The short-term effect of high versus moderate protein intake on recovery after strength training in resistance-trained individuals

Background: Dietary protein intakes up to 2.9 g.kg-1.d-1 and protein consumption before and after resistance training may enhance recovery, resulting in hypertrophy and strength gains. However, it remains unclear whether protein quantity or nutrient timing is central to positive adaptations. This study investigated the effect of total dietary protein content, whilst controlling for protein timing, on recovery in resistance trainees. Methods: Fourteen resistance-trained individuals underwent two 10-day isocaloric dietary regimes with a protein content of 1.8 g.kg-1.d-1 (PROMOD) or 2.9 g.kg-1.d-1 (PROHIGH) in a randomised, counterbalanced, crossover design. On days 8-10 (T1-T3), participants undertook resistance exercise under controlled conditions, performing 3 sets of squat, bench press and bent-over rows at 80% 1 repetition maximum until volitional exhaustion. Additionally, participants consumed a 0.4 g.kg-1 whey protein concentrate/isolate mix 30 minutes before and after exercise sessions to standardise protein timing specific to training. Recovery was assessed via daily repetition performance, muscle soreness, bioelectrical impedance phase angle, plasma creatine kinase (CK) and tumor necrosis factor-α (TNF-α). Results: No significant differences were reported between conditions for any of the performance repetition count variables (p>0.05). However, within PROMOD only, squat performance total repetition count was significantly lower at T3 (19.7 ± 6.8) compared to T1 (23.0 ± 7.5; p=0.006). Pre and post-exercise CK concentrations significantly increased across test days (p≤0.003), although no differences were reported between conditions. No differences for TNF-α or muscle soreness were reported between dietary conditions. Phase angle was significantly greater at T3 for PROHIGH (8.26 ± 0.82°) compared with PROMOD (8.08 ± 0.80°; p=0.012). Conclusions: When energy intake and peri-exercise protein intake was controlled for, a short term PROHIGH diet did not improve markers of muscle damage or soreness in comparison to a PROMOD approach following repeated days of intensive training. Whilst it is therefore likely that protein intakes (1.8g.kg-1.d-1) may be sufficient for resistance-trained individuals, it is noteworthy that both lower body exercise performance and bioelectrical phase angle were maintained with PROHIGH. Longer term interventions are warranted to determine whether PROMOD intakes are sufficient during prolonged training periods or when extensive exercise (e.g. training twice daily) is undertaken

Genetic loss of AMPK-glycogen binding destabilises AMPK and disrupts metabolism

OBJECTIVE: Glycogen is a major energy reserve in liver and skeletal muscle. The master metabolic regulator AMP-activated protein kinase (AMPK) associates with glycogen via its regulatory β subunit carbohydrate-binding module (CBM). However, the physiological role of AMPK-glycogen binding in energy homeostasis has not been investigated in vivo. This study aimed to determine the physiological consequences of disrupting AMPK-glycogen interactions. METHODS: Glycogen binding was disrupted in mice via whole-body knock-in (KI) mutation of either the AMPK β1 (W100A) or β2 (W98A) isoform CBM. Systematic whole-body, tissue and molecular phenotyping was performed in KI and respective wild-type (WT) mice. RESULTS: While β1 W100A KI did not affect whole-body metabolism or exercise capacity, β2 W98A KI mice displayed increased adiposity and impairments in whole-body glucose handling and maximal exercise capacity relative to WT. These KI mutations resulted in reduced total AMPK protein and kinase activity in liver and skeletal muscle of β1 W100A and β2 W98A, respectively, versus WT mice. β1 W100A mice also displayed loss of fasting-induced liver AMPK total and α-specific kinase activation relative to WT. Destabilisation of AMPK was associated with increased fat deposition in β1 W100A liver and β2 W98A skeletal muscle versus WT. CONCLUSIONS: These results demonstrate that glycogen binding plays critical roles in stabilising AMPK and maintaining cellular, tissue and whole-body energy homeostasis

Long-chain fatty acyl-CoA esters regulate metabolism via allosteric control of AMPK beta 1 isoforms

Long-chain fatty acids (LCFAs) play important roles in cellular energy metabolism, acting as both an important energy source and signalling molecules1. LCFA-CoA esters promote their own oxidation by acting as allosteric inhibitors of acetyl-CoA carboxylase, which reduces the production of malonyl-CoA and relieves inhibition of carnitine palmitoyl-transferase 1, thereby promoting LCFA-CoA transport into the mitochondria for β-oxidation2-6. Here we report a new level of regulation wherein LCFA-CoA esters per se allosterically activate AMP-activated protein kinase (AMPK) β1-containing isoforms to increase fatty acid oxidation through phosphorylation of acetyl-CoA carboxylase. Activation of AMPK by LCFA-CoA esters requires the allosteric drug and metabolite site formed between the α-subunit kinase domain and the β-subunit. β1 subunit mutations that inhibit AMPK activation by the small-molecule activator A769662, which binds to the allosteric drug and metabolite site, also inhibit activation by LCFA-CoAs. Thus, LCFA-CoA metabolites act as direct endogenous AMPK β1-selective activators and promote LCFA oxidation

Combining detached watchdog journalism with development ideals: An exploration of Fijian journalism culture

Development journalism has been a key focus of discussion among journalism scholars for around half a decade, but most of the attention has been firmly on African and Asian countries. This paper examines the situation on the little-researched island nation of Fiji, which has experienced considerable political instability since independence in 1970. Based on interviews with 77 of the country’s small population of just over 100 journalists, we find that journalism in Fiji exhibits similarities to Western journalism ideals, but also a significant development journalism orientation. A comparison with six other countries from the global South shows that this mix is not unique, and we argue that Western journalism approaches and development ideals are not by necessity mutually exclusive, as has often been argued. In this way, the article aims to contribute to a reassessment of our understanding of development journalism and how journalists in developing societies view their work

mTORC1 directly inhibits AMPK to promote cell proliferation under nutrient stress

Central to cellular metabolism and cell proliferation are highly conserved signalling pathways controlled by mammalian target of rapamycin (mTOR) and AMP-activated protein kinase (AMPK)1,2, dysregulation of which are implicated in pathogenesis of major human diseases such as cancer and type 2 diabetes. AMPK pathways leading to reduced cell proliferation are well established and, in part, act through inhibition of TOR complex-1 (TORC1) activity. Here we demonstrate reciprocal regulation, specifically that TORC1 directly down-regulates AMPK signalling by phosphorylating the evolutionarily conserved residue Ser367 in the fission yeast AMPK catalytic subunit Ssp2, and AMPK α1Ser347/α2Ser345 in the mammalian homologs, which is associated with reduced phosphorylation of activation loop Thr172. Genetic or pharmacological inhibition of TORC1 signalling led to AMPK activation in the absence of increased AMP:ATP ratios; under nutrient stress conditions this was associated with growth limitation in both yeast and human cell cultures. Our findings reveal fundamental, bi-directional regulation between two major metabolic signalling networks and uncover new opportunity for cancer treatment strategies aimed at suppressing cell proliferation in the nutrient-poor tumor microenvironment

Upscaling of fractured oil reservoirs using homogenization including non-equilibrium capillary pressure and relative permeability

Recovery from incompletely water-wet fractured reservoirs can be extremely low. A reason for the low recovery is related to wetting issues, whereas the reason for slow recovery can be the non-equilibrium behavior of capillary pressure. One of the non-equilibrium theories is developed by Barenblatt et al. and itmodifies both capillary pressure and relative permeabilities. The other theory is developed by Hassanizadeh et al. and it only deals with non-equilibrium effects for capillary pressure. To incorporate non-equilibrium in larger-scale problems, we apply homogenization to derive an upscaled model for fractured reservoirs in which the nonequilibrium effects are included. We formulate a fully implicit three-dimensional upscaled numerical model. Furthermore, we develop a computationally efficient numerical approach to solve the upscaled model. We use simulations to determine the range of delay times and capillary-damping coefficients for which discernable effects occur in terms of oil recovery. It is shown that at low Peclet numbers, i.e., when the residence time of the fluids in the fracture is long with respect to the imbibition time, incorporation of delay times of the order of few months have no significant effect on the oil recovery. However, when the Peclet number is large, the delay times reduce the rate of oil recovery. We discuss for which values of the delay time (Barenblatt) and capillary-damping coefficient (Hassanizadeh), significant delays in oil production occur.Geoscience & EngineeringCivil Engineering and Geoscience

Upscaling of fractured oil reservoirs using homogenization including non-equilibrium capillary pressure and relative permeability

Recovery from incompletely water-wet fractured reservoirs can be extremely low. A reason for the low recovery is related to wetting issues, whereas the reason for slow recovery can be the non-equilibrium behavior of capillary pressure. One of the non-equilibrium theories is developed by Barenblatt et al. and itmodifies both capillary pressure and relative permeabilities. The other theory is developed by Hassanizadeh et al. and it only deals with non-equilibrium effects for capillary pressure. To incorporate non-equilibrium in larger-scale problems, we apply homogenization to derive an upscaled model for fractured reservoirs in which the nonequilibrium effects are included. We formulate a fully implicit three-dimensional upscaled numerical model. Furthermore, we develop a computationally efficient numerical approach to solve the upscaled model. We use simulations to determine the range of delay times and capillary-damping coefficients for which discernable effects occur in terms of oil recovery. It is shown that at low Peclet numbers, i.e., when the residence time of the fluids in the fracture is long with respect to the imbibition time, incorporation of delay times of the order of few months have no significant effect on the oil recovery. However, when the Peclet number is large, the delay times reduce the rate of oil recovery. We discuss for which values of the delay time (Barenblatt) and capillary-damping coefficient (Hassanizadeh), significant delays in oil production occur.Geoscience & EngineeringCivil Engineering and Geoscience