT compared with MICT (P = 0.01). When normalized to cardiolipin (which is found almost exclusively in the inner mitochondrial membrane), the increased abundances of PC and PE were no longer apparent. Therefore, the training-induced increase in these phospholipids may largely reflect increased mitochondrial biosynthesis with training. In contrast, the observed increase in polyunsaturated acylcarnitines may represent an important adaptive response in the coordination of fatty acid metabolism in skeletal muscle after training. Overall, changes in muscle lipid profile were surprisingly similar in HIIT and MICT. Disclosure M.W. Schleh: None. B.J. Ryan: None. A. Ludzki: None. J.B. Gillen: None. J.F. Horowitz: None. Funding National Institutes of Health (R01DK077966, P30DK089503, F32DK117522, U24DK097153, UL1TR002240); Canadian Institutes of Health Research (DFS146190)

Mechanisms underlying the direct effects of exercise on metabolic health (independently of weight loss) are poorly understood, and very little is known about the effects of exercise on adipose tissue. The purpose of this study was to examine the effects of exercise training on the key extracellular matrix (ECM) modifiers, matrix metalloproteinase 2 (MMP2) and MMP9, in abdominal subcutaneous adipose tissue (aSAT) of obese adults. Seven obese adults (BMI=33±4 kg/m2; age=32±6) completed 12 weeks of exercise training (either 45min of steady-state exercise at 70% HRmax or 10x1min intervals at 90% HRmax with 1min recovery between intervals), and they were required to maintain body weight throughout. aSAT biopsies were collected before training (Pre) and twice after training - 1 day post exercise (1d PEX) and again 4 days post exercise (4d PEX; to wash out the acute effects of exercise). Using standard immunoblotting methods, we found no evidence for effects of training on either MMP2 or MMP9. However, using gelatin zymography (a technique with more than 100-fold higher sensitivity than immunoblotting) we found a strong trend for an increased MMP9 abundance 1d PEX (3.7±1.0 vs. 3.0±1.4 arbitrary units (AU), for 1d PEX vs. Pre; P=0.08). Interestingly, however, MMP9 returned to Pre training levels by 4d PEX (1.9±1.3 AU; P In summary, because increased abundance and activity of MMPs may alter the fibrotic content and composition of the ECM, exercise-induced increases in MMP2 and MMP9 within aSAT may contribute to favorable modifications within adipose tissue ECM of obese adults. Disclosure P. Varshney: None. B.J. Ryan: None. C. Ahn: None. M.W. Schleh: None. J.F. Horowitz: None. Funding National Institutes of Health (R01DK077966, P30DK089503, F32DK117522, UL1TR002240)

Objective We compared the effects of high-intensity interval training (HIIT) and moderate-intensity continuous training (MICT) on insulin sensitivity and other important metabolic adaptations in adults with obesity. Methods Thirty-one inactive adults with obesity (age: 31 ± 6 years; body mass index: 33 ± 3 kg/m2) completed 12 weeks (4 sessions/week) of either HIIT (10 × 1-minute at 90%HRmax, 1-minute active recovery; n = 16) or MICT (45 minutes at 70%HRmax; n = 15). To assess the direct effects of exercise independent of weight/fat loss, participants were required to maintain body mass. Results Training increased peak oxygen uptake by ~10% in both HIIT and MICT (P Conclusion Despite large differences in training intensity and exercise time, 12 weeks of HIIT and MICT induce similar acute improvements in peripheral insulin sensitivity the day after exercise, and similar longer term metabolic adaptations in skeletal muscle in adults with obesity. These findings support the notion that the insulin-sensitizing effects of both HIIT and MICT are mediated by factors stemming from the most recent exercise session(s) rather than adaptations that accrue with training.

Purpose This study determined the impact of an exercise-induced energy deficit on postprandial and 24 h glycemic control the day after a session of exercise. Methods Fifteen healthy participants (m/f = 5/10, 27 ± 6 yr, body mass index = 24 ± 3 kg·m, peak oxygen consumption [V˙O2peak] = 36 ± 9 mL·kg·min) completed two separate 5-d experimental trials performed under "free-living" conditions. On day 1 of each trial, participants were fitted with a continuous glucose monitor and abstained from exercise. Day 2 served as a nonexercise control (NoEx). On day 3, participants exercised at 3:00 PM (65% V˙O2peak) until they expended 350 kcals (~45 min). The diet during both experimental trials was identical with the exception of meals after this exercise session. During one trial, the dinner after exercise did not replenish the 350 kcal expended during exercise, thereby establishing an exercise energy deficit (ExDEF). During the other experimental trial, the dinner after exercise contained an additional 350 kcal to compensate for the energy expended during exercise, and thereby maintained energy balance after exercise (ExBAL). Free-living glycemia was measured the day before exercise (NoEx) and the day after exercise under ExDEF and ExBAL conditions. Results The day after exercise, 3 h postprandial area under the curve was lower after breakfast in ExDEF compared with ExBAL (16.0 ± 1.8 vs 17.0 ± 1.6 mmol·L·h per 3 h, P = 0.01), but did not differ between groups after lunch (P = 0.24), dinner (P = 0.39), or evening snack (P = 0.45). Despite differences in the glycemic response to breakfast, 24 h glycemia did not differ between ExDEF and ExBAL (area under the curve = 128 ± 10 vs 131 ± 10 mmol·L·h per 24 h, respectively; P = 0.54). Conclusions An exercise-induced energy deficit lowered the glycemic response to breakfast the next day-but this energy deficit did not impact total 24 h glycemia, the day after exercise in metabolically healthy adults.

Abnormalities in muscle lipid metabolism in obesity have been linked to insulin resistance. Exercise training alters skeletal muscle lipid abundance and localization, but the direct effects of exercise training (independent of weight loss) on skeletal muscle lipolytic proteins are not clearly understood, and data are lacking regarding influence of training intensity on factors regulating muscle lipid metabolism in obesity. Our aim was to examine the effects of high-intensity interval training (HIIT) vs. moderate-intensity continuous training (MICT) on skeletal muscle lipolytic proteins in obese humans. Eighteen sedentary, obese adults completed 12 weeks (4 sessions weekly) of either HIIT (10 x 1 min at 90% HRmax, 1 min recovery; n=8) or MICT (45 min at 70% HRmax; n=10). Muscle biopsies (vastus lateralis) were collected before and after training. Subjects maintained body weight and fat mass and the post-training biopsy occurred 3 days after the final exercise session. Both exercise training programs increased aerobic capacity (VO2max) by ~10% (p=0.003), with no significant difference between HIIT and MICT. In muscle samples, hormone-sensitive lipase (HSL) protein abundance increased ~2-fold after training in HIIT (P In summary, HIIT and MICT result in similar modifications to lipolytic proteins in skeletal muscle, although our findings suggest that HIIT may be a more potent stimulus for increasing HSL abundance. Future work is needed to determine if the concomitant increases in protein abundance of CGI-58 and G0S2 with training may improve lipid handling in obesity. Disclosure B.J. Ryan: None. M.W. Schleh: None. P. Varshney: None. A. Ludzki: None. J.B. Gillen: None. K. Foug: None. B.D. Carr: None. J.F. Horowitz: Research Support; Self; American Diabetes Association. Funding National Institutes of Health (R01DK077966, P30DK089503, T32DK007245); Canadian Institutes of Health Research (DFS146190)

Excessive fatty acid (FA) mobilization from subcutaneous adipose tissue into systemic circulation underlies many metabolic health complications associated with obesity, such as insulin resistance. Exercise is often used to help treat and/or prevent insulin resistance, but the direct effects of exercise training (without weight loss) on systemic FA mobilization are unclear. The aim of this study was to determine the effect of both high-intensity interval training (HIIT) and moderate-intensity continuous training (MICT) on FA rate of appearance (FA Ra) into systemic circulation and factors regulating FA mobilization from subcutaneous adipose tissue. 18 obese adults (33±3 kg•m-2) were randomized to 12 weeks (4 d/week) of either HIIT (10 x 1 min at 90% HRmax with 1 min recovery; n=8) or MICT (45 min at 70% HRmax; n=10), and were required to maintain bodyweight throughout. Resting FA Ra (13C palmitate dilution) and abdominal subcutaneous adipose tissue samples were collected in the overnight fasted state before and after training (72h following their final exercise session). The abundance of key lipolytic and lipid storage proteins in adipose tissue were measured via immunoblot. Aerobic fitness (VO2peak) increased ∼10% after training (P = 0.002), with no difference between HIIT and MICT. Body weight remained unchanged after training (HIIT: 98±12 vs. 98±13 kg, MICT: 101±12 vs. 100±13), as did fat mass (HIIT: 40±5 vs. 39±5 kg, MICT: 42±8 vs. 41±9). Training did not affect resting FA Ra in either HIIT (16.5±3.2 vs. 15.3±1.8 μmol•kg FM-1•min-1) or MICT (16.5±2.6 vs. 15.8±1.4 μmol•kg FM-1•min-1). In line with this finding, neither HIIT nor MICT altered adipose tissue abundance or phosphorylation-state of the lipolytic enzymes ATGL and HSL, or other factors involved in FA mobilization and storage in adipose tissue (e.g., GPAT, DGAT, CGI-58, G0S2, CD36). In summary, in the absence of weight loss, 12 weeks HIIT or MICT did not alter the regulation of resting FA mobilization from subcutaneous adipose tissue. Disclosure M.W. Schleh: None. B.J. Ryan: None. J.B. Gillen: None. P. Varshney: None. K. Foug: None. A. Ludzki: None. J.F. Horowitz: Research Support; Self; American Diabetes Association. Funding National Institutes of Health (R01DK077966, P30DK089503, T32DK007245); Canadian Institutes of Health Research (DFS146190)

Many metabolic health complications in obese adults are linked to abnormalities within their enlarged adipose tissue mass, which include hypertrophic adipocytes, a fibrotic extracellular matrix (ECM), and suppressed capillary density. Exercise training is a first-line treatment for obesity-related diseases, but the direct effects of exercise on adipose tissue structure and metabolic function remain unclear. The purpose of this study was to determine the effects of moderate-intensity continuous training (MICT) and high-intensity interval training (HIIT) on subcutaneous adipose tissue morphology. 17 obese adults were randomly assigned to 12 weeks (4 days/week) of MICT (45 minutes at 70% HRmax, n=9) or HIIT (10 X 1 minutes at 90% HRmax, 1 minute recovery, n=8) and were required to maintain their body weight throughout. Abdominal subcutaneous adipose tissue biopsy samples were collected before and after training for histological and immunoblot measures to assess adipocyte cell size, markers of ECM remodeling and capillarization. Aerobic fitness (VO2peak) improved ∼10% in both MICT and HIIT (P In summary, exercise training, perhaps especially HIIT, may increase adipogenic and angiogenic capacity in adipose tissue, as well as trigger adipose ECM remodeling. Disclosure C. Ahn: None. B.J. Ryan: None. J.B. Gillen: None. A. Ludzki: None. M.W. Schleh: None. B.A. Reinheimer: None. J.F. Horowitz: Research Support; Self; American Diabetes Association. Funding National Institutes of Health (R01DK077966, P30DK089503, T32DK007245); Canadian Institutes of Health Research (DFS146190)

The independent effects of exercise training (without weight loss) on glycemic control are controversial, and the influence of exercise intensity is not well understood. The aim of this study was to determine the effect of 12 weeks (4 sessions/week) of high-intensity interval training (HIIT) or moderate-intensity continuous training (MICT) without weight loss, on “free-living” 24h glycemic control using continuous glucose monitoring (CGM). Eighteen obese adults (33±3 kg·m-2) performed HIIT, involving 10 x 1 min intervals at ∼90% HRmax interspersed with 1 min recovery (n=8), or MICT, involving 45 min at ∼70% HRmax (n=10). CGM was performed under standardized dietary control for 48h before and after training. After training, subjects exercised the day before, but not on Day 1 of CGM measurement. On Day 2 of post-training CGM data collection, participants performed their regular exercise session (HIIT or MICT) before breakfast. This approach allowed us to assess the effects of exercise training on glycemic control on a day with and without exercise. On Day 1 post-training, 24h glucose area under the curve (AUC) was modestly lower than pre-training in both groups (HIIT: 130±11 vs. 126±7 mM·h-1 · 24h; MICT: 138±7 vs. 133±7 mM·h-1 · 24h, p=0.02). There were no differences between HIIT and MICT (p=0.22). The improved 24h glycemic control after training was primarily due to modestly lower postprandial responses to breakfast (p=0.03) and dinner (p=0.002), with no differences between HIIT and MICT. On Day 2 post-training, which included a session of exercise, glycemic control remained better than pre-training in both groups (p=0.006), but interestingly was not improved further by the acute exercise session (p=0.82 for Day 1 vs. Day 2 post-training). In conclusion, exercise training improved 24h “free-living” glycemic responses in the absence of weight loss, and in general, the intensity of exercise training did not impact this improvement in glycemic control. Disclosure M.W. Schleh: None. B.J. Ryan: None. J.B. Gillen: None. A. Ludzki: None. J.F. Horowitz: None.