Genes controlling skeletal muscle glucose uptake and their regulation by endurance and resistance exercise

Verbrugge, Sander A.J.; Alhusen, Julia A.; Kempin, Shimon; Pillon, Nicolas; Rozman, Jan; Wackerhage, Henning; Kleinert, Maximilian

doi:10.1002/jcb.30179

Cited by 11 publications

(9 citation statements)

References 98 publications

(103 reference statements)

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“…Given that the 25 genes causally affect fibre proportions, functionally relevant DNA sequence variants that are related to these genes should affect human muscle fibre type proportions, provided that the function of these genes is conserved between mice and men. Together with a list of muscle hypertrophy genes [ 79 ], endurance genes [ 80 ], and glucose uptake genes [ 81 ] this additional list of causative genes should help to identify causative DNA variants that influence human sport and exercise-related traits [ 82 ] as well as human health—as many exercise-related traits are predictors of health.…”

Section: Discussionmentioning

confidence: 99%

Genes Whose Gain or Loss of Function Changes Type 1, 2A, 2X, or 2B Muscle Fibre Proportions in Mice—A Systematic Review

Kuhnen

Russomanno

Murgia

et al. 2022

IJMS

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Adult skeletal muscle fibres are classified as type 1, 2A, 2X, and 2B. These classifications are based on the expression of the dominant myosin heavy chain isoform. Muscle fibre-specific gene expression and proportions of muscle fibre types change during development and in response to exercise, chronic electrical stimulation, or inactivity. To identify genes whose gain or loss-of-function alters type 1, 2A, 2X, or 2B muscle fibre proportions in mice, we conducted a systematic review of transgenic mouse studies. The systematic review was conducted in accordance with the 2009 PRISMA guidelines and the PICO framework. We identified 25 “muscle fibre genes” (Akirin1, Bdkrb2, Bdnf, Camk4, Ccnd3, Cpt1a, Epas1, Esrrg, Foxj3, Foxo1, Il15, Mapk12, Mstn, Myod1, Ncor1, Nfatc1, Nol3, Ppargc1a, Ppargc1b, Sirt1, Sirt3, Thra, Thrb, Trib3, and Vgll2) whose gain or loss-of-function significantly changes type 1, 2A, 2X or 2B muscle fibre proportions in mice. The fact that 15 of the 25 muscle fibre genes are transcriptional regulators suggests that muscle fibre-specific gene expression is primarily regulated transcriptionally. A reanalysis of existing datasets revealed that the expression of Ppargc1a and Vgll2 increases and Mstn decreases after exercise, respectively. This suggests that these genes help to regulate the muscle fibre adaptation to exercise. Finally, there are many known DNA sequence variants of muscle fibre genes. It seems likely that such DNA sequence variants contribute to the large variation of muscle fibre type proportions in the human population.

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Section: Discussionmentioning

confidence: 99%

Genes Whose Gain or Loss of Function Changes Type 1, 2A, 2X, or 2B Muscle Fibre Proportions in Mice—A Systematic Review

Kuhnen

Russomanno

Murgia

et al. 2022

IJMS

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“…The time taken to consume the meal (approximately 15 min) was replicated in subsequent conditions. At 3:30 into the experiment, participants were provided with a standardized lunch meal (beef rice, 250 mL lemon tea, and 48 g chocolate, consisting of 1100 kcal, where 69.4% energy from carbohydrate (187.9 g), 19.7% energy from fat (23.7 g), and 10.9% energy from protein (29.5 g)). During measurements, participants were allowed to use the internet, work on their computers, or read.…”

Section: Study Protocolmentioning

confidence: 99%

“…18 On the other hand, engaging in diverse muscle activities during both endurance and resistance exercises has been shown to enhance glucose uptake through distinct local pathways. 19 These various patterns of muscle activity, including factors like duration, amplitude, and the absence of contraction, can be effectively measured using wearable electromyography (EMG) devices. [20][21][22] A cross-sectional study has identified associations between EMG patterns, such as average EMG amplitude (aEMG) and EMG activity duration, and glucose metabolism.…”

Section: Introductionmentioning

confidence: 99%

“…Extended periods of muscle inactivity during uninterrupted sedentary behavior contribute to glucose intolerance through local muscle‐contraction mechanisms 18 . On the other hand, engaging in diverse muscle activities during both endurance and resistance exercises has been shown to enhance glucose uptake through distinct local pathways 19 . These various patterns of muscle activity, including factors like duration, amplitude, and the absence of contraction, can be effectively measured using wearable electromyography (EMG) devices 20–22 .…”

Section: Introductionmentioning

confidence: 99%

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Enhanced muscle activity during interrupted sitting improves glycemic control in overweight and obese men

Gao,

Li,

Finni

et al. 2024

Scandinavian Med Sci Sports

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The efficacy of interrupting prolonged sitting may be influenced by muscle activity patterns. This study examined the effects of interrupting prolonged sitting time with different muscle activity patterns on continuously monitored postprandial glycemic response. Eighteen overweight and obese men (21.0 ± 1.2 years; 28.8 ± 2.2 kg/m2) participated in this randomized four‐arm crossover study, including uninterrupted sitting for 8.5 h (SIT) and interruptions in sitting with matched energy expenditure and duration but varying muscle activity: 30‐min walking at 4 km/h (ONE), sitting with 3‐min walking at 4 km/h (WALK) or squatting (SQUAT) every 45 min for 10 times. Net incremental area under the curve (netiAUC) for glucose was compared between conditions. Quadriceps, hamstring, and gluteal muscles electromyogram (EMG) patterns including averaged muscle EMG amplitude (aEMG) and EMG activity duration were used to predict the effects on glucose netiAUC. Compared with SIT (10.2 mmol/L/h [95%CI 6.3 to 11.7]), glucose netiAUC was lower during sitting interrupted with any countermeasure (ONE 9.2 mmol/L/h [8.0 to 10.4], WALK 7.9 mmol/L/h [6.4 to 9.3], and SQUAT 7.9 mmol/L/h [6.4 to 9.3], all p < 0.05). Furthermore, WALK and SQUAT resulted in a lower glucose netiAUC compared with ONE (both p < 0.05). Only increased aEMG in quadriceps (−0.383 mmol/L/h [−0.581 to −0.184], p < 0.001) and gluteal muscles (−0.322 mmol/L/h [−0.593 to −0.051], p = 0.022) was associated with a reduction in postprandial glycemic response. Collectively, short, frequent walking or squatting breaks effectively enhance glycemic control in overweight and obese men compared to a single bout of walking within prolonged sitting. These superior benefits seem to be associated with increased muscle activity intensity in the targeted muscle groups during frequent transitions from sitting to activity.

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“…In order to elucidate the molecular mechanisms responsible for the ET effects [ 14 , 28 ], we identified the genes specifically modulated by ET in elderly muscle compared to young adults, and highlighted the importance of mitochondrial oxidative phosphorylation (OXPHOS) and extracellular matrix (ECM) remodeling in the skeletal muscle [ 16 , 24 , 57 , 59 ]. As shown in Figure 2 , the ET-induced genes in elderly men [ 16 , 24 , 57 , 59 ], SPARC , specifically binds several of the ECM molecules including the collagens [ 60 ]. Thus, they influence lamina organization by binding to the growth factors such as insulin-like growth factor 1 (IGF-1) and transforming growth factor beta 1 (TGF-β1) [ 61 , 62 , 63 ].…”

Section: Sparc -Mediated Effects Among the Exercise Benefitsmentioning

confidence: 99%

Secreted Protein Acidic and Rich in Cysteine (SPARC)—Mediated Exercise Effects: Illustrative Molecular Pathways against Various Diseases

2023

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The strong benefits of exercise, in addition to the development of both the therapeutic applications of physical activity and molecular biology tools, means that it has become very important to explore the underlying molecular patterns linking exercise and its induced phenotypic changes. Within this context, secreted protein acidic and rich in cysteine (SPARC) has been characterized as an exercise-induced protein that would mediate and induce some important effects of exercise. Herein, we suggest some underlying pathways to explain such SPARC-induced exercise-like effects. Such mechanistic mapping would not only allow us to understand the molecular processes of exercise and SPARC effects but would also highlight the potential to develop novel molecular therapies. These therapies would be based on mimicking the exercise benefits via either introducing SPARC or pharmacologically targeting the SPARC-related pathways to produce exercise-like effects. This is of a particular importance for those who do not have the ability to perform the required physical activity due to disabilities or diseases. The main objective of this work is to highlight selected potential therapeutic applications deriving from SPARC properties that have been reported in various publications.

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Genes controlling skeletal muscle glucose uptake and their regulation by endurance and resistance exercise

Cited by 11 publications

References 98 publications

Genes Whose Gain or Loss of Function Changes Type 1, 2A, 2X, or 2B Muscle Fibre Proportions in Mice—A Systematic Review

Genes Whose Gain or Loss of Function Changes Type 1, 2A, 2X, or 2B Muscle Fibre Proportions in Mice—A Systematic Review

Enhanced muscle activity during interrupted sitting improves glycemic control in overweight and obese men

Secreted Protein Acidic and Rich in Cysteine (SPARC)—Mediated Exercise Effects: Illustrative Molecular Pathways against Various Diseases

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