Exercise-Induced Skeletal Muscle Growth

Taylor, Nigel A.S.; Wilkinson, John Gardner

doi:10.2165/00007256-198603030-00003

Cited by 61 publications

(41 citation statements)

References 49 publications

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“…Thus, SMA muscle hypoplasia is likely to result from myogenesis defects, independently from and in addition to neuronal death. The fact that in our experimental conditions exercise fails to counteract muscle hypoplasia is consistent with previous data recording that exercise is unable to activate muscle cell proliferation [32].…”

Section: Exercise In Sma: a Milestone In The Treatment Of Neurogenerasupporting

confidence: 93%

Exercise-Induced Neuroprotection in SMA Model Mice: A Means for Determining New Therapeutic Strategies

Charbonnier

2007

Mol Neurobiol

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Due to the prevalence of neuromuscular disorders such as amyotrophic lateral sclerosis and spinal muscular atrophy in modern societies, defining new and efficient strategies for the treatment of these two neurodegenerative diseases has become a vital and still unfulfilled urge. Several lines of experimental evidence have emphasized the benefits of regular exercise training in mouse models for these affections in terms of life span increase and improvement of both motor capacities and motoneuron survival. Identifying molecules that could mimic the neuroprotective effects of exercise represents a promising way to find novel therapies. Some of the effects of exercise are caused by the overproduction of circulating neurotrophic factors, such as IGF-I, whereas others may be due to modifications of the intrinsic properties of the motoneurons within the spinal cord. The causal relationship that links these potential effects of exercise training and the improvement of motor capacity and life span expectancy is consequently discussed.

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Section: Exercise In Sma: a Milestone In The Treatment Of Neurogenerasupporting

confidence: 93%

Exercise-Induced Neuroprotection in SMA Model Mice: A Means for Determining New Therapeutic Strategies

Charbonnier

2007

Mol Neurobiol

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“…In contrast to these observations, short-term heat acclimation increases the activity of the sweat glands. In short-term heat acclimation trials, Taylor (1986) and Sato et al (1990) observed increased sweat output, increased size of the eccrine sweat glands and increased sensitivity of the sweat glands to methacholine stimulation. These findings confirmed that short and long-term acclimation are mediated by distinct physiological mechanisms.…”

Section: Discussionmentioning

confidence: 96%

Tropical Malaysians and temperate Koreans exhibit significant differences in sweating sensitivity in response to iontophoretically administered acetylcholine

et al. 2008

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Natives of the tropics are able to tolerate high ambient temperatures. This results from their long-term residence in hot and often humid tropical climates. This study was designed to compare the peripheral mechanisms of thermal sweating in tropical natives with that of their temperate counterparts. Fifty-five healthy male subjects including 20 native Koreans who live in the temperate Korean climate (Temperate-N) and 35 native tropical Malaysian men that have lived all of their lives in Malaysia (Tropical-N) were enrolled in this study after providing written informed consent to participate. Quantitative sudomotor axon reflex testing after iontophoresis (2 mA for 5 min) with 10% acetylcholine (ACh) was used to determine directly activated (DIR) and axon reflex-mediated (AXR) sweating during ACh iontophoresis. The sweat rate, activated sweat gland density, sweat gland output per single gland activated, and oral and skin temperature changes were measured. The sweat onset time of AXR (nicotinic-receptor-mediated) was 56 s shorter in the Temperate-N than in the Tropical-N subjects (P < 0.0001). The nicotinic-receptor-mediated sweating activity AXR (1), and the muscarinic-receptor-mediated sweating activity DIR, in terms of sweat volume, were 103% and 59% higher in the Temperate-N compared to the Tropical-N subjects (P < 0.0001). The Temperate-N group also had a 17.8% (P < 0.0001) higher active sweat gland density, 35.4% higher sweat output per gland, 0.24 degrees C higher resting oral temperature, and 0.62 degrees C higher resting forearm skin temperature compared to the Tropical-N subjects (P < 0.01). ACh iontophoresis did not influence oral temperature, but increased skin temperature near where the ACh was administered, in both groups. These results suggest that suppressed thermal sweating in the Tropical-N subjects was, at least in part, due to suppressed sweat gland sensitivity to ACh through both recruitment of active sweat glands and the sweat gland output per each gland. This physiological trait guarantees a more economical use of body fluids, thus ensuring more efficient protection against heat stress.

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“…The primary mechanisms involved in muscle mass increase are the proliferative activation (22,23) and myogenic differentiation of mononuclear satellite cells that fuse with the enlarging myofiber, as well as an increased protein synthesis (10,14,30), although some evidence is present that hyperplasia of existing muscle fibers also plays a role in muscle enlargement along with hypertrophy alone (1).…”

Section: Discussionmentioning

confidence: 99%

Genetic polymorphisms of the enzymes involved in DNA methylation and synthesis in elite athletes

Terruzzi¹,

Senesi

Montesano

et al. 2011

Physiological Genomics

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Terruzzi I, Senesi P, Montesano A, La Torre A, Alberti G, Benedini S, Caumo A, Fermo I, Luzi L. Genetic polymorphisms of the enzymes involved in DNA methylation and synthesis in elite athletes. Physiol Genomics 43: 965-973, 2011. First published June 14, 2011 doi:10.1152/physiolgenomics.00040.2010.-Physical exercise induces adaptive changes leading to a muscle phenotype with enhanced performance. We first investigated whether genetic polymorphisms altering enzymes involved in DNA methylation, probably responsible of DNA methylation deficiency, are present in athletes' DNA. We determined the polymorphic variants C667T/A1298C of 5,10-methylenetetrahydrofolate reductase (MTHFR), A2756G of methionine synthase (MTR), A66G of methionine synthase reductase (MTRR), G742A of betaine:homocysteine methyltransferase (BHMT), and 68-bp ins of cystathionine ␤-synthase (CBS) genes in 77 athletes and 54 control subjects. The frequency of MTHFR (AC), MTR (AG), and MTRR (AG) heterozygous genotypes was found statistically different in the athletes compared with the control group (P ϭ 0.0001, P ϭ 0.018, and P ϭ 0.0001), suggesting a reduced DNA methylating capacity. We therefore assessed whether DNA hypomethylation might increase the expression of myogenic proteins expressed during early (Myf-5 and MyoD), intermediate , and late-phase (MHC) of myogenesis in a cellular model of hypomethylated or unhypomethylated C2C12 myoblasts. Myogenic proteins are largely induced in hypomethylated cells [fold change (FC) ϭ Myf-5: 1.21, 1.35; MyoD: 0.9, 1.47; Myf-6: 1.39, 1.66; MHC: 1.35, 3.10 in GMA, DMA, respectively] compared with the control groups (FC ϭ Myf-5: 1.0, 1.38; MyoD: 1.0, 1.14; Myf-6: 1.0, 1.44; MHC: 1.0, 2.20 in GM, DM, respectively). Diameters and length of hypomethylated myotubes were greater then their respective controls. Our findings suggest that DNA hypomethylation due to lesser efficiency of polymorphic MTHFR, MS, and MSR enzymes induces the activation of factors determining proliferation and differentiation of myoblasts promoting muscle growth and increase of muscle mass. myogenesis; muscle hypertrophy; homocysteine cycle; muscle differentiation; hypertrophy PHYSICAL EXERCISE INDUCES considerable metabolic and morphological adaptive changes leading to an altered muscle phenotype with enhanced performance in trained individuals. The mechanism by which exercise exerts its action in athletes is still unclear. While environmental influences such as training scheme and diet are important, there is increasing evidence for strong genetic influences in athletic subjects. It is suggested that athletes possess some genetic advantage predisposing them to better sport performances than nonathletes. Thus, genotype may predict sport ability and performance (9, 41). Gene expression is controlled by an adequate supply of methyl groups to the DNA. Specific mechanisms (Fig. 1) take part in controlling DNA methylation (35): the methionine synthase enzyme (MS) uses MS-bound cobalamin cofactor as intermediate methyl-carrier and N5-methyltetrahy...

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Exercise-Induced Skeletal Muscle Growth

Cited by 61 publications

References 49 publications

Exercise-Induced Neuroprotection in SMA Model Mice: A Means for Determining New Therapeutic Strategies

Exercise-Induced Neuroprotection in SMA Model Mice: A Means for Determining New Therapeutic Strategies

Tropical Malaysians and temperate Koreans exhibit significant differences in sweating sensitivity in response to iontophoretically administered acetylcholine

Genetic polymorphisms of the enzymes involved in DNA methylation and synthesis in elite athletes

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