ORCID Profile
0000-0002-5620-4788
Current Organisation
Deakin University
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Publisher: Informa UK Limited
Date: 19-07-2022
DOI: 10.1080/02640414.2022.2100676
Abstract: Training interventions often have small effects and are tested in small s les. We used a Bayesian approach to examine the change in jump distance after different resistance training programmes. Thirty-three 18- to 45-year-old males completed one of three lower limb resistance training programmes: deadlift (DL), hip thrust (HT) or back squat (BS). Horizontal and vertical jump performance was assessed over the training intervention. Examination of Bayesian posterior distributions for jump distance estimated that the probability of a change above a horizontal jump smallest worthwhile change (SWC) of 4.7 cm for the DL group was ~12%. For the HT and BS groups, the probability of a change above the SWC was ~87%. The probability of a change above a vertical jump SWC of 1.3 cm for the DL group was ~31%. For the HT and BS groups, the probability of a change above the vertical jump SWC was ~62% and ~67%, respectively. Our study illustrates that a Bayesian approach provides a rich inferential interpretation for small s le training studies with small effects. The extra information from such a Bayesian approach is useful to practitioners in Sport and Exercise Science where small effects are expected and s le size is often constrained.
Publisher: American Physiological Society
Date: 08-2010
DOI: 10.1152/AJPCELL.00438.2009
Abstract: Sodium pyruvate can increase mitochondrial biogenesis in C2C12 myoblasts in a peroxisome proliferator-activated receptor-γ coactivator-1α (PGC1α)-independent manner. The present study examined the effect of 72-h treatment with sodium pyruvate (5–50 mM) or sodium chloride (50 mM) as an osmotic control on the regulation of mitochondrial substrate metabolism and biogenesis in C2C12 myotubes. Pyruvate (50 mM) increased the levels of fatty acid oxidation enzymes (CD36, 61%, and β-oxidative enzyme 3-hydroxyacyl-CoA dehydrogenase, 54%) and the expression of cytochrome- c oxidase subunit I (220%) and cytochrome c (228%), consistent with its previous described role as a promoter of mitochondrial biogenesis. However, in contrast, pyruvate treatment reduced glucose transporter 4 (42%), phosphofructokinase (57%), and PGC1α (72%) protein content as well as PGC1α (48%) and PGC1β (122%) mRNA. The decrease in PGC1α was compensated for by an increase in the PGC1α-related coactivator (PRC 187%). Pyruvate treatment reduced basal and insulin-stimulated glucose uptake (41% and 31%, respectively) and palmitate uptake and oxidation (24% and 31%, respectively). The addition of the pyruvate dehydrogenase activator dichloroacetate (DCA) and the TCA precursor glutamine increased PGC1α expression (368%) and returned PRC expression to basal. Glucose uptake increased by 4.2-fold with DCA and glutamine and palmitate uptake increased by 18%. Coupled to this adaptation was an 80% increase in oxygen consumption. The data suggest that supraphysiological doses of pyruvate decrease mitochondrial function despite limited biogenesis and that anaplerotic agents can reverse this effect.
Publisher: Portland Press Ltd.
Date: 25-10-2007
DOI: 10.1042/BST0351168
Abstract: RONS (reactive oxygen and nitrogen species) have traditionally been perceived to be detrimental to the physiology of the cell, with reports citing mechanisms by which a range of proteins, lipids and DNA are damaged. Consequently, their action has been attributed to many pathologies and the aging process. Opposing these actions are the protective functions held by RONS, as highlighted in microbial destruction, and their role as important cellular signalling molecules. The present paper will focus on the newly emerging field of P2X7R (P2X7 receptor)-induced RONS generation and the current understanding of the signalling pathways from receptor to RONS generators.
Publisher: American Physiological Society
Date: 06-2017
DOI: 10.1152/AJPCELL.00026.2016
Abstract: Mutations in the gene that encodes the principal l-carnitine transporter, OCTN2, can lead to a reduced intracellular l-carnitine pool and the disease Primary Carnitine Deficiency. l-Carnitine supplementation is used therapeutically to increase intracellular l-carnitine. As AMPK and insulin regulate fat metabolism and substrate uptake, we hypothesized that AMPK-activating compounds and insulin would increase l-carnitine uptake in C2C12 myotubes. The cells express all three OCTN transporters at the mRNA level, and immunohistochemistry confirmed expression at the protein level. Contrary to our hypothesis, despite significant activation of PKB and 2DG uptake, insulin did not increase l-carnitine uptake at 100 nM. However, l-carnitine uptake was modestly increased at a dose of 150 nM insulin. A range of AMPK activators that increase intracellular calcium content [caffeine (10 mM, 5 mM, 1 mM, 0.5 mM), A23187 (10 μM)], inhibit mitochondrial function [sodium azide (75 μM), rotenone (1 μM), berberine (100 μM), DNP (500 μM)], or directly activate AMPK [AICAR (250 μM)] were assessed for their ability to regulate l-carnitine uptake. All compounds tested significantly inhibited l-carnitine uptake. Inhibition by caffeine was not dantrolene (10 μM) sensitive despite dantrolene inhibiting caffeine-mediated calcium release. Saturation curve analysis suggested that caffeine did not competitively inhibit l-carnitine transport. To assess the potential role of AMPK in this process, we assessed the ability of the AMPK inhibitor Compound C (10 μM) to rescue the effect of caffeine. Compound C offered a partial rescue of l-carnitine uptake with 0.5 mM caffeine, suggesting that AMPK may play a role in the inhibitory effects of caffeine. However, caffeine likely inhibits l-carnitine uptake by alternative mechanisms independently of calcium release. PKA activation or direct interference with transporter function may play a role.
Publisher: Wiley
Date: 2009
Publisher: Informa UK Limited
Date: 08-2021
DOI: 10.1080/17461391.2021.1953150
Abstract: Many athletes seek to enhance their performance using legal ergogenic aids, including ammonia inhalants (AIs). AIs trigger the inhalation reflex and increase blood pressure, respiration and heart rate but, despite their widespread use, there is little evidence for the benefits of AI on exercise performance. We aimed to determine the psychological and neuromuscular impact of acute ammonia inhalation. Fourteen non-resistance trained males completed three trials: control, experimental (AI), and sham. The order of the sham and experimental trials was randomised. Participants completed handgrip and knee extension maximal voluntary contractions (MVC), and countermovement jump (CMJ). Heart rate and alertness were recorded at rest and immediately following control, experimental or sham treatment, followed by functional performance measurements. Reaction time, electromechanical delay, rate of force development and peak force were calculated from MVCs, and peak power from CMJ. On completion of trials, perceived performance was recorded. Statistical significance was accepted at
Publisher: Wiley
Date: 05-2019
DOI: 10.1113/JP277893
Publisher: American Physiological Society
Date: 15-08-2014
DOI: 10.1152/AJPENDO.00674.2013
Abstract: The goal of the current work was to profile positive (mTORC1 activation, autocrine aracrine growth factors) and negative [AMPK, unfolded protein response (UPR)] pathways that might regulate overload-induced mTORC1 (mTOR complex 1) activation with the hypothesis that a number of negative regulators of mTORC1 will be engaged during a supraphysiological model of hypertrophy. To achieve this, mTORC1-IRS-1/2 signaling, BiP/CHOP/IRE1α, and AMPK activation were determined in rat plantaris muscle following synergist ablation (SA). SA resulted in significant increases in muscle mass of ∼4% per day throughout the 21 days of the experiment. The expression of the insulin-like growth factors (IGF) were high throughout the 21st day of overload. However, IGF signaling was limited, since IRS-1 and -2 were undetectable in the overloaded muscle from day 3 to day 9. The decreases in IRS-1/2 protein were paralleled by increases in GRB10 Ser 501/503 and S6K1 Thr 389 phosphorylation, two mTORC1 targets that can destabilize IRS proteins. PKB Ser 473 phosphorylation was higher from 3–6 days, and this was associated with increased TSC2 Thr 939 phosphorylation. The phosphorylation of TSC2 Thr1345 (an AMPK site) was also elevated, whereas phosphorylation at the other PKB site, Thr 1462 , was unchanged at 6 days. In agreement with the phosphorylation of Thr 1345 , SA led to activation of AMPKα1 during the initial growth phase, lasting the first 9 days before returning to baseline by day 12. The UPR markers CHOP and BiP were elevated over the first 12 days following ablation, whereas IRE1α levels decreased. These data suggest that during supraphysiological muscle loading at least three potential molecular brakes engage to downregulate mTORC1.
Publisher: Informa UK Limited
Date: 19-04-2021
Publisher: Wiley
Date: 05-2016
DOI: 10.14814/PHY2.12803
Publisher: Elsevier BV
Date: 09-2018
DOI: 10.1016/J.JACI.2017.10.024
Abstract: Food allergy naturally resolves in a proportion of food-allergic children without intervention however the underlying mechanisms governing the persistence or resolution of food allergy in childhood are not understood. This study aimed to define the innate immune profiles associated with egg allergy at age 1 year, determine the phenotypic changes that occur with the development of natural tolerance in childhood, and explore the relationship between early life innate immune function and serum vitamin D. This study used longitudinally collected PBMC s les from a population-based cohort of challenge-confirmed egg-allergic infants with either persistent or transient egg allergy outcomes in childhood to phenotype and quantify the functional innate immune response associated with clinical phenotypes of egg allergy. We show that infants with persistent egg allergy exhibit a unique innate immune signature, characterized by increased numbers of circulating monocytes and dendritic cells that produce more inflammatory cytokines both at baseline and following endotoxin exposure when compared with infants with transient egg allergy. Follow-up analysis revealed that this unique innate immune signature continues into childhood in those with persistent egg allergy and that increased serum vitamin D levels correlate with changes in innate immune profiles observed in children who developed natural tolerance to egg. Early life innate immune dysfunction may represent a key immunological driver and predictor of persistent food allergy in childhood. Serum vitamin D may play an immune-modulatory role in the development of natural tolerance.
Publisher: Wiley
Date: 2008
Publisher: American Physiological Society
Date: 11-2014
DOI: 10.1152/AJPENDO.00001.2014
Abstract: Skeletal muscle sirtuin 1 (SIRT1) expression is reduced under insulin-resistant conditions, such as those resulting from high-fat diet (HFD) feeding and obesity. Herein, we investigated whether constitutive activation of SIRT1 in skeletal muscle prevents HFD-induced muscle insulin resistance. To address this, mice with muscle-specific overexpression of SIRT1 (mOX) and wild-type (WT) littermates were fed a control diet (10% calories from fat) or HFD (60% of calories from fat) for 12 wk. Magnetic resonance imaging and indirect calorimetry were used to measure body composition and energy expenditure, respectively. Whole body glucose metabolism was assessed by oral glucose tolerance test, and insulin-stimulated glucose uptake was measured at a physiological insulin concentration in isolated soleus and extensor digitorum longus muscles. Although SIRT1 was significantly overexpressed in muscle of mOX vs. WT mice, body weight and percent body fat were similarly increased by HFD for both genotypes, and energy expenditure was unaffected by diet or genotype. Importantly, impairments in glucose tolerance and insulin-mediated activation of glucose uptake in skeletal muscle that occurred with HFD feeding were not prevented in mOX mice. In contrast, mOX mice showed enhanced postischemic cardiac functional recovery compared with WT mice, confirming the physiological functionality of the SIRT1 transgene in this mouse model. Together, these results demonstrate that activation of SIRT1 in skeletal muscle alone does not prevent HFD-induced glucose intolerance, weight gain, or insulin resistance.
Publisher: Frontiers Media SA
Date: 10-2015
Publisher: Proceedings of the National Academy of Sciences
Date: 13-03-2007
Abstract: Attainment of a brown adipocyte cell phenotype in white adipocytes, with their abundant mitochondria and increased energy expenditure potential, is a legitimate strategy for combating obesity. The unique transcriptional regulators of the primary brown adipocyte phenotype are unknown, limiting our ability to promote brown adipogenesis over white. In the present work, we used microarray analysis strategies to study primary preadipocytes, and we made the striking discovery that brown preadipocytes demonstrate a myogenic transcriptional signature, whereas both brown and white primary preadipocytes demonstrate signatures distinct from those found in immortalized adipogenic models. We found a plausible SIRT1-related transcriptional signature during brown adipocyte differentiation that may contribute to silencing the myogenic signature. In contrast to brown preadipocytes or skeletal muscle cells, white preadipocytes express Tcf21, a transcription factor that has been shown to suppress myogenesis and nuclear receptor activity. In addition, we identified a number of developmental genes that are differentially expressed between brown and white preadipocytes and that have recently been implicated in human obesity. The interlinkage between the myocyte and the brown preadipocyte confirms the distinct origin for brown versus white adipose tissue and also represents a plausible explanation as to why brown adipocytes ultimately specialize in lipid catabolism rather than storage, much like oxidative skeletal muscle tissue.
Publisher: Springer Science and Business Media LLC
Date: 10-07-2017
DOI: 10.1038/S41598-017-05483-X
Abstract: The mechanistic target of rapamycin (mTOR) is a central mediator of protein synthesis in skeletal muscle. We utilized immunofluorescence approaches to study mTOR cellular distribution and protein-protein co-localisation in human skeletal muscle in the basal state as well as immediately, 1 and 3 h after an acute bout of resistance exercise in a fed (FED 20 g Protein/40 g carbohydrate/1 g fat) or energy-free control (CON) state. mTOR and the lysosomal protein LAMP2 were highly co-localised in basal s les. Resistance exercise resulted in rapid translocation of mTOR/LAMP2 towards the cell membrane. Concurrently, resistance exercise led to the dissociation of TSC2 from Rheb and increased in the co-localisation of mTOR and Rheb post exercise in both FED and CON. In addition, mTOR co-localised with Eukaryotic translation initiation factor 3 subunit F (eIF3F) at the cell membrane post-exercise in both groups, with the response significantly greater at 1 h of recovery in the FED compared to CON. Collectively our data demonstrate that cellular trafficking of mTOR occurs in human muscle in response to an anabolic stimulus, events that appear to be primarily influenced by muscle contraction. The translocation and association of mTOR with positive regulators (i.e. Rheb and eIF3F) is consistent with an enhanced mRNA translational capacity after resistance exercise.
Publisher: Springer Science and Business Media LLC
Date: 28-06-2017
Abstract: The purpose of this study was to evaluate the independent and combined associations of moderate-to-vigorous physical activity (MVPA), leisure time sedentary behavior and daily protein consumption on lower extremity muscular strength and lean mass. Data from the 1999-2002 NHANES were utilized (N=1080 adults 50-85 y). Leg lean mass was estimated from dual-energy x-ray absorptiometry scans. Knee extensor strength was assessed objectively using the Kin Com MP dynamometer. MVPA and leisure time sedentary behavior were assessed via questionnaire, with the number of meals per day of ⩾30 g of protein per meal assessed via a 'multiple pass' 24-h dietary interview. Meeting MVPA guidelines (β=16.3, P=0.02) and consuming at least two meals per day of ⩾30 g of protein per meal (β=28.8, P=0.02) were independently associated with greater lower extremity strength, whereas sedentary behavior was not (β=11.6, P=0.23). Finally, there was no evidence of a three-way interaction of these behaviors on lower extremity strength (β=-8.7 P=0.70) or lower extremity lean mass (β=144.5 P=0.75). Although MVPA and frequency of protein consumption of ⩾30 g of protein per meal were independently associated with lower extremity lean mass and strength, the results of the present study do not provide evidence to suggest that there is a three-way interplay between MVPA, sedentary behavior and frequency of protein consumption ⩾30 g of protein per meal on lower extremity lean mass and strength.
Publisher: Springer Science and Business Media LLC
Date: 19-04-2013
Publisher: Wiley
Date: 13-07-2015
DOI: 10.1096/FJ.15-273474
Abstract: We examined how the stimulatory effect of leucine on the mechanistic target of rapamycin complex 1 (mTORC1) pathway is affected by the presence of the remaining essential amino acids (EAAs). Nine male subjects performed resistance exercise on 4 occasions and were randomly supplied EAAs with leucine, EAAs without leucine (EAA-Leu), leucine alone, or flavored water (placebo control). Muscle biopsies were taken from the vastus lateralis before and 60 and 90 min after exercise. Biopsies were analyzed for protein phosphorylation, kinase activity, protein-protein interactions, amino acid concentrations, and tracer incorporation. Leucine alone stimulated ribosomal protein s6 kinase 1 (S6K1) phosphorylation ∼280% more than placebo and EAA-Leu after exercise. Moreover, this response was enhanced by 60-75% after intake of EAAs compared with that of leucine alone (P < 0.05). Kinase activity of S6K1 reflected that of S6K1 phosphorylation 60 min after exercise, the activity was elevated 3.3- and 4.2-fold with intake of leucine alone and with EAAs, respectively (P < 0.05). The interaction between mammalian target of rapamycin and regulatory-associated protein of mammalian target of rapamycin was unaltered in response to both resistance exercise and amino acid provision. Leucine alone stimulates mTORC1 signaling, although this response is enhanced by other EAAs and does not appear to be caused by alterations in mTORC1 assembly.
Publisher: Springer Science and Business Media LLC
Date: 22-05-2014
Publisher: Wiley
Date: 08-2016
DOI: 10.14814/PHY2.12893
Publisher: No publisher found
Date: 2018
Abstract: We examined the effects of whey versus collagen protein on skeletal muscle cell signaling responses associated with mitochondrial biogenesis and protein synthesis in recovery from an acute training session completed with low carbohydrate availability. In a repeated-measures design (after adhering to a 36-hr exercise-dietary intervention to standardize preexercise muscle glycogen), eight males completed a 75-min nonexhaustive cycling protocol and consumed 22 g of a hydrolyzed collagen blend (COLLAGEN) or whey (WHEY) protein 45 min prior to exercise, 22 g during exercise, and 22 g immediately postexercise. Exercise decreased (p < .05) muscle glycogen content by comparable levels from pre- to postexercise in both trials (≈300-150 mmol/kg·dry weight). WHEY protein induced greater increases in plasma branched chain amino acids (p = .03) and leucine (p = .02) than COLLAGEN. Exercise induced (p .05) was observed for p53, Parkin, and Beclin1 mRNA. Exercise suppressed (p < .05) p70S6K1 activity in both conditions immediately postexercise (≈25 fmol·min
Publisher: Springer Science and Business Media LLC
Date: 04-07-2012
Publisher: American Physiological Society
Date: 02-2011
DOI: 10.1152/JAPPLPHYSIOL.00941.2010
Abstract: For over 10 years, we have known that the activation of the mammalian target of rapamycin complex 1 (mTORC1) has correlated with the increase in skeletal muscle size and strength that occurs following resistance exercise. Initial cell culture and rodent models of muscle growth demonstrated that the activation of mTORC1 is common to hypertrophy induced by growth factors and increased loading. The further observation that high loads increased the local production of growth factors led to the paradigm that resistance exercise stimulates the autocrine production of factors that act on membrane receptors to activate mTORC1, and this results in skeletal muscle hypertrophy. Over the last few years, there has been a paradigm shift. From both human and rodent studies, it has become clear that the phenotypic and molecular responses to resistance exercise occur in a growth factor-independent manner. Although the mechanism of load-induced mTORC1 activation remains to be determined, it is clear that it does not require classical growth factor signaling.
Publisher: Wiley
Date: 15-09-2015
DOI: 10.1113/JP271219
Publisher: Wiley
Date: 03-2016
DOI: 10.14814/PHY2.12715
Publisher: American Physiological Society
Date: 15-03-2015
DOI: 10.1152/AJPENDO.00486.2014
Abstract: Combining endurance and strength training in the same session has been reported to reduce the anabolic response to the latter form of exercise. The underlying mechanism, based primarily on results from rodent muscle, is proposed to involve AMPK-dependent inhibition of mTORC1 signaling. This hypothesis was tested in eight trained male subjects who in randomized order performed either resistance exercise only (R) or interval cycling followed by resistance exercise (ER). Biopsies taken from the vastus lateralis before and after endurance exercise and repeatedly after resistance exercise were assessed for glycogen content, kinase activity, protein phosphorylation, and gene expression. Mixed muscle fractional synthetic rate was measured at rest and during 3 h of recovery using the stable isotope technique. In ER, AMPK activity was elevated immediately after both endurance and resistance exercise (∼90%, P 0.05) but was unchanged in R. Thr 389 phosphorylation of S6K1 was increased severalfold immediately after exercise ( P 0.05) in both trials and increased further throughout recovery. After 90 and 180 min recovery, S6K1 activity was elevated (∼55 and ∼110%, respectively, P 0.05) and eukaryotic elongation factor 2 phosphorylation was reduced (∼55%, P 0.05) with no difference between trials. In contrast, markers for protein catabolism were differently influenced by the two modes of exercise ER induced a significant increase in gene and protein expression of MuRF1 ( P 0.05), which was not observed following R exercise only. In conclusion, cycling-induced elevation in AMPK activity does not inhibit mTOR complex 1 signaling after subsequent resistance exercise but may instead interfere with the hypertrophic response by influencing key components in protein breakdown.
Publisher: American Physiological Society
Date: 12-2017
DOI: 10.1152/AJPCELL.00176.2017
Abstract: Mechanistic target of rapamycin (mTOR) resides as two complexes within skeletal muscle. mTOR complex 1 [mTORC1–regulatory associated protein of mTOR (Raptor) positive] regulates skeletal muscle growth, whereas mTORC2 [rapamycin-insensitive companion of mTOR (Rictor) positive] regulates insulin sensitivity. To examine the regulation of these complexes in human skeletal muscle, we utilized immunohistochemical analysis to study the localization of mTOR complexes before and following protein-carbohydrate feeding (FED) and resistance exercise plus protein-carbohydrate feeding (EXFED) in a unilateral exercise model. In basal s les, mTOR and the lysosomal marker lysosomal associated membrane protein 2 (LAMP2) were highly colocalized and remained so throughout. In the FED and EXFED states, mTOR/LAMP2 complexes were redistributed to the cell periphery [wheat germ agglutinin (WGA)-positive staining] (time effect P = 0.025), with 39% (FED) and 26% (EXFED) increases in mTOR/WGA association observed 1 h post-feeding/exercise. mTOR/WGA colocalization continued to increase in EXFED at 3 h (48% above baseline) whereas colocalization decreased in FED (21% above baseline). A significant effect of condition ( P = 0.05) was noted suggesting mTOR/WGA colocalization was greater during EXFED. This pattern was replicated in Raptor/WGA association, where a significant difference between EXFED and FED was noted at 3 h post-exercise/feeding ( P = 0.014). Rictor/WGA colocalization remained unaltered throughout the trial. Alterations in mTORC1 cellular location coincided with elevated S6K1 kinase activity, which rose to a greater extent in EXFED compared with FED at 1 h post-exercise/feeding ( P 0.001), and only remained elevated in EXFED at the 3 h time point ( P = 0.037). Collectively these data suggest that mTORC1 redistribution within the cell is a fundamental response to resistance exercise and feeding, whereas mTORC2 is predominantly situated at the sarcolemma and does not alter localization.
Publisher: MDPI AG
Date: 19-06-2019
DOI: 10.3390/NU11061381
Abstract: Numerous United Kingdom and European Union expert panels recommend that the general adult population consumes ~250 mg of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) per day through the consumption of one portion of oily fish per week. The long-chain omega-3 fatty acids EPA and DHA are only found in appreciable amounts in marine organisms. Increasing oily fish consumption conflicts with sustaining fisheries, so alternative dietary sources of EPA and DHA must be explored. Mussels are high in omega-3 polyunsaturated fatty acids (PUFAs) and a good source of essential amino acids. Therefore, we aimed to investigate the impact of introducing mussels as a protein source in the lunchtime meal three times per week for two weeks on the omega-3 status of free-living participants. Following an initial two-week monitoring period, 12 participants (eight male and four female) attended the nutrition laboratory three times per week for two weeks. Each participant received a personalised lunch constituting one-third of their typical daily calorie consumption with ~20% of the calories supplied as cooked mussels. A portion of cooked mussels from each feeding occasion was tested for total omega-3 content. The mean ± SD mussel EPA + DHA content was 518.9 ± 155.7 mg/100 g cooked weight, meaning that each participant received on average 709.2 ± 252.6 mg of EPA + DHA per meal or 304.0 ± 108.2 mg of EPA + DHA per day. Blood spot analysis revealed a significant increase in the omega-3 index (week 1 = 4.27 ± 0.81 week 4 = 5.07 ± 1.00) and whole blood EPA content during the study (%EPA week 1 = 0.70 ± 0.0.35 %EPA week 4 = 0.98 ± 0.35). Consuming mussels three times per week for two weeks as the protein source in a personalised lunchtime meal is sufficient to moderately improve the omega-3 index and whole blood DHA + EPA content in young healthy adults.
Publisher: Elsevier BV
Date: 09-2016
DOI: 10.1016/J.FREERADBIOMED.2016.01.016
Abstract: Despite over 50 years of research, the field of sports nutrition continues to grow at a rapid rate. Whilst the traditional research focus was one that centred on strategies to maximise competition performance, emerging data in the last decade has demonstrated how both macronutrient and micronutrient availability can play a prominent role in regulating those cell signalling pathways that modulate skeletal muscle adaptations to endurance and resistance training. Nonetheless, in the context of exercise performance, it is clear that carbohydrate (but not fat) still remains king and that carefully chosen ergogenic aids (e.g. caffeine, creatine, sodium bicarbonate, beta-alanine, nitrates) can all promote performance in the correct exercise setting. In relation to exercise training, however, it is now thought that strategic periods of reduced carbohydrate and elevated dietary protein intake may enhance training adaptations whereas high carbohydrate availability and antioxidant supplementation may actually attenuate training adaptation. Emerging evidence also suggests that vitamin D may play a regulatory role in muscle regeneration and subsequent hypertrophy following damaging forms of exercise. Finally, novel compounds (albeit largely examined in rodent models) such as epicatechins, nicotinamide riboside, resveratrol, β-hydroxy β-methylbutyrate, phosphatidic acid and ursolic acid may also promote or attenuate skeletal muscle adaptations to endurance and strength training. When taken together, it is clear that sports nutrition is very much at the heart of the Olympic motto, Citius, Altius, Fortius (faster, higher, stronger).
Publisher: American Physiological Society
Date: 06-2017
DOI: 10.1152/AJPENDO.00438.2015
Abstract: In striated muscle, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) have differential effects on the metabolism of glucose and differential effects on the metabolism of protein. We have shown that, despite similar incorporation, treatment of C 2 C 12 myotubes (CM) with EPA but not DHA improves glucose uptake and protein accretion. We hypothesized that these differential effects of EPA and DHA may be due to ergent shifts in lipidomic profiles leading to altered proteomic profiles. We therefore carried out an assessment of the impact of treating CM with EPA and DHA on lipidomic and proteomic profiles. Fatty acid methyl esters (FAME) analysis revealed that both EPA and DHA led to similar but substantials changes in fatty acid profiles with the exception of arachidonic acid, which was decreased only by DHA, and docosapentanoic acid (DPA), which was increased only by EPA treatment. Global lipidomic analysis showed that EPA and DHA induced large alterations in the cellular lipid profiles and in particular, the phospholipid classes. Subsequent targeted analysis confirmed that the most differentially regulated species were phosphatidylcholines and phosphatidylethanolamines containing long-chain fatty acids with five (EPA treatment) or six (DHA treatment) double bonds. As these are typically membrane-associated lipid species we hypothesized that these treatments differentially altered the membrane-associated proteome. Stable isotope labeling by amino acids in cell culture (SILAC)-based proteomics of the membrane fraction revealed significant ergence in the effects of EPA and DHA on the membrane-associated proteome. We conclude that the EPA-specific increase in polyunsaturated long-chain fatty acids in the phospholipid fraction is associated with an altered membrane-associated proteome and these may be critical events in the metabolic remodeling induced by EPA treatment.
Publisher: Elsevier BV
Date: 08-2018
DOI: 10.1016/J.METABOL.2018.03.005
Abstract: β-secretase/β-site amyloid precursor protein (APP)-cleaving enzyme 1 (BACE1) is a key enzyme involved in Alzheimer's disease that has recently been implicated in insulin-independent glucose uptake in myotubes. However, it is presently unknown whether BACE1 and the product of its activity, soluble APPβ (sAPPβ), contribute to lipid-induced inflammation and insulin resistance in skeletal muscle cells. Studies were conducted in mouse C2C12 myotubes, skeletal muscle from Bace1 We show that BACE1 inhibition or knockdown attenuates palmitate-induced endoplasmic reticulum (ER) stress, inflammation, and insulin resistance and prevents the reduction in Peroxisome Proliferator-Activated Receptor γ Co-activator 1α (PGC-1α) and fatty acid oxidation caused by palmitate in myotubes. The effects of palmitate on ER stress, inflammation, insulin resistance, PGC-1α down-regulation, and fatty acid oxidation were mimicked by soluble APPβ in vitro. BACE1 expression was increased in subcutaneous adipose tissue of obese and type 2 diabetic patients and this was accompanied by a decrease in PGC-1α mRNA levels and by an increase in sAPPβ plasma levels of obese type 2 diabetic patients compared to obese non-diabetic subjects. Acute sAPPβ administration to mice reduced PGC-1α levels and increased inflammation in skeletal muscle and decreased insulin sensitivity. Collectively, these findings indicate that the BACE1 product sAPPβ is a key determinant in ER stress, inflammation and insulin resistance in skeletal muscle and gluconeogenesis in liver.
Publisher: Springer Science and Business Media LLC
Date: 08-06-2022
DOI: 10.1038/S41387-022-00209-Z
Abstract: There is increasing evidence that skeletal muscle microvascular (capillary) blood flow plays an important role in glucose metabolism by increasing the delivery of glucose and insulin to the myocytes. This process is impaired in insulin-resistant in iduals. Studies suggest that in diet-induced insulin-resistant rodents, insulin-mediated skeletal muscle microvascular blood flow is impaired post-short-term high fat feeding, and this occurs before the development of myocyte or whole-body insulin resistance. These data suggest that impaired skeletal muscle microvascular blood flow is an early vascular step before the onset of insulin resistance. However, evidence of this is still lacking in humans. In this review, we summarise what is known about short-term high-calorie and/or high-fat feeding in humans. We also explore selected animal studies to identify potential mechanisms. We discuss future directions aimed at better understanding the ‘early’ vascular mechanisms that lead to insulin resistance as this will provide the opportunity for much earlier screening and timing of intervention to assist in preventing type 2 diabetes.
Publisher: Springer Science and Business Media LLC
Date: 27-05-2010
Abstract: Myogenesis in C2C12 cells requires the activation of the PI3K/mTOR signaling pathways. Since mTOR signaling can feedback through S6K1 to inhibit the activation of PI3K, the aim of this work was to assess whether feedback from S6K1 played a role in myogenesis and determine whether siRNA mediated knockdown of S6K1 would lead to an increased rate of myotube formation. S6K1 activity increased in a linear fashion following plating and was more than 3-fold higher after Day 3 of differentiation (subconfluent = 11.09 ± 3.05, Day 3 = 29.34 ± 3.58). IRS-1 levels tended to increase upon serum withdrawal but decreased approximately 2-fold (subconfluent = 0.88 ± 0.10, Day 3 = 0.42 ± 0.06) 3 days following differentiation whereas IRS-2 protein remained stable. IRS-1 associated p85 was significantly reduced upon serum withdrawal (subconfluent = 0.86 ± 0.07, Day 0 = 0.31 ± 0.05), remaining low through day 1. IRS-2 associated p85 decreased following serum withdrawal (subconfluent = 0.96 ± 0.05, Day 1 = 0.56 ± 0.08) and remained suppressed up to Day 3 following differentiation (0.56 ± 0.05). Phospho-tyrosine associated p85 increased significantly from subconfluent to Day 0 and remained elevated throughout differentiation. siRNA directed against S6K1 and S6K2 did not result in changes in IRS-1 levels after either 48 or 96 hrs. Furthermore, neither 48 nor 96 hrs of S6K1 knockdown caused a change in myotube formation. Even though S6K1 activity increases throughout muscle cell differentiation and IRS-1 levels decrease over this period, siRNA suggests that S6K1 is not mediating the decrease in IRS-1. The decrease in IRS-1/2 associated p85 together with the increase in phospho-tyrosine associated p85 suggests that PI3K associates primarily with scaffolds other than IRS-1/2 during muscle cell differentiation.
Publisher: American Physiological Society
Date: 11-2018
DOI: 10.1152/AJPENDO.00163.2018
Abstract: The aim of this study was to characterize postprandial glucose flux after exercise in the fed versus overnight fasted state and to investigate the potential underlying mechanisms. In a randomized order, twelve men underwent breakfast-rest [(BR) 3 h semirecumbent], breakfast-exercise [(BE) 2 h semirecumbent before 60 min of cycling (50% peak power output)], and overnight fasted exercise [(FE) as per BE omitting breakfast] trials. An oral glucose tolerance test (OGTT) was completed after exercise (after rest on BR). Dual stable isotope tracers ([U- 13 C] glucose ingestion and [6,6- 2 H 2 ] glucose infusion) and muscle biopsies were combined to assess postprandial plasma glucose kinetics and intramuscular signaling, respectively. Plasma intestinal fatty acid binding (I-FABP) concentrations were determined as a marker of intestinal damage. Breakfast before exercise increased postexercise plasma glucose disposal rates during the OGTT, from 44 g/120 min in FE {35 to 53 g/120 min [mean (normalized 95% confidence interval)] to 73 g/120 min in BE [55 to 90 g/120 min P = 0.01]}. This higher plasma glucose disposal rate was, however, offset by increased plasma glucose appearance rates (principally OGTT-derived), resulting in a glycemic response that did not differ between BE and FE ( P = 0.11). Plasma I-FABP concentrations during exercise were 264 pg/ml (196 to 332 pg/ml) lower in BE versus FE ( P = 0.01). Breakfast before exercise increases postexercise postprandial plasma glucose disposal, which is offset (primarily) by increased appearance rates of orally ingested glucose. Therefore, metabolic responses to fed-state exercise cannot be readily inferred from studies conducted in a fasted state.
Publisher: MDPI AG
Date: 16-11-2020
DOI: 10.3390/NU12113527
Abstract: This systematic literature review aimed to determine the protein requirements of pre-menopausal (e.g., 18–45 years) female athletes and identify if the menstrual cycle phase and/or hormonal contraceptive use influence protein requirements. Four databases were searched for original research containing pre-menopausal female athletes that ingested protein alongside exercise. The Academy of Nutrition and Dietetics Quality Criteria Checklist was used to determine study quality. Fourteen studies, which included 204 recreationally active or competitive females, met the eligibility criteria for inclusion in this review, and all were assessed as positive quality. The estimated average requirement (EAR) for protein intake of pre-menopausal recreational and/or competitive female athletes is similar for those undertaking aerobic endurance (1.28–1.63 g/kg/day), resistance (1.49 g/kg/day) and intermittent exercise (1.41 g/kg/day) of ~60–90 min duration. The optimal acute protein intake and influence of menstrual cycle phase or hormonal contraceptive use on protein requirements could not be determined. However, pre- and post-exercise protein intakes of 0.32–0.38 g/kg have demonstrated beneficial physiological responses in recreational and competitive female athletes completing resistance and intermittent exercise. The protein requirements outlined in this review can be used for planning and assessing protein intakes of recreational and competitive pre-menopausal female athletes.
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 05-2017
Publisher: Springer Science and Business Media LLC
Date: 17-09-2013
DOI: 10.1007/S12576-013-0285-4
Abstract: Knockout of Kv1.3 improves glucose homeostasis and confers resistance to obesity. Additionally, Kv1.3 inhibition enhances glucose uptake. This is thought to occur through calcium release. Kv1.3 inhibition in T-lymphocytes alters mitochondrial membrane potential, and, as many agents that induce Ca(2+) release or inhibit mitochondrial function activate AMPK, we hypothesised that Kv1.3 inhibition would activate AMPK and increase glucose uptake. We screened cultured muscle with a range of Kv1.3 inhibitors for their ability to alter glucose uptake. Only Psora4 increased glucose uptake in C2C12 myotubes. None of the inhibitors had any impact on L6 myotubes. Magratoxin activated AMPK in C2C12 myotubes and only Pap1 activated AMPK in the SOL. Kv1.3 inhibitors did not alter cellular respiration, indicating a lack of effect on mitochondrial function. In conclusion, AMPK does not mediate the effects of Kv1.3 inhibitors and they display differential effects in different skeletal muscle cell lines without impairing mitochondrial function.
Publisher: S. Karger AG
Date: 28-03-2012
DOI: 10.1159/000334144
Publisher: Public Library of Science (PLoS)
Date: 16-07-2010
Publisher: Wiley
Date: 12-2017
DOI: 10.14814/PHY2.13498
Publisher: American Physiological Society
Date: 15-05-2016
DOI: 10.1152/JAPPLPHYSIOL.01076.2015
Abstract: The ubiquitous transcriptional coactivators Yap (gene symbol Yap1) and Taz (gene symbol Wwtr1) regulate gene expression mainly by coactivating the Tead transcription factors. Being at the center of the Hippo signaling network, Yap and Taz are regulated by the Hippo kinase cassette and additionally by a plethora of exercise-associated signals and signaling modules. These include mechanotransduction, the AKT-mTORC1 network, the SMAD transcription factors, hypoxia, glucose homeostasis, AMPK, adrenaline/epinephrine and angiotensin II through G protein-coupled receptors, and IL-6. Consequently, exercise should alter Hippo signaling in several organs to mediate at least some aspects of the organ-specific adaptations to exercise. Indeed, Tead1 overexpression in muscle fibers has been shown to promote a fast-to-slow fiber type switch, whereas Yap in muscle fibers and cardiomyocytes promotes skeletal muscle hypertrophy and cardiomyocyte adaptations, respectively. Finally, genome-wide association studies in humans have linked the Hippo pathway members LATS2, TEAD1, YAP1, VGLL2, VGLL3, and VGLL4 to body height, which is a key factor in sports.
Publisher: MDPI AG
Date: 29-03-2021
DOI: 10.3390/NU13041124
Abstract: The world’s ever-growing population presents a major challenge in providing sustainable food options and in reducing pressures on the Earth’s agricultural land and freshwater resources. Current estimates suggest that agriculture contributes ~30% of global greenhouse gas (GHG) emissions. Additionally, there is an increased demand for animal protein, the production of which is particularly polluting. Therefore, the climate-disrupting potential of feeding the planet is likely to substantially worsen in the future. Due to the nutritional value of animal-based protein, it is not a simple solution to recommend a wholesale reduction in production/consumption of animal proteins. Rather, employing strategies which result in the production of low carbon animal protein may be part of the solution to reduce the GHGs associated with our diets without compromising diet quality. We suggest that farmed mussels may present a partial solution to this dilemma. Mussel production has a relatively low GHG production and does not put undue pressure on land or fresh water supplies. By drawing comparisons to other protein sources using the Australian Food and Nutrient Database and other published data, we demonstrate that they are a sustainable source of high-quality protein, long-chain omega-3 fatty acids, phytosterols, and other key micronutrients such as B-12 and iron. The aim of this review is to summarise the current knowledge on the health benefits and potential risks of increasing the consumption of farmed mussels.
Publisher: Springer Science and Business Media LLC
Date: 24-01-2018
Publisher: Elsevier BV
Date: 08-2019
DOI: 10.1093/JN/NXZ018
Publisher: American Physiological Society
Date: 2018
DOI: 10.1152/JAPPLPHYSIOL.00685.2018
Abstract: One of the most striking adaptations to exercise is the skeletal muscle hypertrophy that occurs in response to resistance exercise. A large body of work shows that a mammalian target of rapamycin complex 1 (mTORC1)-mediated increase of muscle protein synthesis is the key, but not sole, mechanism by which resistance exercise causes muscle hypertrophy. While much of the hypertrophy signaling cascade has been identified, the initiating, resistance exercise-induced and hypertrophy-stimulating stimuli have remained elusive. For the purpose of this review, we define an initiating, resistance exercise-induced and hypertrophy-stimulating signal as “hypertrophy stimulus,” and the sensor of such a signal as “hypertrophy sensor.” In this review we discuss our current knowledge of specific mechanical stimuli, damage/injury-associated and metabolic stress-associated triggers, as potential hypertrophy stimuli. Mechanical signals are the prime hypertrophy stimuli candidates, and a filamin-C-BAG3-dependent regulation of mTORC1, Hippo, and autophagy signaling is a plausible albeit still incompletely characterized hypertrophy sensor. Other candidate mechanosensing mechanisms are nuclear deformation-initiated signaling or several mechanisms related to costameres, which are the functional equivalents of focal adhesions in other cells. While exercise-induced muscle damage is probably not essential for hypertrophy, it is still unclear whether and how such muscle damage could augment a hypertrophic response. Interventions that combine blood flow restriction and especially low load resistance exercise suggest that resistance exercise-regulated metabolites could be hypertrophy stimuli, but this is based on indirect evidence and metabolite candidates are poorly characterized.
Publisher: Frontiers Media SA
Date: 16-07-2019
Publisher: American Diabetes Association
Date: 14-05-2012
DOI: 10.2337/DB11-0961
Abstract: In recent decades, the antihyperglycemic biguanide metformin has been used extensively in the treatment of type 2 diabetes, despite continuing uncertainty over its direct target. In this article, using two independent approaches, we demonstrate that cellular actions of metformin are disrupted by interference with its metal-binding properties, which have been known for over a century but little studied by biologists. We demonstrate that copper sequestration opposes known actions of metformin not only on AMP-activated protein kinase (AMPK)-dependent signaling, but also on S6 protein phosphorylation. Biguanide/metal interactions are stabilized by extensive π-electron delocalization and by investigating analogs of metformin we provide evidence that this intrinsic property enables biguanides to regulate AMPK, glucose production, gluconeogenic gene expression, mitochondrial respiration, and mitochondrial copper binding. In contrast, regulation of S6 phosphorylation is prevented only by direct modification of the metal-liganding groups of the biguanide structure, supporting recent data that AMPK and S6 phosphorylation are regulated independently by biguanides. Additional studies with pioglitazone suggest that mitochondrial copper is targeted by both of these clinically important drugs. Together, these results suggest that cellular effects of biguanides depend on their metal-binding properties. This link may illuminate a better understanding of the molecular mechanisms enabling antihyperglycemic drug action.
Publisher: Elsevier BV
Date: 06-2014
DOI: 10.1016/J.PLEFA.2014.03.001
Abstract: The aim of this study was to examine changes in the lipid profile of red blood cells and muscle tissue along with the expression of anabolic signalling proteins in human skeletal muscle. Following a 2-week control period, 10 healthy male participants consumed 5 g d(-1) of fish oil (FO) for 4 weeks. Muscle biopsies and venous blood s les were collected in the fasted state 2 weeks prior (W-2) and immediately before (W0) the initiation of FO supplementation for internal control. Muscle biopsies and venous blood s les were again obtained at week 1 (W1), 2 (W2) and 4 (W4) during FO supplementation for assessment of changes in lipid composition and expression of anabolic signalling proteins. There was no change in the composition of any lipid class between W-2 and W0 confirming control. Following FO supplementation n-3 polyunsaturated fatty acid (n-3 PUFA) muscle lipid composition was increased from W0 to W2 and continued to rise at W4. n-3 PUFA blood lipid composition was increased from W0 to W1 and remained elevated for the remaining time points. Total protein content of focal adhesion kinase (FAK) increased from W0 to W4 whereas total mechanistic target of rapamycin (mTOR) was increased from W0 at W1 with no further significant increases at W2 and W4. These data show that FO supplementation results in discordant changes in the n-3 PUFA composition of skeletal muscle compared to blood that is associated with increases in total FAK content.
Publisher: Informa UK Limited
Date: 27-08-2014
DOI: 10.1080/17461391.2014.950345
Abstract: Concurrent training (the combination of endurance exercise to resistance training) is a common practice for athletes looking to maximise strength and endurance. Over 20 years ago, it was first observed that performing endurance exercise after resistance exercise could have detrimental effects on strength gains. At the cellular level, specific protein candidates have been suggested to mediate this training interference however, at present, the physiological reason(s) behind the concurrent training effect remain largely unknown. Even less is known regarding the optimal nutritional strategies to support concurrent training and whether unique nutritional approaches are needed to support endurance and resistance exercise during concurrent training approaches. In this review, we will discuss the importance of protein supplementation for both endurance and resistance training adaptation and highlight additional nutritional strategies that may support concurrent training. Finally, we will attempt to synergise current understanding of the interaction between physiological responses and nutritional approaches into practical recommendations for concurrent training.
Publisher: Springer Science and Business Media LLC
Date: 31-03-2023
DOI: 10.1186/S13063-023-07199-Y
Abstract: Non-steroidal anti-inflammatory drugs (NSAIDs) and analgesics are used frequently by athletes either prophylactically for the prevention of pain, or to accelerate recovery following an injury. However, these types of pain management strategies have been shown to inhibit signalling pathways (e.g., cyclooxygenase-2) that may hinder muscular adaptations such as hypertrophy and strength. Nutraceuticals such as palmitoylethanolamide (PEA) have analgesic properties that act via different mechanisms to NSAIDS/analgesics. Furthermore, PEA has been shown to have a positive effect on sleep and may contribute positively to muscle hypertrophy via PKB activation. Although PEA has not been widely studied in the athletic or recreationally active population, it may provide an alternative solution for pain management if it is found not to interfere with, or enhance training adaptations. Therefore, the study aim is to investigate the effects of daily PEA supplementation (Levagen + ®) with resistance training on lean body mass, strength, power and physical performance and outcomes of recovery (e.g., sleep) compared to placebo. This double-blind, randomised controlled study will take place over an 11-week period (including 8-weeks of progressive resistance training). Participants for this study will be 18–35 years old, healthy active adults that are not resistance trained. Participants will attend a familiarisation (week 0), pre-testing (week 1) and final-testing (week 11). At the pre-testing and final-testing weeks, total lean body mass (dual-energy X-ray absorptiometry DXA), total mid-thigh cross sectional area (pQCT), maximal muscular strength (1 repetition maximum bench press, isometric mid-thigh pull) and power (countermovement jump and bench throw) will be assessed. Additionally, circulating inflammatory cytokines and anabolic hormones, sleep quality and quantity (ActiGraph), pain and subjective wellbeing (questionnaires) will also be examined. This study is designed to investigate the effects that PEA may have on pre-to post intervention changes in total body and regional lean muscle mass, strength, power, sleep, subjective wellbeing, and pain associated with resistance training and menstruation compared with the placebo condition. Unlike other NSAIDs and analgesics, which may inhibit muscle protein synthesis and training adaptations, PEA which provides analgesia via alternative mechanisms may provide an alternative pain management solution. It is therefore important to determine if this analgesic compound interferes with or enhances training adaptations so that athletes and active in iduals can make an informed decision on their pain management strategies. Australian New Zealand Clinical Trials Registry (ANZCTR: ACTRN12621001726842p).
Publisher: American Physiological Society
Date: 03-2014
DOI: 10.1152/JAPPLPHYSIOL.01072.2013
Abstract: AMPK (AMP-dependant protein kinase)-mTORC1 (mechanistic target of rapamycin in complex 1)-p70S6K1 (ribosomal protein S6 kinase 1 of 70 kDa) signaling plays a crucial role in muscle protein synthesis (MPS). Understanding this pathway has been advanced by the application of the Western blot (WB) technique. However, because many components of the mTORC1 pathway undergo numerous, multisite posttranslational modifications, solely studying the phosphorylation changes of mTORC1 and its substrates may not adequately represent the true metabolic signaling processes. The aim of this study was to develop and apply a quantitative in vitro [γ- 32 P] ATP kinase assay (KA) for p70S6K1 to assess kinase activity in human skeletal muscle to resistance exercise (RE) and protein feeding. In an initial series of experiments the assay was validated in tissue culture and in p70S6K1-knockout tissues. Following these experiments, the methodology was applied to assess p70S6K1 signaling responses to a physiologically relevant stimulus. Six men performed unilateral RE followed by the consumption of 20 g of protein. Muscle biopsies were obtained at pre-RE, and 1 and 3 h post-RE. In response to RE and protein consumption, p70S6K1 activity as assessed by the KA was significantly increased from pre-RE at 1 and 3 h post-RE. However, phosphorylated p70S6K1 thr389 was not significantly elevated. AMPK activity was suppressed from pre-RE at 3 h post-RE, whereas phosphorylated ACC ser79 was unchanged. Total protein kinase B activity also was unchanged after RE from pre-RE levels. Of the other markers we assessed by WB, 4EBP1 thr37/46 phosphorylation was the only significant responder, being elevated at 3 h post-RE from pre-RE. These data highlight the utility of the KA to study skeletal muscle plasticity.
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 03-2018
DOI: 10.1519/JSC.0000000000002866
Abstract: Walsh, JA, Sanders, D, Hamilton, DL, and Walshe, I. Sleep profiles of elite swimmers during different training phases. J Strength Cond Res 33(3): 811–818, 2019—This study aims to describe the sleeping patterns during different training phases in competitive swimmers. Twelve national- and international-level swimmers (3 females and 9 males) were monitored during 4 different phases, consisting of a preparation training phase, a taper phase, a competition phase, and a rest phase. Sleep parameters were assessed using wrist activity monitors and self-reported sleep diaries. There was a moderately higher ( d = 0.70–1.00) sleep onset latency during the competition phase compared with taper, train, and rest phases. Trivial to small differences were observed for total sleep time between phases ( d = 0.05–0.40). Sleep efficiency was moderately higher ( d = 0.60–0.75) in the training and taper phases compared with competition and rest. Restfulness and fragmentation index (FI) were lowest in the rest with differences between phases being small ( d = 0.43–0.51) for restfulness and small to moderate ( d = 0.43–0.62) for FI. Time in and out of bed was very largely later ( d = 1.96–2.34) in rest compared with the other phases. Total nap time was moderately lower in rest ( d = 1.13–1.18) compared with the training and competition phases, whereas there was a small difference ( d = 0.46) compared with taper. To conclude, while there were trivial to small differences in sleep quantity between phases, there are small to moderate differences in other sleep parameters. Specifically, sleep onset latency was higher during the competition phase. In addition, this study highlights the substantial between-in idual variations in sleep responses during different training phases.
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 02-2019
DOI: 10.1519/JSC.0000000000001853
Abstract: Dugdale, JH, Hunter, AM, Di Virgilio, TG, Macgregor, LJ, and Hamilton, DL. Influence of the “Slingshot” bench press training aid on bench press kinematics and neuromuscular activity in competitive powerlifters. J Strength Cond Res 33(2): 327–336, 2019—This study examined the acute effects of the “Slingshot” (SS) on bench press performance, prime mover surface electromyographic (sEMG) litude, and barbell velocity during maximal and submaximal bench pressing in competitive male powerlifters. Fifteen male powerlifters (mean ± SD age: 27.05 ± 5.94 years mass: 94.15 ± 13.43 kg 1 repetition maximum [1RM] bench press: 139.7 ± 16.79 kg) participated in the study. Bench press strength, average barbell velocity, and sEMG litude of the prime mover muscles (triceps brachii, pectoralis major, and anterior deltoid) were measured during 2 conditions “Raw” (without use of any assistance) and “SS” (using the “Slingshot” to perform both the weight achieved during “Raw” 1RM testing [Raw max/SS], and absolute 1RM using the “SS”). The results showed that the “SS” significantly increased bench press 1RM performance by a mean ± SD of 20.67 ± 3.4 kg. Barbell velocity and stick point analysis indicate that this improvement is likely driven by an increase in peak and prestick barbell velocity as triceps root mean square (RMS) was lower throughout all rep max phases with the “SS.” The “SS” also caused reductions in RMS, specifically of the triceps at all rep ranges but barbell velocity was better maintained in the last reps of all sets. These data indicate that the “SS” specifically deloaded the triceps muscle throughout all rep ranges and provide assistance to maintaining barbell velocity under fatigue during later repetitions of multiple repetition sets. The “SS” training aid could therefore be used in deload phases of bench press training or as an overreaching and velocity training aid.
Publisher: American Physiological Society
Date: 15-02-2013
DOI: 10.1152/JAPPLPHYSIOL.00652.2012
Abstract: This study was undertaken to investigate physiological adaptation with two endurance-training periods differing in intensity distribution. In a randomized crossover fashion, separated by 4 wk of detraining, 12 male cyclists completed two 6-wk training periods: 1) a polarized model [6.4 (±1.4 SD) h/wk 80%, 0%, and 20% of training time in low-, moderate-, and high-intensity zones, respectively] and 2) a threshold model [7.5 (±2.0 SD) h/wk 57%, 43%, and 0% training-intensity distribution]. Before and after each training period, following 2 days of diet and exercise control, fasted skeletal muscle biopsies were obtained for mitochondrial enzyme activity and monocarboxylate transporter (MCT) 1 and 4 expression, and morning first-void urine s les were collected for NMR spectroscopy-based metabolomics analysis. Endurance performance (40-km time trial), incremental exercise, peak power output (PPO), and high-intensity exercise capacity (95% maximal work rate to exhaustion) were also assessed. Endurance performance, PPOs, lactate threshold (LT), MCT4, and high-intensity exercise capacity all increased over both training periods. Improvements were greater following polarized rather than threshold for PPO [mean (±SE) change of 8 (±2)% vs. 3 (±1)%, P 0.05], LT [9 (±3)% vs. 2 (±4)%, P 0.05], and high-intensity exercise capacity [85 (±14)% vs. 37 (±14)%, P 0.05]. No changes in mitochondrial enzyme activities or MCT1 were observed following training. A significant multilevel, partial least squares-discriminant analysis model was obtained for the threshold model but not the polarized model in the metabolomics analysis. A polarized training distribution results in greater systemic adaptation over 6 wk in already well-trained cyclists. Markers of muscle metabolic adaptation are largely unchanged, but metabolomics markers suggest different cellular metabolic stress that requires further investigation.
Publisher: Elsevier BV
Date: 12-2017
Publisher: Informa UK Limited
Date: 05-06-2022
DOI: 10.1080/02640414.2022.2080165
Abstract: While proximity-to-failure is considered an important resistance training (RT) prescription variable, its influence on physiological adaptations and short-term responses to RT is uncertain. Given the ambiguity in the literature, a scoping review was undertaken to summarise evidence for the influence of proximity-to-failure on muscle hypertrophy, neuromuscular fatigue, muscle damage and perceived discomfort. Literature searching was performed according to PRISMA-ScR guidelines and identified three themes of studies comparing either: i) RT performed to momentary muscular failure versus non-failure, ii) RT performed to set failure (defined as anything other than momentary muscular failure) versus non-failure, and iii) RT performed to different velocity loss thresholds. The findings highlight that no consensus definition for "failure" exists in the literature, and the proximity-to-failure achieved in "non-failure" conditions is often ambiguous and variable across studies. This poses challenges when deriving practical recommendations for manipulating proximity-to-failure in RT to achieve desired outcomes. Based on the limited available evidence, RT to set failure is likely not superior to non-failure RT for inducing muscle hypertrophy, but may exacerbate neuromuscular fatigue, muscle damage, and post-set perceived discomfort versus non-failure RT. Together, these factors may impair post-exercise recovery and subsequent performance, and may also negatively influence long-term adherence to RT.
Publisher: Elsevier BV
Date: 12-2016
Publisher: MDPI AG
Date: 19-11-2015
DOI: 10.3390/MD13116977
Publisher: Public Library of Science (PLoS)
Date: 02-07-2013
Location: United Kingdom of Great Britain and Northern Ireland
Location: United Kingdom of Great Britain and Northern Ireland
Location: United Kingdom of Great Britain and Northern Ireland
No related grants have been discovered for David Hamilton.