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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

This study assessed the feasibility of a phase II randomized controlled trial of high-intensity interval training (HIIT), resistance training (RT), and usual care (UC) in men with prostate cancer (PCa) on active surveillance and evaluated changes in clinically relevant outcomes. Eighteen men undergoing active surveillance for PCa were randomized to HIIT (n = 5), RT (n = 7), or UC (n = 6). Exercise participants attended 2 supervised sessions weekly and were instructed to complete 1 home-based session weekly for 8 weeks. UC participants were provided with physical activity guidelines. Feasibility was met for attendance, compliance, and retention, but not recruitment. HIIT increased leg press (mean: +8.2 kg, 95% CI 1.1 to 15.3) from baseline to 8 weeks. RT increased seated row (mean: +11.7 kg, 95% CI 6.1 to 17.3), chest press (mean: +10.4 kg, 95% CI 5.3 to 15.5), leg press (mean: +13.1 kg, 95% CI 5.9 to 20.3), serum insulin-like binding protein-3 (IGFBP-3) (mean: +400.0 ng/mL, 95% CI 94.5 to 705.5), and decreased interferon-γ (mean: −3.1 pg/mL, 95% CI −5.7 to −0.4). No changes were observed in the UC group. HIIT and RT may be effective strategies for improving muscle strength; however, only RT may increase serum IGFBP-3. Strategies that can enhance recruitment in men on active surveillance are important prior to conducting a phase II trial. Trial registration number: ClinicalTrials.gov number NCT04266262. Novelty: High-intensity interval training or resistance training are feasible during active surveillance for prostate cancer. Resistance training may suppress the tumour-promoting effects of insulin-like growth factor-I (IGF-I) via increased expression of IGFBP-3.

Type 2 diabetes (T2D) is a rapidly growing yet largely preventable chronic disease. Exaggerated increases in blood glucose concentration following meals is a primary contributor to many long-term complications of the disease that decrease quality of life and reduce lifespan. Adverse health consequences also manifest years prior to the development of T2D due to underlying insulin resistance and exaggerated postprandial concentrations of the glucose-lowering hormone insulin. Postprandial hyperglycemic and hyperinsulinemic excursions can be improved by exercise, which contributes to the well-established benefits of physical activity for the prevention and treatment of T2D. The aim of this review is to describe the postprandial dysmetabolism that occurs in individuals at risk for and with T2D, and highlight how acute and chronic exercise can lower postprandial glucose and insulin excursions. In addition to describing the effects of traditional moderate-intensity continuous exercise on glycemic control, we highlight other forms of activity including low-intensity walking, high-intensity interval exercise, and resistance training. In an effort to improve knowledge translation and implementation of exercise for maximal glycemic benefits, we also describe how timing of exercise around meals and post-exercise nutrition can modify acute and chronic effects of exercise on glycemic control and insulin sensitivity. Novelty: Exaggerated postprandial blood glucose and insulin excursions are associated with disease risk. Both a single session and repeated sessions of exercise improve postprandial glycemic control in individuals with and without T2D. The glycemic benefits of exercise can be enhanced by considering the timing and macronutrient composition of meals around exercise.

Prolonged sitting can impair postprandial glycemia, lipidemia, and insulin sensitivity regardless of previous health status. We demonstrate that interrupting prolonged sitting with brief periods of activity, such as body weight squats or short bouts of walking, improves the efficiency of dietary amino acid utilizations for muscle contractile protein synthesis. This further emphasizes the importance of minimizing sedentary time to improve the postprandial metabolism of all macronutrients.

Breaking up prolonged sitting with intermittent walking breaks can improve glycemic control. Here, we demonstrated that interrupting prolonged sitting every 30 min with 1 min of repeated chair stands was as effective as 2-min treadmill walks for lowering postprandial insulinemia in healthy adults. Markers of contraction- and insulin-mediated muscle glucose uptake were unchanged. Repeated chair stands as a form of body-weight resistance activity may represent a cost- and space-efficient activity break for mitigating cardiometabolic-disease risk.

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.

Interval training is a form of exercise that involves intermittent bouts of relatively intense effort interspersed with periods of rest or lower-intensity exercise for recovery. Low-volume high-intensity interval training (HIIT) and sprint interval training (SIT) induce physiological and health-related adaptations comparable to traditional moderate-intensity continuous training (MICT) in healthy adults and those with chronic disease despite a lower time commitment. However, most studies within the field have been conducted in men, with a relatively limited number of studies conducted in women cohorts across the lifespan. This review summarizes our understanding of physiological responses to low-volume interval training in women, including those with overweight/obesity or type 2 diabetes, with a focus on cardiorespiratory fitness, glycemic control, and skeletal muscle mitochondrial content. We also describe emerging evidence demonstrating similarities and differences in the adaptive response between women and men. Collectively, HIIT and SIT have consistently been demonstrated to improve cardiorespiratory fitness in women, and most sex-based comparisons demonstrate similar improvements in men and women. However, research examining insulin sensitivity and skeletal muscle mitochondrial responses to HIIT and SIT in women is limited and conflicting, with some evidence of blunted improvements in women relative to men. There is a need for additional research that examines physiological adaptations to low-volume interval training in women across the lifespan, including studies that directly compare responses to MICT, evaluate potential mechanisms, and/or assess the influence of sex on the adaptive response. Future work in this area will strengthen the evidence-base for physical activity recommendations in women.

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.

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)

Motor learning may be enhanced when a single session of aerobic exercise is performed immediately before or after motor skill practice. Most research to date has focused on aerobically trained (AT) individuals, but it is unknown if aerobically untrained (AU) individuals would equally benefit. We aimed to: (a) replicate previous studies and determine the effect of rest (REST) versus exercise (EXE) on motor skill retention, and (b) explore the effect of aerobic fitness level (AU, AT), assessed by peak oxygen uptake (VO2peak), on motor skill retention after exercise. Forty-four participants (20–29 years) practiced a visuomotor tracking task (acquisition), immediately followed by 25-min of high-intensity cycling or rest. Twenty-four hours after acquisition, participants completed a motor skill retention test. REST and EXE groups significantly improved motor skill performance during acquisition [F(3.17, 133.22) = 269.13, P = 0.001], but had no group differences in motor skill retention across time. AU-exercise (VO2peak = 31.6 ± 4.2 ml kg−1 min−1) and AT-exercise (VO2peak = 51.5 ± 7.6 ml kg−1 min−1) groups significantly improved motor skill performance during acquisition [F(3.07, 61.44) = 155.95, P = 0.001], but had no group differences in motor skill retention across time. Therefore, exercise or aerobic fitness level did not modify motor skill retention.

There are limited and equivocal data regarding potential fiber type-specific differences in the human skeletal muscle response to sprint interval training (SIT), including how this compares with moderate-intensity continuous training (MICT). We examined mixed-muscle and fiber type-specific responses to a single session (study 1) and to 12 wk (study 2) of MICT and SIT using Western blot analysis. MICT consisted of 45 min of cycling at ∼70% of maximal heart rate, and SIT involved 3 × 20-s "all-out" sprints interspersed with 2 min of recovery. Changes in signaling proteins involved in mitochondrial biogenesis in mixed-muscle and pooled fiber samples were similar after acute MICT and SIT. This included increases in the ratios of phosphorylated to total acetyl-CoA carboxylase and p38 mitogen-activated protein kinase protein content (main effects, P < 0.05). Following training, mitochondrial content markers including the protein content of cytochrome c oxidase subunit IV and NADH:ubiquinone oxidoreductase subunit A9 were increased similarly in mixed-muscle and type IIa fibers (main effects, P < 0.05). In contrast, only MICT increased these markers of mitochondrial content in type I fibers (interactions, P < 0.05). MICT and SIT also similarly increased the content of mitochondrial fusion proteins optic atrophy 1 (OPA1) and mitofusin 2 in mixed-muscle, and OPA1 in pooled fiber samples (main effects, P < 0.02). In summary, acute MICT and SIT elicited similar fiber type-specific responses of signaling proteins involved in mitochondrial biogenesis, whereas 12 wk of training revealed differential responses of mitochondrial content markers in type I but not type IIa fibers.NEW & NOTEWORTHY We examined mixed-muscle and fiber type-specific responses to a single session and to 12 wk of moderate-intensity continuous training (MICT) and sprint interval training (SIT) in humans. Both interventions elicited generally similar responses, although the training-induced increases in type I fiber-specific markers of mitochondrial content were greater in MICT than in SIT. These findings advance our understanding of the potential role of fiber type-specific changes in determining the human skeletal muscle response to intermittent and continuous exercise.

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)

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.

Protein recommendations for resistance-trained athletes are generally lower than their habitual intakes. Excess protein consumption increases the capacity to oxidize amino acids, which can attenuate post-exercise anabolism and may impact protein requirements determined by stable isotope techniques predicated on amino acid tracer oxidation. We aimed to determine the impact of an acute (5d) reduction in dietary protein intake on post-exercise anabolism in high habitual consumers using the indicator amino acid oxidation (IAAO) technique. Resistance trained men [n = 5; 25 ± 7 y; 73.0 ± 5.7 kg; 9.9 ± 2.9% body fat; 2.69 ± 0.38 g·kg−1·d−1 habitual protein intake) consumed a high (H; 2.2 g·kg−1·d−1) and moderate (M; 1.2 g·kg−1·d−1) protein diet while training every other day. During the High protein phase, participants consumed a 2d controlled diet prior to determining whole body phenylalanine turnover, net balance (NB), and 13CO2 excretion (F13CO2) after exercise via oral [13C]phenylalanine. During the Moderate phase, participants consumed 2.2 g protein·kg−1·d−1 for 2d prior to consuming 1.2 g protein·kg−1·d−1 for 5d. Phenylalanine metabolism was measured on days 1, 3, and 5 (M1, M3, and M5, respectively) of the moderate intake. F13CO2, the primary outcome for IAAO, was ~72 and ~55% greater on the 1st day (M1, P < 0.05) and the third day of the moderate protein diet (M3, P = 0.07), respectively, compared to the High protein trial. Compared to the High protein trial, NB was ~25% lower on the 1st day (M1, P < 0.01) and 15% lower on the third day of the moderate protein diet (M3, P = 0.09). High habitual protein consumption may bias protein requirements determined by traditional IAAO methods that use only a 2d pre-trial controlled diet. Post-exercise whole body anabolism is attenuated following a reduction in protein intake in resistance trained men and may require ~3–5d to adapt. This trial is registered at clinicaltrials.gov as NCT03845569.

High intensity interval training (HIIT) boosts natural killer (NK) cell number and activity in normal weight breast cancer patients; however, whether this occurs in obese individuals is not well established. The goal of this study was to determine whether HIIT effectively boosts NK cells as a therapeutic strategy against breast cancer in an obese mouse model and in overweight/obese women. Diet induced female C57Bl/6 obese mice were assigned to undergo HIIT for four weeks or remain sedentary. Female participants were subjected to a six weeks HIIT protocol. HIIT mice acclimatized to treadmill running were subsequently injected with 5 × 105 polyoma middle T (MT) breast cancer cells intravenously. NK cell number and activation were monitored using flow cytometry, and tumor burden or lipid content evaluated from histological lung and liver tissues, respectively. In both mice and humans, circulating NK cell number and activation (CD3-NK1.1+CD27+ and CD3-CD56+, respectively) markedly increased immediately after HIIT. HIIT obese mice had reduced lung tumor burden compared to controls following MT challenge, and had diminished hepatic lipid deposition despite minimal body weight loss. Our findings demonstrate that HIIT can benefit obese individuals by enhancing NK cell number and activity, reducing tumor burden, and enhancing metabolic health.

Moderate-intensity continuous training (MICT) improves peripheral artery function in healthy adults, a phenomenon that reverses as continued training induces structural remodeling. Sprint interval training (SIT) elicits physiological adaptations similar to MICT, despite a lower exercise volume and time commitment; however, its effect on peripheral artery function and structure is largely unexplored. We compared peripheral artery responses to 12 wk of MICT and SIT in sedentary, healthy men (age = 27 ± 8 yr). Participants performed MICT (45 min of cycling at 70% peak heart rate; n = 10) or SIT (3 × 20-s “all out” cycling sprints with 2 min of recovery; n = 9), and responses were compared with a nontraining control group (CTL, n = 6). Allometrically scaled brachial flow-mediated dilation (FMD) increased 2.2% after 6 wk of MICT and returned to baseline levels by 12 wk, but did not change in SIT or CTL (group × time interaction, P = 0.04). Brachial artery diameter increased after 6 and 12 wk (main effect, P = 0.03), with the largest increases observed in MICT. Neither training protocol affected popliteal relative FMD and diameter, or central and lower limb arterial stiffness (carotid distensibility, central and leg pulse wave velocity) ( P > 0.05 for all). Whereas earlier and more frequent measurements are needed to establish the potential presence and time course of arterial responses to low-volume SIT, our findings suggest that MICT was superior to the intense, but brief and intermittent SIT stimulus at inducing brachial artery responses in healthy men. NEW & NOTEWORTHY We compared the effects of 12 wk of moderate-intensity continuous training (MICT) and sprint interval training (SIT) on peripheral artery endothelial function and diameter, and central and lower limb stiffness in sedentary, healthy men. Whereas neither training program affected the popliteal artery or stiffness indexes, we observed changes in brachial artery function and diameter with MICT but not SIT. Brachial artery responses to SIT may follow a different time course or may not occur at all.

New Findings What is the central question of this study? Are there sex-based differences in the acute skeletal muscle response to sprint interval training (SIT)? What is the main finding and its importance? In response to a SIT protocol that involved three 20 s bouts of ‘all-out’ cycling, the expression of multiple genes associated with mitochondrial biogenesis, metabolic control and structural remodelling was largely similar between men and women matched for fitness. Our findings cannot explain previous reports of sex-based differences in the adaptive response to SIT and suggest that the mechanistic basis for these differences remains to be elucidated. A few studies have reported sex-based differences in response to several weeks of sprint interval training (SIT). These findings may relate to sex-specific responses to an acute session of SIT. We tested the hypothesis that the acute skeletal muscle response to SIT differs between sexes. Sedentary but healthy men (n = 10) and women (n = 9) were matched for age (22 ± 3 versus 22 ± 3 years old) and cardiorespiratory fitness [45 ± 7 versus 43 ± 10 ml O2 (kg fat-free mass)−1 min−1], with women tested in the mid-follicular phase of their menstrual cycles. Subjects performed three 20 s ‘all-out’ cycling efforts against a resistance of 5% of body mass, interspersed with 2 min of recovery. Relative mean power outputs [7.6 ± 0.5 versus 7.5 ± 0.9 W (kg fat-free mass)−1] were similar between men and women (P > 0.05). Furthermore, there were no differences in the exercise-induced changes in mRNA expression of PGC-1α, PRC, PPARD, SIRT1, RIP140, HSL, HKII, PDK4, PDP1, FOXO3, MURF-1, Myf5, MyoD and VEGFA at 3 h of recovery versus rest (P

Carotid artery longitudinal wall motion (CALM) exhibits reduced magnitude in older adults and in individuals with chronic diseases, although longitudinal data are lacking to indicate how changes in CALM might develop over time. Therefore, the aim of this study was to investigate the effect of exercise training in healthy men on CALM using a retrospective design. Carotid ultrasound data were analysed from two previous studies in which men performed 12 wk of moderate-intensity continuous exercise training (n = 9), sprint-interval training (n = 7), higher-repetition resistance exercise training (n = 15) or lower-repetition resistance exercise training (n = 15). The CALM pattern was unaltered after 12 wk of exercise training, regardless of exercise mode, with no differences in systolic or diastolic CALM magnitudes (p > 0.05), similar to carotid intima-media thickness (p > 0.05). Our findings suggest that CALM is resistant to transient changes in lifestyle factors, similar to wall thickness in otherwise healthy populations.

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)

Training with low-carbohydrate (CHO) availability enhances markers of aerobic adaptation and has become popular to periodize throughout an endurance-training program. However, exercise-induced amino acid oxidation is increased with low muscle glycogen, which may limit substrate availability for postexercise protein synthesis. We aimed to determine the impact of training with low-CHO availability on estimates of dietary protein requirements.Eight endurance-trained males (27 ± 4 yr, 75 ± 10 kg, 67 ± 10 mL·kg body mass·min) completed two trials matched for energy and macronutrient composition but with differing CHO periodization. In the low-CHO availability trial (LOW), participants consumed 7.8 g CHO·kg before evening high-intensity interval training (10 × 5 min at 10-km race pace, 1 min rest) and subsequently withheld CHO postexercise (0.2 g·kg). In the high-CHO availability trial (HIGH), participants consumed 3 g CHO·kg during the day before high-intensity interval training, and consumed 5 g CHO·kg that evening to promote muscle glycogen resynthesis. A 10-km run (~80% HRmax) was performed the following morning, fasted (LOW) or 1 h after consuming 1.2 g CHO·kg (HIGH). Whole-body phenylalanine flux and oxidation were determined over 8 h of recovery via oral [C]phenylalanine ingestion, according to standard indicator amino acid oxidation methodology, while consuming sufficient energy, 7.8 g CHO·kg·d, and suboptimal protein (0.93 g·kg·d).Fat oxidation (indirect calorimetry) during the 10-km run was higher in LOW compared with HIGH (0.99 ± 0.35 g·min vs 0.60 ± 0.26 g·min, P0.05). phenylalanine flux during recovery was not different between trials (P0.05) whereas phenylalanine oxidation (reciprocal of protein synthesis) was higher in LOW compared with HIGH (8.8 ± 2.7 μmol·kg·h vs 7.9 ± 2.4 μmol·kg·h, P0.05), suggesting a greater amino acid requirement to support rates of whole-body protein synthesis.Our findings suggest that performing endurance exercise with low-CHO availability increases protein requirements of endurance athletes.

We tested the hypothesis that ingestion of sodium bicarbonate (NaHCO3) prior to an acute session of high-intensity interval training (HIIT) would augment signaling cascades and gene expression linked to mitochondrial biogenesis in human skeletal muscle. On two occasions separated by ∼1 wk, nine men (mean ± SD: age 22 ± 2 yr, weight 78 ± 13 kg, V̇o2 peak 48 ± 8 ml·kg−1·min−1) performed 10 × 60-s cycling efforts at an intensity eliciting ∼90% of maximal heart rate (263 ± 40 W), interspersed with 60 s of recovery. In a double-blind, crossover manner, subjects ingested a total of 0.4 g/kg body weight NaHCO3 before exercise (BICARB) or an equimolar amount of a placebo, sodium chloride (PLAC). Venous blood bicarbonate and pH were elevated at all time points after ingestion ( P < 0.05) in BICARB vs. PLAC. During exercise, muscle glycogen utilization (126 ± 47 vs. 53 ± 38 mmol/kg dry weight, P < 0.05) and blood lactate accumulation (12.8 ± 2.6 vs. 10.5 ± 2.8 mmol/liter, P < 0.05) were greater in BICARB vs. PLAC. The acute exercise-induced increase in the phosphorylation of acetyl-CoA carboxylase, a downstream marker of AMP-activated protein kinase activity, and p38 mitogen-activated protein kinase were similar between treatments ( P > 0.05). However, the increase in PGC-1α mRNA expression after 3 h of recovery was higher in BICARB vs. PLAC (approximately sevenfold vs. fivefold compared with rest, P < 0.05). We conclude that NaHCO3 before HIIT alters the mRNA expression of this key regulatory protein associated with mitochondrial biogenesis. The elevated PGC-1α mRNA response provides a putative mechanism to explain the enhanced mitochondrial adaptation observed after chronic HIIT supplemented with NaHCO3 in rats.

Sprint interval training (SIT), repeated bouts of high-intensity exercise, improves skeletal muscle oxidative capacity and exercise performance. β-alanine (β-ALA) supplementation has been shown to enhance exercise performance, which led us to hypothesize that chronic β-ALA supplementation would augment work capacity during SIT and augment training-induced adaptations in skeletal muscle and performance. Twenty-four active but untrained men (23 ± 2 yr; VO2peak = 50 ± 6 mL·kg−1·min−1) ingested 3.2 g/day of β-ALA or a placebo (PLA) for a total of 10 weeks (n = 12 per group). Following 4 weeks of baseline supplementation, participants completed a 6-week SIT intervention. Each of 3 weekly sessions consisted of 4–6 Wingate tests, i.e., 30-s bouts of maximal cycling, interspersed with 4 min of recovery. Before and after the 6-week SIT program, participants completed a 250-kJ time trial and a repeated sprint test. Biopsies (v. lateralis) revealed that skeletal muscle carnosine content increased by 33% and 52%, respectively, after 4 and 10 weeks of β-ALA supplementation, but was unchanged in PLA. Total work performed during each training session was similar across treatments. SIT increased markers of mitochondrial content, including cytochome c oxidase (40%) and β-hydroxyacyl-CoA dehydrogenase maximal activities (19%), as well as VO2peak (9%), repeated-sprint capacity (5%), and 250-kJ time trial performance (13%), but there were no differences between treatments for any measure (p < .01, main effects for time; p > .05, interaction effects). The training stimulus may have overwhelmed any potential influence of β-ALA, or the supplementation protocol was insufficient to alter the variables to a detectable extent.

Accumulating evidence suggests obese women maintain higher insulin sensitivity than obese men, but factors underlying this sex difference in insulin resistance remain unclear. We recently developed a semi-automated method for quantifying visceral and hepatic fat using advanced chemical shift-encoded magnetic resonance imaging (MRI). Using this method, we explored whether sex differences in ectopic fat accumulation may contribute to differences in insulin resistance. Twenty-one obese women (32 ± 6 year, 34.5 ± 3.1 kg/m2, 43.1 ± 5.5 kg fat mass (FM)) and a well-matched cohort of fifteen obese men (29 ± 6 year, 34.5 ± 3.3 kg/m2, 42.0 ± 7.8 kg FM) underwent an MRI scan during which 5mm axial slices were acquired from the abdominal region. Using 3D Slicer software, visceral fat area was quantified on three axial slices from the L2-L3 vertebrae region and averaged. Hepatic fat was quantified as the average percentage fat from three axial slices of the liver. On a separate day, subjects underwent a hyperinsulinemic-euglycemic clamp to quantify insulin sensitivity. Compared with men, women had lower hepatic (4.2 ± 5.5 vs. 13.1 ± 9.7%, p Disclosure J.B. Gillen: None. B.J. Ryan: None. R.A. Gioscia-Ryan: None. A. Ludzki: None. T.L. Chenevert: None. J.F. Horowitz: None.

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.

High‐intensity interval training (HIIT) enhances skeletal muscle oxygen delivery and utilization but data are limited regarding fiber‐specific adaptations in humans. We examined the effect of 18 sessions of HIIT (10 × 60‐sec cycling intervals at ~90% HR max , interspersed by 60‐sec of recovery) over 6 weeks on markers of microvascular density and oxidative capacity in type I and II fibers in healthy but sedentary young women (Age: 26 ± 7 years; BMI: 30 ± 4 kg·m −2 ; VO 2peak : 2.16 ± 0.45 L·m −1 ). Immunohistochemical analyses of muscle cross sections revealed a training‐induced increase in capillary contacts per fiber in type I fibers (PRE: 4.38 ± 0.37 vs. POST: 5.17 ± 0.80; main effect, P 0.05) and type II fibers (PRE: 4.24 ± 0.55 vs. POST: 4.92 ± 0.54; main effect, P 0.05). The capillary‐to‐fiber ratio also increased after training in type I fibers (PRE: 1.53 ± 1.44 vs. POST: 1.88 ± 0.38; main effect, P 0.05) and type II fibers (PRE: 1.45 ± 0.19 vs. POST: 1.76 ± 0.27; main effect, P 0.05). Muscle oxidative capacity as reflected by the protein content of cytochrome oxidase IV also increased after training in type I fibers (PRE: 3500 ± 858 vs. POST: 4442 ± 1377 arbitrary units; main effect, P 0.01) and type II fibers (PRE: 2632 ± 629 vs. POST: 3863 ± 1307 arbitrary units; main effect, P 0.01). We conclude that short‐term HIIT in previously inactive women similarly increases markers of capillary density and mitochondrial content in type I and type II fibers.

Lifestyle interventions incorporating both diet and exercise strategies remain cornerstone therapies for treating metabolic disease. Carbohydrate-restriction and high-intensity interval training (HIIT) have independently been shown to improve cardiovascular and metabolic health. Carbohydrate-restriction reduces postprandial hyperglycemia, thereby limiting potential deleterious metabolic and cardiovascular consequences of excessive glucose excursions. Additionally, carbohydrate-restriction has been shown to improve body composition and blood lipids. The benefits of exercise for improving insulin sensitivity are well known. In this regard, HIIT has been shown to rapidly improve glucose control, endothelial function, and cardiorespiratory fitness. Here, we report the available evidence for each strategy and speculate that the combination of carbohydrate-restriction and HIIT will synergistically maximize the benefits of both approaches. We hypothesize that this lifestyle strategy represents an optimal intervention to treat metabolic disease; however, further research is warranted in order to harness the potential benefits of carbohydrate-restriction and HIIT for improving cardiometabolic health.

Dietary protein intake should be optimized in all athletes to ensure proper recovery and enhance the skeletal muscle adaptive response to exercise training. In addition to total protein intake, the use of specific proteincontaining food sources and the distribution of protein throughout the day are relevant for optimizing protein intake in athletes. In the present study, we examined the daily intake and distribution of various proteincontaining food sources in a large cohort of strength, endurance and team-sport athletes. Well-trained male (n=327) and female (n=226) athletes completed multiple web-based 24-hr dietary recalls over a 2-4 wk period. Total energy intake, the contribution of animal- and plant-based proteins to daily protein intake, and protein intake at six eating moments were determined. Daily protein intake averaged 108±33 and 90±24 g in men and women, respectively, which corresponded to relative intakes of 1.5±0.4 and 1.4±0.4 g/kg. Dietary protein intake was correlated with total energy intake in strength (r=0.71, p r=0.79, p r=0.77, p 1.2 g protein/kg/d, but the distribution throughout the day may be suboptimal to maximize the skeletal muscle adaptive response to training.

What is the central question of this study? Are there sex-based differences in the acute skeletal muscle response to sprint interval training (SIT)? What is the main finding and its importance? In response to a SIT protocol that involved three 20 s bouts of 'all-out' cycling, the expression of multiple genes associated with mitochondrial biogenesis, metabolic control and structural remodelling was largely similar between men and women matched for fitness. Our findings cannot explain previous reports of sex-based differences in the adaptive response to SIT and suggest that the mechanistic basis for these differences remains to be elucidated. A few studies have reported sex-based differences in response to several weeks of sprint interval training (SIT). These findings may relate to sex-specific responses to an acute session of SIT. We tested the hypothesis that the acute skeletal muscle response to SIT differs between sexes. Sedentary but healthy men (n = 10) and women (n = 9) were matched for age (22 ± 3 versus 22 ± 3 years old) and cardiorespiratory fitness [45 ± 7 versus 43 ± 10 ml O

Green tea extract (GTE) ingestion improves glucose homeostasis in healthy and diabetic humans, but the interactive effect of GTE and exercise is unknown. The present study examined the effect of short-term GTE supplementation on the glycemic response to an oral glucose load at rest and following an acute bout of exercise, as well as substrate oxidation during exercise. Eleven sedentary, overweight men with fasting plasma glucose (FPG) ≥5.6 mmol·L−1 (age, 34 ± 13 years; body mass index = 32 ± 5 kg·m−2; FPG = 6.8 ± 1.0; mean ± SD) ingested GTE (3× per day, 1050 mg·day–1 total) or placebo (PLA) for 7 days in a double-blind, crossover design. The effects of a 75-g glucose drink were assessed on 4 occasions during both GTE and PLA treatments: On days 1 and 5 at rest, and again following an acute bout of exercise on days 3 and 8. The glycemic response was assessed via an indwelling continuous glucose monitor (CGM) and venous blood draws. At rest, 1-h CGM glucose area under the curve was not different (P > 0.05), but the postexercise response was lower after GTE versus PLA (330 ± 53 and 393 ± 65 mmol·L−1·min−1, main effect of treatment, P < 0.05). The 1-h postprandial peaks in venous blood glucose (8.6 ± 1.6 and 9.8 ± 2.2 mmol·L−1) and insulin (96 ± 59 and 124 ± 68 μIU·ml−1) were also lower postexercise with GTE versus PLA (time × treatment interactions, P < 0.05). In conclusion, short-term GTE supplementation did not affect postprandial glucose at rest; however, GTE was associated with an attenuated glycemic response following a postexercise oral glucose load. These data suggest that GTE might alter skeletal muscle glucose uptake in humans.

Aims We investigated whether sprint interval training (SIT) was a time-efficient exercise strategy to improve insulin sensitivity and other indices of cardiometabolic health to the same extent as traditional moderate-intensity continuous training (MICT). SIT involved 1 minute of intense exercise within a 10-minute time commitment, whereas MICT involved 50 minutes of continuous exercise per session. Methods Sedentary men (27±8y; BMI = 26±6kg/m2) performed three weekly sessions of SIT (n = 9) or MICT (n = 10) for 12 weeks or served as non-training controls (n = 6). SIT involved 3x20-second ‘all-out’ cycle sprints (~500W) interspersed with 2 minutes of cycling at 50W, whereas MICT involved 45 minutes of continuous cycling at ~70% maximal heart rate (~110W). Both protocols involved a 2-minute warm-up and 3-minute cool-down at 50W. Results Peak oxygen uptake increased after training by 19% in both groups (SIT: 32±7 to 38±8; MICT: 34±6 to 40±8ml/kg/min; p