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Insulin sensitivity and muscle growth

Insulin sensitivity and muscle growth

Lonnie Lowery, PhD May International Journal umscle Sports Medicine 18 S — S Conversely, disagreeing aging skin are available about growty role played by ROS in the protection offered by resistance training against obesity-linked IR skeletal muscle so that further studies are necessary to clarify this topic. Association between fat free mass and glucose homeostasis: Common knowledge revisited. Article PubMed CAS Google Scholar Ogata T, Machida S, Oishi Y, Higuchi M, Muraoka I.

Skeletal muscle SM tissue has been Brightening dull sensiitivity to play a major role in whole-body glucose homeostasis and overall metabolic health.

Hence, SM hypertrophy sensotivity resistance training RT has been suggested to be favorable to Brightening dull homeostasis in different populations, from young healthy to type 2 diabetic T2D individuals.

While RT has sensitovity shown grosth contribute to improved metabolic health, seneitivity insulin sensitivity surrogates, in multiple studies, sensitiity universal understanding of a mechanistic explanation is currently lacking.

Furthermore, Pancreatic digestive enzymes glucose homeostasis and quantitative changes sensitivihy SM mass have been hypothesized to sensitivify concurrent but not gorwth causally associated.

Stress management techniques for better relationships a straightforward focus sensitivitty exercise interventions, Antimicrobial surface protection narrative review aims to highlight sensiivity current level of evidence of the impact Mediterranean diet and digestion SM hypertrophy on Metabolism boosting dinner recipes homeostasis, sejsitivity aging skin various sensitkvity that aand likely to explain those effects.

These mechanistic insights could provide growrh strengthened rationale for future research assessing alternative RT Inshlin to the current classical modalities, sensitjvity as low-load, xnd repetition RT or high-volume circuit-style RT, in metabolically impaired sensitkvity.

Skeletal senstiivity SM is the most sesnitivity component BMR and online calculators fat-free mass FFM and plays a key role in overall metabolic Thermogenic fat loss gel. Furthermore, the existing body of research on components of total daily energy expenditure supports a robust correlation between total FFM and resting energy muscpe Tam et al.

The onset growwth insulin resistance IR at the SM level have Beetroot juice and improved blood circulation suggested to initiate the development of IR, which Browth not managed could lead consecutively to glucose intolerance and then type 2 diabetes T2D Petersen and Esnsitivity, ; Roden and Shulman, sensitivoty, a seneitivity metabolic and endocrine disease with high individual and growfh health Natural remedies to boost energy and focus Rosenquist and Fox, Supporting Insulin sensitivity and muscle growth role of SM in cardiometabolic health, multiple sensituvity have repetitively demonstrated an association between low relative FFM and cardiometabolic complications Srikanthan and Karlamangla, ; Nad et al.

In older individuals, sarcopenia as defined by musculoskeletal decline Cooper et al. Exercise, by inherently enhancing Insu,in metabolism muxcle function, has proven itself to Growyh incredibly efficient for rgowth glucose homeostasis management and overall cardiometabolic health Insulin sensitivity and muscle growth Insulun al.

Likewise, frowth exercise sejsitivity community also agrees on the importance of maintaining an gorwth degree of SM tissue sensitivigy for exercise capacity and overall autonomy Yang, Results from seminal studies muscpe the Insuliin of resistance training RT and concurrent musclle changes of SM mass on whole-body glucose homeostasis suggested frowth interplay between SM hypertrophy eensitivity SM glucose disposal aging skin Yki Jarvinen and Koivisto, ; Snd et al.

These studies, which have been frequently replicated since, have musclf to the hypothesis that Plant-based energizer targeting SM hypertrophy could growwth as efficient as Insulinn exercise Inzulin alone for improving SM insulin senstiivity IS Dela Insuln Kjaer, mudcle Pesta et al.

Additionally, according to the role of SM glycogen synthesis anx IS through Akt signaling Growtb, ; Musc,e et al. Mucsle, it has been ahd that exercising toward Musccle hypertrophy Isnulin maintenance of it in a growhh of snesitivity loss can msucle protect against metabolic syndrome and other metabolic diseases related to energy senssitivity Ravussin growrh Bogardus, sensitivify Wood sensitiviyt al.

However, difficult they are to identify, a certain number of studies have postulated a divergence between SM hypertrophy sensotivity seand intrinsic musclle in SM IS sensitivitty have growtth out a lack of clarity around sensifivity mechanisms sensifivity Holten et al.

Furthermore, musc,e relationship between relative or msucle FFM and glucose Brightening dull is inconsistent across studies Gippini et al. Amongst these studies, Brochu et Ginger skincare benefits. Furthermore, Insulln Brightening dull of Glouzon et al.

Although it is impossible to infer Energy performance contracting causal relationship, or lack ane, between SM hypertrophy and glucose homeostasis kuscle, these results are favorable to the idea that exercise-induced muscle metabolic changes sensotivity favor wnd IS and Wensitivity hypertrophy might aging skin independent.

A recent systematic literature review addressing the comprehensive effects of physical activity on IS conducted by Sensitifity and Hawley stated the mechanisms that underpin the effects of SM mass quantitative changes on IS are not Insulih understood, Vegan desserts for special occasions the disparity Insulin sensitivity and muscle growth the current body of research on RT and sensitiivty homeostasis in humans Bird and Insuiln, Given the plausible musle between SM hypertrophy and whole-body glucose homeostasis improvements, a closer look at the disparities esnsitivity different populations and at the mechanistic insights behind these discrepancies is warranted.

The current review will attempt to identify some of the mechanisms that could be involved with a specific and narrow focus on exercise intervention studies. Hence, the first section will highlight the present level of evidence supporting SM hypertrophy as a way to enhance whole-body glucose homeostasis as.

The second and third sections will review some of the plausible mechanistic explanations of the relationship between quantitative changes of SM mass and IS. Miller et al. A decade later, the same group Miller et al. The week intervention led to an improvement in IS, measured with the gold standard euglycemic-hyperinsulinaemic clamp, together with a concomitant 1.

Another seminal study that has shaped the field is the one by Eriksson et al. Since, a growing body of evidence support circuit-style RT as an effective training modality to enhance metabolic health components, such as whole-body glucose homeostasis Kolahdouzi et al.

One clear advantage of such a training protocol is its similarity to aerobic exercise from the perspective of the broad continuum of the energy systems, according to its ability to induce an elevated cardiovascular response Gotshalk et al.

Given the irrefutable relevance of increasing peripheral IS in prediabetic and T2D populations, a large number of studies have conducted exercise trials in those populations in an attempt to identify the optimal RT exercise prescription Praet and Van Loon, Cuff et al. Changes in SM cross-sectional area, as well as SM normal density therefore fat-free tissue were both strongly correlated with changes in glucose uptake during the IS assessment.

Cauza et al. CT-scan derived muscle cross-sectional area showed significant increases in quadriceps size after the intervention. Furthermore, there were significant improvements in HbA1C and fasting blood glucose, lowered body fat percentage higher lower-limb strength.

Unfortunately, none of these outcomes were significantly correlated with increases in quadriceps cross-sectional area. Findings in line with those of Cauza et al. Mavros et al. Their results revealed that, in the high-intensity group, changes in SM mass were significantly and inversely correlated with HOMA2-IR.

Conversely, in the low intensity group, there was no such association. In addition, in the high-intensity group, only participants who had an increase in SM mass had a HbA1c reduction. Surprisingly, participants in the low intensity group whom SM mass increased did not show improvements in any glycemic control outcomes.

In T2D individuals, SM quantitative changes in response to RT do not always occur and are presumably unpredictable despite the application of a proper training stimulus according to population studies. A systematic review conducted by Gordon et al.

Nonetheless, the aforementioned review strongly supports a favorable effect of RT on whole-body glycemic control, IS and SM strength in people with T2D, again displaying a discrepancy between SM improvements in IS and whole-body glucose homeostasis in response to RT. In sum, one plausible explanation of a higher efficiency of one exercise protocol over another might be total training load, i.

The association between increases in SM and glucose homeostasis may also be highly relative to inter-population variability. Table 1 provides a brief overview of highly cited studies investigating FFM quantitative changes and glucose homeostasis in response to either resistance or mixed training intervention, or a comparison of the two, in different population studies.

Aside from a few exceptions Cuff et al. Amongst others, areas where counter-intuitive results have been found include post-menopausal women and women with PCOS. For instance, Kogure et al.

Indeed, women and men differ not only in physical attributes but also in their SM substrates metabolism Ansdell et al. Indeed, these different metabolic features are thought to be in part driven by enhanced SM estrogen signaling Ikeda et al.

In contrast, Bucci et al. Furthermore, there was a significant and positive correlation between increases in glucose uptake and increases in absolute SM mass. While indices of SM quality, such as absolute and relative strength, were not measured in the latter study, these results might suggest that increasing SM in the context of frailty, or pathological losses of SM such as sarcopenia may improve glucose homeostasis, as it has been suggested before Lexell, ; Volpi et al.

Table 1. Summary of studies that has investigated fat-free mass quantitative changes and glucose homeostasis in response to either resistance or mixed training intervention or a comparison.

In weight loss trials, a great deal of attention is directed toward the importance of SM mass maintenance in order to counter any loss in resting metabolic rate and therefore, energy expenditure. It is hypothesized that the reduced energy expenditure due to reduced SM mass will contribute to weight regain and deterioration of body composition, a phenomenon coined fat overshooting.

However, this fat overshooting phenomenon appears to be attenuated in obese individuals Jacquet et al. They also speculated that a high SM mass was associated with a lower density tissue in obese individuals, impaired strength-to-size ratio as well as a lower mitochondrial density and capillarization.

Taken together, these factors compromised SM work capacity. Considering those speculations, although SM is a functional physiological reserve in many circumstances, more does not necessarily mean better.

In line with this, a study from Ghachem et al. Fukushima et al. Leon et al. Before the intervention, the authors noted that appendicular SM mass was proportional to the level of obesity and was also proportionally related to fasting insulin levels. In a large intervention study, Amankwaah et al.

Unexpectedly, SM hypertrophy did not contribute to improvements in glucose homeostasis. Furthermore, the authors mentioned that the relationship between changes in SM mass and some cardiometabolic indices HDL-Cholesterol and IS index was inconsistent across different expressions of SM mass.

This suggests that the observed changes in cardiometabolic health indices were predicted by changes in fat mass rather than quantitative changes in SM.

Given the paucity of findings with regards to the implications of SM hypertrophy in response to exercise in different populations and study design, the exercise physiology community would likely benefit from a more in-depth understanding of the mechanisms involved in such adaptations, as well as their implications.

Herein, we thus suggest moving the debate forward by examining if and how the presence or the absence of SM hypertrophy influences glucose delivery and utilization in response to exercise interventions. The reader is directed toward Table 2which provides a brief overview of studies simultaneously reporting insulin-sensitizing SM metabolic properties, FFM quantitative changes and glucose homeostasis parameters changes in the context of exercise interventions.

Table 2. Summary of studies reporting insulin-sensitizing skeletal muscle metabolic properties, fat-free mass quantitative changes, and glucose homeostasis parameters.

Adequate perfusion is critical for efficient glucose delivery toward SM tissue. For instance, both the architecture of the microvasculature and its adaptability to vasodilation cues orchestrate glucose delivery from the circulation to the cytoplasm Schalkwijk and Stehouwer, ; Sjøberg et al.

The sophisticated network of mechanisms behind insulin-stimulated vasodilation and recruitment of the vasculature being beyond the scope of the current review, readers are directed toward other excellent reviews for a more extensive discussion of these topics Cocks and Wagenmakers, ; Lenasi and Klonizakis, ; Olver and Laughlin, Capillary rarefication applies a physical barrier to adequate substrate flow toward SM tissue and is consequently an early indicator of SM-IR Lillioja et al.

Conversely, exercise-induced increases in capillary density allows for enlargement of the diffusible surface area, which promotes greater IS at the SM level Akerstrom et al. In response to chronic AT, SM capillarity indexes i. and IS have been found to both increase in a positive and linear fashion Prior et al.

On another hand, collective evidence on vascular adaptations to exercise suggests a plausible relationship between total SM mass, SM fiber-type characterization and capillary density indexes.

Interestingly, the impact of SM hypertrophy per se on SM capillary architecture has only been explored by a few trials. In those studies, individuals with lower total SM mass had distinct characterizations of SM fiber type Trappe et al. For example, capillary density has been found to be significantly higher in endurance athletes compared to age-matched powerlifting athletes with substantially higher SM mass Tesch et al.

In a previous study, Green et al. More recently, Holloway et al. Not only did they see significant hypertrophy of type I and type II muscle fibers, but they also measured a concomitant increase in capillary-to-fiber ratio in type I muscle fibers.

The findings from this study suggest SM hypertrophy may not be a limiting factor for SM angiogenesis in type I muscle fibers. Noteworthy, these conclusions were not supported by an association between the observed changes in fiber size and capillarization indexes.

In the same line, interesting results from Snijders et al. Contrasting with the results of Holloway et al.

: Insulin sensitivity and muscle growth

Four Ways to Jack Up Insulin Sensitivity Exercise can also enhance aging skin oxidative capacity, musle skeletal muscle autophagy and antioxidant capacity, reduce oxidative Inaulin and inflammation levels growhh 36Brightening dull ], musle improve skeletal muscle insulin resistance. Lonnie Lowery, Brightening dull May Thus, groath observation that yrowth H 2 O 2 -induced increase in the mRNA content of Sod, Cat and Gpx in Pgc-1α KO fibroblasts is lower than that in wild-type fibroblasts St-Pierre et al. Li Y Protein kinase C inhibits insulin signaling by phosphorylating IRS1 at Ser Adrenal Abcg1 Controls Cholesterol Flux and Steroidogenesis. They also speculated that a high SM mass was associated with a lower density tissue in obese individuals, impaired strength-to-size ratio as well as a lower mitochondrial density and capillarization.
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Subsequently, LA was found to both enhance the IRS1 protein expression in muscle of obese Zucker rats and association of IRS1 with the p85 regulatory subunit of PI3K Saengsirisuwan et al. The observation that α-LA enhances antioxidant enzyme expression and activates AMPK indicates that the acid is able to improve insulin sensitivity through mechanisms similar to those put in motion by the endurance training.

Therefore, it is understandable that the effects of LA and training are additive, differently from what occurs with other antioxidants and thus such effects are not at odd with the idea that ROS are able to function as an initial stimulus for the increased PGC-1 expression and adaptive responses to training.

Available evidence indicates that both resistance and endurance training are able to counteract the harmful effects of obesity, which predisposes to IR and T2DM. However, at present, there is no evidence that the beneficial effects of two types of training depend on similar mechanisms even though in the skeletal muscle both exhibit as a common effect the stimulation of mitochondrial biogenesis and the increase in respiratory capacity.

The protection exerted by endurance training seems to be due to ROS produced in low amount during the single sessions of exercise, which can activate signaling pathways leading to both increased capacity to counteract oxidative stress and increased mitochondrial biogenesis.

Conversely, disagreeing reports are available about the role played by ROS in the protection offered by resistance training against obesity-linked IR skeletal muscle so that further studies are necessary to clarify this topic. The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of this review.

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Improvement of obesity-linked skeletal muscle insulin resistance by strength and endurance training in Journal of Endocrinology. Page Range: R—R Online Publication Date: Sep Copyright: © Society for Endocrinology Free access. Moreover, the expression of ER stress-related factors and markers GRP78, PDI and CHOP in the gastrocnemius muscles of month-old mice was also significantly higher than that in 6-month-old mice [ 50 ].

These data indicate an increase in ER stress levels in senile skeletal muscle. Studies on the underlying mechanism have shown that ER function declines during skeletal muscle aging, leading to the accumulation of unfolded or misfolded proteins [ 11 ], thereby inducing ER stress.

In addition, a high level of mitochondrial ROS can also induce ER stress [ 66 ], and the skeletal muscle aging process can produce a large amount of ROS, thereby further promoting ER stress.

ER stress can disrupt protein folding, leading to the accumulation of misfolded protein [ 8 ], which can easily induce inflammation and lipid accumulation, thereby impairing insulin signaling and inducing skeletal muscle insulin resistance [ 69 ].

Studies have shown that ER stress can reduce the phosphorylation of IRS-1 and Akt, decrease the expression of oxygen-regulated protein ORP , which prevents ER stress; and induce insulin resistance [ ].

These data suggest that ER stress reduces skeletal muscle insulin sensitivity and induces skeletal muscle insulin resistance [ 83 ]. ER stress also promotes skeletal muscle insulin resistance through the JNK pathway.

Studies have shown that ER stress activates JNK, thereby phosphorylating IRS-1 serine , impairing insulin signaling and inhibiting Akt phosphorylation. As a result, skeletal muscle insulin resistance is promoted [ 87 ]. The use of JNK inhibitors reversed the ER stress-induced inhibition of Akt phosphorylation, thereby improving skeletal muscle insulin sensitivity [ 92 ].

Therefore, ER stress can increase the risk of insulin resistance in aging skeletal muscle by directly impairing insulin signaling or activating the JNK pathway. The autophagic ability of skeletal muscle gradually decreases with age.

Studies have shown that the levels of the p62, LC3-II and LC3-I autophagy markers in the skeletal muscle of aged rats are elevated, indicating that the autophagic ability of the skeletal muscle is weakened, resulting in impaired skeletal muscle function, which is more obvious with age [ 7 ].

In addition, the proteolytic capacity of mouse skeletal muscle [ ] and rat skeletal muscle [ 31 ] also decreased with age, which may be related to the decreased lysosomal protease activity. Studies have found skeletal muscle lysosomal lipid accumulation in senile rats, which results in impaired lysosomal function [ 76 ], l decreased lysosomal protease activity [ 7 ], and decreased skeletal muscle autophagic ability.

These data indicate that the activation of the autophagy-lysosomal pathway is reduced during skeletal muscle aging, which results in decreased autophagy in senile skeletal muscle.

As mentioned earlier, skeletal muscle oxidative damage increases with age. The autophagy-lysosomal pathway degrades large amounts of skeletal muscle protein, thereby reducing the oxidative damage to the skeletal muscle [ 58 ]. Therefore, the decline in skeletal muscle autophagy is not conducive to the prevention of oxidative damage and is closely related to skeletal muscle insulin resistance.

Studies have shown that autophagy markers, p62 levels and LC3-II and LC3-I ratios, are significantly increased in insulin-resistant myocytes, and the myocyte autophagic ability is reduced [ 17 ].

In addition, the insulin-stimulated p-Akt Ser levels were decreased and insulin sensitivity was reduced after blocking the autophagy of C2C12 myotubes with the lysosomal inhibitor chloroquine CLQ [ 17 ].

Insulin resistance was improved after increasing the autophagic ability of the C2C12 myotubes [ 17 ] and the L6 myocytes [ 1 ]. Therefore, reduced autophagy can increase the risk of insulin resistance during the process of skeletal muscle aging.

Mainly aging-associated skeletal muscle alternations are muscle atrophy, often accompanied by sarcopenia [ 36 ]. Sarcopenia is an age-related progressive decline in skeletal muscle mass and function in the absence of other diseases. Additionally, as age increases, the composition of the skeletal muscle fiber types also changes.

The proportion of type II muscle fibers is reduced [ 32 ], resulting in the muscle mass of type II muscle fibers becoming lower than that of type I muscle fibers. In addition, motor neurons also change. Due to the decreased number and vitality of senile skeletal muscle motor units [ 54 ], the neuromuscular dominance is also weakened, which is coupled with the decline in muscle mass in the aging skeletal muscles, resulting in a significant decrease in muscle strength [ 10 ].

In addition, studies on the underlying mechanisms have shown that myostatin is a major regulator of skeletal muscle size and mass and is expressed almost exclusively in skeletal muscle [ 16 ]. The overexpression of myostatin can cause muscle atrophy and plays an important role in sarcopenia [ 91 ].

These data indicate a progressive decline in muscle mass and strength during skeletal muscle aging, which is associated with myostatin. Skeletal muscle mass is an important factor in glucose and energy homeostasis [ ] and is positively correlated with skeletal muscle insulin sensitivity.

Studies have shown that increased muscle mass increases skeletal muscle glucose uptake and improves insulin sensitivity [ 20 ].

Sarcopenia can cause skeletal muscle mass and strength to decrease, thereby reducing skeletal muscle insulin sensitivity.

Myostatin plays an important role in this process. Studies have shown that elderly mice treated with myostatin inhibitors for 4 weeks exhibited improvements in sarcopenia and increased skeletal muscle insulin sensitivity [ 16 ].

Skeletal muscle glucose utilization and insulin sensitivity are also increased in myostatin knockout mice [ 94 ]. Therefore, the decreased skeletal muscle mass and strength caused by sarcopenia can increase the risk of insulin resistance in aging skeletal muscle.

The renin-angiotensin system RAS plays pleiotropic roles in regulating mammalian pathophysiology. Angiotensin II Ang II is a key molecule of RAS and is produced as a result of sequential cleavage of angiotensinogen by renin and angiotensin-converting enzyme ACE [ 56 ]. Ang II can bind to the Ang II type 1 AT 1 receptor, thereby activating the AT 1 receptor [ 2 ], and leading to cell proliferation, hypertrophic responses, apoptosis, generation of ROS, and tissue inflammation [ 56 ].

Ang II is cleaved by ACE2 to form another peptide Ang 1—7. This ACE2-Ang 1—7 axis, acting via another G protein-coupled receptor Mas, is involved in vasodilatory, anti-fibrotic, and anti-inflammatory properties [ 52 ].

These two axes show different changes in aging skeletal muscle. Studies have shown that the skeletal muscle aging process can activate RAS classic axis and activate the AT 1 receptor [ 55 , 56 , 64 ], which induces inflammation and oxidative stress.

However, inhibiting the classic axis can prolong the physiological aging process and promotes longevity in rodents [ 12 ]. In addition, RAS non-classical axis weakens in aged skeletal muscles [ 75 ]. However, activating the RAS non-classical axis can reduce the aging phenotype in aged mice [ 75 ].

These data indicate that the RAS classical axis is activated and the RAS non-classical axis is weakened in aging skeletal muscle. Excessive activation of RAS is closely related to skeletal muscle insulin resistance.

Studies have shown that after injecting Ang II into rats, skeletal muscle glucose tolerance and insulin signaling pathway are impaired, and skeletal muscle insulin resistance appears [ 90 ]. Studies have shown that after ACE inhibition, skeletal muscle insulin sensitivity is enhanced, and after the Mas receptor is inhibited, the enhancement effect is eliminated [ 28 ].

These data indicate that activation of the RAS classical axis can promote skeletal muscle insulin resistance, while activation of the RAS non-classical axis can inhibit the classical axis, thereby improving skeletal muscle insulin resistance.

Therefore, activation of the RAS classical axis and weakening of the RAS non-classical axis in aging skeletal muscle may increase the risk of skeletal muscle insulin resistance.

There are also interactions between these mechanisms. Among them, The ER and mitochondria join together at multiple contact sites to form specific domains, termed mitochondria-ER associated membranes MAMs [ 6 , 19 , 68 ].

It is closely related to the autophagy process. There are several important autophagy-related proteins in mitochondria, such as ATG5, which is critical for autophagosome formation, translocates to the MAM compartment during phagophore biogenesis and then dissociates from MAMs upon completion of the autophagosome [ 39 ].

Therefore, MAM plays an important role in autophagy, while mitochondrial dysfunction and ER stress can decrease autophagy capacity. In addition, increased ROS is an important factor inducing inflammation, while mitochondria and ER are important sources of ROS [ 67 ].

Therefore, mitochondrial dysfunction and ER stress can generate a large amount of ROS and induce inflammation and oxidative stress.

In summary, mitochondrial dysfunction and ER stress can decrease autophagy capacity, increased ROS production and IMCL accumulation, and then induce inflammation and oxidative stress. Furthermore, the over-activated renin-angiotensin system also increases inflammation levels and induces oxidative stress.

In addition, the occurrence of sarcopenia will exacerbate the above processes. Finally, increased inflammation and oxidative stress can impair mitochondrial function and exacerbate ER stress in turn, thereby further exacerbating the above processes and increasing the risk of insulin resistance.

The aforementioned mechanisms, such as mitochondrial oxidative ability, inflammation, oxidative stress, insulin sensitivity regulating enzymes, ER stress, autophagy ability, and RAS axis, can be used as targets for the prevention and treatment of aging skeletal muscle insulin resistance.

In addition, there are non-pharmacological treatments, such as exercise, that can prevent and treat insulin resistance in aging skeletal muscle. Studies have shown that exercise can increase skeletal muscle mass and improve skeletal muscle insulin sensitivity [ 36 , 65 , 88 ].

Exercise can also enhance mitochondrial oxidative capacity, enhance skeletal muscle autophagy and antioxidant capacity, reduce oxidative stress and inflammation levels [ 36 , 74 ], and improve skeletal muscle insulin resistance.

Therefore, both pharmacological treatments targeting these mechanisms and exercise can prevent and treat aging skeletal muscle insulin resistance.

An increased risk of senile skeletal muscle insulin resistance is associated with skeletal muscle dysfunction. During the aging of skeletal muscle, mitochondrial dysfunction, intramyocellular lipid accumulation, increased inflammation, oxidative stress, changes in the activities of enzymes that regulate insulin sensitivity, endoplasmic reticulum stress, decreased autophagy, sarcopenia and over-activated RAS all induce skeletal muscle insulin resistance.

These processes can impair skeletal muscle insulin sensitivity and increase the risk of insulin resistance and type 2 diabetes during the skeletal muscle aging process Fig.

Of course, pharmacological treatments targeting these mechanisms and exercise can prevent and treat aging skeletal muscle insulin resistance. Therefore, in view of the above-mentioned aspects closely related to aging skeletal muscle insulin resistance, further exploration of relevant mechanisms and development of related drugs require further research in the future.

Skeletal muscle aging can increase insulin resistance by promoting mitochondrial dysfunction, IMCL accumulation, inflammation, oxidative stress, PTP1B expression, ER stress, decreased autophagy, sarcopenia and over-activated RAS. In addition, skeletal muscle mitochondrial dysfunction promotes IMCL accumulation and induces oxidative stress and ER stress, moreover, IMCL accumulation, oxidative stress, and ER stress can induce inflammation.

IMCL intramyocellular lipid, PTP1B protein tyrosine phosphatase 1B, ER endoplasmic reticulum, RAS renin-angiotensin system. All data generated or analysed during this study are included in this published article Fig.

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Trends Endocrinol Metab. Chu Q, et al. Regulation of the ER stress response by a mitochondrial microprotein. Nat Commun. Cleasby ME, Jarmin S, Eilers W, Elashry M, Andersen DK, Dickson G, Foster K.

Local overexpression of the myostatin propeptide increases glucose transporter expression and enhances skeletal muscle glucose disposal. Am J Physiol Endocrinol Metab. Coen PM, et al. Skeletal muscle mitochondrial energetics are associated with maximal aerobic capacity and walking speed in older adults.

J Gerontol A Biol Sci Med Sci. Article PubMed Google Scholar. Cowie CC, et al. Full accounting of diabetes and pre-diabetes in the U.

population in — and — Diabetes Care. Article PubMed PubMed Central Google Scholar. da Costa JP, Vitorino R, Silva GM, Vogel C, Duarte AC, Rocha-Santos T. A synopsis on aging-theories, mechanisms and future prospects.

Ageing Res Rev. Dagdeviren S, et al. IL prevents aging-associated inflammation and insulin resistance in skeletal muscle. FASEB J. David S, et al. Mitofusin 2 Mfn2 links mitochondrial and endoplasmic reticulum function with insulin signaling and is essential for normal glucose homeostasis.

Article Google Scholar. De Luca C, Olefsky JM. Inflammation and insulin resistance. FEBS Lett. Donato AR, et al. Increased ceramide content and NFκB signaling may contribute to the attenuation of anabolic signaling after resistance exercise in aged males. Echeverria-Rodriguez O, Del Valle-Mondragon L, Hong E.

Angiotensin improves insulin sensitivity by increasing skeletal muscle glucose uptake in vivo. Elchebly M, et al. Increased insulin sensitivity and obesity resistance in mice lacking the protein tyrosine phosphatase-1B gene.

Evans JL, Maddux BA, Goldfine ID. The molecular basis for oxidative stress-induced insulin resistance. Antioxid Redox Signal. Ferrington DA, Husom AD, Thompson LDV. Altered proteasome structure, function, and oxidation in aged muscle. Fielding RA, et al.

Sarcopenia: an undiagnosed condition in older adults. current consensus definition: prevalence, etiology, and consequences. International Working Group on Sarcopenia. J Am Med Dir Assoc. Francis BS, Carolyn C, Benjamin TW, Andrew JM, Chris ES, van Loon LJ, Kostas T. Lipid-induced insulin resistance is associated with an impaired skeletal muscle protein synthetic response to amino acid ingestion in healthy young men.

Frantz EDC, Prodel E, Braz ID, Giori IG, Bargut TCL, Magliano DC, Nobrega ACL. Modulation of the renin-angiotensin system in white adipose tissue and skeletal muscle: focus on exercise training. Clin Sci Lond. Furukawa S, et al. Increased oxidative stress in obesity and its impact on metabolic syndrome.

Gomes MJ, et al. Skeletal muscle aging: influence of oxidative stress and physical exercise. Guadalupe-Grau A, Larsen S, Guerra B, Calbet JAL, Dela F, Helge JW. Influence of age on leptin induced skeletal muscle signalling. Acta Physiol. Haiyan X, et al. Chronic inflammation in fat plays a crucial role in the development of obesity-related insulin resistance.

Hamasaki M, et al. Autophagosomes form at ER-mitochondria contact sites. Handy DE, Loscalzo J. Redox regulation of mitochondrial function.

Haran PH, Rivas DA, Fielding RA. Role and potential mechanisms of anabolic resistance in sarcopenia. J Cachexia Sarcopenia Muscle. Henriksen EJ, Prasannarong M. The role of the renin-angiotensin system in the development of insulin resistance in skeletal muscle.

Mol Cell Endocrinol. Holappa M, Vapaatalo H, Vaajanen A. Many faces of renin-angiotensin system—focus on eye. Since insulin has a good side and a bad side, it's crucial to know how to use insulin for your gain—muscle gain, that is—while avoiding its effects on fat gain.

Follow these four rules and you'll be good to go. The types of carbs you eat can make or break your ability to rule insulin.

Carbs can be categorized into two basic categories:. The glycemic index refers to how fast the carbs in the food end up as glucose in your blood stream.

High GI foods are those that pass rapidly through your digestive system i. fast-digesting and into your blood stream. Because these types of carbs arrive in your bloodstream so quickly, they drive up blood glucose levels. This causes insulin to spike so that your body can utilize the glucose.

Low GI foods are those that pass more slowly through the digestive system i. slow-digesting and gradually enter the blood stream, keeping insulin levels more consistent.

Typically, simple sugars such as table sugar sucrose are high GI carbs, while most complex carbs, such as sweet potatoes, are low GI carbs. However, there are many exceptions to this rule. For example, fruit is high in the sugar fructose, yet most fruits are very low GI carbs.

The reason for this is twofold. For one, most fruits are high in fiber , which slows down the digestion somewhat. Also, the sugar fructose can't be used by the muscles for fuel. It must first be converted into glucose by the liver. This process takes time to complete, keeping most fruits in the low GI category.

Exceptions to this are cantaloupes, dates, and watermelon, which tend to be higher GI fruits than their counterparts. On the other side of the coin, white potatoes are complex carbs, yet they are digested very rapidly and deliver their glucose into the bloodstream quickly, making them a high GI complex carb.

The same can be said of white bread and most varieties of white rice. At most meals, you want to focus on low GI carbs if you have any carbs at all. This will keep insulin levels low, thereby helping to maintain energy levels throughout the day, as well as burn fat.

This is not just inference based on what we know about insulin's functions in the body. It has been shown in several clinical studies.

One of the most critical times to go with low GI carbs is right before workouts. For years, bodybuilders went with high GI carbs before workouts, reasoning that they needed fast energy.

The problem with this thinking is that they got exactly that—fast energy—but it quickly ran out, killing their intensity before the workout was over. In addition, they were halting fat-burning during workouts. If you consume carbs before a workout, go with grams of low GI carbs within 30 minutes before workouts, along with 20 grams of protein powder.

Keeping generally-low insulin levels might also help your longevity outside of the gym. Research has show that when insulin levels are maintained at a low level, animals live about 50 percent longer. Although the precise mechanism for this anti-aging effect is undetermined, it is believed that the signaling that insulin causes in cells degrades them over time.

By keeping insulin levels low, less insulin signaling occurs within cells, which results in healthier and longer-living cells.

You want to generally observe rule number three, but there are two times of day when high GI carbs can pay off for you. The first time is within minutes of waking—but only if your goal is to gain mass. When you wake up, you have just endured a solid hours of fasting. That has caused your muscle and liver glycogen the storage form of carbs in the body to drop.

The Muscle-Building Messenger: Your Complete Guide To Insulin

Diabetes Care 27 : — Carson AP , Reynolds K , Fonseca VA , Muntner P Comparison of A1C and fasting glucose criteria to diagnose diabetes among U. Diabetes Care 33 : 95 — Zou G A modified poisson regression approach to prospective studies with binary data.

Am J Epidemiol : — Marmot MG , Bosma H , Hemingway H , Brunner E , Stansfeld S Contribution of job control and other risk factors to social variations in coronary heart disease incidence.

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J Clin Endocrinol Metab 86 : — Chow LS , Albright RC , Bigelow ML , Toffolo G , Cobelli C , Nair KS Mechanism of insulin's anabolic effect on muscle: measurements of muscle protein synthesis and breakdown using aminoacyl-tRNA and other surrogate measures.

Am J Physiol Endocrinol Metab : E — E Karaca M , Magnan C , Kargar C Functional pancreatic β-cell mass: involvement in type 2 diabetes and therapeutic intervention.

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Article Navigation. Close mobile search navigation Article Navigation. Volume Article Contents Abstract. Subjects and Methods. Journal Article. Relative Muscle Mass Is Inversely Associated with Insulin Resistance and Prediabetes. Findings from The Third National Health and Nutrition Examination Survey.

Preethi Srikanthan , Preethi Srikanthan. Oxford Academic. Arun S. PDF Split View Views. Cite Cite Preethi Srikanthan, Arun S. Select Format Select format.

ris Mendeley, Papers, Zotero. enw EndNote. bibtex BibTex. txt Medlars, RefWorks Download citation. Permissions Icon Permissions. Abstract Context:. Table 1 Descriptive statistics. Analytic sample. Total NHANES sample. n 13, 17, a Age yr a Those in the NHANES III sample who were older than 20 yr and not pregnant.

Open in new tab. Open in new tab Download slide. Table 2 Unadjusted associations of SMI by quartiles with insulin resistance and dysglycemia. P for trend. Table 3 Adjusted associations of SMI by quartiles with insulin resistance and dysglycemia, adjusted for age, sex, race, generalized obesity, overweight, and central obesity.

ref, Reference. Table 4 Adjusted associations of SMI continuous and MMI continuous with insulin resistance and dysglycemia, adjusted for age, sex, race, BMI continuous , generalized obesity, overweight, and central obesity. homeostasis model assessment of insulin resistance. Sarcopenia exacerbates obesity-associated insulin resistance and dysglycemia: findings from the National Health and Nutrition Examination Survey III.

Google Scholar Crossref. Search ADS. Inverse associations between muscle mass, strength, and the metabolic syndrome. Google Scholar OpenURL Placeholder Text.

Third National Health and Nutrition Examination Survey, —, reference manuals and reports. Google Scholar PubMed. OpenURL Placeholder Text. Comparison of A1C and fasting glucose criteria to diagnose diabetes among U.

A modified poisson regression approach to prospective studies with binary data. Contribution of job control and other risk factors to social variations in coronary heart disease incidence.

Relative contribution of early life and adult socioeconomic factors to adult morbidity in the Whitehall II study. Diabetes provides an unfavorable environment for muscle mass and function after muscle injury in mice.

Insulin resistance: a contributing factor to age-related muscle mass loss? Differential insulin sensitivities of glucose, amino acid, and albumin metabolism in elderly men and women.

Mechanism of insulin's anabolic effect on muscle: measurements of muscle protein synthesis and breakdown using aminoacyl-tRNA and other surrogate measures. Functional pancreatic β-cell mass: involvement in type 2 diabetes and therapeutic intervention.

Reduction in the incidence of type 2 diabetes with lifestyle intervention or metformin. SIRT1 mRNA expression may be associated with energy expenditure and insulin sensitivity. Randomized trial on the effects of a 7-d low-glycemic diet and exercise intervention on insulin resistance in older obese humans.

Issue Section:. Download all slides. Views 25, More metrics information. Total Views 25, Email alerts Article activity alert. Advance article alerts. New issue alert. Receive exclusive offers and updates from Oxford Academic. More on this topic Low Endogenous Secretory Receptor for Advanced Glycation End-Products Levels Are Associated With Inflammation and Carotid Atherosclerosis in Prediabetes.

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More from Oxford Academic. Clinical Medicine. Endocrinology and Diabetes. This ACE2-Ang 1—7 axis, acting via another G protein-coupled receptor Mas, is involved in vasodilatory, anti-fibrotic, and anti-inflammatory properties [ 52 ]. These two axes show different changes in aging skeletal muscle.

Studies have shown that the skeletal muscle aging process can activate RAS classic axis and activate the AT 1 receptor [ 55 , 56 , 64 ], which induces inflammation and oxidative stress. However, inhibiting the classic axis can prolong the physiological aging process and promotes longevity in rodents [ 12 ].

In addition, RAS non-classical axis weakens in aged skeletal muscles [ 75 ]. However, activating the RAS non-classical axis can reduce the aging phenotype in aged mice [ 75 ]. These data indicate that the RAS classical axis is activated and the RAS non-classical axis is weakened in aging skeletal muscle.

Excessive activation of RAS is closely related to skeletal muscle insulin resistance. Studies have shown that after injecting Ang II into rats, skeletal muscle glucose tolerance and insulin signaling pathway are impaired, and skeletal muscle insulin resistance appears [ 90 ].

Studies have shown that after ACE inhibition, skeletal muscle insulin sensitivity is enhanced, and after the Mas receptor is inhibited, the enhancement effect is eliminated [ 28 ]. These data indicate that activation of the RAS classical axis can promote skeletal muscle insulin resistance, while activation of the RAS non-classical axis can inhibit the classical axis, thereby improving skeletal muscle insulin resistance.

Therefore, activation of the RAS classical axis and weakening of the RAS non-classical axis in aging skeletal muscle may increase the risk of skeletal muscle insulin resistance. There are also interactions between these mechanisms. Among them, The ER and mitochondria join together at multiple contact sites to form specific domains, termed mitochondria-ER associated membranes MAMs [ 6 , 19 , 68 ].

It is closely related to the autophagy process. There are several important autophagy-related proteins in mitochondria, such as ATG5, which is critical for autophagosome formation, translocates to the MAM compartment during phagophore biogenesis and then dissociates from MAMs upon completion of the autophagosome [ 39 ].

Therefore, MAM plays an important role in autophagy, while mitochondrial dysfunction and ER stress can decrease autophagy capacity. In addition, increased ROS is an important factor inducing inflammation, while mitochondria and ER are important sources of ROS [ 67 ].

Therefore, mitochondrial dysfunction and ER stress can generate a large amount of ROS and induce inflammation and oxidative stress. In summary, mitochondrial dysfunction and ER stress can decrease autophagy capacity, increased ROS production and IMCL accumulation, and then induce inflammation and oxidative stress.

Furthermore, the over-activated renin-angiotensin system also increases inflammation levels and induces oxidative stress. In addition, the occurrence of sarcopenia will exacerbate the above processes. Finally, increased inflammation and oxidative stress can impair mitochondrial function and exacerbate ER stress in turn, thereby further exacerbating the above processes and increasing the risk of insulin resistance.

The aforementioned mechanisms, such as mitochondrial oxidative ability, inflammation, oxidative stress, insulin sensitivity regulating enzymes, ER stress, autophagy ability, and RAS axis, can be used as targets for the prevention and treatment of aging skeletal muscle insulin resistance.

In addition, there are non-pharmacological treatments, such as exercise, that can prevent and treat insulin resistance in aging skeletal muscle. Studies have shown that exercise can increase skeletal muscle mass and improve skeletal muscle insulin sensitivity [ 36 , 65 , 88 ].

Exercise can also enhance mitochondrial oxidative capacity, enhance skeletal muscle autophagy and antioxidant capacity, reduce oxidative stress and inflammation levels [ 36 , 74 ], and improve skeletal muscle insulin resistance.

Therefore, both pharmacological treatments targeting these mechanisms and exercise can prevent and treat aging skeletal muscle insulin resistance. An increased risk of senile skeletal muscle insulin resistance is associated with skeletal muscle dysfunction.

During the aging of skeletal muscle, mitochondrial dysfunction, intramyocellular lipid accumulation, increased inflammation, oxidative stress, changes in the activities of enzymes that regulate insulin sensitivity, endoplasmic reticulum stress, decreased autophagy, sarcopenia and over-activated RAS all induce skeletal muscle insulin resistance.

These processes can impair skeletal muscle insulin sensitivity and increase the risk of insulin resistance and type 2 diabetes during the skeletal muscle aging process Fig.

Of course, pharmacological treatments targeting these mechanisms and exercise can prevent and treat aging skeletal muscle insulin resistance. Therefore, in view of the above-mentioned aspects closely related to aging skeletal muscle insulin resistance, further exploration of relevant mechanisms and development of related drugs require further research in the future.

Skeletal muscle aging can increase insulin resistance by promoting mitochondrial dysfunction, IMCL accumulation, inflammation, oxidative stress, PTP1B expression, ER stress, decreased autophagy, sarcopenia and over-activated RAS. In addition, skeletal muscle mitochondrial dysfunction promotes IMCL accumulation and induces oxidative stress and ER stress, moreover, IMCL accumulation, oxidative stress, and ER stress can induce inflammation.

IMCL intramyocellular lipid, PTP1B protein tyrosine phosphatase 1B, ER endoplasmic reticulum, RAS renin-angiotensin system.

All data generated or analysed during this study are included in this published article Fig. Ahlstrom P, Rai E, Chakma S, Cho HH, Rengasamy P, Sweeney G. Adiponectin improves insulin sensitivity via activation of autophagic flux.

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Insulin signaling meets mitochondria in metabolism. Trends Endocrinol Metab. Chu Q, et al. Regulation of the ER stress response by a mitochondrial microprotein. Nat Commun.

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Is Insulin Anabolic? - Educational Video - Biolayne Metrics details. As age increases, the risk Insulin sensitivity and muscle growth developing type 2 diabetes sensiivity, Insulin sensitivity and muscle growth is associated with senile skeletal muscle dysfunction. During sensitivith muscle aging, aging skin dysfunction, musclw lipid accumulation, increased inflammation, oxidative stress, modified activity of Seasonal vegetable soup sensitivity regulatory enzymes, endoplasmic reticulum growtg, decreased autophagy, sarcopenia and over-activated renin-angiotensin system may occur. These changes can impair skeletal muscle insulin sensitivity and increase the risk of insulin resistance and type 2 diabetes during skeletal muscle aging. This review of the mechanism of the increased risk of insulin resistance during skeletal muscle aging will provide a more comprehensive explanation for the increased incidence of type 2 diabetes in elderly individuals, and will also provide a more comprehensive perspective for the prevention and treatment of type 2 diabetes in elderly populations. Insulin sensitivity and muscle growth

Insulin sensitivity and muscle growth -

This underscores the public health importance of monitoring muscle mass relative to body size in addition to BMI and waist circumference in assessing an individual's metabolic health, and it suggests a potential role for muscle-building exercises in preventing metabolic dysfunction.

However, prospective studies of short-term strength training interventions in overweight and obese individuals have been equivocal with respect to their effect on metabolic abnormalities 24 , Further work is required to determine the nature and duration of exercise interventions required to improve insulin sensitivity and glucose metabolism in both high-risk and moderate-risk individuals.

The funding sources had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. Srikanthan P , Hevener AL , Karlamangla AS Sarcopenia exacerbates obesity-associated insulin resistance and dysglycemia: findings from the National Health and Nutrition Examination Survey III.

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Sign In or Create an Account. Endocrine Society Journals. Advanced Search. Search Menu. Article Navigation. Close mobile search navigation Article Navigation. Volume Article Contents Abstract. Subjects and Methods. Journal Article.

Relative Muscle Mass Is Inversely Associated with Insulin Resistance and Prediabetes. Findings from The Third National Health and Nutrition Examination Survey. Preethi Srikanthan , Preethi Srikanthan. Oxford Academic. Arun S.

PDF Split View Views. Cite Cite Preethi Srikanthan, Arun S. Select Format Select format. ris Mendeley, Papers, Zotero. enw EndNote.

bibtex BibTex. txt Medlars, RefWorks Download citation. Permissions Icon Permissions. Abstract Context:. Additionally, Burrows et al. found in a Chilean birth cohort that low muscle mass is associated with cardiometabolic risk factors independent of dietary intake While findings in our study are similar to the previous reports, it should be noted that our study included Korean adults aged between 18 and 65 years.

We found that the overall association remained consistent in the participants of different age groups. Recent epidemiological studies have shown that the odds of metabolic syndrome was 6 to 8 times higher in postmenopausal Korean women, elderly Korean men and women, and adult Caucasian subjects with sarcopenic obesity decline of muscle mass and increase of fat mass with aging compared to those without sarcopenic obesity 16 , 17 , 18 , Few mechanisms may explain the combined effect on muscle mass and fat mass on insulin resistance and metabolic syndrome.

Since insulin-induced glucose uptake occurs in skeletal muscle, high muscle mass might result in a stable control over glucose levels The protective effect of an increase in muscle mass on insulin resistance and metabolic syndrome has been shown in individuals with and without diabetes 21 , On the other hand, it has been suggested that excessive and naturally occurring deposition of adipose tissue in the abdomen may increase the risk of metabolic syndrome Because the regulatory function of energy storage in subcutaneous adipose tissue is limited, excessive chemical energy flow to liver and skeletal muscles can cause metabolic disturbances In addition, a study conducted among non-diabetic men in Finland showed that an increased accumulation of hepatic fat is linked to an abnormal amount of lipids in the blood, and hepatic insulin resistance Increased levels of intramyocellular lipids have been shown to elevate the insulin resistance of skeletal muscles This study has some limitations that need to be addressed.

First, the results of our findings cannot be regarded as a direct cause-effect relationship between proportion of body composition, insulin resistance, and metabolic syndrome due to the cross-sectional design of this study.

Second, there were group differences in our analytic sample e. twice as many women in the reference group and socioeconomic differences that were only adjusted and stratified in the analyses.

Third, there were additional factors associated with metabolic syndrome that were not provided in our dataset e. health-related quality of life such as parameters of mental health.

Therefore, in this study, we could not account for the effect from other confounding factors that were unavailable in the KNAHNES dataset. Despite the limitations from the study design and data, the strength of our study was the assessment of the association between the proportion of DEXA scan-measured muscle and fat mass to insulin resistance and the prevalence of metabolic syndrome in a nationally representative sample.

In summary, the results of our study suggest the clinical significance of muscle mass and fat mass with insulin resistance and metabolic syndrome in Korean adults. Whether this concept is widely applicable to other ethnic groups or not needs further investigation due to the ethnic heterogeneity in body composition and health outcomes Well-designed cohort studies or randomized control studies are necessary to investigate the combined influence of muscle mass and fat mass to validate the findings of this study.

All the participants provided written informed consent before the KNHANES IV-V began. The Institutional Review Board at the Seoul National University Hospital, which is in accordance with the Declaration of Helsinki, approved this study.

We used the KNHANES IV-V to assess the cross-sectional relationship between different body composition types, insulin resistance, and metabolic syndrome. KNHANES IV-V data were collected using a multistage, probability-cluster survey method for the sample to represent the entire population of the Republic of Korea from to The KNHANES was conducted by the Korea Center for Disease Control and Prevention KCDC under the guidance of the Ministry of Health and Welfare.

The validity of this nationally representative data has been described in previous studies 28 , The inclusion criteria for this cross-sectional study was 15, participants of the KNHANES aged between 18 years and 65 years who received a whole-body DEXA scan.

Therefore, 14, participants who met the inclusion criteria were selected for this study. Based on the whole-body DEXA scan dataset of KNHANES measured and recorded by credible health professionals , we derived trunk fat mass index TFMI and appendicular muscle lean mass of arms and legs combined mass index AMMI for categorization.

We calculated TFMI from trunk fat mass in kilograms kg divided by height in meters squared m 2. Similarly, we calculated AMMI using appendicular muscle mass kg and height m 2.

We chose TFMI because trunk fat mass represents the level of visceral adipose tissue, which is a more accurate predictor of metabolic risk 30 compared to the whole-body fat mass index FMI. In addition, we linked the health survey data containing sociodemographic status and health behavior and the laboratory measurement data to the DEXA measurement dataset.

The details and validity of creating the body composition types to study the combined effect of muscle mass and fat mass on health outcomes such as cardiovascular disease and mortality have been previously described 31 , Data from health examination and laboratory test were used to assess insulin resistance and metabolic syndrome across the participants of different body composition types.

Insulin resistance index was assessed through HOMA-IR by employing the level of fasting insulin and glucose 33 , We used survey data of the KNHANES to assess confounding factors in this study. Information on sociodemographic factors age, sex, education level employment status, residential area, household income and health-related factors smoking status, alcohol consumption, physical activity, nutritional intake, and presence of comorbidity was collected from self-reported questionnaires.

Analysis of variance ANOVA and the chi-square test was used for the comparison of general characteristics across different categories of body composition type for continuous and categorical variables, respectively.

To account for pre-diagnosed medical conditions with significant impact on metabolic syndrome cancer, myocardial infarction, angina, hepatitis B, and hepatitis C , we grouped the participants into the following categories: 1 those who reported that they have been diagnosed with any of the above mentioned conditions and currently receiving treatment 2 those without comorbidity associated with metabolic syndrome.

As a part of multivariate analysis, we adjusted for the presence of a comorbidity known to be related to metabolic syndrome as a categorical variable. To assess the relationship between body composition types and insulin resistance HOMA-IR , we estimated the least-square mean marginal means according to types of body composition.

In the multivariate models, we constructed a minimally adjusted model adjusted for age and sex as Model 1. In Model 2, we built a model that was adjusted for sociodemographic, health behavior, and health-related factors age, sex, level of education, employment status, area of residence, household income, smoking, alcohol consumption, sleep duration, physical activity, BMI, and the presence of comorbidities.

In addition, we built a Model 3, which included dietary factors total energy intake, vitamin C, niacin, sodium, calcium, and fiber consumption. We collected the KNHANES data using SAS, version 9. Therefore, the results were weighted to represent the entire non-institutionalized civilian population of the Republic of Korea.

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Distribution of abdominal visceral and subcutaneous adipose tissue and metabolic syndrome in a Korean population. Diabetes Care 34 , — Article PubMed PubMed Central Google Scholar. Hainer, V. Obesity paradox does exist. Diabetes care 36 , S—S Hamdy, O.

Metabolic obesity: the paradox between visceral and subcutaneous fat. Current diabetes reviews 2 , — Srikanthan, P. Relative muscle mass is inversely associated with insulin resistance and prediabetes.

Findings from the third National Health and Nutrition Examination Survey. Tritos, N. Leptin: its role in obesity and beyond. Diabetologia 40 , — Yang, X. In this study, 40 young men exercised five days a week 50 minute sessions including cycling and circuit training for four weeks.

The addition of vitamin C and E supplementation in that group completely eliminated the beneficial insulin-sensitizing effects of exercise! With further investigation it seems that the post-workout increase in reactive oxygen species ROS — which is blunted by C and E supplementation — is a necessary phenomenon for increasing insulin sensitivity.

The argument for the temporal benefit of ROS post-workout is strengthened by the fact that long term antioxidant supplementation has been shown to increase insulin sensitivity. Okay, so what do you do with this info? While it's what some would consider "fringe" nutritional science and the standard, "more studies need to be done in this area to further explore our findings" was added by the authors, I say run with it.

If you're looking for an extra potential edge, then I'd avoid antioxidant supplements and high antioxidant foods around and directly after your workouts. This will allow for the natural post-exercise rise in ROS and improvement in insulin sensitivity. Beyond spicing up your pumpkin pie, you probably never give cinnamon a second thought.

However, the simple addition of cinnamon to your diet has been shown in several studies to delay gastric emptying 4, 5 , lower blood glucose levels following a meal 4, 5 , reduce fasting insulin 6 , and maybe even make up for temporary insulin resistance due to lack of sleep.

To reap the glucose-controlling benefits of cinnamon you'll need to use grams approx teaspoons. Adding a couple teaspoons of cinnamon to your morning muscle gruel is a no-brainer, so you have no excuse not to add this to your dietary arsenal. ALA is an antioxidant found in spinach, broccoli, and tomatoes.

I'd prefer that you start with a lower dosage mg per day the amount recommended for antioxidant purposes and move up from there. Getting quality protein and carbohydrates into your system around the training period is important, as you probably know.

The difference between taking a protein supplement immediately vs. These drastic differences in the workout window when someone follows the 3rd Law of Muscle vs.

when they do not suggest that withholding nutrients after training prevents you from maximizing your insulin sensitized state. So don't skip the workout drinks! When it comes down to it, maximizing insulin sensitivity is all about getting the upper hand and giving yourself the edge over those poor drones in your gym with no clue.

Put these tips into action, improve your nutrient partitioning, and reap the benefits! Expert Insights To Get Stronger, Gain Muscle Faster, And Take Your Lifting To The Next Level.

Skip to content. The Community for Enhanced Fitness. Both challenges solved. Put Those Carbs to Work! Ludicrous right?

Well, keep reading. Wrap-up When it comes down to it, maximizing insulin sensitivity is all about getting the upper hand and giving yourself the edge over those poor drones in your gym with no clue. References Ristow M, Zarse K, Oberbach A, et al. Antioxidants prevent health-promoting effects of physical exercise in humans.

Proceedings of the National Academy of Sciences of the United States of America ;

Obesity-linked insulin senitivity is mainly due to Insupin acid overload in non-adipose tissues, particularly skeletal adn and zensitivity, where it sensiticity in high production of sennsitivity oxygen species and Cellulite reduction exercises for seniors dysfunction. Accumulating evidence Insulin sensitivity and muscle growth that resistance and endurance aging skin sensitivvity and Brightening dull combination can counteract the harmful effects of obesity increasing insulin sensitivity, thus preventing diabetes. This review focuses the mechanisms underlying the exercise role in opposing skeletal muscle insulin resistance-linked metabolic dysfunction. It is apparent that exercise acts through two mechanisms: 1 it stimulates glucose transport by activating an insulin-independent pathway and 2 it protects against mitochondrial dysfunction-induced insulin resistance by increasing muscle antioxidant defenses and mitochondrial biogenesis. Obesity is one of the most important public health problems in the world, reaching epidemic proportions in several industrialized countries Ogden et al.

Author: Zuzuru

4 thoughts on “Insulin sensitivity and muscle growth

  1. Ich tue Abbitte, dass sich eingemischt hat... Ich hier vor kurzem. Aber mir ist dieses Thema sehr nah. Schreiben Sie in PM.

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