bims-exemet 2021-03-07 papers

bims-exemet

Biomed News

on Exercise metabolism

Issue of 2021–03–07
ten papers selected by
Javier Botella Ruiz, Victoria University

Mapping of the contraction-induced phosphoproteome identifies TRIM28 as a significant regulator of skeletal muscle size and function.
Glycogen supercompensation is due to increased number, not size, of glycogen particles in human skeletal muscle.
Acute and delayed hormonal and blood cell count responses to high-intensity exercise before and after short-term high-intensity interval training.
Resistance Training Diminishes the Expression of Exosome CD63 Protein without Modification of Plasma miR-146a-5p and cfDNA in the Elderly.
Effect of the order of concurrent training combined with resistance and high-intensity interval exercise on mTOR signaling and glycolytic metabolism in mouse skeletal muscle.
Effects of Resistance Training on the Redox Status of Skeletal Muscle in Older Adults.
The Acute Effects of Swimming Exercise on PGC-1α-FNDC5/Irisin-UCP1 Expression in Male C57BL/6J Mice.
Protective Effects of Voluntary Exercise on Hepatic Fat Accumulation Induced by Dietary Restriction in Zucker Fatty Rats.
Influence of low-dose aspirin, resistance exercise, and sex on human skeletal muscle PGE2 /COX pathway activity.
An Antioxidant Nanoparticle Enhances Exercise Performance in Rat High-intensity Running Models.

Cell Rep. 2021 Mar 02. pii: S2211-1247(21)00110-8. [Epub ahead of print]34(9): 108796

Mapping of the contraction-induced phosphoproteome identifies TRIM28 as a significant regulator of skeletal muscle size and function.

Nathaniel D Steinert, Gregory K Potts, Gary M Wilson, Amelia M Klamen, Kuan-Hung Lin, Jake B Hermanson, Rachel M McNally, Joshua J Coon, Troy A Hornberger.

  Mechanical signals, such as those evoked by maximal-intensity contractions (MICs), can induce an increase in muscle mass. Rapamycin-sensitive signaling events are widely implicated in the regulation of this process; however, recent studies indicate that rapamycin-insensitive signaling events are also involved. Thus, to identify these events, we generate a map of the MIC-regulated and rapamycin-sensitive phosphoproteome. In total, we quantify more than 10,000 unique phosphorylation sites and find that more than 2,000 of these sites are significantly affected by MICs, but remarkably, only 38 of the MIC-regulated events are mediated through a rapamycin-sensitive mechanism. Further interrogation of the rapamycin-insensitive phosphorylation events identifies the S473 residue on Tripartite Motif-Containing 28 (TRIM28) as one of the most robust MIC-regulated phosphorylation sites, and extensive follow-up studies suggest that TRIM28 significantly contributes to the homeostatic regulation of muscle size and function as well as the hypertrophy that occurs in response to increased mechanical loading.

Keywords:  atrophy; contraction; exercise; growth; hypertrophy; mTOR; mechanical loading; phosphorylation; rapamycin; signal transduction

DOI:  https://doi.org/10.1016/j.celrep.2021.108796
Exp Physiol. 2021 Mar 06.

Glycogen supercompensation is due to increased number, not size, of glycogen particles in human skeletal muscle.

Rasmus Jensen, Niels Ørtenblad, Marie-Louise H Stausholm, Mette C Skjaerbaek, Daniel N Larsen, Mette Hansen, Hans-Christer Holmberg, Peter Plomgaard, Joachim Nielsen.

   NEW FINDINGS: What is the central question of this study? Glycogen supercompensation following glycogen-depleting exercise can be achieved by consuming a carbohydrate-enriched diet, but the associated effects on the size, number and localization of intramuscular glycogen particles is unknown. What is the main finding and its importance? Using transmission electron microscopy to visually inspect individual glycogen particles, we show that glycogen supercompensation is achieved by increasing the number of particles while keeping them at submaximal sizes. This may be a strategy to ensure that glycogen particles can be utilised fast as too large particles may impair utilisation rate.
ABSTRACT: Glycogen supercompensation following glycogen-depleting exercise can be achieved by consuming a carbohydrate-enriched diet, but the associated effects on the size, number and localization of intramuscular glycogen particles is unknown. We investigated how a glycogen loading protocol affects fibre type-specific glycogen volume density, particle diameter and numerical density in three subcellular pools: between (intermyofibrillar) or within (intramyofibrillar) the myofibrils or beneath the sarcolemma (subsarcolemmal). Resting muscle biopsies from 11 physically active men were analysed using transmission electron microscopy after mixed (MIX), LOW, or HIGH carbohydrate consumption separated by glycogen lowering cycling at 75% of V̇O2 max until exhaustion. After HIGH, the total volumetric glycogen content was 40% [95% CI 16;68] higher than after MIX in type 1 fibres (P<0.001) with little to no difference in type 2 fibres (9% [-9;27]). Median particle diameter was 22.5 (IQR 20.8;24.7) nm across glycogen pools and fibre types, while the numerical density was 61% [25;107] and 40% [9;80] higher in the subsarcolemmal (P<0.001) and intermyofibrillar (P<0.01) pools of type 1 fibres, respectively, with little to no difference in the intramyofibrillar pool (3% [-20;32]). In LOW, total glycogen was in the range of 21-23% lower, relative to MIX, in both fibre types reflected in a 21-46% lower numerical density across pools. Compared to MIX, particle diameter was unaffected by other diets ([-1.4;1.3] nm). In conclusion, glycogen supercompensation after prolonged cycling is exclusive to type 1 fibres, predominantly in the subsarcolemmal pool, and involves an increase in the numerical density rather than the size of existing glycogen particles. This article is protected by copyright. All rights reserved.

Keywords:  carbohydrate; compartmentalisation; diet; glycogen loading; transmission electron microscopy

DOI:  https://doi.org/10.1113/EP089317
Res Sports Med. 2021 Mar 04. 1-15

Acute and delayed hormonal and blood cell count responses to high-intensity exercise before and after short-term high-intensity interval training.

Gregory C Bogdanis, Anastassios Philippou, Pinelopi S Stavrinou, Roxane Tenta, Maria Maridaki.

  The acute and delayed hormonal and blood cell responses to a high-intensity interval training (HIIT) session, were examined before and after a 3-week intervention (9 HIIT sessions of 4-6 × 30 s high-intensity cycling bouts) in eight recreationally active male volunteers (age: 24.3 ± 1.4 y, VO2max: 41.2 ± 3.2 ml/kg/min). Blood samples were collected before and 0.5, 24, 48 h following the first and last training session. Before training, the HIIT session induced acute increases in cortisol, prolactin and TSH concentration, while free-T4 peaked 24 h later (p < 0.001) and testosterone remained unchanged. White blood cell count was increased 0.5 h after exercise (p < 0.001), while lymphocyte percentage decreased 24 h post exercise (p < 0.01). After three weeks of HIIT, cortisol, WBC and lymphocyte responses were decreased by ~42% (p = 0.002), 8.6% (p = 0.032) and 9.6% (p = 0.039), respectively, despite an increase in total work. These findings show that short-term HIIT may induce rapid adaptations of the hypothalamic-pituitary-adrenal axis and may blunt exercise-induced immune responses.

Keywords:  Cortisol; exercise; power output; testosterone; thyroid

DOI:  https://doi.org/10.1080/15438627.2021.1895783
Nutrients. 2021 Feb 19. pii: 665. [Epub ahead of print]13(2):

Resistance Training Diminishes the Expression of Exosome CD63 Protein without Modification of Plasma miR-146a-5p and cfDNA in the Elderly.

Brisamar Estébanez, Nishant P Visavadiya, José A de Paz, Michael Whitehurst, María J Cuevas, Javier González-Gallego, Chun-Jung Huang.

  Aging-associated inflammation is characterized by senescent cell-mediated secretion of high levels of inflammatory mediators, such as microRNA (miR)-146a. Moreover, a rise of circulating cell-free DNA (cfDNA) is also related to systemic inflammation and frailty in the elderly. Exosome-mediated cell-to-cell communication is fundamental in cellular senescence and aging. The plasma changes in exercise-promoted miR-146a-5p, cfDNA, and exosome release could be the key to facilitate intercellular communication and systemic adaptations to exercise in aging. Thirty-eight elderly subjects (28 trained and 10 controls) volunteered in an 8-week resistance training protocol. The levels of plasma miR-146a-5p, cfDNA, and exosome markers (CD9, CD14, CD63, CD81, Flotillin [Flot]-1, and VDAC1) were measured prior to and following training. Results showed no changes in plasma miR-146a-5p and cfDNA levels with training. The levels of exosome markers (Flot-1, CD9, and CD81) as well as exosome-carried proteins (CD14 and VDAC1) remained unchanged, whereas an attenuated CD63 response was found in the trained group compared to the controls. These findings might partially support the anti-inflammatory effect of resistance training in the elderly as evidenced by the diminishment of exosome CD63 protein expression, without modification of plasma miR-146a-5p and cfDNA.

Keywords:  aging; cell-free DNA; exercise-promoted exosomes; extracellular vesicles; inflammaging; microRNAs; physical activity; strength training

DOI:  https://doi.org/10.3390/nu13020665
Physiol Rep. 2021 Mar;9(5): e14770

Effect of the order of concurrent training combined with resistance and high-intensity interval exercise on mTOR signaling and glycolytic metabolism in mouse skeletal muscle.

Takanaga Shirai, Hideto Hanakita, Kazuki Uemichi, Tohru Takemasa.

  Athletes train to improve strength and endurance to demonstrate maximum performance during competitions. Training methods vary but most focus on strength, endurance, or both. Concurrent training is a combination of two different modes of training. In this study, we combined resistance exercise (RE) and high-intensity interval exercise (HIIE) to investigate the influence of the order of the concurrent training on signal molecules on hypertrophy and glycolysis in the skeletal muscle. The phosphorylation levels of mechanistic target of rapamycin (mTOR) signals, p70 S6 kinase (p70S6 K), ribosomal protein S6 (S6), and glycogen synthase kinase beta (GSK-3β) were significantly increased in the HIIE first group compared with the control group. The combined training course did not affect the glycogen content and expression levels of proteins concerning glycolytic and metabolic capacity, suggesting that a combination of HIIE and RE on the same day, with HIIE prior to RE, improves hypertrophy response and glycolysis enhancement.

Keywords:  concurrent training; glycolysis; high-intensity interval exercise; mTOR signaling; resistance exercise

DOI:  https://doi.org/10.14814/phy2.14770
Antioxidants (Basel). 2021 Feb 26. pii: 350. [Epub ahead of print]10(3):

Effects of Resistance Training on the Redox Status of Skeletal Muscle in Older Adults.

Paulo H C Mesquita, Donald A Lamb, Joshua S Godwin, Shelby C Osburn, Bradley A Ruple, Johnathon H Moore, Christopher G Vann, Kevin W Huggins, Andrew D Fruge, Kaelin C Young, Andreas N Kavazis, Michael D Roberts.

  The aim of this study was to investigate the effects of resistance training (RT) on the redox status of skeletal muscle in older adults. Thirteen males aged 64 ± 9 years performed full-body RT 2x/week for 6 weeks. Muscle biopsies were obtained from the vastus lateralis prior to and following RT. The mRNA, protein, and enzymatic activity levels of various endogenous antioxidants were determined. In addition, skeletal muscle 4-hydroxynonenal and protein carbonyls were determined as markers of oxidative damage. Protein levels of heat shock proteins (HSPs) were also quantified. RT increased mRNA levels of all assayed antioxidant genes, albeit protein levels either did not change or decreased. RT increased total antioxidant capacity, catalase, and glutathione reductase activities, and decreased glutathione peroxidase activity. Lipid peroxidation also decreased and HSP60 protein increased following RT. In summary, 6 weeks of RT decreased oxidative damage and increased antioxidant enzyme activities. Our results suggest the older adult responses to RT involve multi-level (transcriptional, post-transcriptional, and post-translational) control of the redox status of skeletal muscle.

Keywords:  antioxidants; exercise; oxidative damage; oxidative stress; redox homeostasis

DOI:  https://doi.org/10.3390/antiox10030350
Metabolites. 2021 Feb 16. pii: 111. [Epub ahead of print]11(2):

The Acute Effects of Swimming Exercise on PGC-1α-FNDC5/Irisin-UCP1 Expression in Male C57BL/6J Mice.

Eunhee Cho, Da Yeon Jeong, Jae Geun Kim, Sewon Lee.

  Irisin is a myokine primarily secreted by skeletal muscles and is known as an exercise-induced hormone. The purpose of this study was to determine whether the PGC-1α -FNDC5 /Irisin-UCP1 expression which is an irisin-related signaling pathway, is activated by an acute swimming exercise. Fourteen to sixteen weeks old male C57BL/6J mice (n = 20) were divided into control (CON, n = 10) and swimming exercise groups (SEG, n = 10). The SEG mice performed 90 min of acute swimming exercise, while control (non-exercised) mice were exposed to shallow water (2 cm of depth) for 90 min. The mRNA and protein expression of PGC-1α, FNDC5 and browning markers including UCP1 were evaluated by quantitative real-time PCR and western blotting. Serum irisin concentration was measured by enzyme-linked immunosorbent assay. An acute swimming exercise did not lead to alterations in the mRNA and protein expression of PGC-1α in both soleus and gastrocnemius muscles, the mRNA and protein expression of UCP1 in brown adipose tissue, mRNA browning markers in visceral adipose tissue and circulating irisin when compared with the control group. On the other hand, an acute swimming exercise led to increases in the mRNA and protein expressions of FNDC5 in the soleus muscle, the protein expression of FNDC5 in the gastrocnemius muscles and the protein expression of UCP1 in subcutaneous adipose tissue.

Keywords:  FNDC5; PGC-1α; UCP1; irisin; swimming exercise

DOI:  https://doi.org/10.3390/metabo11020111
Int J Mol Sci. 2021 Feb 18. pii: 2014. [Epub ahead of print]22(4):

Protective Effects of Voluntary Exercise on Hepatic Fat Accumulation Induced by Dietary Restriction in Zucker Fatty Rats.

Yuka Kurosaka, Shuichi Machida, Yoko Shiroya, Hideki Yamauchi, Kumiko Minato.

  Weight control based on dietary restriction (DR) alone can cause lipid metabolic failure and progression to fatty liver. This study aimed to investigate the effect of exercise on preventing DR-induced hepatic fat accumulation in Zucker fatty (ZF) rats by focusing on the relationship between adipose tissue lipolysis and hepatic fat uptake. Six-week-old male ZF rats were randomly assigned to obese, DR, or DR with exercise (DR + Ex) groups. The DR and DR + Ex groups were fed a restricted diet, with the latter also undergoing voluntary exercise. After 6 weeks, hepatic fat accumulation was observed in the DR group, whereas intrahepatic fat was markedly reduced in the DR + Ex group. Compared with the obese (Ob) group, the DR group exhibited 2.09-fold expression of hepatic fatty acid translocase (FAT)/CD36 proteins (p < 0.01) and 0.14-fold expression of hepatic fatty acid-binding protein (FABP)1 (p < 0.01). There were no significant differences between the DR + Ex group and the Ob group. FAT/CD36 and hepatic triglyceride (TG) expression levels were strongly positively correlated (r = 0.81, p < 0.001), whereas there was a strong negative correlation between FABP1 and hepatic TG expression levels (r = -0.65, p < 0.001). Our results suggest that hepatic fat accumulation induced by DR in ZF rats might be prevented through exercise-induced modifications in FAT/CD36 and FABP1 expression.

Keywords:  CD36; FABP1; diet restriction; exercise; fatty liver; hepatocyte ultrastructure; obesity

DOI:  https://doi.org/10.3390/ijms22042014
Physiol Rep. 2021 Mar;9(5): e14790

Influence of low-dose aspirin, resistance exercise, and sex on human skeletal muscle PGE2 /COX pathway activity.

Masatoshi Naruse, William A Fountain, Alex Claiborne, Toby L Chambers, Andrew M Jones, Andrew M Stroh, Cristhian F Montenegro, Colleen E Lynch, Kiril Minchev, Scott Trappe, Todd A Trappe.

  Prostaglandin (PG) E2 has been linked to increased inflammation and attenuated resistance exercise adaptations in skeletal muscle. Nonaspirin cyclooxygenase (COX) inhibitors have been shown to reduce these effects. This study examined the effect of low-dose aspirin on skeletal muscle COX production of PGE2 at rest and following resistance exercise. Skeletal muscle (vastus lateralis) biopsies were taken from six individuals (4 M/2 W) before and 3.5 hr after a single bout of resistance exercise for ex vivo PGE2 production under control and low (10 μM)- or standard (100 μM)-dose aspirin conditions. Sex-specific effects of aspirin were also examined by combining the current findings with our previous similar ex vivo skeletal muscle investigations (n = 20, 10 M/10 W). Low-dose aspirin inhibited skeletal muscle PGE2 production (p < 0.05). This inhibition was similar to standard-dose aspirin (p > 0.05) and was not influenced by resistance exercise (p > 0.05) (overall effect: -18 ± 5%). Men and women had similar uninhibited skeletal muscle PGE2 production at rest (men: 1.97 ± 0.33, women: 1.96 ± 0.29 pg/mg wet weight/min; p > 0.05). However, skeletal muscle of men was 60% more sensitive to aspirin inhibition than women (p < 0.05). In summary, the current findings 1) confirm low-dose aspirin inhibits the PGE2 /COX pathway in human skeletal muscle, 2) show that resistance exercise does not alter aspirin inhibitory efficacy, and 3) suggest the skeletal muscle of men and women could respond differently to long-term consumption of low-dose aspirin, one of the most common chronically consumed drugs in the world.

Keywords:  cyclooxygenase; low-dose aspirin; prostaglandin E2; resistance exercise; skeletal muscle

DOI:  https://doi.org/10.14814/phy2.14790
Adv Healthc Mater. 2021 Mar 04. e2100067

An Antioxidant Nanoparticle Enhances Exercise Performance in Rat High-intensity Running Models.

Takuto Toriumi, Ahram Kim, Shoichi Komine, Ikuru Miura, Suminori Nagayama, Hajime Ohmori, Yukio Nagasaki.

  Although the adverse effects of excessively generated reactive oxygen species (ROS) on the body during aerobic exercise have been debated, there are few reports on the remarkable effects of the application of conventional antioxidants on exercise performance. The conventional antioxidants could not enhance exercise performance due to their rapid excretion from the body and serious adverse effects on the cellular respiratory system. In this study, impact of the original antioxidant self-assembling nanoparticle, redox-active nanoparticle (RNP), is investigated on the exercise performance of rats during running experiments. With an increase in the dose of the administered RNP, the all-out time of the rat running extends in a dose-dependent manner. In contrast, with an increase in the dose of the low-molecular-weight (LMW) antioxidant, the all-out running time of the rats decreases. The control group and LMW antioxidant treated group decrease in the number of red blood cells (RBCs) and increase oxidative stress after running. However, the RNP group maintains a similar RBC level and oxidative stress as that of the sedentary group. The results suggest that RNP, which shows long-blood circulation without disturbance of mitohormesis, effectively removes ROS from the bloodstream to suppresses RBC oxidative stress and damage, thus improving exercise performance.

Keywords:  Fenton reaction; exercise performance; oxidative stress; polymeric nanoparticles; reactive oxygen species; red blood cells; self-assembling antioxidants

DOI:  https://doi.org/10.1002/adhm.202100067