Marine Vertebrates and Low Frequency Sound: Technical Report for LFA EIS

Over the past 50 years, economic and technological developments have dramatically increased the human contribution to ambient noise in the ocean. The dominant frequencies of most human-made noise in the ocean is in the low-frequency range (defined as sound energy below 1000Hz), and low-frequency sound (LFS) may travel great distances in the ocean due to the unique propagation characteristics of the deep ocean (Munk et al. 1989). For example, in the Northern Hemisphere oceans low-frequency ambient noise levels have increased by as much as 10 dB during the period from 1950 to 1975 (Urick 1986; review by NRC 1994). Shipping is the overwhelmingly dominant source of low-frequency manmade noise in the ocean, but other sources of manmade LFS including sounds from oil and gas industrial development and production activities (seismic exploration, construction work, drilling, production platforms), and scientific research (e.g., acoustic tomography and thermography, underwater communication). The SURTASS LFA system is an additional source of human-produced LFS in the ocean, contributing sound energy in the 100-500 Hz band. When considering a document that addresses the potential effects of a low-frequency sound source on the marine environment, it is important to focus upon those species that are the most likely to be affected. Important criteria are: 1) the physics of sound as it relates to biological organisms; 2) the nature of the exposure (i.e. duration, frequency, and intensity); and 3) the geographic region in which the sound source will be operated (which, when considered with the distribution of the organisms will determine which species will be exposed). The goal in this section of the LFA/EIS is to examine the status, distribution, abundance, reproduction, foraging behavior, vocal behavior, and known impacts of human activity of those species may be impacted by LFA operations. To focus our efforts, we have examined species that may be physically affected and are found in the region where the LFA source will be operated. The large-scale geographic location of species in relation to the sound source can be determined from the distribution of each species. However, the physical ability for the organism to be impacted depends upon the nature of the sound source (i.e. explosive, impulsive, or non-impulsive); and the acoustic properties of the medium (i.e. seawater) and the organism. Non-impulsive sound is comprised of the movement of particles in a medium. Motion is imparted by a vibrating object (diaphragm of a speaker, vocal chords, etc.). Due to the proximity of the particles in the medium, this motion is transmitted from particle to particle in waves away from the sound source. Because the particle motion is along the same axis as the propagating wave, the waves are longitudinal. Particles move away from then back towards the vibrating source, creating areas of compression (high pressure) and areas of rarefaction (low pressure). As the motion is transferred from one particle to the next, the sound propagates away from the sound source. Wavelength is the distance from one pressure peak to the next. Frequency is the number of waves passing per unit time (Hz). Sound velocity (not to be confused with particle velocity) is the impedance is loosely equivalent to the resistance of a medium to the passage of sound waves (technically it is the ratio of acoustic pressure to particle velocity). A high impedance means that acoustic particle velocity is small for a given pressure (low impedance the opposite). When a sound strikes a boundary between media of different impedances, both reflection and refraction, and a transfer of energy can occur. The intensity of the reflection is a function of the intensity of the sound wave and the impedances of the two media. Two key factors in determining the potential for damage due to a sound source are the intensity of the sound wave and the impedance difference between the two media (impedance mis-match). The bodies of the vast majority of organisms in the ocean (particularly phytoplankton and zooplankton) have similar sound impedence values to that of seawater. As a result, the potential for sound damage is low; organisms are effectively transparent to the sound – it passes through them without transferring damage-causing energy. Due to the considerations above, we have undertaken a detailed analysis of species which met the following criteria: 1) Is the species capable of being physically affected by LFS? Are acoustic impedence mis-matches large enough to enable LFS to have a physical affect or allow the species to sense LFS? 2) Does the proposed SURTASS LFA geographical sphere of acoustic influence overlap the distribution of the species? Species that did not meet the above criteria were excluded from consideration. For example, phytoplankton and zooplankton species lack acoustic impedance mis-matches at low frequencies to expect them to be physically affected SURTASS LFA. Vertebrates are the organisms that fit these criteria and we have accordingly focused our analysis of the affected environment on these vertebrate groups in the world’s oceans: fishes, reptiles, seabirds, pinnipeds, cetaceans, pinnipeds, mustelids, sirenians (Table 1).

Genes and the ageing muscle: a review on genetic association studies

Western populations are living longer. Ageing decline in muscle mass and strength (i.e. sarcopenia) is becoming a growing public health problem, as it contributes to the decreased capacity for independent living. It is thus important to determine those genetic factors that interact with ageing and thus modulate functional capacity and skeletal muscle phenotypes in older people. It would be also clinically relevant to identify 'unfavourable' genotypes associated with accelerated sarcopenia. In this review, we summarized published information on the potential associations between some genetic polymorphisms and muscle phenotypes in older people. A special emphasis was placed on those candidate polymorphisms that have been more extensively studied, i.e. angiotensin-converting enzyme (ACE) gene I/D, α-actinin-3 (ACTN3) R577X, and myostatin (MSTN) K153R, among others. Although previous heritability studies have indicated that there is an important genetic contribution to individual variability in muscle phenotypes among old people, published data on specific gene variants are controversial. The ACTN3 R577X polymorphism could influence muscle function in old women, yet there is controversy with regards to which allele (R or X) might play a 'favourable' role. Though more research is needed, up-to-date MSTN genotype is possibly the strongest candidate to explain variance among muscle phenotypes in the elderly. Future studies should take into account the association between muscle phenotypes in this population and complex gene-gene and gene-environment interactions.

Activity in Geriatric acute CARe (AGECAR): Rationale, design and methods

The Activity in GEriatric acute CARe (AGECAR) is a randomised control trial to assess the effectiveness of an intrahospital strength and walk program during short hospital stays for improving functional capacity of patients aged 75 years or older. Patien

Exercise training can induce cardiac autophagy at end-stage chronic conditions: Insights from a graft-versus-host-disease mouse model

Chronic graft-versus-host disease (cGVHD) is a frequent cause of morbimortality after allogeneic hematopoietic stem cell transplantation (allo-HSCT), and severely compromises patients' physical capacity. Despite the aggressive nature of the disease, aerobic exercise training can positively impact survival as well as clinical and functional parameters. We analyzed potential mechanisms underlying the recently reported cardiac function improvement in an exercise-trained cGVHD murine model receiving lethal total body irradiation and immunosuppressant treatment (Fiuza-Luces et al., 2013. Med Sci Sports Exerc 45, 1703-1711). We hypothesized that a cellular quality-control mechanism that is receiving growing attention in biomedicine, autophagy, was involved in such improvement. Our results suggest that exercise training elicits a positive autophagic adaptation in the myocardium that may help preserve cardiac function even at the end-stage of a devastating disease like cGVHD. These preliminary findings might provide new insights into the cardiac exercise benefits in chronic/debilitating conditions.

Short-term changes in light distortion in orthokeratology subjects

Quantifying adaptation to light distortion of subjects undergoing orthokeratology (OK) for myopia during the first month of treatment. Twenty-nine healthy volunteers (age: 22.34 ± 8.08 years) with mean spherical equivalent refractive error −2.10 ± 0.93D were evaluated at baseline and days 1, 7, 15, and 30 of OK treatment. Light distortion was determined using an experimental prototype. Corneal aberrations were derived from corneal topography for different pupil sizes. Contrast sensitivity function (CSF) was analyzed for frequencies of 1.50, 2.12, 3.00, 4.24, 6.00, 8.49, 12.00, 16.97, and 24.00 cpd under photopic conditions.

Cancer is essentially due to bad luck...but not so much if you don’t exercise or are overweight

2.241 JCR (2015) Q3, 140/213 Oncology, 45/80 Nutrition & dietetics

Phenotype consequences of myophosphorylase dysfunction: insights from the McArdle mouse model

McArdle disease, caused by inherited deficiency of the enzyme muscle glycogen phosphorylase (GP-MM), is arguably the paradigm of exercise intolerance. The recent knock-in (p.R50X/p.R50X) mouse disease model allows an investigation of the phenotypic consequences of muscle glycogen unavailability and the physiopathology of exercise intolerance. We analysed, in 2-month-old mice [wild-type (wt/wt), heterozygous (p.R50X/wt) and p.R50X/p.R50X)], maximal endurance exercise capacity and the molecular consequences of an absence of GP-MM in the main glycogen metabolism regulatory enzymes: glycogen synthase, glycogen branching enzyme and glycogen debranching enzyme, as well as glycogen content in slow-twitch (soleus), intermediate (gastrocnemius) and glycolytic/fast-twitch (extensor digitorum longus; EDL) muscles.

McArdle disease: a unique study model in sports medicine

McArdle disease is arguably the paradigm of exercise intolerance in humans. This disorder is caused by inherited deficiency of myophosphorylase, the enzyme isoform that initiates glycogen breakdown in skeletal muscles. Because patients are unable to obtain energy from their muscle glycogen stores, this disease provides an interesting model of study for exercise physiologists, allowing insight to be gained into the understanding of glycogen-dependent muscle functions. Of special interest in the field of muscle physiology and sports medicine are also some specific (if not unique) characteristics of this disorder, such as the so-called 'second wind' phenomenon, the frequent exercise-induced rhabdomyolysis and myoglobinuria episodes suffered by patients (with muscle damage also occurring under basal conditions), or the early appearance of fatigue and contractures, among others. In this article we review the main pathophysiological features of this disorder leading to exercise intolerance as well as the currently available therapeutic possibilities.

Corrigendum to "Short-term changes in light distortion in orthokeratology subjects"

2.134 JCR (2015) Q3, 74/124 Medicine, research & experimental, 81/161 Biotechnology & applied microbiology

Rodent models for resolving extremes of exercise and health

The extremes of exercise capacity and health are considered a complex interplay between genes and the environment. In general, the study of animal models has proven critical for deep mechanistic exploration that provides guidance for focused and hypothesis driven discovery in humans. Hypotheses underlying molecular mechanisms of disease, and gene/tissue function can be tested in rodents in order to generate sufficient evidence to resolve and progress our understanding of human biology. Here we provide examples of three alternative uses of rodent models that have been applied successfully to advance knowledge that bridges our understanding of the connection between exercise capacity and health status. Firstly we review the strong association between exercise capacity and all-cause morbidity and mortality in humans through artificial selection on low and high exercise performance in the rat and the consequent generation of the "energy transfer hypothesis". Secondly we review specific transgenic and knock-out mouse models that replicate the human disease condition and performance. This includes human glycogen storage diseases (McArdle and Pompe) and α-actinin-3 deficiency. Together these rodent models provide an overview of the advancements of molecular knowledge required for clinical translation. Continued study of these models in conjunction with human association studies will be critical to resolving the complex gene-environment interplay linking exercise capacity, health, and disease.

Exercise as a polypill for chronic diseases

Exercise may be described as a polypill to prevent and/or treat almost every chronic disease, with obvious benefits such as its low cost and practical lack of adverse effects. Implementing physical activity interventions in public health is therefore a goal at the medical, social, and economic levels. This chapter describes the importance of health promotion through physical activity and discusses the impacts of exercise on the most prevalent chronic diseases, namely metabolic syndrome-related disorders, cardiovascular diseases, cancer, and Alzheimer's disease. For each of these chronic conditions, we discuss the epidemiological evidence supporting a beneficial role of exercise, provide guidelines for exercise prescription, and describe the biological mechanisms whereby exercise exerts its modulatory effects.

Blood and urinary abnormalities induced during and after 24-hour continuous running: A case report

In this reported clinical case, a healthy and well-trained male subject [aged 37 years, maximal oxygen uptake (V[Combining Dot Above]O2max) 64 mL·kg·min] ran for 23 hours and 35 minutes covering 160 km (6.7 km/h average running speed). The analysis of hematological and biochemical parameters 3 days before the event, just after termination of exercise, and after 24 and 48 hours of recovery revealed important changes on muscle and liver function, and hemolysis. The analysis of urine sediments showed an increment of red and white blood cells filtrations, compatible with transient nephritis. After 48 hours, most of these alterations were recovered. Physicians and health professionals who monitor such athletic events should be aware that these athletes could exhibit transient symptoms compatible with severe pathologies and diseases, although the genesis of these blood and urinary abnormalities are attributable to transient physiological adaptations rather to pathological status.

Limits of ventricular function: from athlete's heart to a failing heart

The interest in the study of ventricular function has grown considerably in the last decades. In this review, we analyse the extreme values of ventricular function as obtained with Doppler echocardiography. We mainly focus on the parameters that have been used throughout the history of Doppler echocardiography to assess left ventricular (LV) systolic and diastolic function. The ‘athlete's heart’ would be the highest expression of ventricular function whereas its lowest expression is represented by the failing heart, independently from the original aetiology leading to this condition. There are, however, morphological similarities (dilation and hypertrophy) between the athlete's and the failing heart, which emerge as physiological and pathophysiological adaptations, respectively. The introduction of new assessment techniques, specifically speckle tracking, may provide new insight into the properties that determine ventricular filling, specifically left ventricular twisting. The concept of ventricular function must be always considered, although it may not be always possible to distinguish the normal heart of sedentary individuals from that of highly trained hearts based solely on echocardiographic or basic studies.

Xanthine oxidase pathway and muscle damage: Insights from McArdle disease

The intent of this review is to summarize current body of knowledge on the potential implication of the xanthine oxidase pathway (XO) on skeletal muscle damage. The possible involvement of the XO pathway in muscle damage is exemplified by the role of XO inhibitors (e.g., allopurinol) in attenuating muscle damage. Reliance on this pathway (as well as on the purine nucleotide cycle) could be exacerbated in conditions of low muscle glycogen availability. Thus, we also summarize current hypotheses on the etiology of both baseline and exertional muscle damage in McArdle disease, a condition caused by inherited deficiency of myophosphorylase. Because myophosphorylase catalyzes the first step of muscle glycogen breakdown, patients are unable to obtain energy from their muscle glycogen stores. Finally, we provide preliminary data from our laboratory on the potential implication of the XO pathway in the muscle damage that is commonly experienced by these patients.

'Adipaging': Aging and obesity share biological hallmarks related to a dysfunctional adipose tissue

The increasing aging of our societies is accompanied by a pandemic of obesity and related cardiometabolic disorders. Progressive dysfunction of the white adipose tissue is increasingly recognized as an important hallmark of the aging process which in turn contributes to metabolic alterations, multi-organ damage, and a systemic pro-inflammatory state ('inflammaging'). On the other hand, obesity, the paradigm of adipose tissue dysfunction, shares numerous biological similarities with the normal aging process such as chronic inflammation and multi-system alterations. Accordingly, understanding the interplay between accelerated aging related to obesity and adipose tissue dysfunction is critical to gain insight into the aging process in general as well as into the pathophysiology of obesity and other related conditions. Here we postulate the concept of 'adipaging' to illustrate the common links between aging and obesity and the fact that, to a great extent, obese adults are prematurely aged individuals.