Effects of reduced-volume of sprint interval training and the time course of physiological and performance adaptations

This study sought to determine the time course of training adaptations to two different sprint interval training programmes with the same sprint: rest ratio (1:8) but different sprint duration. Nine participants (M: 7; F: 2) were assigned to 15-s training group (15TG) consisting of 4 to 6 x 15-s sprints interspersed with 2-min recovery, whereas eight participants (M: 5; F: 3) were assigned to 30-s training group (30TG) consisting of 4 to 6 30-s sprints interspersed with 4-min recovery. Both groups performed their respective training twice per week over 9 weeks and changes in peak oxygen uptake (V̇O2peak) and time to exhaustion (TTE) were assessed every 3 weeks. Additional 8 healthy active adults (M: 6; F: 2) completed the performance assessments 9 weeks apart without performing training (control group, CON). Following 9 weeks of training, both groups improved V̇O2peak (15TG: 12.1%; 30TG: 12.8%, P < 0.05) and TTE (15TG: 16.2%; 30TG: 12.8%, P < 0.01) to a similar extent. However, while both groups showed the greatest gains in V̇O2peak at 3 weeks (15TG: 16.6%; 30TG: 17.0%, P < 0.001), those in TTE were greatest at 9 weeks. CON did not change any of performance variables following 9 weeks. This study demonstrated that whilst the changes in cardiorespiratory function plateau within several weeks with sprint interval training, endurance capacity (TTE) is more sensitive to such training over a longer time frame in moderately-trained individuals. Furthermore, a 50% reduction in sprint duration does not diminish overall training adaptations over 9 weeks

Influence of recovery intensity on oxygen demand and repeated sprint performance

AIM: This study aimed to determine effects of recovery intensity (passive, 20, 30 and 40%V̇ O2peak) on oxygen uptake kinetics, performance and blood lactate accumulation during repeated sprints. METHODS: 7 moderately-trained male participants (V̇O2peak: 48.1 ± 5.1 ml·kg-1·min-1) performed 4 x 30-s repeated Wingate tests on 4 separate occasions. RESULTS: Recovery of V̇ O2 between sprints was prolonged with recovery intensity (time required to reach 50% V̇O2peak: Passive: 50 ± 9; 20%: 81 ± 17; 30%: 130 ± 43; 40%: 188 ± 62 sec, P<0.001), while V̇O2-to-sprint work ratio was mainly increased by the higher intensities (Passive: 138 ± 17; 20%: 149 ± 14; 30%: 159 ± 15; 40%: 158 ± 17 ml·min-1·kJ-1, P=0.001). The decline in peak power tended to be greater in the higher intensity conditions during sprint 2 (Passive: 7.4 ± 5.4; 20%: 5.8 ± 7.9; 30%: 12.7 ± 7.4; 40%: 12.7 ± 5.5%, P=0.052), whereas average power was less decreased with recovery intensity during sprint 4 (Passive: 22.4 ± 8.9; 20%: 19.9 ± 6.1; 30%: 18.4 ± 7.3; 40%: 16.6 ± 6.2%, P=0.036). Blood lactate was not different with recovery intensity (P=0.251). CONCLUSION: The present study demonstrated that while the higher recovery intensities induce prolonged oxygen recovery and impaired peak power restoration during the initial sprints, those intensities provide a greater aerobic contribution to sprint performance, resulting in better power maintenance during the latter sprints

Anabolic resistance does not explain sarcopenia in patients with type 2 diabetes mellitus, compared with healthy controls, despite reduced mTOR pathway activity

BackgroundAgeing and type 2 diabetes mellitus (T2DM) are risk factors for skeletal muscle loss. We investigated whether anabolic resistance to feeding might underlie accelerated muscle loss in older people with T2DM and whether dysregulated mTOR signalling was implicated.Subjects8 obese men with T2DM, and 12 age-matched controls were studied (age 68±3 vs. 68±6y; BMI: 30±2 vs. 27±5 kg·m-2).MethodsBody composition was measured by dual-X-ray absorptiometry. Insulin and glucose were clamped at post-absorptive concentrations (13±2 vs. 9±3 mU·l-1; 7.4±1.9 vs. 4.6±0.4 mmol·l-1; T2DM vs. controls). Fractional synthetic rates (FSR) of myofibrillar and sarcoplasmic proteins were measured as the rate of incorporation of [13C] leucine during a primed, constant infusion of [1-13C] α-ketoisocaproic acid, 3 h after 10 or 20g of essential amino acids (EAA) were orally administered. Protein expression of total and phosphorylated mTOR signalling proteins was determined by Western blot analysis.ResultsDespite a significantly lower appendicular lean mass index and a greater fat mass index in T2DM vs. controls, basal myofibrillar and sarcoplasmic and post-prandial myofibrillar FSR were similar. After 20g EAA, stimulation of sarcoplasmic FSR was slightly blunted in T2DM patients. Furthermore, feeding 20g EAA increased phosphorylation of mTOR, p70S6k and 4E-BP1 by 60-100% in controls with no response observed in T2DM.ConclusionsThere was clear dissociation between changes in mTOR signalling versus changes in protein synthesis rates. However, the intact anabolic response of myofibrillar FSR to feeding in both groups suggests anabolic resistance may not explain accelerated muscle loss in T2DM

The effect of low volume sprint interval training in patients with non-alcoholic fatty liver disease

Objectives: Exercise is an important part of disease management in patients with non-alcoholic fatty liver disease (NAFLD), but adherence to current exercise recommendations is poor. Novel low-volume sprint interval training (SIT) protocols with total training time commitments of ≤30 min per week have been shown to improve cardiometabolic risk and functional capacity in healthy sedentary participants, but the efficacy of such protocols in the management of NAFLD remains unknown. The aim of the present study was to examine whether a low-volume SIT protocol can be used to improve liver function, insulin resistance, body composition, physical fitness, cognitive function and general well-being in patients with NAFLD.Methods: In the present study, 7 men and 2 women with NAFLD (age: 45±8 y, BMI: 28.7±4.1 kg·m−2) completed a 6-week control period followed by 6 weeks of twice-weekly SIT sessions (5-10×6-s ‘all-out’ cycle sprints). Body composition, blood pressure, liver function, metabolic function, functional capacity, cognitive function and quality of life were assessed at baseline, following the control period, and following the SIT intervention.Results: Walking speed during the walk test (+12%), estimated V̇O2max (+8%), verbal fluency (+44%), and blood platelet count (+12%; all p<0.05) significantly increased during the control period. These measures remained significantly raised compared to baseline following the SIT intervention, but did not significantly change any further compared to the post-control time-point. Diastolic blood pressure decreased from 87±10 to 77±8 mm Hg from the end of the control period to the end of the SIT intervention (p<0.05).Conclusion: This study does not support the use of 6 weeks of a low volume SIT protocol involving twice-weekly sessions with 5-10×6-s ‘all-out’ cycle sprints as an intervention for NAFLD disease management

Vitamin D3 supplementation combined with sprint interval training improves aerobic and anaerobic exercise performance over sprint interval training alone in recreational combat sport athletes

Objectives: Correcting vitamin D deficiency might improve aerobic and anaerobic exercise performance. However, it is unclear if vitamin D 3 supplementation can convey a positive ergogenic benefit to aerobic and anaerobic exercise performance when combined with sprint interval training (SIT). Methods: Twenty-seven recreational male combat sport athletes were recruited (age: 25 ± 5 years, stature: 178 ± 7 cm, weight: 77 ± 10 kg). Participants completed baseline haematocrit and haemoglobin testing, lower body and upper body VO 2peak testing and two consecutive lower and upper body Wingate tests separated by five minutes rest. Participants were randomly assigned to either the vitamin D 3 group (VITD) or placebo group (CON) and underwent 6 weeks of twice-weekly SIT and weekly supplementation (50,000 IU.week −1). Following the intervention, testing was repeated. Results: Haemoglobin (P &lt; 0.001), haematocrit (P &lt; 0.001) and LB VO 2peak (P = 0.016) increased in VITD, remaining unchanged in CON (haemoglobin P = 0.981; haematocrit P = 0.947, LB VO 2peak P = 0.750). UB VO 2peak was unchanged in both groups (P = 0.284). LB and UB time to exhaustion increased in both groups (P &lt; 0.001). LB oxygen kinetics was not affected in either group (P = 0.063) with UB oxygen kinetics improved in VITD (P = 0.028). LB and UB Wingate peak power improved in both groups (P &lt; 0.001). LB Wingate average power improved in both groups (P &lt; 0.001) with VITD increasing average power over CON. Conclusion: Given the results, supplementing 50,000 IU of vitamin D 3 per week for six weeks combined with six weeks of SIT may improve markers of aerobic and anaerobic performance in recreational male combat sport athletes. </p

Effect of an acute dose of omega-3 fish oil following exercise-induced muscle damage

Purpose The purpose of this double-blind, placebo-controlled study was to examine the effect of two fish oil supplements, one high in EPA (750 mg EPA, 50 mg DHA) and one low in EPA (150 mg EPA, 100 mg DHA), taken acutely as a recovery strategy following EIMD. Methods Twenty-seven physically active males (26 ± 4 year, 1.77 ± 0.07 m, 80 ± 10 kg) completed 100 plyometric drop jumps to induce muscle damage. Perceptual (perceived soreness) and functional (isokinetic muscle strength at 60° and 180° s−1, squat jump performance and countermovement jump performance) indices of EIMD were recorded before, and 1, 24, 48, 72, and 96h after the damaging protocol. Immediately after the damaging protocol, volunteers ingested either a placebo (Con), a low-EPA fish oil (Low EPA) or a high-EPA fish oil (High EPA) at a dose of 1 g per 10 kg body mass. Results A significant group main effect was observed for squat jump, with the High EPA group performing better than Con and Low EPA groups (average performance decrement, 2.1, 8.3 and 9.8%, respectively), and similar findings were observed for countermovement jump performance, (average performance decrement, 1.7, 6.8 and 6.8%, respectively, p = 0.07). Significant time, but no interaction main effects were observed for all functional and perceptual indices measured, although large effect sizes demonstrate a possible ameliorating effect of high dose of EPA fish supplementation (effect sizes ≥0.14). Conclusion This study indicates that an acute dose of high-EPA fish oil may ameliorate the functional changes following EIMD

Integration of microRNA changes in vivo identifies novel molecular features of muscle insulin resistance in type 2 diabetes

Skeletal muscle insulin resistance (IR) is considered a critical component of type II diabetes, yet to date IR has evaded characterization at the global gene expression level in humans. MicroRNAs (miRNAs) are considered fine-scale rheostats of protein-coding gene product abundance. The relative importance and mode of action of miRNAs in human complex diseases remains to be fully elucidated. We produce a global map of coding and non-coding RNAs in human muscle IR with the aim of identifying novel disease biomarkers. We profiled &gt;47,000 mRNA sequences and &gt;500 human miRNAs using gene-chips and 118 subjects (n = 71 patients versus n = 47 controls). A tissue-specific gene-ranking system was developed to stratify thousands of miRNA target-genes, removing false positives, yielding a weighted inhibitor score, which integrated the net impact of both up- and down-regulated miRNAs. Both informatic and protein detection validation was used to verify the predictions of in vivo changes. The muscle mRNA transcriptome is invariant with respect to insulin or glucose homeostasis. In contrast, a third of miRNAs detected in muscle were altered in disease (n = 62), many changing prior to the onset of clinical diabetes. The novel ranking metric identified six canonical pathways with proven links to metabolic disease while the control data demonstrated no enrichment. The Benjamini-Hochberg adjusted Gene Ontology profile of the highest ranked targets was metabolic (P &lt; 7.4 × 10-8), post-translational modification (P &lt; 9.7 × 10-5) and developmental (P &lt; 1.3 × 10-6) processes. Protein profiling of six development-related genes validated the predictions. Brain-derived neurotrophic factor protein was detectable only in muscle satellite cells and was increased in diabetes patients compared with controls, consistent with the observation that global miRNA changes were opposite from those found during myogenic differentiation. We provide evidence that IR in humans may be related to coordinated changes in multiple microRNAs, which act to target relevant signaling pathways. It would appear that miRNAs can produce marked changes in target protein abundance in vivo by working in a combinatorial manner. Thus, miRNA detection represents a new molecular biomarker strategy for insulin resistance, where micrograms of patient material is needed to monitor efficacy during drug or life-style interventions

Obesity-induced insulin resistance in human skeletal muscle is characterised by defective activation of p42/p44 MAP kinase

Insulin resistance (IR), an impaired cellular, tissue and whole body response to insulin, is a major pathophysiological defect of type 2 diabetes mellitus. Although IR is closely associated with obesity, the identity of the molecular defect(s) underlying obesity-induced IR in skeletal muscle remains controversial; reduced post-receptor signalling of the insulin receptor substrate 1 (IRS1) adaptor protein and downstream effectors such as protein kinase B (PKB) have previously been implicated. We examined expression and/or activation of a number of components of the insulin-signalling cascade in skeletal muscle of 22 healthy young men (with body mass index (BMI) range, 20–37 kg/m2). Whole body insulin sensitivity (M value) and body composition was determined by the hyperinsulinaemic (40 mU. min−1.m−2.), euglycaemic clamp and by dual energy X-ray absorptiometry (DEXA) respectively. Skeletal muscle (vastus lateralis) biopsies were taken before and after one hour of hyperinsulinaemia and the muscle insulin signalling proteins examined by western blot and immunoprecipitation assay. There was a strong inverse relationship between M-value and BMI. The most striking abnormality was significantly reduced insulin-induced activation of p42/44 MAP kinase, measured by specific assay, in the volunteers with poor insulin sensitivity. However, there was no relationship between individuals' BMI or M-value and protein expression/phosphorylation of IRS1, PKB, or p42/44 MAP kinase protein, under basal or hyperinsulinaemic conditions. In the few individuals with poor insulin sensitivity but preserved p42/44 MAP kinase activation, other signalling defects were evident. These findings implicate defective p42/44 MAP kinase signalling as a potential contributor to obesity-related IR in a non-diabetic population, although clearly multiple signalling defects underlie obesity associated IR

Use of Cis-[18F]Fluoro-Proline for Assessment of Exercise-Related Collagen Synthesis in Musculoskeletal Connective Tissue

Protein turnover in collagen rich tissue is influenced by exercise, but can only with difficulty be studied in vivo due to use of invasive procedure. The present study was done to investigate the possibility of applying the PET-tracer, cis-[18F]fluoro-proline (cis-Fpro), for non-invasive assessment of collagen synthesis in rat musculoskeletal tissues at rest and following short-term (3 days) treadmill running. Musculoskeletal collagen synthesis was studied in rats at rest and 24 h post-exercise. At each session, rats were PET scanned at two time points following injection of cis-FPro: (60 and 240 min p.i). SUV were calculated for Achilles tendon, calf muscle and tibial bone. The PET-derived results were compared to mRNA expression of collagen type I and III. Tibial bone had the highest SUV that increased significantly (p<0.001) from the early (60 min) to the late (240 min) PET scan, while SUV in tendon and muscle decreased (p<0.001). Exercise had no influence on SUV, which was contradicted by an increased gene expression of collagen type I and III in muscle and tendon. The clearly, visible uptake of cis-Fpro in the collagen-rich musculoskeletal tissues is promising for multi-tissue studies in vivo. The tissue-specific differences with the highest basal uptake in bone are in accordance with earlier studies relying on tissue incorporation of isotopic-labelled proline. A possible explanation of the failure to demonstrate enhanced collagen synthesis following exercise, despite augmented collagen type I and III transcription, is that SUV calculations are not sensitive enough to detect minor changes in collagen synthesis. Further studies including kinetic compartment modeling must be performed to establish whether cis-Fpro can be used for non-invasive in-vivo assessment of exercise-induced changes in musculoskeletal collagen synthesis

Appetite, gut hormone and energy intake responses to low volume sprint interval and traditional endurance exercise.

Sprint interval exercise improves several health markers but the appetite and energy balance response is unknown. This study compared the effects of sprint interval and endurance exercise on appetite, energy intake and gut hormone responses. Twelve healthy males [mean (SD): age 23 (3) years, body mass index 24.2 (2.9) kg m(-2), maximum oxygen uptake 46.3 (10.2) mL kg(-1) min(-1)] completed three 8 h trials [control (CON), endurance exercise (END), sprint interval exercise (SIE)] separated by 1 week. Trials commenced upon completion of a standardised breakfast. Sixty minutes of cycling at 68.1 (4.3) % of maximum oxygen uptake was performed from 1.75-2.75 h in END. Six 30-s Wingate tests were performed from 2.25-2.75 h in SIE. Appetite ratings, acylated ghrelin and peptide YY (PYY) concentrations were measured throughout each trial. Food intake was monitored from buffet meals at 3.5 and 7 h and an overnight food bag. Appetite (P 0.05). Therefore, relative energy intake (energy intake minus the net energy expenditure of exercise) was lower in END than that in CON (15.7 %; P = 0.006) and SIE (11.5 %; P = 0.082). An acute bout of endurance exercise resulted in lower appetite perceptions in the hours after exercise than sprint interval exercise and induced a greater 24 h energy deficit due to higher energy expenditure during exercise