Endurance

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Twins Tashi and Nungshi Malik on endurance trek at the foothills of the Himalayas Endurance training for Mt Carstensz Pyramid.JPG
Twins Tashi and Nungshi Malik on endurance trek at the foothills of the Himalayas

Endurance (also related to sufferance, forbearance, resilience, constitution, fortitude, persistence, tenacity, steadfastness, perseverance, stamina, and hardiness) is the ability of an organism to exert itself and remain active for a long period of time, as well as its ability to resist, withstand, recover from and have immunity to trauma, wounds, or fatigue.

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The term is often used in the context of aerobic or anaerobic exercise. The definition of "long" varies according to the type of exertion – minutes for high intensity anaerobic exercise, hours or days for low intensity aerobic exercise. Training for endurance can reduce endurance strength [ verification needed ] [1] unless an individual also undertakes resistance training to counteract this effect.

When a person is able to accomplish or withstand more effort than previously, their endurance is increasing. To improve their endurance they may slowly increase the amount of repetitions or time spent; in some exercises, more repetitions taken rapidly improve muscle strength but have less effect on endurance. [2] Increasing endurance has been proven to release endorphins resulting in a positive mind.[ citation needed ] The act of gaining endurance through physical activity decreases anxiety, depression, and stress, or any chronic disease [ dubious – discuss ]. [3] Although a greater endurance can assist the cardiovascular system this does not imply that endurance is guaranteed to improve any cardiovascular disease. [4] "The major metabolic consequences of the adaptations of muscle to endurance exercise are a slower utilization of muscle glycogen and blood glucose, a greater reliance on fat oxidation, and less lactate production during exercise of a given intensity." [5]

The term stamina is sometimes used synonymously and interchangeably with endurance. Endurance may also refer to an ability to persevere through a difficult situation, to "endure hardship".

In military settings, endurance is the ability of a force[ clarification needed ] to sustain high levels of combat potential relative to its opponent over the duration of a campaign. [6]

Philosophy

Aristotle noted similarities between endurance and self control: To have self control is to resist the temptation of things that seem immediately appealing, while to endure is to resist the discouragement of things that seem immediately uncomfortable. [7]

Endurance training

Different types of endurance performance can be trained in specific ways. Adaptation of exercise plans should follow individual goals.

Calculating the intensity of exercise the individual capabilities should be considered[ by whom? ]. Effective training starts within half the individual performance capability.[ further explanation needed ] Performance capability is expressed by maximum heart rate. Best[ clarification needed ] results can be achieved in the range between 55% and 65% of maximum heart rate. Aerobic, anaerobic and further thresholds are not to be mentioned within extensive endurance exercises.[ why? ] Training intensity is measured via the heart rate. [8]

Endurance-trained effects are mediated by epigenetic mechanisms

Between 2012 and 2019 at least 25 reports indicated a major role of epigenetic mechanisms in skeletal muscle responses to exercise. [9]

Regulation of transcription in mammals An active enhancer regulatory region is enabled to interact with the promoter region of its target gene by formation of a chromosome loop. This can allow initiation of messenger RNA (mRNA) synthesis by RNA polymerase II (RNAP II) bound to the promoter at the transcription start site of the gene. The loop is stabilized by one architectural protein anchored to the enhancer and one anchored to the promoter, and these proteins are joined together to form a dimer (red zigzags). Specific regulatory transcription factors bind to DNA sequence motifs on the enhancer. General transcription factors bind to the promoter. When a transcription factor is activated by a signal (here indicated as phosphorylation shown by a small red star on a transcription factor on the enhancer) the enhancer is activated and can now activate its target promoter. The active enhancer is transcribed on each strand of DNA in opposite directions by bound RNAP IIs. Mediator (a complex consisting of about 26 proteins in an interacting structure) communicates regulatory signals from the enhancer DNA-bound transcription factors to the promoter. Regulation of transcription in mammals.jpg
Regulation of transcription in mammals
An active enhancer regulatory region is enabled to interact with the promoter region of its target gene by formation of a chromosome loop. This can allow initiation of messenger RNA (mRNA) synthesis by RNA polymerase II (RNAP II) bound to the promoter at the transcription start site of the gene. The loop is stabilized by one architectural protein anchored to the enhancer and one anchored to the promoter, and these proteins are joined together to form a dimer (red zigzags). Specific regulatory transcription factors bind to DNA sequence motifs on the enhancer. General transcription factors bind to the promoter. When a transcription factor is activated by a signal (here indicated as phosphorylation shown by a small red star on a transcription factor on the enhancer) the enhancer is activated and can now activate its target promoter. The active enhancer is transcribed on each strand of DNA in opposite directions by bound RNAP IIs. Mediator (a complex consisting of about 26 proteins in an interacting structure) communicates regulatory signals from the enhancer DNA-bound transcription factors to the promoter.

Gene expression in muscle is largely regulated, as in tissues generally, by regulatory DNA sequences, especially enhancers. Enhancers are non-coding sequences in the genome that activate the expression of distant target genes, [10] by looping around and interacting with the promoters of their target genes [11] (see Figure "Regulation of transcription in mammals"). As reported by Williams et al., [12] the average distance in the loop between the connected enhancers and promoters of genes is 239,000 nucleotide bases.

Endurance exercise-induced long-term alteration of gene expression by histone acetylation or deacetylation

A nucleosome with histone tails set for transcriptional activation DNA in the nucleus generally consists of segments of 146 base pairs of DNA wrapped around nucleosomes connected to adjacent nucleosomes by linker DNA. Nucleosomes consist of four pairs of histone proteins in a tightly assembled core region plus up to 30% of each histone remaining in a loosely organized polypeptide tail (only one tail of each pair is shown). The pairs of histones, H2A, H2B, H3 and H4, each have lysines (K) in their tails, some of which are subject to post-translational modifications consisting, usually, of acetylations [Ac] and methylations {me}. The lysines (K) are designated with a number showing their position as, for instance, (K4), indicating lysine as the 4th amino acid from the amino (N) end of the tail in the histone protein. The particular acetylations [Ac] and methylations {Me} shown are those that occur on nucleosomes close to, or at, some DNA regions undergoing transcriptional activation of the DNA wrapped around the nucleosome. Histone tails set for transcriptional activation.jpg
A nucleosome with histone tails set for transcriptional activation
DNA in the nucleus generally consists of segments of 146 base pairs of DNA wrapped around nucleosomes connected to adjacent nucleosomes by linker DNA. Nucleosomes consist of four pairs of histone proteins in a tightly assembled core region plus up to 30% of each histone remaining in a loosely organized polypeptide tail (only one tail of each pair is shown). The pairs of histones, H2A, H2B, H3 and H4, each have lysines (K) in their tails, some of which are subject to post-translational modifications consisting, usually, of acetylations [Ac] and methylations {me}. The lysines (K) are designated with a number showing their position as, for instance, (K4), indicating lysine as the 4th amino acid from the amino (N) end of the tail in the histone protein. The particular acetylations [Ac] and methylations {Me} shown are those that occur on nucleosomes close to, or at, some DNA regions undergoing transcriptional activation of the DNA wrapped around the nucleosome.

After exercise, epigenetic alterations to enhancers alter long-term expression of hundreds of muscle genes. This includes genes producing proteins and other products secreted into the systemic circulation, many of which may act as endocrine messengers. [12] Of 817 genes with altered expression, 157 (according to Uniprot) or 392 (according to Exocarta) of the proteins produced according to those genes were known to be secreted from the muscles. Four days after an endurance type of exercise, many genes have persistently altered epigentically regulated expression. [12] Four pathways altered were in the platelet/coagulation system, the cognitive system, the cardiovascular system, and the renal system. Epigenetic regulation of these genes was indicated by epigenetic alterations in the distant upstream DNA regulatory sequences of the enhancers of these genes.

Up-regulated genes had epigenetic acetylations added at histone 3 lysine 27 (H3k27ac) of nucleosomes located at the enhancers controlling those up-regulated genes, while down-regulated genes had epigenetic acetylations removed from H3K27 in nucleosomes located at the enhancers that control those genes (see Figure "A nucleosome with histone tails set for transcriptional activation"). Biopsies of the vastus lateralis muscle showed expression of 13,108 genes at baseline before an exercise training program. Six sedentary 23-year-old Caucasian males provided vastus lateralis biopsies before entering an exercise program (six weeks of 60-minute sessions of riding a stationary cycle, five days per week). Four days after the exercise program was completed, biopsies of the same muscles had altered gene expression, with 641 genes up-regulated and 176 genes down-regulated. Williams et al. [12] identified 599 enhancer-gene interactions, covering 491 enhancers and 268 genes, where both the enhancer and the connected target gene were coordinately either upregulated or downregulated after exercise training.

Endurance exercise-induced alteration to gene expression by DNA methylation or demethylation

Endurance muscle training also alters muscle gene expression through epigenetic DNA methylation or de-methylation of CpG sites within enhancers. [13] In a study by Lindholm et al., [13] twenty-three 27-year-old, sedentary, male and female volunteers had endurance training on only one leg during three months. The other leg was used as an untrained control leg. Skeletal muscle biopsies from the vastus lateralis were taken both before training began and 24 hours after the last training session from each of the legs. The endurance-trained leg, compared to the untrained leg, had significant DNA methylation changes at 4,919 sites across the genome. The sites of altered DNA methylation were predominantly in enhancers. Transcriptional analysis, using RNA sequencing, identified 4,076 differentially expressed genes.

The transcriptionally upregulated genes were associated with enhancers that had a significant decrease in DNA methylation, while transcriptionally downregulated genes were associated with enhancers that had increased DNA methylation. In this study, the differentially methylated positions in enhancers with increased methylation were mainly associated with genes involved in structural remodeling of the muscle and glucose metabolism. The differentially decreased methylated positions in enhancers were associated with genes functioning in inflammatory/immunological processes and transcriptional regulation.

Related Research Articles

<span class="mw-page-title-main">Epigenetics</span> Study of DNA modifications that do not change its sequence

In biology, epigenetics is the study of heritable traits, or a stable change of cell function, that happen without changes to the DNA sequence. The Greek prefix epi- in epigenetics implies features that are "on top of" or "in addition to" the traditional genetic mechanism of inheritance. Epigenetics usually involves a change that is not erased by cell division, and affects the regulation of gene expression. Such effects on cellular and physiological phenotypic traits may result from environmental factors, or be part of normal development. They can lead to cancer.

<span class="mw-page-title-main">Euchromatin</span> Lightly packed form of chromatin that is enriched in genes

Euchromatin is a lightly packed form of chromatin that is enriched in genes, and is often under active transcription. Euchromatin stands in contrast to heterochromatin, which is tightly packed and less accessible for transcription. 92% of the human genome is euchromatic.

<span class="mw-page-title-main">Cellular differentiation</span> Developmental biology

Cellular differentiation is the process in which a stem cell changes from one type to a differentiated one. Usually, the cell changes to a more specialized type. Differentiation happens multiple times during the development of a multicellular organism as it changes from a simple zygote to a complex system of tissues and cell types. Differentiation continues in adulthood as adult stem cells divide and create fully differentiated daughter cells during tissue repair and during normal cell turnover. Some differentiation occurs in response to antigen exposure. Differentiation dramatically changes a cell's size, shape, membrane potential, metabolic activity, and responsiveness to signals. These changes are largely due to highly controlled modifications in gene expression and are the study of epigenetics. With a few exceptions, cellular differentiation almost never involves a change in the DNA sequence itself. However, metabolic composition does get altered quite dramatically where stem cells are characterized by abundant metabolites with highly unsaturated structures whose levels decrease upon differentiation. Thus, different cells can have very different physical characteristics despite having the same genome.

A regulatory sequence is a segment of a nucleic acid molecule which is capable of increasing or decreasing the expression of specific genes within an organism. Regulation of gene expression is an essential feature of all living organisms and viruses.

<span class="mw-page-title-main">Skeletal muscle</span> One of three major skeletal system types that connect to bones

Skeletal muscles are organs of the vertebrate muscular system and typically are attached by tendons to bones of a skeleton. The muscle cells of skeletal muscles are much longer than in the other types of muscle tissue, and are often known as muscle fibers. The muscle tissue of a skeletal muscle is striated – having a striped appearance due to the arrangement of the sarcomeres.

<span class="mw-page-title-main">Regulation of gene expression</span> Modifying mechanisms used by cells to increase or decrease the production of specific gene products

Regulation of gene expression, or gene regulation, includes a wide range of mechanisms that are used by cells to increase or decrease the production of specific gene products. Sophisticated programs of gene expression are widely observed in biology, for example to trigger developmental pathways, respond to environmental stimuli, or adapt to new food sources. Virtually any step of gene expression can be modulated, from transcriptional initiation, to RNA processing, and to the post-translational modification of a protein. Often, one gene regulator controls another, and so on, in a gene regulatory network.

Histone methylation is a process by which methyl groups are transferred to amino acids of histone proteins that make up nucleosomes, which the DNA double helix wraps around to form chromosomes. Methylation of histones can either increase or decrease transcription of genes, depending on which amino acids in the histones are methylated, and how many methyl groups are attached. Methylation events that weaken chemical attractions between histone tails and DNA increase transcription because they enable the DNA to uncoil from nucleosomes so that transcription factor proteins and RNA polymerase can access the DNA. This process is critical for the regulation of gene expression that allows different cells to express different genes.

The histone code is a hypothesis that the transcription of genetic information encoded in DNA is in part regulated by chemical modifications to histone proteins, primarily on their unstructured ends. Together with similar modifications such as DNA methylation it is part of the epigenetic code. Histones associate with DNA to form nucleosomes, which themselves bundle to form chromatin fibers, which in turn make up the more familiar chromosome. Histones are globular proteins with a flexible N-terminus that protrudes from the nucleosome. Many of the histone tail modifications correlate very well to chromatin structure and both histone modification state and chromatin structure correlate well to gene expression levels. The critical concept of the histone code hypothesis is that the histone modifications serve to recruit other proteins by specific recognition of the modified histone via protein domains specialized for such purposes, rather than through simply stabilizing or destabilizing the interaction between histone and the underlying DNA. These recruited proteins then act to alter chromatin structure actively or to promote transcription. For details of gene expression regulation by histone modifications see table below.

<span class="mw-page-title-main">CTCF</span> Transcription factor

Transcriptional repressor CTCF also known as 11-zinc finger protein or CCCTC-binding factor is a transcription factor that in humans is encoded by the CTCF gene. CTCF is involved in many cellular processes, including transcriptional regulation, insulator activity, V(D)J recombination and regulation of chromatin architecture.

Chromatin remodeling is the dynamic modification of chromatin architecture to allow access of condensed genomic DNA to the regulatory transcription machinery proteins, and thereby control gene expression. Such remodeling is principally carried out by 1) covalent histone modifications by specific enzymes, e.g., histone acetyltransferases (HATs), deacetylases, methyltransferases, and kinases, and 2) ATP-dependent chromatin remodeling complexes which either move, eject or restructure nucleosomes. Besides actively regulating gene expression, dynamic remodeling of chromatin imparts an epigenetic regulatory role in several key biological processes, egg cells DNA replication and repair; apoptosis; chromosome segregation as well as development and pluripotency. Aberrations in chromatin remodeling proteins are found to be associated with human diseases, including cancer. Targeting chromatin remodeling pathways is currently evolving as a major therapeutic strategy in the treatment of several cancers.

Epigenomics is the study of the complete set of epigenetic modifications on the genetic material of a cell, known as the epigenome. The field is analogous to genomics and proteomics, which are the study of the genome and proteome of a cell. Epigenetic modifications are reversible modifications on a cell's DNA or histones that affect gene expression without altering the DNA sequence. Epigenomic maintenance is a continuous process and plays an important role in stability of eukaryotic genomes by taking part in crucial biological mechanisms like DNA repair. Plant flavones are said to be inhibiting epigenomic marks that cause cancers. Two of the most characterized epigenetic modifications are DNA methylation and histone modification. Epigenetic modifications play an important role in gene expression and regulation, and are involved in numerous cellular processes such as in differentiation/development and tumorigenesis. The study of epigenetics on a global level has been made possible only recently through the adaptation of genomic high-throughput assays.

<span class="mw-page-title-main">EHMT1</span> Protein-coding gene in the species Homo sapiens

Euchromatic histone-lysine N-methyltransferase 1, also known as G9a-like protein (GLP), is a protein that in humans is encoded by the EHMT1 gene.

While the cellular and molecular mechanisms of learning and memory have long been a central focus of neuroscience, it is only in recent years that attention has turned to the epigenetic mechanisms behind the dynamic changes in gene transcription responsible for memory formation and maintenance. Epigenetic gene regulation often involves the physical marking of DNA or associated proteins to cause or allow long-lasting changes in gene activity. Epigenetic mechanisms such as DNA methylation and histone modifications have been shown to play an important role in learning and memory.

In recent years it has become apparent that the environment and underlying mechanisms affect gene expression and the genome outside of the central dogma of biology. It has been found that many epigenetic mechanisms are involved in the regulation and expression of genes such as DNA methylation and chromatin remodeling. These epigenetic mechanisms are believed to be a contributing factor to pathological diseases such as type 2 diabetes. An understanding of the epigenome of Diabetes patients may help to elucidate otherwise hidden causes of this disease.

Even before the very beginning of human space exploration, serious and reasonable concerns were expressed about exposure of humans to the microgravity of space due to the potential systemic effects on terrestrially-evolved life forms adapted to Earth gravity. Unloading of skeletal muscle, both on Earth via bed-rest experiments and during spaceflight, result in remodeling of muscle. As a result, decrements occur in skeletal muscle strength, fatigue resistance, motor performance, and connective tissue integrity. In addition, there are cardiopulmonary and vascular changes, including a significant decrease in red blood cell mass, that affect skeletal muscle function. This normal adaptive response to the microgravity environment may become a liability resulting in increased risk of an inability or decreased efficiency in crewmember performance of physically demanding tasks during extravehicular activity (EVA) or upon return to Earth.

Epigenetic regulation of neurogenesis is the role that epigenetics plays in the regulation of neurogenesis.

Epigenetics of physical exercise is the study of epigenetic modifications to the cell genome resulting from physical exercise. Environmental factors, including physical exercise, have been shown to have a beneficial influence on epigenetic modifications. Generally, it has been shown that acute and long-term exercise has a significant effect on DNA methylation, an important aspect of epigenetic modifications.

H3K4me3 is an epigenetic modification to the DNA packaging protein Histone H3 that indicates tri-methylation at the 4th lysine residue of the histone H3 protein and is often involved in the regulation of gene expression. The name denotes the addition of three methyl groups (trimethylation) to the lysine 4 on the histone H3 protein.

Pharmacoepigenetics is an emerging field that studies the underlying epigenetic marking patterns that lead to variation in an individual's response to medical treatment.

Epigenetics of autoimmune disorders is the role that epigenetics play in autoimmune diseases. Autoimmune disorders are a diverse class of diseases that share a common origin. These diseases originate when the immune system becomes dysregulated and mistakenly attacks healthy tissue rather than foreign invaders. These diseases are classified as either local or systemic based upon whether they affect a single body system or if they cause systemic damage.

References

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  2. ↑ "Muscular Strength and Endurance". HealthLinkBC: Physical Activity Services. 29 November 2016. Archived from the original on 18 December 2018. Retrieved 4 April 2013.
  3. ↑ Hansen, Cheryl J.; et al. (2001). "Exercise Duration and Mood State: How Much Is Enough to Feel Better?" (PDF). Health Psychology . 20 (4): 267–75. doi:10.1037/0278-6133.20.4.267. PMID   11515738. Archived from the original (PDF) on 2010-03-31. Retrieved 2017-10-08.
  4. ↑ Iwasaki, Ken-ichi; Zhang, Rong; Zuckerman, Julie H.; Levine, Benjamin D. (2003-10-01). "Dose-response relationship of the cardiovascular adaptation to endurance training in healthy adults: how much training for what benefit?". Journal of Applied Physiology. 95 (4): 1575–1583. doi:10.1152/japplphysiol.00482.2003. ISSN   8750-7587. PMID   12832429. S2CID   8493563. Archived from the original on 2017-12-03. Retrieved 2017-10-08.
  5. ↑ Holloszy, J.O.; Coyle, E.F. (1 April 1984). "Adaptations of skeletal muscle to endurance exercise and their metabolic consequences". Journal of Applied Physiology. 56 (4): 831–838. doi:10.1152/jappl.1984.56.4.831. PMID   6373687. Archived from the original on 9 July 2019. Retrieved 4 April 2013.
  6. ↑ Headquarter, Department of the Army (1994), Leader's Manual for Combat Stress Control, FM 22-51, Washington D.C.{{citation}}: CS1 maint: location missing publisher (link)
  7. ↑ Aristotle. Nicomachean Ethics. VII.7.
  8. ↑ Tomasits, Josef; Haber, Paul (2008). Leistungsphysiologie – Grundlagen für Trainer, Physiotherapeuten und Masseure (in German). Springer-Verlag. ISBN   9783211720196.
  9. ↑ Widmann M, Nieß AM, Munz B (April 2019). "Physical Exercise and Epigenetic Modifications in Skeletal Muscle". Sports Med. 49 (4): 509–523. doi:10.1007/s40279-019-01070-4. PMID   30778851. S2CID   73481438.
  10. ↑ Panigrahi A, O'Malley BW (April 2021). "Mechanisms of enhancer action: the known and the unknown". Genome Biol. 22 (1): 108. doi: 10.1186/s13059-021-02322-1 . PMC   8051032 . PMID   33858480.
  11. ↑ Marsman J, Horsfield JA (2012). "Long distance relationships: enhancer-promoter communication and dynamic gene transcription". Biochim Biophys Acta. 1819 (11–12): 1217–27. doi:10.1016/j.bbagrm.2012.10.008. PMID   23124110.
  12. 1 2 3 4 Williams K, Carrasquilla GD, Ingerslev LR, Hochreuter MY, Hansson S, Pillon NJ, Donkin I, Versteyhe S, Zierath JR, Kilpeläinen TO, Barrès R (November 2021). "Epigenetic rewiring of skeletal muscle enhancers after exercise training supports a role in whole-body function and human health". Mol Metab. 53: 101290. doi:10.1016/j.molmet.2021.101290. PMC   8355925 . PMID   34252634.
  13. 1 2 Lindholm ME, Marabita F, Gomez-Cabrero D, Rundqvist H, Ekström TJ, Tegnér J, Sundberg CJ (December 2014). "An integrative analysis reveals coordinated reprogramming of the epigenome and the transcriptome in human skeletal muscle after training". Epigenetics. 9 (12): 1557–69. doi:10.4161/15592294.2014.982445. PMC   4622000 . PMID   25484259.

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