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The aims of this study were (1) to determine how stair-climbing-based exercise snacks (ES) compared to moderate-intensity continuous training (MICT) for improving cardiorespiratory fitness (CRF), and (2) to explore whether ES could improve maximal fat oxidation rate (MFO) in inactive adults. Healthy, young, inactive adults ( n : 42, age: 21.6 ± 2.3 years, BMI: 22.5 ± 3.6 kg·m -2 , peak oxygen uptake (VO 2 peak): 33.6 ± 6.3 mL·kg -1 ·min -1 ) were randomly assigned to ES, MICT, or Control. ES ( n  = 14) and MICT ( n  = 13) groups performed three sessions per week over 6 weeks, while the control group ( n  = 15) maintained their habitual lifestyle. ES involved 3 × 30 s "all-out" stair-climbing (6 flight, 126 steps, and 18.9 m total height) bouts separated by >1 h rest, and MICT involved 40 min × 60%-70% HR max stationary cycling. A significant group × time interaction was found for relative VO 2 peak ( p  < 0.05) with ES significantly increasing by 7% compared to baseline (MD = 2.5 mL·kg -1 ·min -1 (95% CI = 1.2, 3.7), Cohen's d  = 0.44), while MICT had no significant effects (MD = 1.0 mL·kg -1 ·min -1 (-1.1, 3.2), Cohen's d  = 0.17), and Control experienced a significant decrease (MD = -1.7 mL·kg -1 ·min -1 (-2.9, -0.4), Cohen's d  = 0.26). MFO was unchanged among the three groups (group × time interaction, p  > 0.05 for all). Stair climbing-based ES are a time-efficient alternative to MICT for improving CRF among inactive adults, but the tested ES intervention appears to have limited potential to increase MFO., Competing Interests: No conflicts and interests are relevant to the content of this research.

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., (© 2022 The Authors. The Journal of Physiology © 2022 The Physiological Society.)

Background: The term immunometabolism describes cellular and molecular metabolic processes that control the immune system and the associated immune responses. Acute exercise and regular physical activity have a substantial influence on the metabolism and the immune system, so that both processes are closely associated and influence each other bidirectionally., Scope of Review: We limit the review here to focus on metabolic phenotypes and metabolic plasticity of T cells and macrophages to describe the complex role of acute exercise stress and regular physical activity on these cell types. The metabolic and immunological consequences of the social problem of inactivity and how, conversely, an active lifestyle can break this vicious circle, are then described. Finally, these aspects are evaluated against the background of an aging society., Major Conclusions: T cells and macrophages show high sensitivity to changes in their metabolic environment, which indirectly or directly affects their central functions. Physical activity and sedentary behaviour have an important influence on metabolic status, thereby modifying immune cell phenotypes and influencing immunological plasticity. A detailed understanding of the interactions between acute and chronic physical activity, sedentary behaviour, and the metabolic status of immune cells, can help to target the dysregulated immune system of people who live in a much too inactive society., (Copyright © 2022 International Society of Exercise and Immunology. All rights reserved.)

The global pandemics of obesity and sedentarism are associated with poor quality of life and increased risks for development of inflammatory chronic diseases, including type 2 diabetes, cardiovascular diseases, and cancer. Physical activity is considered as an antidote to counteract the development of chronic sterile inflammatory diseases. Thus, we review the most promising exercise training protocols for promoting weight loss, improving glucose homeostasis, and reducing inflammation. We discuss the advantages and disadvantages of moderate-intensity continuous aerobic training, high-intensity aerobic training, and combined (aerobic + resistance) training. Our aim with this chapter is to provide evidence and guidance for choosing the most appropriate protocols of exercise training according to the goals of the patient., (© 2022. The Author(s), under exclusive license to Springer Science+Business Media, LLC, part of Springer Nature.)

Background: Low cardiorespiratory fitness (V̇O 2peak ) is highly associated with chronic disease and mortality from all causes. Whilst exercise training is recommended in health guidelines to improve V̇O 2peak , there is considerable inter-individual variability in the V̇O 2peak response to the same dose of exercise. Understanding how genetic factors contribute to V̇O 2peak training response may improve personalisation of exercise programs. The aim of this study was to identify genetic variants that are associated with the magnitude of V̇O 2 peak response following exercise training., Methods: Participant change in objectively measured V̇O 2 peak from 18 different interventions was obtained from a multi-centre study (Predict-HIIT). A genome-wide association study was completed (n = 507), and a polygenic predictor score (PPS) was developed using alleles from single nucleotide polymorphisms (SNPs) significantly associated (P < 1 × 10 -5 ) with the magnitude of V̇O 2 peak response. Findings were tested in an independent validation study (n = 39) and compared to previous research., Results: No variants at the genome-wide significance level were found after adjusting for key covariates (baseline V̇O 2 peak , individual study, principal components which were significantly associated with the trait). A Quantile-Quantile plot indicates there was minor inflation in the study. Twelve novel loci showed a trend of association with V̇O 2 peak response that reached suggestive significance (P < 1 × 10 -5 ). The strongest association was found near the membrane associated guanylate kinase, WW and PDZ domain containing 2 (MAGI2) gene (rs6959961, P = 2.61 × 10 -7 ). A PPS created from the 12 lead SNPs was unable to predict V̇O 2 peak response in a tenfold cross validation, or in an independent (n = 39) validation study (P > 0.1). Significant correlations were found for beta coefficients of variants in the Predict-HIIT (P < 1 × 10 -4 ) and the validation study (P <  × 10 -6 ), indicating that general effects of the loci exist, and that with a higher statistical power, more significant genetic associations may become apparent., Conclusions: Ongoing research and validation of current and previous findings is needed to determine if genetics does play a large role in V̇O 2 peak response variance, and whether genomic predictors for V̇O 2 peak response trainability can inform evidence-based clinical practice. Trial registration Australian New Zealand Clinical Trials Registry (ANZCTR), Trial Id: ACTRN12618000501246, Date Registered: 06/04/2018, http://www.anzctr.org.au/Trial/Registration/TrialReview.aspx?id=374601&isReview=true .

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 < 0.0001), and body weight/fat mass were unchanged. Peripheral insulin sensitivity (hyperinsulinemic-euglycemic clamp) was ~20% greater the day after the final exercise session compared to pretraining (P < 0.01), with no difference between HIIT and MICT. When trained participants abstained from exercise for 4 days, insulin sensitivity returned to pretraining levels in both groups. HIIT and MICT also induced similar increases in abundance of many skeletal muscle proteins involved in mitochondrial respiration and lipid and carbohydrate metabolism. Training-induced alterations in muscle lipid profile were also similar between groups., 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., (© Endocrine Society 2020. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)

Exercise-induced increases in peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) and p53 protein content in the nucleus mediate the initial phase of exercise-induced mitochondrial biogenesis. Here, we investigated whether exercise-induced increases in these and other markers of mitochondrial biogenesis were altered after 40 sessions of twice-daily high-volume, high-intensity interval training (HVT) in human skeletal muscle. Vastus lateralis muscle biopsies were collected from 10 healthy recreationally active participants before, immediately postexercise, and 3 h after a session of high-intensity interval exercise (HIIE) performed at the same absolute exercise intensity before and after HVT (pre-HVT and post-HVT, respectively). The protein content of common markers of exercise-induced mitochondrial biogenesis was assessed in nuclear- and cytosolic-enriched fractions by immunoblotting; mRNA contents of key transcription factors and mitochondrial genes were assessed by qPCR. Despite exercise-induced increases in PGC-1α, p53, and plant homeodomain finger-containing protein 20 (PHF20) protein content, the phosphorylation of p53 and acetyl-CoA carboxylase (p-p53 Ser 15 and p-ACC Ser 79 , respectively), and PGC-1α mRNA Pre-HVT, no significant changes were observed post-HVT. Forty sessions of twice-daily high-intensity interval training blunted all of the measured exercise-induced molecular events associated with mitochondrial biogenesis that were observed pre-HVT. Future studies should determine whether this loss relates to the decrease in relative exercise intensity, habituation to the same exercise stimulus, or a combination of both.

This review considers the physiological basis of brief vigorous exercise to improve health, with a focus on cardiorespiratory fitness (CRF) and glycaemic control, and the potential underlying mechanisms involved. We defined 'brief' as a protocol lasting ≤15 min including warm-up, cool-down and recovery, and involving a total of ≤5 min of 'vigorous' exercise, which was classified as meeting or exceeding the lower end of the range for this relative intensity as per the criteria from the American College of Sports Medicine. The physiological mechanisms responsible for the increase in CRF, as measured by maximal oxygen update ( V ̇ O 2 max ), after brief vigorous exercise are unclear and likely depend on various factors including the specific nature of the intervention as well as the time course of the response. Limited available evidence suggests the potential for an increased oxygen extraction by active muscle (i.e. greater arterio-venous oxygen difference), since an increase in V ̇ O 2 max has been reported after several weeks of brief vigorous exercise despite no measurable change in cardiac output. Emerging evidence indicates that brief vigorous exercise can improve glycaemic control, suggesting that this type of exercise could potentially play a role in the prevention and management of type 2 diabetes. The acute response is not well characterized but several studies have shown that several weeks of vigorous exercise improves estimates of insulin sensitivity as determined by various methods including by hyperinsulinaemic-euglycaemic clamp. The physiological mechanisms underlying improved CRF and glycaemic control after brief vigorous exercise, and the broader impact on health, remain fruitful areas of investigation., (© 2019 The Authors. The Journal of Physiology © 2019 The Physiological Society.)

A key pathological component of obesity is chronic low-grade inflammation, which is propagated by infiltration of immune cells into tissues and overproduction of pro-inflammatory cytokines. Cytokines that possess anti-inflammatory properties, such as interleukin (IL)-10 and IL6, may also play an important role. This study was designed to determine the impact of short-term exercise on the anti-inflammatory action of IL10 and IL6. Thirty-three inactive obese adults were randomized to two weeks of high-intensity interval training (HIIT) or moderate-intensity continuous training (MICT). Fasting blood samples were collected before and after training. Lipopolysaccharide (LPS)-induced tumor necrosis factor (TNF)-α production was measured in whole blood cultures in the presence or absence of IL10 or IL6. IL10 and IL6 receptor expression were measured on circulating monocytes, neutrophils, and T cells. HIIT and MICT reduced the ability of IL10 to inhibit LPS-induced TNFα production, with a greater effect with HIIT (Group × Time and IL10 × Time interactions, p's < 0.05). This reduction in IL10 function was not explained by altered IL10R1 expression, which was unchanged after training (p > 0.05). HIIT and MICT differentially affected IL6 function (Group × Time and IL6 × Time interactions, p's < 0.05) with evidence of reductions in the anti-inflammatory ability of IL6 with HIIT. Neither HIIT nor MICT altered levels of circulating IL10, IL6, or TNFα. The impact of short-term HIIT and MICT resulted in differential effects on anti-inflammatory cytokine function. The clinical implications remain to be determined but these novel findings indicate that measuring anti-inflammatory cytokine action could reveal important immunomodulatory effects of exercise., (Copyright © 2018 Elsevier Ltd. All rights reserved.)

Purpose: High-intensity interval training (HIIT) may lead to superior cardiometabolic improvements when compared with moderate-intensity continuous training (MICT). However, adherence to HIIT requires examination. The purpose of this pilot study was to examine moderate-to-vigorous physical activity (MVPA) adherence 24 wk after a brief counseling intervention combined with either HIIT or MICT., Methods: Individuals at high risk of type 2 diabetes (T2D) were randomized to HIIT (n = 15) or MICT (n = 17) and completed 10 exercise sessions accompanied by a brief 10-min counseling intervention over a 2-wk period. Objectively measured purposeful MVPA (accelerometry) and cardiorespiratory fitness (V˙O2peak) were assessed at baseline and 24 wk postintervention. Self-regulatory efficacy and task self-efficacy were examined at baseline, postintervention, and 24 wk postintervention. Using an intention-to-treat analysis, change scores were calculated for HIIT and MICT and compared between groups., Results: Individuals assigned to HIIT increased their MVPA by 53 min (Cohen's d = 1.52) at 24 wk compared with 19 min in MICT. Both HIIT and MICT increased relative V˙O2peak by 2 and 1 mL·kg·min, respectively. Participants in both groups increased in their self-regulatory and task self-efficacy postintervention, but both groups demonstrated similar decline at 24 wk., Conclusion: This pilot intervention was successful in increasing, and maintaining, free-living MVPA over a 24-wk period in individuals at high risk of T2D. Speculation that HIIT is inappropriate or unattainable for overweight individuals at high risk of T2D may be unfounded.

High-intensity interval training (HIIT) elicits health benefits but it is unclear how HIIT impacts sedentary behaviour. In this preliminary study, we compared the effects of supervised HIIT or moderate-intensity continuous training (MICT) on sedentary time in overweight/obese adults. In both groups, percentage of time spent in sedentary activities was significantly reduced during the supervised exercise intervention (time main effect, P = 0.03), suggesting that both HIIT and MICT replaced time spent previously being sedentary.

New Findings: What is the central question of this study? Does exercise training impact resting and postexercise cardiac troponin T (cTnT) concentration? What is the main finding and its importance? This randomized controlled intervention study demonstrated that 12 weeks of either high-intensity interval training or moderate-intensity continuous training largely abolished the exercise-induced elevation in cTnT when exercise was performed at the same absolute intensity. There was no impact of training on resting cTnT or postexercise appearance of cTnT when exercise was performed at the same relative intensity. These findings provide new information that might help clinicians with decision-making in relationship to basal and postexercise values of cTnT in individuals with different training status., Abstract: We evaluated the influence of 12 weeks of high-intensity interval training [HIIT; repeated 4 min cycling at 90% of maximal oxygen uptake (V̇O2max) interspersed with 3 min rest, 200-300 kJ per session, 3 or 4 days each week] and work-equivalent moderate-intensity continuous training (MICT; continuous cycling at 60% V̇O2max) on resting cardiac troponin T (cTnT) and the appearance of exercise-induced cTnT. Forty-eight sedentary obese young women were randomly assigned to HIIT, MICT or a control group. The V̇O2max and body composition were measured before and after training. At baseline, cTnT was assessed using a high-sensitivity assay at rest and immediately, 2 and 4 h after 45 min cycling at 60% V̇O2max. After a 12 week training period, cTnT was assessed before and after 45 min cycling at the same relative and absolute intensities as before training. Training led to higher V̇O2max and lower fat mass in both HIIT and MICT groups (all P < 0.05). Before training, cTnT was significantly elevated in all three groups (by 35-118%, all P < 0.05) with acute exercise. After training, both resting and postexercise cTnT concentrations (same relative intensity) were similar to pretraining values. In contrast, postexercise cTnT (same absolute intensity, which represented a smaller exercise stimulus) was not elevated from rest in both HIIT and MICT groups. In conclusion, 12 weeks of either HIIT or MICT largely abolished the postexercise elevation of cTnT concentration when exercise was performed at the same absolute intensity. There was, however, no impact of training on resting cTnT or postexercise appearance of cTnT for exercise performed at the same relative intensity., (© 2017 The Authors. Experimental Physiology © 2017 The Physiological Society.)

Background: Cardiorespiratory fitness (VO 2max ) is an excellent predictor of chronic disease morbidity and mortality risk. Guidelines recommend individuals undertake exercise training to improve VO 2max for chronic disease reduction. However, there are large inter-individual differences between exercise training responses. This systematic review is aimed at identifying genetic variants that are associated with VO 2max trainability., Methods: Peer-reviewed research papers published up until October 2016 from four databases were examined. Articles were included if they examined genetic variants, incorporated a supervised aerobic exercise intervention; and measured VO 2max /VO 2peak pre and post-intervention., Results: Thirty-five articles describing 15 cohorts met the criteria for inclusion. The majority of studies used a cross-sectional retrospective design. Thirty-two studies researched candidate genes, two used Genome-Wide Association Studies (GWAS), and one examined mRNA gene expression data, in addition to a GWAS. Across these studies, 97 genes to predict VO 2max trainability were identified. Studies found phenotype to be dependent on several of these genotypes/variants, with higher responders to exercise training having more positive response alleles than lower responders (greater gene predictor score). Only 13 genetic variants were reproduced by more than two authors. Several other limitations were noted throughout these studies, including the robustness of significance for identified variants, small sample sizes, limited cohorts focused primarily on Caucasian populations, and minimal baseline data. These factors, along with differences in exercise training programs, diet and other environmental gene expression mediators, likely influence the ideal traits for VO 2max trainability., Conclusion: Ninety-seven genes have been identified as possible predictors of VO 2max trainability. To verify the strength of these findings and to identify if there are more genetic variants and/or mediators, further tightly-controlled studies that measure a range of biomarkers across ethnicities are required.

This study investigated the impact of raising plasma beta-hydroxybutyrate (β-OHB) through ingestion of ketone salts on substrate oxidation and performance during cycling exercise. Ten healthy adult males (age, 23 ± 3 years; body mass index, 25 ± 3 kg/m 2 , peak oxygen uptake, 45 ± 10 mL/(kg·min) -1 ) were recruited to complete 2 experimental trials. Before enrollment in the experimental conditions, baseline anthropometrics and cardiorespiratory fitness (peak oxygen uptake) were assessed and familiarization to the study protocol was provided. On experimental days, participants reported to the laboratory in the fasted state and consumed either 0.3 g/kg β-OHB ketone salts or a flavour-matched placebo at 30 min prior to engaging in cycling exercise. Subjects completed steady-state exercise at 30%, 60%, and 90% ventilatory threshold (VT) followed by a 150-kJ cycling time-trial. Respiratory exchange ratio (RER) and total substrate oxidation were derived from indirect calorimetry. Plasma glucose, lactate, and ketones were measured at baseline, 30 min post-supplement, post-steady-state exercise, and immediately following the time-trial. Plasma β-OHB was elevated from baseline and throughout the entire protocol in the ketone condition (p < 0.05). RER was lower at 30% and 60% VT in the ketone compared with control condition. Total fat oxidation was greater in the ketone versus control (p = 0.05). Average time-trial power output was ∼7% lower (-16 W, p = 0.029) in the ketone condition. Ingestion of ketone salts prior to exercise increases fat oxidation during steady-state exercise but impairs high-intensity exercise performance.

Metformin is used clinically to reduce fasting glucose with minimal effects on postprandial glucose. Postmeal exercise reduces postprandial glucose and may offer additional glucose-lowering benefit beyond that of metformin alone, yet controversy exists surrounding exercise and metformin interactions. It is currently unknown how postmeal exercise and metformin monotherapy in combination will affect postprandial glucose. Thus, we examined the independent and combined effects of postmeal exercise and metformin monotherapy on postprandial glucose. A randomized crossover design was used to assess the influence of postmeal exercise on postprandial glucose excursions in 10 people treated with metformin monotherapy (57 ± 10 yr, HbA 1C  = 6.3 ± 0.6%). Each participant completed the following four conditions: sedentary and postmeal exercise (5 × 10-min bouts of treadmill walking at 60% V̇o 2max ) with metformin and sedentary and postmeal exercise without metformin. Peak postprandial glucose within a 2-h time window and 2-h total area under the curve was assessed after a standardized breakfast meal, using continuous glucose monitoring. Postmeal exercise significantly blunted 2-h peak ( P = 0.001) and 2-h area under the curve ( P = 0.006), with the lowest peak postprandial glucose excursion observed with postmeal exercise and metformin combined ( P < 0.05 vs. all other conditions: metformin/sedentary: 12 ± 3.4, metformin/exercise: 9.7 ± 2.3, washout/sedentary: 13.3 ± 3.2, washout/exercise: 11.1 ± 3.4 mmol/l). Postmeal exercise and metformin in combination resulted in the lowest peak postprandial glucose excursion compared with either treatment modality alone. Exercise timed to the postprandial phase may be important for optimizing glucose control during metformin monotherapy. NEW & NOTEWORTHY The interactive effects of metformin and exercise on key physiological outcomes remain an area of controversy. Findings from this study show that the combination of metformin monotherapy and moderate-intensity postmeal exercise led to beneficial reductions in postprandial glucose excursions. Postmeal exercise may be a useful strategy for the management of postprandial glucose in people on metformin., (Copyright © 2017 the American Physiological Society.)

Aims: Type 2 diabetes treatment primarily focuses on reducing hyperglycemia, including postprandial glucose excursions. Hypoglycemic agents are used clinically to lower fasting and postprandial glucose. Metformin is the first-line therapy; however, if metformin is inadequate then 'add-on' hypoglycemic agents are implemented. Postmeal exercise has been shown to lower postprandial glucose. The aim of this study was to assess if postmeal exercise provides additional glucose-lowering benefit, beyond medication alone, in those on add-on hypoglycemic agents., Methods: Postprandial glucose excursions in eight participants with type 2 diabetes (Age: 60±10.7, HbA 1C : 7.9±2.3) being treated with add-on hypoglycemic agents were assessed during both drug-treated sedentary and drug-treated postmeal exercise conditions. Continuous glucose monitoring was used to assess peak and area under the glucose curve (AUC) during exercise, as well as peak within a 2-h time window, 2-h total and 2-h incremental AUC after a standardized breakfast meal. Postmeal exercise consisted of 3×10-min intervals of treadmill walking at 50% maximal oxygen uptake., Results: Glucose peak (drug only: 13.8±3.7, drug/exercise: 9.9±2.7mmol/L; p=0.02) and AUC (drug only: 500±136, drug/exercise: 357±89mmol/L×40min; p=0.03) were reduced during postmeal exercise. Breakfast 2-h incremental AUC was also reduced (drug only: 585±291, drug/exercise: 330±294; p=0.047)., Discussion: Post-breakfast exercise lowered glucose during the exercise bout, although this effect was not sustained on later meals., (Copyright © 2017 Elsevier B.V. All rights reserved.)

Increased mitochondrial content and respiration have both been reported after exercise training. However, no study has directly compared how different training volumes influence mitochondrial respiration and markers of mitochondrial biogenesis. Ten healthy men performed high-intensity interval cycling during 3 consecutive training phases; 4 wk of normal-volume training (NVT; 3/wk), followed by 20 d of high-volume training (HVT; 2/d) and 2 wk of reduced-volume training (RVT; 5 sessions). Resting biopsy samples (vastus lateralis) were obtained at baseline and after each phase. No mitochondrial parameter changed after NVT. After HVT, mitochondrial respiration and citrate synthase activity (∼40-50%), as well as the protein content of electron transport system (ETS) subunits (∼10-40%), and that of peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α), NRF1, mitochondrial transcription factor A (TFAM), PHF20, and p53 (∼65-170%) all increased compared to baseline; mitochondrial specific respiration remained unchanged. After RVT, all the mitochondrial parameters measured except citrate synthase activity (∼36% above initial) were not significantly different compared to baseline (all P > 0.05). Our findings demonstrate that training volume is an important determinant of training-induced mitochondrial adaptations and highlight the rapid reversibility of human skeletal muscle to a reduction in training volume.-Granata, C., Oliveira, R. S. F., Little, J. P., Renner, K., Bishop, D. J. Mitochondrial adaptations to high-volume exercise training are rapidly reversed after a reduction in training volume in human skeletal muscle., (© FASEB.)

Major depressive disorder (MDD), schizophrenia (SCH), Alzheimer's disease (AD), and Parkinson's disease (PD) are devastating neurological disorders, which increasingly contribute to global morbidity and mortality. Although the pathogenic mechanisms of these conditions are quite diverse, chronic neuroinflammation is one underlying feature shared by all these diseases. Even though the specific root causes of these diseases remain to be identified, evidence indicates that the observed neuroinflammation is initiated by unique pathological features associated with each specific disease. If the initial acute inflammation is not resolved, a chronic neuroinflammatory state develops and ultimately contributes to disease progression. Chronic neuroinflammation is characterized by adverse and non-specific activation of glial cells, which can lead to collateral damage of nearby neurons and other glia. This misdirected neuroinflammatory response is hypothesized to contribute to neuropathology in MDD, SCH, AD, and PD. Physical activity (PA), which is critical for maintenance of whole body and brain health, may also beneficially modify neuroimmune responses. Since PA has neuroimmune-modifying properties, and the common underlying feature of MDD, SCH, AD, and PD is chronic neuroinflammation, we hypothesize that PA could minimize brain diseases by modifying glia-mediated neuroinflammation. This review highlights current evidence supporting the disease-altering potential of PA and exercise through modifications of neuroimmune responses, specifically in MDD, SCH, AD and PD., (Copyright © 2016 Elsevier Inc. All rights reserved.)

Background: Exercise helps individuals with prediabetes or type 2 diabetes (T2D) manage their blood glucose (BG); however, exercise adherence in this population is dismal. In this pilot study we tested the efficacy of a self-monitoring group-based intervention using continuous glucose monitors (CGMs) at increasing exercise adherence in individuals with impaired BG., Materials and Methods: Thirteen participants with prediabetes or T2D were randomized to an 8-week standard care exercise program (CON condition) (n = 7) or self-monitoring exercise intervention (SM condition) (n = 6). Participants in the SM condition were taught how to self-monitor their exercise and BG, to goal set, and to use CGM to observe how exercise influences BG. We hypothesized that compared with the CON condition, using a real-time CGM would facilitate self-monitoring behavior, resulting in increased exercise adherence., Results: Repeated-measures analysis of variance revealed significant Condition × Time interactions for self-monitoring (P < 0.01), goal setting (P = 0.01), and self-efficacy to self-monitor (P = 0.01), such that the SM condition showed greater increases in these outcomes immediately after the program and at the 1-month follow-up compared with the CON condition. The SM condition had higher program attendance rates (P = 0.03), and a greater proportion of participants reregistered for additional exercise programs (P = 0.048) compared with the CON condition. Participants in both conditions experienced improvements in health-related quality of life, waist circumference, and fitness (P values <0.05)., Conclusions: These findings provide promising initial support for the use of a real-time CGM to foster self-monitoring and exercise behavior in individuals living with prediabetes or T2D.

Exercise training has been associated with increased mitochondrial content and respiration. However, no study to date has compared in parallel how training at different intensities affects mitochondrial respiration and markers of mitochondrial biogenesis. Twenty-nine healthy men performed 4 wk (12 cycling sessions) of either sprint interval training [SIT; 4-10 × 30-s all-out bouts at ∼200% of peak power output (WPeak)], high-intensity interval training (HIIT; 4-7 × 4-min intervals at ∼90% WPeak), or sublactate threshold continuous training (STCT; 20-36 min at ∼65% WPeak). The STCT and HIIT groups were matched for total work. Resting biopsy samples (vastus lateralis) were obtained before and after training. The maximal mitochondrial respiration in permeabilized muscle fibers increased significantly only after SIT (25%). Similarly, the protein content of peroxisome proliferator-activated receptor γ coactivator (PGC)-1α, p53, and plant homeodomain finger-containing protein 20 (PHF20) increased only after SIT (60-90%). Conversely, citrate synthase activity, and the protein content of TFAM and subunits of the electron transport system complexes remained unchanged throughout. Our findings suggest that training intensity is an important factor that regulates training-induced changes in mitochondrial respiration and that there is an apparent dissociation between training-induced changes in mitochondrial respiration and mitochondrial content. Moreover, changes in the protein content of PGC-1α, p53, and PHF20 are more strongly associated with training-induced changes in mitochondrial respiration than mitochondrial content., (© FASEB.)

Exercise can have anti-inflammatory effects in obesity, but the optimal type and intensity of exercise are not clear. This study compared short-term high-intensity interval training (HIIT) with moderate-intensity continuous training (MICT) in terms of improvement in cardiorespiratory fitness, markers of inflammation, and glucose control in previously inactive adults at elevated risk of developing type 2 diabetes. Thirty-nine inactive, overweight/obese adults (32 women) were randomly assigned to 10 sessions over 2 wk of progressive HIIT (n = 20, four to ten 1-min sessions at ∼90% peak heart rate, 1-min rest periods) or MICT (n = 19, 20-50 min at ∼65% peak heart rate). Before and 3 days after training, participants performed a peak O2 uptake test, and fasting blood samples were obtained. Both HIIT (1.8 ± 0.4 vs. 1.9 ± 0.4 l/min, pre vs. post) and MICT (1.8 ± 0.5 vs. 1.9 ± 0.5 l/min, pre vs. post) improved peak O2 uptake (P < 0.001) and lowered plasma fructosamine (P < 0.05). Toll-like receptor (TLR) 4 (TLR4) expression was reduced on lymphocytes and monocytes after both HIIT and MICT (P < 0.05) and on neutrophils after MICT (P < 0.01). TLR2 on lymphocytes was reduced after HIIT and MICT (P < 0.05). Plasma inflammatory cytokines were unchanged after training in both groups, but MICT led to a reduction in fasting plasma glucose (P < 0.05, 5.9 ± 1.0 vs. 5.6 ± 1.0 mmol/l, pre vs. post). Ten days of either HIIT or MICT can improve cardiorespiratory fitness and glucose control and lead to reductions in TLR2 and TLR4 expression. MICT, which involved a longer duration of exercise, may be superior for reducing fasting glucose., (Copyright © 2015 the American Physiological Society.)

High-intensity interval training (HIIT) has many known physiological benefits, but research investigating the psychological aspects of this training is limited. The purpose of the current study is to investigate the affective and enjoyment responses to continuous and high-intensity interval exercise sessions. Twenty overweight-to-obese, insufficiently active adults completed four counterbalanced trials: a 20-min trial of heavy continuous exercise and three 24-min HIIT trials that used 30-s, 60-s, and 120-s intervals. Affect declined during all trials (p < .05), but affect at the completion of trials was more positive in the shorter interval trials (p < .05). Enjoyment declined in the 120-s interval and heavy continuous conditions only (p < .05). Postexercise enjoyment was higher in the 60-s trial than in the 120-s trial and heavy continuous condition (p < .05). Findings suggest that pleasure and enjoyment are higher during shorter interval trials than during a longer interval or heavy continuous exercise.

Background: An acute bout of exercise can improve endothelial function and insulin sensitivity when measured on the day following exercise. Our aim was to compare acute high-intensity continuous exercise (HICE) to high-intensity interval exercise (HIIE) on circulating endothelial microparticles (EMPs) and insulin sensitivity in overweight/obese men and women., Methods: Inactive males (BMI = 30 ± 3, 25 ± 6 yr, n = 6) and females (BMI = 28 ± 2, 21 ± 3 yr, n = 7) participated in three experimental trials in a randomized counterbalanced crossover design: 1) No exercise control (Control); 2) HICE (20 min cycling @ just above ventilatory threshold); 3) HIIE (10 X 1-min @ ∼ 90% peak aerobic power). Exercise conditions were matched for external work and diet was controlled post-exercise. Fasting blood samples were obtained ∼ 18 hr after each condition. CD62E(+) and CD31(+)/CD42b- EMPs were assessed by flow cytometry and insulin resistance (IR) was estimated by homeostasis model assessment (HOMA-IR)., Results: There was a significant sex X exercise interaction for CD62E(+) EMPs, CD31(+)/CD42b- EMPs, and HOMA-IR (all P < 0.05). In males, both HICE and HIIE reduced EMPs compared to Control (P ≤ 0.05). In females, HICE increased CD62E(+) EMPs (P < 0.05 vs. Control) whereas CD31(+)/CD42b- EMPs were unaltered by either exercise type. There was a significant increase in HOMA-IR in males but a decrease in females following HIIE compared to Control (P<0.05)., Conclusions: Overweight/obese males and females appear to respond differently to acute bouts of high-intensity exercise. A single session of HICE and HIIE reduced circulating EMPs measured on the morning following exercise in males but in females CD62E(+) EMPs were increased following HICE. Next day HOMA-IR paradoxically increased in males but was reduced in females following HIIE. Future research is needed to investigate mechanisms responsible for potential differential responses between males and females.

Aims: High-intensity interval training (HIIT) leads to improvements in various markers of cardiometabolic health but adherence to HIIT following a supervised laboratory intervention has yet to be tested. We compared self-report and objective measures of physical activity after one month of independent exercise in individuals with prediabetes who were randomized to HIIT (n = 15) or traditional moderate-intensity continuous training (MICT, n = 17)., Method: After completing 10 sessions of supervised training participants were asked to perform HIIT or MICT three times per week for four weeks., Results: Individuals in HIIT (89 ± 11%) adhered to their prescribed protocol to a greater extent than individuals in MICT (71 ± 31%) as determined by training logs completed over one-month follow-up (P = 0.05, Cohen's d = 0.75). Minutes spent in vigorous physical activity per week measured by accelerometer were higher in HIIT (24 ± 18) as compared to MICT (11 ± 10) at one-month follow-up (P = 0.049, Cohen's d = 0.92). Cardiorespiratory fitness and systolic blood pressure assessed at one-month follow-up were equally improved (P's < 0.05)., Conclusions: This study provides preliminary evidence that individuals with prediabetes can adhere to HIIT over the short-term and do so at a level that is greater than MICT.

Affect experienced during an exercise session is purported to predict future exercise behaviour. Compared to continuous moderate-intensity exercise (CMI), the affective response to continuous vigorous-intensity exercise (CVI) has consistently been shown to be more aversive. The affective response, and overall tolerability to high-intensity interval training (HIT), is less studied. To date, there has yet to be a comparison between HIT, CVI, and CMI. The purpose of this study was to compare the tolerability and affective responses during HIT to CVI and CMI. This study utilized a repeated measures, randomized, counter-balanced design. Forty-four participants visited the laboratory on four occasions. Baseline fitness testing was conducted to establish peak power output in Watts (W peak). Three subsequent visits involved a single bout of a) HIT, corresponding to 1-minute at ∼ 100% W peak and 1-minute at ∼ 20% W peak for 20 minutes, b) CMI, corresponding to ∼ 40% W peak for 40 minutes, and c) CVI, corresponding to ∼ 80% W peak for 20 minutes. The order of the sessions was randomized. Affective responses were measured before, during and after each session. Task self-efficacy, intentions, enjoyment and preference were measured after sessions. Participants reported greater enjoyment of HIT as compared to CMI and CVI, with over 50% of participants reporting a preference to engage in HIT as opposed to either CMI or CVI. HIT was considered more pleasurable than CVI after exercise, but less pleasurable than CMI at these times. Despite this participants reported being just as confident to engage in HIT as they were CMI, but less confident to engage in CVI. This study highlights the utility of HIT in inactive individuals, and suggests that it may be a viable alternative to traditionally prescribed continuous modalities of exercise for promoting self-efficacy and enjoyment of exercise.

High-intensity interval training (HIIT) has garnered attention in recent years as a time-efficient exercise option for improving cardiovascular and metabolic health. New research demonstrates that HIIT may be particularly effective for improving postprandial hyperglycemia in individuals with, or at risk for, type 2 diabetes (T2D). These findings have clinical relevance because elevated postprandial hyperglycemia is a significant risk factor for cardiovascular morbidity and mortality. This article summarizes the latest evidence demonstrating that HIIT can improve postprandial glucose control to highlight the potential application of HIIT in the prevention and management of T2D and associated cardiovascular complications.

The purpose of this study was to examine the impact of acute high-intensity interval training (HIIT) compared with continuous moderate-intensity (CMI) exercise on postprandial hyperglycemia in overweight or obese adults. Ten inactive, overweight or obese adults (41 ± 11 yrs, BMI = 36 ± 7 kg/m(2)) performed an acute bout of HIIT (10 × 1 min at approximately 90% peak heart rate (HRpeak) with 1-min recovery periods) or matched work CMI (30 min at approximately 65% HRpeak) in a randomized, counterbalanced fashion. Exercise was performed 2 h after breakfast, and glucose control was assessed by continuous glucose monitoring under standardized dietary conditions over 24 h. Postprandial glucose (PPG) responses to lunch, dinner, and the following day's breakfast were analyzed and compared with a no-exercise control day. Exercise did not affect the PPG responses to lunch, but performing both HIIT and CMI in the morning significantly reduced the PPG incremental area under the curve (AUC) following dinner when compared with control (HIIT = 110 ± 35, CMI = 125 ± 34, control = 162 ± 46 mmol/L × 2 h, p < 0.05). The PPG AUC (HIIT = 125 ± 53, CMI = 186 ± 55, control = 194 ± 96 mmol/L × 2 h) and the PPG spike (HIIT = Δ2.1 ± 0.9, CMI = Δ3.0 ± 0.9, control = Δ3.0 ± 1.5 mmol/l) following breakfast on the following day were significantly lower following HIIT compared with both CMI and control (p < 0.05). Absolute AUC and absolute glucose spikes were not different between HIIT, CMI, or control for any meal (p > 0.05 for all). We conclude that a single session of HIIT has greater and more lasting effects on reducing incremental PPG when compared with CMI.

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., (© 2014 The Authors. Experimental Physiology © 2014 The Physiological Society.)

The purpose of this study was to investigate the acute effects of endurance exercise (END; 65% V̇O2peak for 60 min) and high-intensity interval exercise (HIE; four 30 s Wingates separated by 4.5 min of active rest) on cardiorespiratory, hormonal, and subjective appetite measures that may account for the previously reported superior fat loss with low volume HIE compared with END. Recreationally active males (n = 18) completed END, HIE, and control (CON) protocols. On each test day, cardiorespiratory measures including oxygen uptake (V̇O2), respiratory exchange ratio (RER), and heart rate were recorded and blood samples were obtained at baseline (BSL), 60 min after exercise, and 180 min after exercise (equivalent times for CON). Subjective measures of appetite (hunger, fullness, nausea, and prospective consumption) were assessed using visual analogue scales, administered at BSL, 0, 60, 120, and 180 min after exercise. No significant differences in excess postexercise oxygen consumption (EPOC) were observed between conditions. RER was significantly (P < 0.05) depressed in HIE compared with CON at 60 min after exercise, yet estimates of total fat oxidation over CON were not different between HIE and END. No differences in plasma adiponectin concentrations between protocols or time points were present. Epinephrine and norepinephrine were significantly (P < 0.05) elevated immediately after exercise in HIE compared with CON. Several subjective measures of appetite were significantly (P < 0.05) depressed immediately following HIE. Our data indicate that increases in EPOC or fat oxidation following HIE appear unlikely to contribute to the reported superior fat loss compared with END.

Type 2 diabetes has progressed into a major contributor to preventable death, and developing optimal therapeutic strategies to prevent future type 2 diabetes and its primary clinical manifestation of cardiovascular disease is a major public health challenge. This article will provide a brief overview of the role of activity and exercise in modulating insulin sensitivity and will outline the effect of physical activity, high-intensity interval training, and resistance training on insulin sensitivity and glycemic control.

Muscle activation as well as changes in peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC-1α) following high-intensity interval exercise (HIIE) were examined in young healthy men (n  = 8; age, 21.9±2.2 yrs; VO2peak, 53.1±6.4 ml/min/kg; peak work rate, 317±23.5 watts). On each of 3 visits HIIE was performed on a cycle ergometer at a target intensity of 73, 100, or 133% of peak work rate. Muscle biopsies were taken at rest and three hours after each exercise condition. Total work was not different between conditions (∼730 kJ) while average power output (73%, 237±21; 100%, 323±26; 133%, 384±35 watts) and EMG derived muscle activation (73%, 1262±605; 100%, 2089±737; 133%, 3029±1206 total integrated EMG per interval) increased in an intensity dependent fashion. PGC-1α mRNA was elevated after all three conditions (p<0.05), with a greater increase observed following the 100% condition (∼9 fold, p<0.05) compared to both the 73 and 133% conditions (∼4 fold). When expressed relative to muscle activation, the increase in PGC-1α mRNA for the 133% condition was less than that for the 73 and 100% conditions (p<0.05). SIRT1 mRNA was also elevated after all three conditions (∼1.4 fold, p<0.05), with no difference between conditions. These findings suggest that intensity-dependent increases in PGC-1α mRNA following submaximal exercise are largely due to increases in muscle recruitment. As well, the blunted response of PGC-1α mRNA expression following supramaximal exercise may indicate that signalling mediated activation of PGC-1α may also be blunted. We also indentify that increases in PDK4, SIRT1, and RIP140 mRNA following acute exercise are dissociated from exercise intensity and muscle activation, while increases in EGR1 are augmented with supramaximal HIIE (p<0.05).

Lower skeletal muscle mitochondrial oxidative phosphorylation capacity (OXPHOS) and intramyocellular lipid (IMCL) accumulation have been implicated in the etiology of insulin resistance (IR) in obesity. The purpose of this study was to examine the impact of endurance exercise on biochemical and morphological measures of IMCL and mitochondrial content, and their relationship to IR in obese individuals. We examined mitochondrial content (subunit protein abundance and maximal activity of electron transport chain enzymes), IMCL/mitochondrial morphology in both subsarcolemmal (SS) and intermyofibrillar (IMF) regions by transmission electron microscopy, and intracellular lipid metabolites (diacylglycerol and ceramide) in vastus lateralis biopsies, as well as, the homeostasis model assessment index of IR (HOMA-IR) prior to and following twelve weeks of an endurance exercise regimen in healthy age- and physical activity-matched lean and obese men. Obese men did not show evidence of mitochondrial OXPHOS dysfunction, disproportionate IMCL content in sub-cellular regions, or diacylglycerol/ceramide accretion despite marked IR vs. lean controls. Endurance exercise increased OXPHOS and mitochondrial size and density, but not number of individual mitochondrial fragments, with moderate improvements in HOMA-IR. Exercise reduced SS IMCL content (size, number and density), increased IMF IMCL content, while increasing IMCL/mitochondrial juxtaposition in both regions. HOMA-IR was inversely associated with SS (r = -0.34; P = 0.051) and IMF mitochondrial density (r = -0.29; P = 0.096), IMF IMCL/mitochondrial juxtaposition (r = -0.30; P = 0.086), and COXII (r = -0.32; P = 0.095) and COXIV protein abundance (r = -0.35; P = 0.052); while positively associated with SS IMCL size (r = 0.28; P = 0.119) and SS IMCL density (r = 0.25; P = 0.152). Our findings suggest that once physical activity and cardiorespiratory fitness have been controlled for, skeletal muscle mitochondrial and IMCL profile in obesity may only partially contribute to the development of IR.

The current study evaluated changes in aerobic fitness and muscular endurance following endurance training and very low volume, whole-body, high-intensity, interval-style aerobic-resistance training. Subjects' enjoyment and implementation intentions were also examined prior to and following training. Subjects (22 recreationally active females (20.3 ± 1.4 years)) completed 4 weeks of exercise training 4 days per week consisting of either 30 min of endurance treadmill training (~85% maximal heart rate; n = 7) or whole-body aerobic-resistance training involving one set of 8 × 20 s of a single exercise (burpees, jumping jacks, mountain climbers, or squat thrusts) separated by 10 s of rest per session (n = 7). A third group was assigned to a nontraining control group (n = 8). Following training, [Formula: see text]O(2peak) was increased in both the endurance (~7%) and interval (~8%) groups (p < 0.05), whereas muscle endurance was improved (p < 0.05) in the interval group (leg extensions, +40%; chest presses, +207%; sit-ups, +64%; push-ups, +135%; and back extensions, +75%). Perceived enjoyment of, and intentions to engage in, very low volume, high-intensity, whole-body interval exercise were both increased following training (p < 0.05). No significant changes were observed for any variable in the control (nontraining) group. These data demonstrate that although improvements in cardiovascular fitness are induced by both endurance and extremely low volume interval-style training, whole-body aerobic-resistance training imparted addition benefit in the form of improved skeletal muscle endurance.

Skeletal muscle mass declines with age (i.e., sarcopenia) resulting in muscle weakness and functional limitations. Sarcopenia has been associated with physiological changes in muscle morphology, protein and hormonal kinetics, insulin resistance, inflammation, and oxidative stress. The purpose of this review is to highlight how exercise and nutritional intervention strategies may benefit aging muscle. It is well known that resistance exercise training increases muscle strength and size and evidence also suggests that resistance training can increase mitochondrial content and decrease oxidative stress in older adults. Recent findings suggest that fast-velocity resistance exercise may be an effective intervention for older adults to enhance muscle power and functional capacity. Aerobic exercise training may also benefit aging skeletal muscle by enhancing mitochondrial bioenergetics, improving insulin sensitivity, and/or decreasing oxidative stress. In addition to exercise, creatine monohydrate, milk-based proteins, and essential fatty acids all have biological effects which could enhance some of the physiological adaptations from exercise training in older adults. Additional research is needed to determine whether skeletal muscle adaptations to increased activity in older adults are further enhanced with effective nutritional interventions and whether this is due to enhanced muscle protein synthesis, improved mitochondrial function, and/or a reduced inflammatory response.

Exercise training is a clinically proven, cost-effective, primary intervention that delays and in many cases prevents the health burdens associated with many chronic diseases. However, the precise type and dose of exercise needed to accrue health benefits is a contentious issue with no clear consensus recommendations for the prevention of inactivity-related disorders and chronic diseases. A growing body of evidence demonstrates that high-intensity interval training (HIT) can serve as an effective alternate to traditional endurance-based training, inducing similar or even superior physiological adaptations in healthy individuals and diseased populations, at least when compared on a matched-work basis. While less well studied, low-volume HIT can also stimulate physiological remodelling comparable to moderate-intensity continuous training despite a substantially lower time commitment and reduced total exercise volume. Such findings are important given that 'lack of time' remains the most commonly cited barrier to regular exercise participation. Here we review some of the mechanisms responsible for improved skeletal muscle metabolic control and changes in cardiovascular function in response to low-volume HIT. We also consider the limited evidence regarding the potential application of HIT to people with, or at risk for, cardiometabolic disorders including type 2 diabetes. Finally, we provide insight on the utility of low-volume HIT for improving performance in athletes and highlight suggestions for future research.

We aimed to determine if the time that muscle is under loaded tension during low intensity resistance exercise affects the synthesis of specific muscle protein fractions or phosphorylation of anabolic signalling proteins. Eight men (24 ± 1 years (sem), BMI = 26.5 ± 1.0 kg m(-2)) performed three sets of unilateral knee extension exercise at 30% of one-repetition maximum strength involving concentric and eccentric actions that were 6 s in duration to failure (SLOW) or a work-matched bout that consisted of concentric and eccentric actions that were 1 s in duration (CTL). Participants ingested 20 g of whey protein immediately after exercise and again at 24 h recovery. Needle biopsies (vastus lateralis) were obtained while fasted at rest and after 6, 24 and 30 h post-exercise in the fed-state following a primed, constant infusion of l-[ring-(13)C(6)]phenylalanine. Myofibrillar protein synthetic rate was higher in the SLOW condition versus CTL after 24-30 h recovery (P < 0.001) and correlated to p70S6K phosphorylation (r = 0.42, P = 0.02). Exercise-induced rates of mitochondrial and sarcoplasmic protein synthesis were elevated by 114% and 77%, respectively, above rest at 0-6 h post-exercise only in the SLOW condition (both P < 0.05). Mitochondrial protein synthesis rates were elevated above rest during 24-30 h recovery in the SLOW (175%) and CTL (126%) conditions (both P < 0.05). Lastly, muscle PGC-1α expression was increased at 6 h post-exercise compared to rest with no difference between conditions (main effect for time, P < 0.001). These data show that greater muscle time under tension increased the acute amplitude of mitochondrial and sarcoplasmic protein synthesis and also resulted in a robust, but delayed stimulation of myofibrillar protein synthesis 24-30 h after resistance exercise.

It has been known for more than 4 decades that exercise causes increases in skeletal muscle mitochondrial enzyme content and activity (i.e., mitochondrial biogenesis). Increasing evidence now suggests that exercise can induce mitochondrial biogenesis in a wide range of tissues not normally associated with the metabolic demands of exercise. Perturbations in mitochondrial content and (or) function have been linked to a wide variety of diseases, in multiple tissues, and exercise may serve as a potent approach by which to prevent and (or) treat these pathologies. In this context, the purpose of this review is to highlight the effects of exercise, and the underlying mechanisms therein, on the induction of mitochondrial biogenesis in skeletal muscle, adipose tissue, liver, brain, and kidney.

Receptor interacting protein 1 (RIP140) has recently been demonstrated to be a key player in the regulation of skeletal muscle mitochondrial content. We have shown that β-guanadinopropionic acid (β-GPA) feeding reduces RIP140 protein content and mRNA levels concomitant with increases in mitochondrial content (Williams DB, Sutherland LN, Bomhof MR, Basaraba SA, Thrush AB, Dyck DJ, Field CJ, Wright DC. Am J Physiol Endocrinol Metab 296: E1400-E1408, 2009). Since β-GPA feeding reduces high-energy phosphate levels and activates AMPK, alterations reminiscent of exercise, we hypothesized that exercise training would reduce RIP140 protein content. We further postulated that an acute bout of exercise, or interventions known to induce the expression of mitochondrial enzymes or genes involved in mitochondrial biogenesis, would result in decreases in nuclear RIP140 content. Two weeks of daily swim training increased markers of mitochondrial content in rat skeletal muscle independent of reductions in RIP140 protein. Similarly, high-intensity exercise training in humans failed to reduce RIP140 content despite increasing skeletal muscle mitochondrial enzymes. We found that 6 wk of daily 5-aminoimidazole-4-carboxamide-1-β-D-ribofuranoside (AICAR) injections had no effect on RIP140 protein content in rat skeletal muscle while RIP140 content from LKB1 knockout mice was unaltered despite reductions in mitochondria. An acute bout of exercise, AICAR treatment, and epinephrine injections increased the mRNA levels of PGC-1α, COXIV, and lipin1 independent of decreases in nuclear RIP140 protein. Surprisingly these interventions increased RIP140 mRNA expression. In conclusion our results demonstrate that decreases in RIP140 protein content are not required for exercise and AMPK-dependent increases in skeletal muscle mitochondrial content, nor do acute perturbations alter the cellular localization of RIP140 in parallel with the induction of genes involved in mitochondrial biogenesis.

Low-volume, high-intensity interval training (HIT) increases skeletal muscle mitochondrial capacity, yet little is known regarding potential mechanisms promoting this adaptive response. Our purpose was to examine molecular processes involved in mitochondrial biogenesis in human skeletal muscle in response to an acute bout of HIT. Eight healthy men performed 4 × 30-s bursts of all-out maximal intensity cycling interspersed with 4 min of rest. Muscle biopsy samples (vastus lateralis) were obtained immediately before and after exercise, and after 3 and 24 h of recovery. At rest, the majority of peroxisome proliferator-activated receptor γ coactivator (PGC)-1α, a master regulator of mitochondrial biogenesis, was detected in cytosolic fractions. Exercise activated p38 MAPK and AMPK in the cytosol. Nuclear PGC-1α protein increased 3 h into recovery from exercise, a time point that coincided with increased mRNA expression of mitochondrial genes. This was followed by an increase in mitochondrial protein content and enzyme activity after 24 h of recovery. These findings support the hypothesis that an acute bout of low-volume HIT activates mitochondrial biogenesis through a mechanism involving increased nuclear abundance of PGC-1α.

Consuming carbohydrate-rich meals before continuous endurance exercise improves performance, yet few studies have evaluated the ideal preexercise meal for high-intensity intermittent exercise, which is characteristic of many team sports. The authors' purpose was to investigate the effects of low- and high-glycemic-index (GI) meals on metabolism and performance during high-intensity, intermittent exercise. Sixteen male participants completed three 90-min high-intensity intermittent running trials in a single-blinded random order, separated by ~7 d, while fasted (control) and 2 hr after ingesting an isoenergetic low-GI (lentil), or high-GI (potato and egg white) preexercise meal. Serum free fatty acids were higher and insulin lower throughout exercise in the fasted condition (p < .05), but there were no differences in blood glucose during exercise between conditions. Distance covered on a repeated-sprint test at the end of exercise was significantly greater in the low-GI and high-GI conditions than in the control (p < .05). Rating of perceived exertion was lower in the low-GI condition than in the control (p = .01). In a subsample of 5 participants, muscle glycogen availability was greater in the low-and high-GI conditions versus fasted control before the repeated-sprint test (p < .05), with no differences between low and high GI. When exogenous carbohydrates are not provided during exercise both low- and high-GI preexercise meals improve high-intensity, intermittent exercise performance, probably by increasing the availability of muscle glycogen. However, the GI does not influence markers of substrate oxidation during high-intensity, intermittent exercise.

High-intensity interval training (HIT) induces skeletal muscle metabolic and performance adaptations that resemble traditional endurance training despite a low total exercise volume. Most HIT studies have employed 'all out', variable-load exercise interventions (e.g. repeated Wingate tests) that may not be safe, practical and/or well tolerated by certain individuals. Our purpose was to determine the performance, metabolic and molecular adaptations to a more practical model of low-volume HIT. Seven men (21 + or - 0.4 years, V(O2peak) = 46 + or - 2 ml kg(-1) min(-1)) performed six training sessions over 2 weeks. Each session consisted of 8-12 x 60 s intervals at approximately 100% of peak power output elicited during a ramp V(O2) peak test (355 + or - 10 W) separated by 75 s of recovery. Training increased exercise capacity, as assessed by significant improvements on both 50 kJ and 750 kJ cycling time trials (P < 0.05 for both). Skeletal muscle (vastus lateralis) biopsy samples obtained before and after training revealed increased maximal activity of citrate synthase (CS) and cytochrome c oxidase (COX) as well as total protein content of CS, COX subunits II and IV, and the mitochondrial transcription factor A (Tfam) (P < 0.05 for all). Nuclear abundance of peroxisome proliferator-activated receptor gamma co-activator 1alpha (PGC-1alpha) was approximately 25% higher after training (P < 0.05), but total PGC-1alpha protein content remained unchanged. Total SIRT1 content, a proposed activator of PGC-1alpha and mitochondrial biogenesis, was increased by approximately 56% following training (P < 0.05). Training also increased resting muscle glycogen and total GLUT4 protein content (both P < 0.05). This study demonstrates that a practical model of low volume HIT is a potent stimulus for increasing skeletal muscle mitochondrial capacity and improving exercise performance. The results also suggest that increases in SIRT1, nuclear PGC-1alpha, and Tfam may be involved in coordinating mitochondrial adaptations in response to HIT in human skeletal muscle.

Exercise training under conditions of reduced carbohydrate (CHO) availability has been reported to augment gains in skeletal muscle oxidative capacity; however, the underlying mechanisms are unclear. We examined the effect of manipulating CHO intake on the acute metabolic response to high-intensity interval exercise, including signaling cascades linked to mitochondrial biogenesis. Ten men performed two trials in random order separated by >or=1 wk. Each trial consisted of a morning (AM) and afternoon (PM) training session (5 x 4 min cycling at approximately 90-95% of heart rate reserve) separated by 3 h of recovery during which subjects ingested a high-CHO drink (HI-HI) or nonenergetic placebo (HI-LO) before PM exercise. Biopsies (vastus lateralis) revealed that muscle phosphocreatine and ATP content were similar after AM exercise but decreased to a greater extent during PM exercise in HI-LO vs. HI-HI. Phosphorylation of p38 mitogen-activated protein kinase (MAPK) and AMP-activated protein kinase (AMPK) increased approximately 4-fold and 2-fold, respectively, during AM exercise with no difference between conditions. After PM exercise, p38 MAPK phosphorylation was higher in HI-LO vs. HI-HI, whereas AMPK was not different between conditions. Peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1 alpha) gene expression increased approximately 8-fold during recovery from AM exercise and remained elevated during PM exercise with no differences between conditions. Cytochrome oxidase subunit 4 (COXIV) mRNA was also elevated 3 h after AM exercise, with no difference between conditions. These data provide evidence that p38 MAPK is a nutrient-sensitive signaling molecule that could be involved in the altered skeletal muscle adaptive response reported after exercise training under conditions of restricted CHO intake, but further research is required to confirm this hypothesis.

Unlabelled: The glycemic index (GI) of a preexercise meal may affect substrate utilization and performance during continuous exercise., Purpose: To examine the effects of low- and high-GI foods on metabolism and performance during high-intensity, intermittent exercise., Methods: Seven male athletes participated in three experimental trials (low-GI, high-GI, and fasted control) separated by approximately 7 days. Foods were consumed 3 h before (approximately 1.3 g x kg(-1) carbohydrate) and halfway through (approximately 0.2 g x kg(-1) carbohydrate) 90 min of intermittent treadmill running designed to simulate the activity pattern of soccer. Expired gas was collected during exercise to estimate substrate oxidation. Performance was assessed by the distance covered on five 1-min sprints during the last 15 min of exercise., Results: Respiratory exchange ratio was higher and fat oxidation lower during exercise in the high-GI condition compared with fasting (P < .05). The mean difference in total distance covered on the repeated sprint test between low GI and fasting (247 m; 90% confidence limits +/-352 m) represented an 81% (likely, probable) chance that the low-GI condition improved performance over fasting. The mean difference between high GI and fasted control (223 m; +/- 385 m) represented a 76% (likely, probable) chance of improved performance. There were no differences between low and high GI., Conclusions: When compared with fasting, both low- and high-GI foods consumed 3 h before and halfway through prolonged, high-intensity intermittent exercise improved repeated sprint performance. High-GI foods impaired fat oxidation during exercise but the GI did not appear to influence high-intensity, intermittent exercise performance.

Brief, intense exercise training may induce metabolic and performance adaptations comparable to traditional endurance training. However, no study has directly compared these diverse training strategies in a standardized manner. We therefore examined changes in exercise capacity and molecular and cellular adaptations in skeletal muscle after low volume sprint-interval training (SIT) and high volume endurance training (ET). Sixteen active men (21 +/- 1 years, ) were assigned to a SIT or ET group (n = 8 each) and performed six training sessions over 14 days. Each session consisted of either four to six repeats of 30 s 'all out' cycling at approximately 250% with 4 min recovery (SIT) or 90-120 min continuous cycling at approximately 65% (ET). Training time commitment over 2 weeks was approximately 2.5 h for SIT and approximately 10.5 h for ET, and total training volume was approximately 90% lower for SIT versus ET ( approximately 630 versus approximately 6500 kJ). Training decreased the time required to complete 50 and 750 kJ cycling time trials, with no difference between groups (main effects, P

Type 2 diabetes (T2D) is a complex and multifaceted condition clinically characterized by high blood glucose. The management of T2D requires a holistic approach, typically involving a combination of pharmacological interventions as well as lifestyle changes, such as incorporating regular exercise, within an overall patient-centred approach. However, several condition-specific and contextual factors can modulate the glucoregulatory response to acute or chronic exercise. In an era of precision medicine, optimizing exercise prescription in an effort to maximize glucose lowering effects holds promise for reducing the risk of T2D complications and improving the overall quality of life of individuals living with this condition. Reflecting on the main pathophysiological features of T2D, we review the evidence to highlight how factors related to exercise prescription can be modulated to target improved glucose control in T2D, including the frequency, intensity, total volume, and timing (e.g., pre- vs. post-prandial) of exercise, as well as exercise modality (e.g., aerobic vs. resistance training). We also propose a step-by-step, general framework for clinicians and practitioners on how to personalize exercise prescription to optimize glycemic control in individuals living with T2D. [ABSTRACT FROM AUTHOR]