Both moderate- and high-intensity exercise training increase intramyocellular lipid droplet abundance and modify myocellular distribution in adults with obesity.

Exercise training modifies lipid metabolism in skeletal muscle, but the effect of exercise training on intramyocellular lipid droplet (LD) abundance, size, and intracellular distribution in adults with obesity remains elusive. This study compared high-intensity interval training (HIIT) with more conventional moderate-intensity continuous training (MICT) on intramyocellular lipid content, as well as LD characteristics (size and number) and abundance within the intramyofibrillar (IMF) and subsarcolemmal (SS) regions of type I and type II skeletal muscle fibers in adults with obesity. Thirty-six adults with obesity [body mass index (BMI) = 33 ± 3 kg/m2] completed 12 wk (4 days/wk) of either HIIT (10 × 1 min, 90% HRmax + 1-min active recovery; n = 19) or MICT (45-min steady-state exercise, 70% HRmax; n = 17), while on a weight-maintaining diet throughout training. Skeletal muscle biopsies were collected from the vastus lateralis before and after training, and intramyocellular lipid content and intracellular LD distribution were measured by immunofluorescence microscopy. Both MICT and HIIT increased total intramyocellular lipid content by more than 50% (P < 0.01), which was attributed to a greater LD number per µm2 in the IMF region of both type I and type II muscle fibers (P < 0.01). Our findings also suggest that LD lipophagy (autophagy-mediated LD degradation) may be transiently upregulated the day after the last exercise training session (P < 0.02 for both MICT and HIIT). In summary, exercise programs for adults with obesity involving either MICT or HIIT increased skeletal muscle LD abundance via a greater number of LDs in the IMF region of the myocyte, thereby providing more lipid in close proximity to the site of energy production during exercise.NEW & NOTEWORTHY In this study, 12 wk of either moderate-intensity continuous training (MICT) or high-intensity interval training (HIIT) enhanced skeletal muscle lipid abundance by increasing lipid droplet number within the intramyofibrillar (IMF) region of muscle. Because the IMF associates with high energy production during muscle contraction, this adaptation may enhance lipid oxidation during exercise. Despite differences in training intensity and energy expenditure between MICT and HIIT, their effects on muscle lipid abundance and metabolism were remarkably similar.

Exercise training remodels subcutaneous adipose tissue in adults with obesity even without weight loss.

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-2 ) were assigned to 12 weeks (4 days week-1 ) of either moderate-intensity continuous training (MICT; 70% maximal heart rate, 45 min; n = 17) or high-intensity interval training (HIIT; 90% maximal heart rate, 10 × 1 min; n = 19), maintaining their body weight throughout. Abdominal subcutaneous adipose tissue (aSAT) biopsy samples were collected once before and twice after training (1 day after last exercise and again 4 days later). Exercise training modified aSAT morphology (i.e. reduced fat cell size, increased collagen type 5a3, both P ≤ 0.05, increased capillary density, P = 0.05) and altered protein abundance of factors that regulate aSAT remodelling (i.e. reduced matrix metallopeptidase 9; P = 0.02; increased angiopoietin-2; P < 0.01). Exercise training also increased protein abundance of factors that regulate lipid metabolism (e.g. hormone sensitive lipase and fatty acid translocase; P ≤ 0.03) and key proteins involved in the mitogen-activated protein kinase pathway when measured the day after the last exercise session. However, most of these exercise-mediated changes were no longer significant 4 days after exercise. Importantly, MICT and HIIT induced remarkably similar adaptations in aSAT. Collectively, even in the absence of weight loss, 12 weeks of exercise training induced changes in aSAT structure, as well as factors that regulate metabolism and the inflammatory signal pathway in adults with obesity. KEY POINTS: Exercise training is well-known to improve metabolic health in obesity, although how exercise modifies the structure and metabolic function of adipose tissue, in the absence of weight loss, remains unclear. We report that both 12 weeks of moderate-intensity continuous training (MICT) and 12 weeks of high-intensity interval training (HIIT) induced modifications in adipose tissue structure and factors that regulate adipose tissue remodelling, metabolism and the inflammatory signal pathway in adults with obesity, even without weight loss (with no meaningful differences between MICT and HIIT). The modest modifications in adipose tissue structure in response to 12 weeks of MICT or HIIT did not lead to changes in the rate of fatty acid release from adipose tissue. These results expand our understanding about the effects of two commonly used exercise training prescriptions (MICT and HIIT) on adipose tissue remodelling that may lead to advanced strategies for improving metabolic health outcomes in adults with obesity.

Exercise training decreases whole-body and tissue iron storage in adults with obesity.

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.

Skeletal muscle ferritin abundance is tightly related to plasma ferritin concentration in adults with obesity.

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.

Effect of sex on the acute skeletal muscle response to sprint interval exercise.

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 < 0.05, main effect of time). The only sex-specific responses to exercise were an increase in the mRNA expression of GLUT4 and LPL in women only and Atrogin-1 in men only (P < 0.05). Women also had higher expression of HKII and lower expression of FOXO3 compared with men (P < 0.05, main effect of sex). We conclude that the acute skeletal muscle response to SIT is largely similar in young men and women. The mechanistic basis for sex-based differences in response to several weeks of SIT that has been previously reported remains to be elucidated.

Dietary Protein Intake and Distribution Patterns of Well-Trained Dutch Athletes.

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 <.001), endurance (r=0.79, p <.001) and team-sport (r=0.77, p <.001) athletes. Animal and plant-based sources of protein intake was 57% and 43%, respectively. The distribution of protein intake was 19% (19±8 g) at breakfast, 24% (25±13 g) at lunch and 38% (38±15 g) at dinner. Protein intake was below the recommended 20 g for 58% of athletes at breakfast, 36% at lunch and 8% at dinner. In summary, this survey of athletes revealed they habitually consume > 1.2 g protein/kg/d, but the distribution throughout the day may be suboptimal to maximize the skeletal muscle adaptive response to training.

Satellite cell activity, without expansion, after nonhypertrophic stimuli.

The purpose of the present studies was to determine the effect of various nonhypertrophic exercise stimuli on satellite cell (SC) pool activity in human skeletal muscle. Previously untrained men and women (men: 29 ± 9 yr and women: 29 ± 2 yr, n = 7 each) completed 6 wk of very low-volume high-intensity sprint interval training. In a separate study, recreationally active men (n = 16) and women (n = 3) completed 6 wk of either traditional moderate-intensity continuous exercise (n = 9, 21 ± 4 yr) or low-volume sprint interval training (n = 10, 21 ± 2 yr). Muscle biopsies were obtained from the vastus lateralis before and after training. The fiber type-specific SC response to training was determined, as was the activity of the SC pool using immunofluorescent microscopy of muscle cross sections. Training did not induce hypertrophy, as assessed by muscle cross-sectional area, nor did the SC pool expand in any group. However, there was an increase in the number of active SCs after each intervention. Specifically, the number of activated (Pax7(+)/MyoD(+), P ≤ 0.05) and differentiating (Pax7(-)/MyoD(+), P ≤ 0.05) SCs increased after each training intervention. Here, we report evidence of activated and cycling SCs that may or may not contribute to exercise-induced adaptations while the SC pool remains constant after three nonhypertrophic exercise training protocols.

Multiplexed separations for biomarker discovery in metabolomics: Elucidating adaptive responses to exercise training.

High efficiency separations are needed to enhance selectivity, mass spectral quality, and quantitative performance in metabolomic studies. However, low sample throughput and complicated data preprocessing remain major bottlenecks to biomarker discovery. We introduce an accelerated data workflow to identify plasma metabolite signatures of exercise responsiveness when using multisegment injection-capillary electrophoresis-mass spectrometry (MSI-CE-MS). This multiplexed separation platform takes advantage of customizable serial injections to enhance sample throughput and data fidelity based on temporally resolved ion signals derived from seven different sample segments analyzed within a single run. MSI-CE-MS was applied to explore the adaptive metabolic responses of a cohort of overweight/obese women (BMI > 25, n = 9) performing a 6-wk high-intensity interval training intervention using a repeated measures/cross-over study design. Venous blood samples were collected from each subject at three time intervals (baseline, postexercise, recovery) in their naïve and trained states while completing standardized cycling trials at the same absolute workload. Complementary statistical methods were used to classify dynamic changes in plasma metabolism associated with strenuous exercise and training status. Positive adaptations to exercise were associated with training-induced upregulation in plasma l-carnitine at rest due to improved muscle oxidative capacity, and greater antioxidant capacity as reflected by lower circulating glutathionyl-l-cysteine mixed disulfide. Attenuation in plasma hypoxanthine and higher O-acetyl-l-carnitine levels postexercise also indicated lower energetic stress for trained women.

ß-Alanine Supplementation Does Not Augment the Skeletal Muscle Adaptive Response to 6 Weeks of Sprint Interval Training.

Sprint interval training (SIT), repeated bouts of high-intensity exercise, improves skeletal muscle oxidative capacity and exercise performance. ß-alanine (ß-ALA) supplementation has been shown to enhance exercise performance, which led us to hypothesize that chronic ß-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 ß-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 ß-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 ß-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 ß-ALA, or the supplementation protocol was insufficient to alter the variables to a detectable extent.

Evidence for the contribution of muscle stem cells to nonhypertrophic skeletal muscle remodeling in humans.

The purpose of this study was to explore the possible role of muscle stem cells, also referred to as satellite cells (SCs), in adaptation and remodeling following a nonhypertrophic stimulus in humans. Muscle biopsies were obtained from the vastus lateralis of previously untrained women (n=15; age: 27±8 yr, BMI: 29±6 kg/m(2)) before and after 6 wk of aerobic interval training. The fiber type-specific SC response to training was analyzed using immunofluorescent microscopy of muscle cross sections. Following training, the number of SCs associated with fibers expressing myosin heavy-chain type I and II isoforms (hybrid fibers) increased (pre: 0.062±0.035 SC/hybrid fiber; post: 0.38±0.063 SC/hybrid fiber; P<0.01). In addition, there was a greater number of MyoD(+)/Pax7(-) SCs, indicative of differentiating SCs, associated with hybrid fibers (0.18±0.096 MyoD(+)/Pax7(-) SC/hybrid fiber) compared to type I (0.015±0.00615 MyoD(+)/Pax7(-) SC/type I fiber) or II (0.012±0.00454 MyoD(+)/Pax7(-) SC/type II fiber) fibers (P<0.05). There was also a training-induced increase in the number of hybrid fibers containing centrally located nuclei (15.1%) compared to either type I (3.4%) or II fibers (3.6%) (P<0.01). These data are consistent with the hypothesis that SCs contribute to the remodeling of muscle fibers even in the absence of hypertrophy.

Intermittent and continuous high-intensity exercise training induce similar acute but different chronic muscle adaptations.

High-intensity interval training (HIIT) performed in an 'all-out' manner (e.g. repeated Wingate tests) is a time-efficient strategy to induce skeletal muscle remodelling towards a more oxidative phenotype. A fundamental question that remains unclear, however, is whether the intermittent or 'pulsed' nature of the stimulus is critical to the adaptive response. In study 1, we examined whether the activation of signalling cascades linked to mitochondrial biogenesis was dependent on the manner in which an acute high-intensity exercise stimulus was applied. Subjects performed either four 30 s Wingate tests interspersed with 4 min of rest (INT) or a bout of continuous exercise (CONT) that was matched for total work (67 ± 7 kJ) and which required ∼4 min to complete as fast as possible. Both protocols elicited similar increases in markers of adenosine monophosphate-activated protein kinase (AMPK) and p38 mitogen-activated protein kinase activation, as well as Peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) mRNA expression (main effects for time, P ≤ 0.05). In study 2, we determined whether 6 weeks of the CONT protocol (3 days per week) would increase skeletal muscle mitochondrial content to a similar extent to what we have previously reported after 6 weeks of INT. Despite similar acute signalling responses to the CONT and INT protocols, training with CONT did not increase the maximal activity or protein content of a range of mitochondrial markers. However, peak oxygen uptake was higher after CONT training (from 45.7 ± 5.4 to 48.3 ± 6.5 ml kg(-1) min(-1); P < 0.05) and 250 kJ time trial performance was improved (from 26:32 ± 4:48 to 23:55 ± 4:16 min:s; P < 0.001) in our recreationally active participants. We conclude that the intermittent nature of the stimulus is important for maximizing skeletal muscle adaptations to low-volume, all-out HIIT. Despite the lack of skeletal muscle mitochondrial adaptations, our data show that a training programme based on a brief bout of high-intensity exercise, which lasted <10 min per session including warm-up, and performed three times per week for 6 weeks, improved peak oxygen uptake in young healthy subjects.

No effect of short-term green tea extract supplementation on metabolism at rest or during exercise in the fed state.

UNLABELLED: Supplementation with green tea extract (GTE) in animals has been reported to induce numerous metabolic adaptations including increased fat oxidation during exercise and improved performance. However, data regarding the metabolic and physiological effects of GTE during exercise in humans are limited and equivocal. PURPOSE: To examine the effects of short-term GTE treatment on resting energy expenditure (REE), wholebody substrate utilization during exercise and time trial performance. METHODS: Fifteen active men (24 ± 3 y; VO(2)peak = 48 ± 7 ml · kg · min(-1); BMI = 26 ± 3 kg · m(2)((-1))) ingested GTE (3x per day = 1,000 mg/d) or placebo (PLA) for 2 day in a double-blind, crossover design (each separated by a 1 week wash-out period). REE was assessed in the fasted state. Subjects then ingested a standardized breakfast (~5.0 kcal · kg(-1)) and 90 min later performed a 60 min cycling bout at an intensity corresponding to individual maximal fat oxidation (44 ± 11% VO(2)peak), followed by a 250 kJ TT. RESULTS: REE, whole-body oxygen consumption (VO2) and substrate oxidation rates during steady-state exercise were not different between treatments. However, mean heart rate (HR) was lower in GTE vs. PLA (115 ± 16 vs. 118 ± 17 beats · min(-1); main effect, p = .049). Mixed venous blood [glycerol] was higher during rest and exercise after GTE vs. PLA (p = .006, main effect for treatment) but glucose, insulin and free-fatty acids were not different. Subsequent time trial performance was not different between treatments (GTE = 25:38 ± 5:32 vs. PLA = 26:08 ± 8:13 min; p = .75). CONCLUSION: GTE had minimal effects on whole-body substrate metabolism but significantly increased plasma glycerol and lowered heart rate during steady-state exercise, suggesting a potential increase in lipolysis and a cardiovascular effect that warrants further investigation.

Interactive effects of low-volume interval exercise and nutrition on glycemic control.

Low-volume interval training has been demonstrated to improve indices of 24 h glycemic control using continuous glucose monitoring in individuals with or at risk for metabolic diseases. Nonetheless, there are inconsistencies in the literature with respect to the effects of interval exercise on 24 h glycemia, which may partly result from different nutritional conditions and/or controls adopted across various studies. This current opinion aims to provide a concise overview of the effects of acute and chronic interval exercise on 24 h glycemic control, while also describing how nutrition can influence and modify these responses. Given the distinct impact of dietary intake on blood glucose regulation, the adoption of diverse dietary control strategies during measurement of 24 h glycemia-spanning from using the participant's habitual diet to providing standardized meals customized to individual energy requirements-may contribute to varying conclusions across studies regarding the influence of interval exercise on 24 h glycemia. In addition, nutritional manipulations surrounding exercise, including whether interval exercise commences in the fasted or fed state, the macronutrient composition of post-exercise meals, and the presence of an energy and/or carbohydrate deficit among participants, offer important context when considering the effects of interval exercise on 24 h glycemia. Additional well-controlled studies are warranted to explore the interactive effects of interval exercise and nutrition on 24 h glycemia. These efforts will assist in refining exercise and nutrition recommendations aimed at improving glycemic control.

At-home bodyweight interval exercise in the fed versus fasted state lowers postprandial glycemia and appetite perceptions in females.

Limited research has characterized the metabolic health benefits of bodyweight interval exercise (BWE) performed outside of a laboratory setting. Metabolic responses to exercise can also be influenced by meal timing around exercise, but the interactive effects of BWE and nutrition are unknown. This study investigated the effects of BWE performed in the fasted or fed state on postprandial glycemia, post-exercise fat oxidation and appetite perceptions. Twelve females (23 ± 2 years; 22 ± 2 kg/m2) underwent two virtually-monitored trials that involved completing BWE (10 × 1 min, 1 min recovery) 5 min before (FastEX) or beginning BWE 10 min after (FedEX) a standardized breakfast. Heart rate and rating of perceived exertion (RPE) were measured during exercise and capillary glucose concentrations were measured for 2 h postprandial. Following exercise, appetite perceptions were assessed and Lumen expired carbon dioxide percentage (L%CO2) was measured as an index of fat oxidation. Heart rate (85 ± 5%) and RPE (14 ± 2) did not differ between conditions (p > 0.05). Postprandial glucose mean (6.1 ± 0.6 vs. 6.8 ± 0.8 mmol/L, p = 0.03), peak (7.4 ± 1.2 vs. 8.5 ± 1.5 mmol/L, p = 0.01), and area under the curve (AUC) (758 ± 72 vs. 973 ± 82 mmol/L × 2 h, p = 0.004) were lower in FedEX versus FastEX. Appetite perceptions were lower in FedEX versus FastEX (-87.63 ± 58.51 vs. -42.06 ± 34.96 mm, p = 0.029). Post-exercise L%CO2 was transiently decreased 30 min post-exercise in both conditions (4.03 ± 0.38 vs. 4.29 ± 0.34%, p = 0.0023), reflective of increased fat oxidation following BWE. These findings demonstrate that BWE performed in the fed compared to the fasted state lowered postprandial glycemia and appetite perceptions in females.

Protein requirements may be lower on a training compared to rest day but are not influenced by moderate training volumes in endurance trained males.

The impact of training volume on protein requirements in endurance trained males was investigated with indicator amino acid oxidation (IAAO) methodology on a recovery day (REST) or after a 10 or 20 km run while consuming a single suboptimal protein intake (0.93 g/kg/day). Phenylalanine excretion (F13CO2; inverse proxy for whole body protein synthesis) was greatest and phenylalanine net balance was lowest on REST compared to post-exercise recovery with no difference between training volumes. Single point F13CO2 was indistinguishable from past IAAO studies using multiple protein intakes. Our results suggest that protein requirements may be greatest on recovery days but are not influenced by moderate training volumes in endurance athletes.

Skeletal muscle mechanisms contributing to improved glycemic control following intense interval exercise and training.

High-intensity and sprint interval training (HIIT and SIT, respectively) enhance insulin sensitivity and glycemic control in both healthy adults and those with cardiometabolic diseases. The beneficial effects of intense interval training on glycemic control include both improvements seen in the hours to days following a single session of HIIT/SIT and those which accrue with chronic training. Skeletal muscle is the largest site of insulin-stimulated glucose uptake and plays an integral role in the beneficial effects of exercise on glycemic control. Here we summarize the skeletal muscle responses that contribute to improved glycemic control during and following a single session of interval exercise and evaluate the relationship between skeletal muscle remodelling and improved insulin sensitivity following HIIT/SIT training interventions. Recent evidence suggests that targeting skeletal muscle mechanisms via nutritional interventions around exercise, particularly with carbohydrate manipulation, can enhance the acute glycemic benefits of HIIT. There is also some evidence of sex-based differences in the glycemic benefits of intense interval exercise, with blunted responses observed after training in females relative to males. Differences in skeletal muscle metabolism between males and females may contribute to sex differences in insulin sensitivity following HIIT/SIT, but well-controlled studies evaluating purported muscle mechanisms alongside measurement of insulin sensitivity are needed. Given the greater representation of males in muscle physiology literature, there is also a need for more research involving female-only cohorts to enhance our basic understanding of how intense interval training influences muscle insulin sensitivity in females across the lifespan.

Metabolic dysfunction in obesity is related to impaired suppression of fatty acid release from adipose tissue by insulin.

OBJECTIVE: The aims of this study were: 1) to assess relationships among insulin-mediated glucose uptake with standard clinical outcomes and deep-phenotyping measures (including fatty acid [FA] rate of appearance [FA Ra] into the systemic circulation); and 2) to examine the contribution of adipocyte size, fibrosis, and proteomic profile to FA Ra regulation. METHODS: A total of 66 adults with obesity (BMI = 34 [SD 3] kg/m2 ) were assessed for insulin sensitivity (hyperinsulinemic-euglycemic clamp), and stable isotope dilution methods quantified glucose, FA, and glycerol kinetics in vivo. Abdominal subcutaneous adipose tissue (aSAT) and skeletal muscle biopsies were collected, and magnetic resonance imaging quantified liver and visceral fat content. RESULTS: Insulin-mediated FA Ra suppression associated with insulin-mediated glucose uptake (r = 0.51; p < 0.01) and negatively correlated with liver (r = -0.36; p < 0.01) and visceral fat (r = -0.42; p < 0.01). aSAT proteomics from subcohorts of participants with low FA Ra suppression (n = 8) versus high FA Ra suppression (n = 8) demonstrated greater extracellular matrix collagen protein in low versus high FA Ra suppression. Skeletal muscle lipidomics (n = 18) revealed inverse correlations of FA Ra suppression with acyl-chain length of acylcarnitine (r = -0.42; p = 0.02) and triacylglycerol (r = -0.51; p < 0.01), in addition to insulin-mediated glucose uptake (acylcarnitine: r = -0.49; p < 0.01, triacylglycerol: r = -0.40; p < 0.01). CONCLUSIONS: Insulin's ability to suppress FA release from aSAT in obesity is related to enhanced insulin-mediated glucose uptake and metabolic health in peripheral tissues.

Carbohydrate-Energy Replacement Following High-Intensity Interval Exercise Blunts Next-Day Glycemic Control in Untrained Women.

Background: Improved glycemic control has been reported for ∼24 h following low-volume high-intensity interval exercise (HIIE), but it is unclear if this is a direct effect of exercise or an indirect effect of the exercise-induced energy deficit. The purpose of this study was to investigate the effect of carbohydrate-energy replacement after low-volume HIIE on 24 h glycemic control in women. Methods: Seven untrained women (age: 22 ± 2 yr; BMI: 22 ± 3 kg/m2; VO2peak: 33 ± 7 ml/kg/min) completed three 2-day trials in the mid-follicular phase of the menstrual cycle. Continuous glucose monitoring was used to measure blood glucose concentrations during, and for 24 h following three conditions: (1) HIIE followed by a high-carbohydrate energy replacement drink (EX-HC); (2) HIIE followed by a non-caloric taste-matched placebo drink (EX-NC); and (3) seated control with no drink (CTL). HIIE involved an evening session (1,700 h) of 10 × 1-min cycling efforts at ∼90% maximal heart rate with 1 min recovery. Diet was standardized and identical across all three 2-day trials, apart from the post-exercise carbohydrate drink in EX-HC, which was designed to replenish the exercise-induced energy expenditure. Postprandial glycemic responses to the following days breakfast, snack, lunch, and dinner, as well as 24 h indices of glycemic control, were analyzed. Results: The day after HIIE, postprandial glycemia following breakfast and snack were reduced in EX-NC compared to EX-HC, as reflected by lower 3 h glucose mean (breakfast: 5.5 ± 0.5 vs. 6.7 ± 1, p = 0.01, Cohen's d = 1.4; snack: 4.9 ± 0.3 vs. 5.7 ± 0.8 mmol/L, p = 0.02, d = 1.4) and/or area under the curve (AUC) (breakfast: 994 ± 86 vs. 1,208 ± 190 mmol/L x 3 h, p = 0.01, d = 1.5). Postprandial glycemic responses following lunch and dinner were not different across conditions (p > 0.05). The 24 h glucose mean (EX-NC: 5.2 ± 0.3 vs. EX-HC: 5.7 ± 0.7 mmol/L; p = 0.02, d = 1.1) and AUC (EX-NC: 7,448 ± 425 vs. EX-HC: 8,246 ± 957 mmol/L × 24 h; p = 0.02, d = 1.1) were reduced in EX-NC compared to EX-HC. Conclusion: Post-exercise carbohydrate-energy replacement attenuates glycemic control the day following a single session of low-volume HIIE in women.