Eccentric exercise testing and training

Some researchers and practitioners have touted the benefits of including eccentric exercise in strength training programs. However, others have challenged its use because they believe that eccentric actions are dangerous and lead to injuries. Much of the controversy may be based on a lack of understanding of the physiology of eccentric actions. This review will present data concerning eccentric exercise in strength training, the physiological characteristics of eccentric exercise, and the possible stimulus for strength development. Also a discussion of strength needs for extended exposure to microgravity will be presented. Not only is the use of eccentric exercise controversial, but the name itself is fraught with problems. The correct pronunciation is with a hard 'c' so that the word sounds like ekscentric. The confusion in pronunciation may have been prevented if the spelling that Asmussen used in 1953, excentric, had been adopted. Another problem concerns the expressions used to describe eccentric exercise. Commonly used expressions are negatives, eccentric contractions, lengthening contractions, resisted muscle lengthenings, muscle lengthening actions, and eccentric actions. Some of these terms are cumbersome (i.e., resisted muscle lengthenings), one is slang (negatives), and another is an oxymoron (lengthening contractions). Only eccentric action is appropriate and adoption of this term has been recommended by Cavanagh. Despite the controversy that surrounds eccentric exercise, it is important to note that these types of actions play an integral role in normal daily activities. Eccentric actions are used during most forms of movement, for example, in walking when the foot touches the ground and the center of mass is decelerated and in lowering objects, such as placing a bag of groceries in the car

Bringing nature back into cities: urban land environments, indigenous cover and urban restoration

1. The restoration of urban ecosystems is an increasingly important strategy to maintain and enhance indigenous biodiversity as well as reconnecting people to the environment. High levels of endemism, the sensitivity of species that have evolved without humans, and the invasion of exotic species have all contributed to severe depletion of indigenous biodiversity in New Zealand. In this work, we analysed national patterns of urban biodiversity in New Zealand and the contribution that urban restoration can make to maximising and enhancing indigenous biodiversity. 2. We analysed data from two national databases in relation to the 20 largest New Zealand cities. We quantified existing indigenous biodiversity within cities, both within the core built up matrix and in centroid buffer zones of 5, 10 and 20 km around this urban centre. We analysed the type and frequency of land environments underlying cities as indicators of the range of native ecosystems that are (or can potentially be) represented within the broader environmental profile of New Zealand. We identified acutely threatened land environments that are represented within urban and periurban areas and the potential role of cities in enhancing biodiversity from these land environments. 3. New Zealand cities are highly variable in both landform and level of indigenous resource. Thirteen of 20 major land environments in New Zealand are represented in cities, and nearly three-quarters of all acutely threatened land environments are represented within 20 km of city cores nationally. Indigenous land cover is low within urban cores, with less than 2% on average remaining, and fragmentation is high. However, indigenous cover increases to more than 10% on average in the periurban zone, and the size of indigenous remnants also increases. The number of remaining indigenous landcover types also increases from only 5 types within the urban centre, to 14 types within 20 km of the inner urban cores. 4. In New Zealand, ecosystem restoration alone is not enough to prevent biodiversity loss from urban environments, with remnant indigenous cover in the urban core too small (and currently too degraded) to support biodiversity long-term. For some cities, indigenous cover in the periurban zone is also extremely low. This has significant ramifications for the threatened lowland and coastal environments that are most commonly represented in cities. Reconstruction of ecosystems is required to achieve a target of 10% indigenous cover in cities: the addition of land to land banks for this purpose is crucial. Future planning that protects indigenous remnants within the periurban zone is critical to the survival of many species within urban areas, mitigating the homogenisation and depletion of indigenous flora and fauna typical of urbanisation. A national urban biodiversity plan would help city councils address biodiversity issues beyond a local and regional focus, while encouraging predominantly local solutions to restoration challenges, based on the highly variable land environments, ecosystems and patch connectivity present within different urban areas

Perspectives on Exertional Rhabdomyolysis

© 2017, The Author(s). Exertional (exercise-induced) rhabdomyolysis is a potentially life threatening condition that has been the subject of research, intense discussion, and media attention. The causes of rhabdomyolysis are numerous and can include direct muscle injury, unaccustomed exercise, ischemia, extreme temperatures, electrolyte abnormalities, endocrinologic conditions, genetic disorders, autoimmune disorders, infections, drugs, toxins, and venoms. The objective of this article is to review the literature on exertional rhabdomyolysis, identify precipitating factors, and examine the role of the dietary supplement creatine monohydrate. PubMed and SPORTDiscus databases were searched using the terms rhabdomyolysis, muscle damage, creatine, creatine supplementation, creatine monohydrate, and phosphocreatine. Additionally, the references of papers identified through this search were examined for relevant studies. A meta-analysis was not performed. Although the prevalence of rhabdomyolysis is low, instances still occur where exercise is improperly prescribed or used as punishment, or incomplete medical history is taken, and exertional rhabdomyolysis occurs. Creatine monohydrate does not appear to be a precipitating factor for exertional rhabdomyolysis. Healthcare professionals should be able to recognize the basic signs of exertional rhabdomyolysis so prompt treatment can be administered. For the risk of rhabdomyolysis to remain low, exercise testing and prescription must be properly conducted based on professional standards

Pericyte NF-κB Activation Enhances Endothelial Cell Proliferation and Proangiogenic Cytokine Secretion in Vitro

Pericytes are skeletal muscle resident, multipotent stem cells that are localized to the microvasculature. In vivo, studies have shown that they respond to damage through activation of nuclear-factor kappa-B (NF-κB), but the downstream effects of NF-κB activation on endothelial cell proliferation and cell–cell signaling during repair remain unknown. The purpose of this study was to examine pericyte NF-κB activation in a model of skeletal muscle damage; and use genetic manipulation to study the effects of changes in pericyte NF-κB activation on endothelial cell proliferation and cytokine secretion. We utilized scratch injury to C2C12 cells in coculture with human primary pericytes to assess NF-κB activation and monocyte chemoattractant protein-1 (MCP-1) secretion from pericytes and C2C12 cells. We also cocultured endothelial cells with pericytes that expressed genetically altered NF-κB activation levels, and then quantified endothelial cell proliferation and screened the conditioned media for secreted cytokines. Pericytes trended toward greater NF-κB activation in injured compared to control cocultures (P = 0.085) and in comparison to C2C12 cells (P = 0.079). Second, increased NF-κB activation in pericytes enhanced the proliferation of cocultured endothelial cells (1.3-fold,P = 0.002). Finally, we identified inflammatory signaling molecules, including MCP-1 and interleukin 8 (IL-8) that may mediate the crosstalk between pericytes and endothelial cells. The results of this study show that pericyte NF-κB activation may be an important mechanism in skeletal muscle repair with implications for the development of therapies for musculoskeletal and vascular diseases, including peripheral artery disease

PPAR alpha L162V underlies variation in serum triglycerides and subcutaneous fat volume in young males

Background: Of the five sub-phenotypes defining metabolic syndrome, all are known to have strong genetic components ( typically 50 - 80% of population variation). Studies defining genetic predispositions have typically focused on older populations with metabolic syndrome and/or type 2 diabetes. We hypothesized that the study of younger populations would mitigate many confounding variables, and allow us to better define genetic predisposition loci for metabolic syndrome. Methods: We studied 610 young adult volunteers ( average age 24 yrs) for metabolic syndrome markers, and volumetric MRI of upper arm muscle, bone, and fat pre- and post-unilateral resistance training. Results: We found the PPARa L162V polymorphism to be a strong determinant of serum triglyceride levels in young White males, where carriers of the V allele showed 78% increase in triglycerides relative to L homozygotes ( LL = 116 +/- 11 mg/ dL, LV = 208 +/- 30 mg/ dL; p = 0.004). Men with the V allele showed lower HDL ( LL = 42 +/- 1 mg/ dL, LV = 34 +/- 2 mg/ dL; p = 0.001), but women did not. Subcutaneous fat volume was higher in males carrying the V allele, however, exercise training increased fat volume of the untrained arm in V carriers, while LL genotypes significantly decreased in fat volume ( LL = - 1,707 +/- 21 mm(3), LV = 17,617 +/- 58 mm(3); p = 0.002), indicating a systemic effect of the V allele on adiposity after unilateral training. Our study suggests that the primary effect of PPARa L162V is on serum triglycerides, with downstream effects on adiposity and response to training. Conclusion: Our results on association of PPARa and triglycerides in males showed a much larger effect of the V allele than previously reported in older and less healthy populations. Specifically, we showed the V allele to increase triglycerides by 78% ( p = 0.004), and this single polymorphism accounted for 3.8% of all variation in serum triglycerides in males ( p = 0.0037)

Electromagnetic signatures of far-field gravitational radiation in the 1+3 approach

Gravitational waves from astrophysical sources can interact with background electromagnetic fields, giving rise to distinctive and potentially detectable electromagnetic signatures. In this paper, we study such interactions for far-field gravitational radiation using the 1+3 approach to relativity. Linearised equations for the electromagnetic field on perturbed Minkowski space are derived and solved analytically. The inverse Gertsenshtein conversion of gravitational waves in a static electromagnetic field is rederived, and the resultant electromagnetic radiation is shown to be significant for highly magnetised pulsars in compact binary systems. We also obtain a variety of nonlinear interference effects for interacting gravitational and electromagnetic waves, although wave-wave resonances previously described in the literature are absent when the electric-magnetic self-interaction is taken into account. The fluctuation and amplification of electromagnetic energy flux as the gravitational wave strength increases towards the gravitational-electromagnetic frequency ratio is a possible signature of gravitational radiation from extended astrophysical sources.Comment: Published versio

PPARα L162V underlies variation in serum triglycerides and subcutaneous fat volume in young males

<p>Abstract</p> <p>Background</p> <p>Of the five sub-phenotypes defining metabolic syndrome, all are known to have strong genetic components (typically 50–80% of population variation). Studies defining genetic predispositions have typically focused on older populations with metabolic syndrome and/or type 2 diabetes. We hypothesized that the study of younger populations would mitigate many confounding variables, and allow us to better define genetic predisposition loci for metabolic syndrome.</p> <p>Methods</p> <p>We studied 610 young adult volunteers (average age 24 yrs) for metabolic syndrome markers, and volumetric MRI of upper arm muscle, bone, and fat pre- and post-unilateral resistance training.</p> <p>Results</p> <p>We found the PPARα L162V polymorphism to be a strong determinant of serum triglyceride levels in young White males, where carriers of the V allele showed 78% increase in triglycerides relative to L homozygotes (LL = 116 ± 11 mg/dL, LV = 208 ± 30 mg/dL; p = 0.004). Men with the V allele showed lower HDL (LL = 42 ± 1 mg/dL, LV = 34 ± 2 mg/dL; p = 0.001), but women did not. Subcutaneous fat volume was higher in males carrying the V allele, however, exercise training increased fat volume of the untrained arm in V carriers, while LL genotypes significantly decreased in fat volume (LL = -1,707 ± 21 mm³, LV = 17,617 ± 58 mm³; p = 0.002), indicating a systemic effect of the V allele on adiposity after unilateral training. Our study suggests that the primary effect of PPARα L162V is on serum triglycerides, with downstream effects on adiposity and response to training.</p> <p>Conclusion</p> <p>Our results on association of PPARα and triglycerides in males showed a much larger effect of the V allele than previously reported in older and less healthy populations. Specifically, we showed the V allele to increase triglycerides by 78% (p = 0.004), and this single polymorphism accounted for 3.8% of all variation in serum triglycerides in males (p = 0.0037).</p

MC4R Variant Is Associated With BMI but Not Response to Resistance Training in Young Females

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/93697/1/oby_2147_sm_1.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/93697/2/oby.2010.180.pd

INSIG2 gene polymorphism is associated with increased subcutaneous fat in women and poor response to resistance training in men

Background A common SNP upstream of the INSIG2 gene, rs7566605 (g.-10,1025G\u3eC, Chr2:118,552,255, NT_022135.15), was reported to be associated with obesity (Body Mass Index, [BMI]) in a genome-wide association scan using the Framingham Heart Study but has not been reproduced in other cohorts. As BMI is a relatively insensitive measure of adiposity that is subject to many confounding variables, we sought to determine the relationship between the INSIG2 SNP and subcutaneous fat volumes measured by MRI in a young adult population. Methods We genotyped the INSIG2 SNP rs7566605 in college-aged population enrolled in a controlled resistance-training program, (the Functional Polymorphism Associated with Human Muscle Size and Strength, FAMuSS cohort, n = 752 volunteers 18–40 yrs). In this longitudinal study, we examined the effect of the INSIG2 polymorphism on subcutaneous fat and muscle volumes of the upper arm measured by magnetic resonance imaging (MRI) before and after 12 wks of resistance training. Gene/phenotype associations were tested using an analysis of covariance model with age and weight as covariates. Further, the % variation in each phenotype attributable to genotype was determined using hierarchical models and tested with a likelihood ratio test. Results Women with a copy of the C allele had higher levels of baseline subcutaneous fat (GG: n = 139; 243473 ± 5713 mm3 vs. GC/CC: n = 181; 268521 ± 5003 mm3; p = 0.0011); but men did not show any such association. Men homozygous for the G ancestral allele showed a loss of subcutaneous fat, while those with one or two copies of the C allele gained a greater percentage of subcutaneous fat with resistance training (GG: n = 103; 1.02% ± 1.74% vs. GC/CC: n = 93; 6.39% ± 1.82%; p = 0.035). Conclusion Our results show that the INSIG2 rs7566605 polymorphism underlies variation in subcutaneous adiposity in young adult women and suppresses the positive effects of resistance training on men. This supports and extends the original finding that there is an association between measures of obesity and INSIG2 rs7566605 and further implicates this polymorphism in fat regulation