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Background: A typical training plan is a mix of many training sessions with different intensities and durations to achieve a specific goal, like running a marathon in a certain time. Scientific publications provide little specific information to aid in writing a comprehensive training plan. This review aims to systematically and quantitatively analyse the last 12 weeks before a marathon as recommended in 92 sub-elite training plans. Methods: We retrieved 92 marathon training plans and linked their running training sessions to five intensity zones. Subsequently, each training plan was grouped based on the total running volume in peak week into high (> 90 km/week), middle (65–90 km/week), and low (< 65 km/week) training volume plan categories. Results: In the final 12 weeks before a race, recommended weekly running volume averaged 108 km, 59 km, and 43 km for high, middle, and low distance marathon training plans. The intensity distribution of these plans followed a pyramidal training structure with 15–67–10–5–3%, 14–63–18–2–3%, and 12–67–17–2–2% in zones 1, 2, 3, 4, and 5, for high, middle, and low volume training plans, respectively. Conclusions: By quantitatively analysing 92 recommended marathon training plans, we can specify typical recommendations for the last 12 weeks before a marathon race. Whilst this approach has obvious limitations such as no evidence for the effectiveness of the training plans investigated, it is arguably a useful strategy to narrow the gap between science and practice. Key points: This review links science and best practice recommendations by quantitatively analysing 92 publicly available marathon training plans for sub-elite marathon runners. Weekly planned running distance in the last 12 weeks before the marathon ranged from 107.7 km for high volume, 58.5 km for middle volume, to 42.9 km for low volume training plans, with the longest run in these plans ranging from 35.2 km for high to 30.9 km for low volume plans. Following a five-zone intensity model, training intensity distribution for all volume categories followed a low, middle, and high intensity pyramidal structure with 13.2% in zone 1, 65.6% in zone 2, 15.1% in zone 3, 3.0% in zone 4, and 3.0% in zone 5. Most of the training volume was recommended to be run in zone 2. [ABSTRACT FROM AUTHOR]

In skeletal muscle, the Hippo effector Yap promotes satellite cell, myoblast, and rhabdomyoblast proliferation but prevents myogenic differentiation into multinucleated muscle fibres. We previously noted that Yap drives expression of the first enzyme of the serine biosynthesis pathway, phosphoglycerate dehydrogenase (Phgdh). Here, we examined the regulation and function of Phgdh in satellite cells and myoblasts and found that Phgdh protein increased during satellite cell activation. Analysis of published data reveal that Phgdh mRNA in mouse tibialis anterior muscle was highly expressed at day 3 of regeneration after cardiotoxin injection, when markers of proliferation are also robustly expressed and in the first week of synergist-ablated muscle. Finally, siRNA-mediated knockdown of PHGDH significantly reduced myoblast numbers and the proliferation rate. Collectively, our data suggest that Phgdh is a proliferation-enhancing metabolic enzyme that is induced when quiescent satellite cells become activated. [ABSTRACT FROM AUTHOR]

Airborne transmission of pathogens plays a major role in the spread of infectious diseases. Aerosol particle production from the lung is thought to occur in the peripheral airways. In the present study we investigated eighty lung-healthy subjects of two age groups (20–39, 60–76 years) at rest and during exercise whether lung function parameters indicative of peripheral airway function were correlated with individual differences in aerosol particle emission. Lung function comprised spirometry and impulse oscillometry during quiet breathing and an expiratory vital capacity manoeuvre, using resistance (R5) and reactance at 5 Hz (X5) as indicators potentially related to peripheral airway function. The association between emission at different ventilation rates relative to maximum ventilation and lung function was assessed by regression analysis. In multiple regression analyses including age group, only vital capacity manoeuvre R5 at 15% to 50% of end-expiratory vital capacity as well as quiet breathing X5 were independently linked to particle emission at 20% to 50% of maximum ventilation, in addition to age group. The fact that age as predictive factor was still significant, although to a lower degree, points towards further effects of age, potentially involving surface properties not accounted for by impulse oscillometry parameters. [ABSTRACT FROM AUTHOR]

Purpose: Exercise typically reduces tumour growth, proliferation and improves outcomes. Many of these effects require exercise to change gene expression within a tumour, but whether exercise actually affects gene expression within a tumour has not been investigated yet. The aim of this study was, therefore, to find out whether one bout of endurance exercise alters gene expression and proliferation in a C26 carcinoma in immunocompetent mice. Methods: BALB/c were injected with C26 colon carcinoma cells. Once the tumours had formed, the mice either ran for 65 min with increasing intensity or rested before the tumour was dissected. The tumours were then analysed by RNA-Seq and stained for the proliferation marker KI67. Results: One bout of running for 65 min did not systematically change gene expression in C26 carcinomas of BALB/c mice when compared to BALB/c mice that were rested. However, when analysed for sex, the expression of 17, mostly skeletal muscle-related genes was higher in the samples of the female mice taken post-exercise. Further histological analysis showed that this signal likely comes from the presence of muscle fibres from the panniculus carnosus muscle inside the tumours. Also, we found no differences in the positivity for the proliferation marker KI67 in the control and exercise C26 carcinomas. Conclusion: A bout of exercise did not systematically affect gene expression or proliferation in C26 carcinomas in immunocompetent BALB/c mice. [ABSTRACT FROM AUTHOR]

Background: Advanced footwear technology improves average running economy compared with racing flats in sub-elite athletes. However, not all athletes benefit as performance changes vary from a 10% drawback to a 14% improvement. The main beneficiaries from such technologies, world-class athletes, have only been analyzed using race times. Objective: The aim of this study was to measure running economy on a laboratory treadmill in advanced footwear technology compared to a traditional racing flat in world-class Kenyan (mean half-marathon time: 59:30 min:s) versus European amateur runners. Methods: Seven world-class Kenyan and seven amateur European male runners completed a maximal oxygen uptake assessment and submaximal steady-state running economy trials in three different models of advanced footwear technology and a racing flat. To confirm our results and better understand the overall effect of new technology in running shoes, we conducted a systematic search and meta-analysis. Results: Laboratory results revealed large variability in both world-class Kenyan road runners, which ranged from a 11.3% drawback to a 11.4% benefit, and amateur Europeans, which ranged from a 9.7% benefit to a 1.1% drawback in running economy of advanced footwear technology compared to a flat. The post-hoc meta-analysis revealed an overall significant medium benefit of advanced footwear technology on running economy compared with traditional flats. Conclusions: Variability of advanced footwear technology performance appears in both world-class and amateur runners, suggesting further testing should examine such variability to ensure validity of results and explain the cause as a more personalized approach to shoe selection might be necessary for optimal benefit. [ABSTRACT FROM AUTHOR]

In 1924, Otto Warburg asked "How does the metabolism of a growing tissue differ from that of a non-growing tissue?" Currently, we know that proliferating healthy and cancer cells reprogramme their metabolism. This typically includes increased glucose uptake, glycolytic flux and lactate synthesis. A key function of this reprogramming is to channel glycolytic intermediates and other metabolites into anabolic reactions such as nucleotide-RNA/DNA synthesis, amino acid-protein synthesis and the synthesis of, for example, acetyl and methyl groups for epigenetic modification. In this review, we discuss evidence that a hypertrophying muscle similarly takes up more glucose and reprogrammes its metabolism to channel energy metabolites into anabolic pathways. We specifically discuss the functions of the cancer-associated enzymes phosphoglycerate dehydrogenase and pyruvate kinase muscle 2 in skeletal muscle. In addition, we ask whether increased glucose uptake by a hypertrophying muscle explains why muscularity is often negatively associated with type 2 diabetes mellitus and obesity. [ABSTRACT FROM AUTHOR]

The Hippo signal transduction network regulates transcription through Yap/Taz-Tead1-4 in many tissues including skeletal muscle. Whilst transgenic mice have been generated for many Hippo genes, the resultant skeletal muscle phenotypes were not always characterized. Here, we aimed to phenotype the hindlimb muscles of Hippo gene-mutated Lats1−/−, Mst2−/−, Vgll3−/−, and Vgll4+/− mice. This analysis revealed that Lats1−/− mice have 11% more slow type I fibers than age and sex-matched wild-type controls. Moreover, the mRNA expression of slow Myh7 increased by 50%, and the concentration of type I myosin heavy chain is 80% higher in Lats1−/− mice than in age and sex-matched wild-type controls. Second, to find out whether exercise-related stimuli affect Lats1, we stimulated C2C12 myotubes with the hypertrophy agent clenbuterol or the energy stress agent AICAR. We found that both stimulated Lats1 expression by 1.2 and 1.3 fold respectively. Third, we re-analyzed published datasets and found that Lats1 mRNA in muscle is 63% higher in muscular dystrophy, increases by 17–77% after cardiotoxin-induced muscle injury, by 41–71% in muscles during overload-induced hypertrophy, and by 19–21% after endurance exercise when compared to respective controls. To conclude, Lats1 contributes to the regulation of muscle fiber type proportions, and its expression is regulated by physiological and pathological situations in skeletal muscle. [ABSTRACT FROM AUTHOR]

A training plan, or an exercise prescription, is the point where we translate sport and exercise science into practice. As in medicine, good practice requires writing a training plan or prescribing an exercise programme based on the best current scientific evidence. A key issue, however, is that a training plan or exercise prescription is typically a mix of many interacting interventions (e.g. exercises and nutritional recommendations) that additionally change over time due to periodisation or tapering. Thus, it is virtually impossible to base a complex long-term training plan fully on scientific evidence. We, therefore, speak of evidence-informed training plans and exercise prescriptions to highlight that only some of the underlying decisions are made using an evidence-based decision approach. Another challenge is that the adaptation to a given, e.g. endurance or resistance training programme is often highly variable. Until biomarkers for trainability are identified, we must therefore continue to test athletes, clients, or patients, and monitor training variables via a training log to determine whether an individual sufficiently responds to a training intervention or else re-plan. Based on these ideas, we propose a subjective, pragmatic six-step approach that details how to write a training plan or exercise prescription that is partially based on scientific evidence. Finally, we advocate an athlete, client and patient-centered approach whereby an individual's needs and abilities are the main consideration behind all decision-making. This implies that sometimes the most effective form of training is eschewed if the athlete, client or patient has other wishes. [ABSTRACT FROM AUTHOR]

Background: Exercise changes the concentrations of many metabolites, which are small molecules (< 1.5 kDa) metabolized by the reactions of human metabolism. In recent years, especially mass spectrometry-based metabolomics methods have allowed researchers to measure up to hundreds of metabolites in a single sample in a non-biased fashion. To summarize human exercise metabolomics studies to date, we conducted a systematic review that reports the results of experiments that found metabolite concentrations changes after a bout of human endurance or resistance exercise. Methods: We carried out a systematic review following PRISMA guidelines and searched for human metabolomics studies that report metabolite concentrations before and within 24 h after endurance or resistance exercise in blood, urine, or sweat. We then displayed metabolites that significantly changed their concentration in at least two experiments. Results: Twenty-seven studies and 57 experiments matched our search criteria and were analyzed. Within these studies, 196 metabolites changed their concentration significantly within 24 h after exercise in at least two experiments. Human biofluids contain mainly unphosphorylated metabolites as the phosphorylation of metabolites such as ATP, glycolytic intermediates, or nucleotides traps these metabolites within cells. Lactate, pyruvate, TCA cycle intermediates, fatty acids, acylcarnitines, and ketone bodies all typically increase after exercise, whereas bile acids decrease. In contrast, the concentrations of proteinogenic and non-proteinogenic amino acids change in different directions. Conclusion: Across different exercise modes and in different subjects, exercise often consistently changes the average concentrations of metabolites that belong to energy metabolism and other branches of metabolism. This dataset is a useful resource for those that wish to study human exercise metabolism. [ABSTRACT FROM AUTHOR]

How force development and time under tension (TUT) during resistance exercise (RE) influence anabolic signalling of skeletal muscle is incompletely understood. We hypothesized that high force development during RE is more important for post-exercise-induced signalling than submaximal and fatiguing RE with lower force development but similar TUT. Twenty-two male subjects (24 ± 6 years, 181 ± 9 cm, 79 ± 2 kg) performed three distinct RE modes in the fed state with equal TUT but distinct force output: (i) maximal eccentric RE (ECC, n = 7) three sets, eight reps, 100 % eccentric dynamic force; (ii) standard RE (STD, n = 7), three sets, 10 reps, 75 % dynamic force; and (iii) high fatiguing single-set RE (HIT, n = 8), 20 reps, 100 % eccentric-concentric force; vastus lateralis biopsies were collected at baseline, 15, 30, 60, 240 min and 24 h after RE, and the signalling of mechanosensitive and mammalian target of rapamycin (mTOR)-related proteins was determined. The phosphorylation levels of pFAK, pJNK, pAKT, pmTOR, p4E-BP1, p70s6k/ and pS6 were significantly higher in ECC than those in STD and HIT at several time points ( P < 0.01). pJNK and pS6 levels were significantly higher in type II myofibres in ECC compared with STD and HIT. HIT exerted throughout the weakest signalling response. We conclude that high force development during acute RE is superior for anabolic skeletal muscle signalling than fatiguing RE with lower force output but similar TUT. Our results suggest that this response is substantially driven by the higher activation of type II myofibres during RE. [ABSTRACT FROM AUTHOR]

Activation of either the calcineurin or the extracellular signal-regulated kinase (ERK1/2) pathway increases the percentage of slow fibres in vivo suggesting that both pathways can regulate fibre phenotypes in skeletal muscle. We investigated the effect of calcineurin blockade with cyclosporin A and mitogen-activated protein kinase kinase (MEK1/2) blockade with U0126 upon myosin heavy chain (MHC) isoform mRNA levels and activities of metabolic enzymes after 1 day, 3 days and 7 days of treatment in primary cultures of spontaneously twitching rat skeletal muscle. U0126 treatment significantly decreased MHC Iβ mRNA levels and significantly increased MHC IIX, MHC IIB, embryonal MHC and perinatal MHC mRNA levels when compared to control. In addition, U0126 treatment significantly increased lactate dehydrogenase, creatine kinase, hexokinase, malate dehydrogenase and β-hydroxyacyl-CoA dehydrogenase activities above control values while a significant reduction in the percentage of pyruvate dehydrogenase in the active form was also observed. Calcineurin blockade significantly decreased both MHC Iβ and embryonal mRNA levels below control and significantly increased MHC IIX mRNA levels. Significant increases in the activities of both lactate dehydrogenase and creatine kinase above control values were also seen following cyclosporin A treatment. In conclusion, the results suggest that calcineurin upregulates slow-fibre genes and suppresses fast-fibre genes. Similarly, the ERK1/2 pathway upregulates slow-fibre MHC and suppresses fast-fibre MHC isoforms. However, the effect on enzyme activities is not fibre-type specific. The effect of U0126 on the percentage of pyruvate dehydrogenase in the active form suggests that the ERK1/2 pathway may also be involved in regulation of the phosphorylation state of this enzyme. [ABSTRACT FROM AUTHOR]

Persistent hyperactivity of the Hippo effector YAP in activated satellite cells is sufficient to cause embryonal rhabdomyosarcoma (ERMS) in mice. In humans, YAP is abundant and nuclear in the majority of ERMS cases, and high YAP expression is associated with poor survival. However, YAP1 is rarely mutated in human ERMS. Instead, the most common mutations in ERMS are oncogenic RAS mutations. First, to compare YAP1S127A and KRASG12V-driven rhabdomyosarcomas, we re-analysed gene expression microarray datasets from mouse rhabdomyosarcomas caused by these genes. This revealed that only 20% of the up or downregulated genes are identical, suggesting substantial differences in gene expression between YAP and KRAS-driven rhabdomyosarcomas. As oncogenic RAS has been linked to YAP in other types of cancer, we also tested whether KRAS G12V alone or in combination with loss of p53 and p16 activates YAP in myoblasts. We found that neither KRAS G12V alone nor KRAS G12V combined with loss of p53 and p16 activated Yap or Yap/Taz-Tead1-4 transcriptional activity in C2C12 myoblasts or U57810 cells. In conclusion, whilst oncogenic KRAS mutation might activate Yap in other cell types, we could find no evidence for this in myoblasts because the expression of KRAS G12V expression did not change Yap/Taz activity in myoblasts and there was a limited overlap in gene expression between KRAS G12V and YAP1 S127A-driven tumours. [ABSTRACT FROM AUTHOR]