Training Monitoring for Resistance Exercise: Theory and Applications

Resistance exercise is difficult to quantify owing to its inherent complexity with numerous training variables contributing to the training dose (type of exercise, load lifted, training volume, inter-set rest periods, and repetition velocity). In addition, the intensity of resistance training is often inadequately determined as the relative load lifted (% 1-repetition maximum), which does not account for the effects of inter-set recovery periods, repetition velocity, or the number of repetitions performed in each set at a given load. Methods to calculate the volume load associated with resistance training, as well as the perceived intensity of individual sets and entire training sessions have been shown to provide useful information regarding the actual training stimulus. In addition, questionnaires to subjectively assess how athletes are coping with the stressors of training and portable technologies to quantify performance variables such as concentric velocity may also be valuable. However, while several methods have been proposed to quantify resistance training, there is not yet a consensus regarding how these methods can be best implemented and integrated to complement each other. Therefore, the purpose of this review is to provide practical information for strength coaches to highlight effective methods to assess resistance training, and how they can be integrated into a comprehensive monitoring program

Factors that influence running intensity in interchange players in professional rugby league

Background: Rugby league coaches adopt replacement strategies for their interchange players to maximize running intensity; however, it is important to understand the factors that may influence match performance. Purpose: To assess the independent factors affecting running intensity sustained by interchange players during professional rugby league. Methods: Global positioning system (GPS) data were collected from all interchanged players (starters and nonstarters) in a professional rugby league squad across 24 matches of a National Rugby League season. A multilevel mixed-model approach was employed to establish the effect of various technical (attacking and defensive involvements), temporal (bout duration, time in possession, etc), and situational (season phase, recovery cycle, etc) factors on the relative distance covered and average metabolic power (Pmet) during competition. Significant effects were standardized using correlation coefficients, and the likelihood of the effect was described using magnitude-based inferences. Results: Superior intermittent running ability resulted in very likely large increases in both relative distance and Pmet. As the length of a bout increased, both measures of running intensity exhibited a small decrease. There were at least likely small increases in running intensity for matches played after short recovery cycles and against strong opposition. During a bout, the number of collision-based involvements increased running intensity, whereas time in possession and ball time out of play decreased demands. Conclusions: These data demonstrate a complex interaction of individual- and match-based factors that require consideration when developing interchange strategies, and the manipulation of training loads during shorter recovery periods and against stronger opponents may be beneficial

Acceleration-Based Running Intensities of Professional Rugby League Match-Play

Purpose: To quantify the energetic cost of running and acceleration efforts during rugby league competition to aid in prescription and monitoring of training. Methods: Global positioning system (GPS) data were collected from 37 professional rugby league players across 2 seasons. Peak values for relative distance, average acceleration/deceleration, and metabolic power (P_met) were calculated for 10 different moving-average durations (1–10 min) for each position. A mixed-effects model was used to assess the effect of position for each duration, and individual comparisons were made using a magnitude-based-inference network. Results: There were almost certainly large differences in relative distance and P_met between the 10-min window and all moving averages <5 min in duration (ES = 1.21–1.88). Fullbacks, halves, and hookers covered greater relative distances than outside backs, edge forwards, and middle forwards for moving averages lasting 2–10 min. Acceleration/deceleration demands were greatest in hookers and halves compared with fullbacks, middle forwards, and outside backs. P_met was greatest in hookers, halves, and fullbacks compared with middle forwards and outside backs. Conclusions: Competition running intensities varied by both position and moving-average duration. Hookers exhibited the greatest P_met of all positions, due to high involvement in both attack and defense. Fullbacks also reached high P_met, possibly due to a greater absolute volume of running. This study provides coaches with match data that can be used for the prescription and monitoring of specific training drills

Sleep Hygiene and Light Exposure Can Improve Performance Following Long-Haul Air Travel.

PURPOSE:To assess the efficacy of a combined light exposure and sleep hygiene intervention to improve team-sport performance following eastward long-haul transmeridian travel. METHODS:Twenty physically trained males underwent testing at 09:00 and 17:00 hours local time on 4 consecutive days at home (baseline) and the first 4 days following 21 hours of air travel east across 8 time zones. In a randomized, matched-pairs design, participants traveled with (INT; n = 10) or without (CON; n = 10) a light exposure and sleep hygiene intervention. Performance was assessed via countermovement jump, 20-m sprint, T test, and Yo-Yo Intermittent Recovery Level 1 tests, together with perceptual measures of jet lag, fatigue, mood, and motivation. Sleep was measured using wrist activity monitors in conjunction with self-report diaries. RESULTS:Magnitude-based inference and standardized effect-size analysis indicated there was a very likely improvement in the mean change in countermovement jump peak power (effect size 1.10, ±0.55), and likely improvement in 5-m (0.54, ±0.67) and 20-m (0.74, ±0.71) sprint time in INT compared with CON across the 4 days posttravel. Sleep duration was most likely greater in INT both during travel (1.61, ±0.82) and across the 4 nights following travel (1.28, ±0.58) compared with CON. Finally, perceived mood and motivation were likely worse (0.73, ±0.88 and 0.63, ±0.87) across the 4 days posttravel in CON compared with INT. CONCLUSIONS:Combined light exposure and sleep hygiene improved speed and power but not intermittent-sprint performance up to 96 hours following long-haul transmeridian travel. The reduction of sleep disruption during and following travel is a likely contributor to improved performance

Dysregulation in Retinal Para-Inflammation and Age-Related Retinal Degeneration in CCL2 or CCR2 Deficient Mice

We have shown previously that a para-inflammatory response exists at the retinal/choroidal interface in the aging eye; and this response plays an important role in maintaining retinal homeostasis under chronic stress conditions. We hypothesized that dysregulation of the para-inflammatory response may result in an overt pro-inflammatory response inducing retinal degeneration. In this study, we examined this hypothesis in mice deficient in chemokine CCL2 or its cognate receptor CCR2. CCL2- or CCR2-deficient mice developed retinal degenerative changes with age, characterized as retinal pigment epithelial (RPE) cell and photoreceptor cell death. Retinal cell death was associated with significantly more subretinal microglial accumulation and increased complement activation. In addition, monocytes from CCL2- or CCR2-deficient mice had reduced capacity for phagocytosis and chemotaxis, expressed less IL-10 but more iNOS, IL-12 and TNF-α when compared to monocytes from WT mice. Complement activation at the site of RPE cell death resulted in C3b/C3d but not C5b-9 deposition, indicating only partial activation of the complement pathway. Our results suggest that altered monocyte functions may convert the protective para-inflammatory response into an overtly harmful inflammation at the retina/choroidal interface in CCL2- or CCR2-deficient mice, leading to RPE and photoreceptor degeneration. These data support a concept whereby a protective para-inflammatory response relies upon a normally functioning innate immune system. If the innate immune system is deficient chronic stress may tip the balance towards an overt inflammatory response causing cell/tissue damage

Measuring oxytocin and vasopressin:bioassays, immunoassays and random numbers

In this review, we consider the ways in which vasopressin and oxytocin have been measured since their first discovery. Two different ways of measuring oxytocin in widespread use currently give values in human plasma that differ by two orders of magnitude, and the values measured by these two methods in the same samples show no correlation. The notion that we should accept this seems absurd. Either one (or both) methods is not measuring oxytocin, or, by ‘oxytocin’, the scientists that use these different methods mean something very different. If these communities are to talk to each other, it is important to validate one method and invalidate the other, or else to establish exactly what each community understands by ‘oxytocin’. A similar issue concerns vasopressin: again, different ways of measuring vasopressin give values in human plasma that differ by two orders of magnitude, and it appears that the same explanation for discrepant oxytocin measurements applies to discrepant vasopressin measurements. The first assays for oxytocin and vasopressin measured biological activity directly. When immunoassays were introduced, they encountered problems: high molecular weight factors in raw plasma interfered with the binding of antibodies to the hormones, leading to high and erroneous readings. When these interfering factors were removed by extraction of plasma samples, immunoassays gave measurements consistent with bioassays, with measures of turnover and with the sensitivity of target tissues to exogenous hormone. However, many recent papers use an enzyme‐linked immunoassay to measure plasma levels without extracting the samples. Like the first radioimmunassays of unextracted plasma, this generates impossibly high and wholly erroneous measurements

Attribution: how is it relevant for loss and damage policy and practice?

Attribution has become a recurring issue in discussions about Loss and Damage (L&D). In this highly-politicised context, attribution is often associated with responsibility and blame; and linked to debates about liability and compensation. The aim of attribution science, however, is not to establish responsibility, but to further scientific understanding of causal links between elements of the Earth System and society. This research into causality could inform the management of climate-related risks through improved understanding of drivers of relevant hazards, or, more widely, vulnerability and exposure; with potential benefits regardless of political positions on L&D. Experience shows that it is nevertheless difficult to have open discussions about the science in the policy sphere. This is not only a missed opportunity, but also problematic in that it could inhibit understanding of scientific results and uncertainties, potentially leading to policy planning which does not have sufficient scientific evidence to support it. In this chapter, we first explore this dilemma for science-policy dialogue, summarising several years of research into stakeholder perspectives of attribution in the context of L&D. We then aim to provide clarity about the scientific research available, through an overview of research which might contribute evidence about the causal connections between anthropogenic climate change and losses and damages, including climate science, but also other fields which examine other drivers of hazard, exposure, and vulnerability. Finally, we explore potential applications of attribution research, suggesting that an integrated and nuanced approach has potential to inform planning to avert, minimise and address losses and damages. The key messages are In the political context of climate negotiations, questions about whether losses and damages can be attributed to anthropogenic climate change are often linked to issues of responsibility, blame, and liability. Attribution science does not aim to establish responsibility or blame, but rather to investigate drivers of change. Attribution science is advancing rapidly, and has potential to increase understanding of how climate variability and change is influencing slow onset and extreme weather events, and how this interacts with other drivers of risk, including socio-economic drivers, to influence losses and damages. Over time, some uncertainties in the science will be reduced, as the anthropogenic climate change signal becomes stronger, and understanding of climate variability and change develops. However, some uncertainties will not be eliminated. Uncertainty is common in science, and does not prevent useful applications in policy, but might determine which applications are appropriate. It is important to highlight that in attribution studies, the strength of evidence varies substantially between different kinds of slow onset and extreme weather events, and between regions. Policy-makers should not expect the later emergence of conclusive evidence about the influence of climate variability and change on specific incidences of losses and damages; and, in particular, should not expect the strength of evidence to be equal between events, and between countries. Rather than waiting for further confidence in attribution studies, there is potential to start working now to integrate science into policy and practice, to help understand and tackle drivers of losses and damages, informing prevention, recovery, rehabilitation, and transformation

Multiple Neural Oscillators and Muscle Feedback Are Required for the Intestinal Fed State Motor Program

After a meal, the gastrointestinal tract exhibits a set of behaviours known as the fed state. A major feature of the fed state is a little understood motor pattern known as segmentation, which is essential for digestion and nutrient absorption. Segmentation manifests as rhythmic local constrictions that do not propagate along the intestine. In guinea-pig jejunum in vitro segmentation constrictions occur in short bursts together with other motor patterns in episodes of activity lasting 40–60 s and separated by quiescent episodes lasting 40–200 s. This activity is induced by luminal nutrients and abolished by blocking activity in the enteric nervous system (ENS). We investigated the enteric circuits that regulate segmentation focusing on a central feature of the ENS: a recurrent excitatory network of intrinsic sensory neurons (ISNs) which are characterized by prolonged after-hyperpolarizing potentials (AHPs) following their action potentials. We first examined the effects of depressing AHPs with blockers of the underlying channels (TRAM-34 and clotrimazole) on motor patterns induced in guinea-pig jejunum, in vitro, by luminal decanoic acid. Contractile episode durations increased markedly, but the frequency and number of constrictions within segmenting bursts and quiescent period durations were unaffected. We used these observations to develop a computational model of activity in ISNs, excitatory and inhibitory motor neurons and the muscle. The model predicted that: i) feedback to ISNs from contractions in the circular muscle is required to produce alternating activity and quiescence with the right durations; ii) transmission from ISNs to excitatory motor neurons is via fast excitatory synaptic potentials (EPSPs) and to inhibitory motor neurons via slow EPSPs. We conclude that two rhythm generators regulate segmentation: one drives contractions within segmentation bursts, the other the occurrence of bursts. The latter depends on AHPs in ISNs and feedback to these neurons from contraction of the circular muscle

Resource Quantity Affects Benthic Microbial Community Structure and Growth Efficiency in a Temperate Intertidal Mudflat

Estuaries cover <1% of marine habitats, but the carbon dioxide (CO2) effluxes from these net heterotrophic systems contribute significantly to the global carbon cycle. Anthropogenic eutrophication of estuarine waterways increases the supply of labile substrates to the underlying sediments. How such changes affect the form and functioning of the resident microbial communities remains unclear. We employed a carbon-13 pulse-chase experiment to investigate how a temperate estuarine benthic microbial community at 6.5°C responded to additions of marine diatom-derived organic carbon equivalent to 4.16, 41.60 and 416.00 mmol C m−2. The quantities of carbon mineralized and incorporated into bacterial biomass both increased significantly, albeit differentially, with resource supply. This resulted in bacterial growth efficiency increasing from 0.40±0.02 to 0.55±0.04 as substrates became more available. The proportions of diatom-derived carbon incorporated into individual microbial membrane fatty acids also varied with resource supply. Future increases in labile organic substrate supply have the potential to increase both the proportion of organic carbon being retained within the benthic compartment of estuaries and also the absolute quantity of CO2 outgassing from these environments