scholarly journals Resistance Training in Hypoxia as a New Therapeutic Modality for Sarcopenia—A Narrative Review

Life ◽  
2021 ◽  
Vol 11 (2) ◽  
pp. 106
Author(s):  
Won-Sang Jung ◽  
Sung-Woo Kim ◽  
Jeong-Weon Kim ◽  
Hun-Young Park
Keyword(s):  
Resistance Training ◽  
Resistance Exercise ◽  
Intracellular Signaling ◽  
Exercise Intervention ◽  
Muscle Size ◽  
Therapeutic Modality ◽  
Bodily Function ◽  
Muscular Function ◽  
Low Altitude

Hypoxic training is believed to be generally useful for improving exercise performance in various athletes. Nowadays, exercise intervention in hypoxia is recognized as a new therapeutic modality for health promotion and disease prevention or treatment based on the lower mortality and prevalence of people living in high-altitude environments than those living in low-altitude environments. Recently, resistance training in hypoxia (RTH), a new therapeutic modality combining hypoxia and resistance exercise, has been attempted to improve muscle hypertrophy and muscle function. RTH is known to induce greater muscle size, lean mass, increased muscle strength and endurance, bodily function, and angiogenesis of skeletal muscles than traditional resistance exercise. Therefore, we examined previous studies to understand the clinical and physiological aspects of sarcopenia and RTH for muscular function and hypertrophy. However, few investigations have examined the combined effects of hypoxic stress and resistance exercise, and as such, it is difficult to make recommendations for implementing universal RTH programs for sarcopenia based on current understanding. It should also be acknowledged that a number of mechanisms proposed to facilitate the augmented response to RTH remain poorly understood, particularly the role of metabolic, hormonal, and intracellular signaling pathways. Further RTH intervention studies considering various exercise parameters (e.g., load, recovery time between sets, hypoxic dose, and intervention period) are strongly recommended to reinforce knowledge about the adaptational processes and the effects of this type of resistance training for sarcopenia in older people.

scholarly journals Resistance Exercise Regulates Hepatic Lipolytic Factors as Effective as Aerobic Exercise in Obese Mice

2020 ◽  
Vol 17 (22) ◽  
pp. 8307
Author(s):  
Ju Yong Bae
Keyword(s):  
Resistance Training ◽  
Resistance Exercise ◽  
Aerobic Exercise ◽  
Exercise Intervention ◽  
Cannabinoid Receptor ◽  
Regulatory Element ◽  
Obese Mice ◽  
Alcoholic Fatty Liver ◽  
Protein Levels ◽  
Type Of Exercise

Non-alcoholic fatty liver disease (NAFLD) is associated with obesity. The effect of resistance exercise without dietary restriction on the regulation of hepatic lipolytic factors is unclear. This study aimed to analyze the effects of aerobic and resistance exercise on hepatic lipolytic factors of obese mice. High-fat diet (HFD)-induced obese mice were divided into HFD + sedentary (HF), HFD + aerobic exercise, and HFD + resistance exercise groups. Exercise group mice were subjected to treadmill or ladder climbing exercise for 8 weeks. Fat mass and liver triglycerides were significantly decreased in both aerobic and resistance training groups. In the results of protein levels related to hepatic steatosis, HFD significantly increased liver cannabinoid receptor 1 and sterol-regulatory element binding protein 1 (SREBP-1). Both aerobic and resistance training significantly (p < 0.05) increased liver carnitine palmitoyltransferase-1, phosphor-AMP-activated protein kinase (p-AMPK), and p-AMPK/AMPK and decreased liver SREBP-1. However, the type of exercise did not exert any significant effects on these protein levels. Thus, resistance exercise, similarly to aerobic exercise, effectively regulated hepatic lipolytic factors of obese mice. Therefore, a sustainable type of exercise selected based on the fitness level, disease type, musculoskeletal disorder status, and preference of the patients is the best exercise intervention for alleviating NAFLD.

mTOR signaling response to resistance exercise is altered by chronic resistance training and detraining in skeletal muscle

2013 ◽  
Vol 114 (7) ◽  
pp. 934-940 ◽  
Author(s):  
Riki Ogasawara ◽  
Koji Kobayashi ◽  
Arata Tsutaki ◽  
Kihyuk Lee ◽  
Takashi Abe ◽  
...  
Keyword(s):  
Resistance Training ◽  
Resistance Exercise ◽  
Intracellular Signaling ◽  
Gastrocnemius Muscle ◽  
Male Rats ◽  
Exercise Session ◽  
Signaling Proteins ◽  
Signaling Mechanisms ◽  
Exercise Induced ◽  
Training And Detraining

Resistance training-induced muscle anabolism and subsequent hypertrophy occur most rapidly during the early phase of training and become progressively slower over time. Currently, little is known about the intracellular signaling mechanisms underlying changes in the sensitivity of muscles to training stimuli. We investigated the changes in the exercise-induced phosphorylation of hypertrophic signaling proteins during chronic resistance training and subsequent detraining. Male rats were divided into four groups: 1 bout (1B), 12 bouts (12B), 18 bouts (18B), and detraining (DT). In the DT group, rats were subjected to 12 exercise sessions, detrained for 12 days, and then were subjected to 1 exercise session before being killed. Isometric training consisted of maximum isometric contraction, which was produced by percutaneous electrical stimulation of the gastrocnemius muscle every other day. Muscles were removed 24 h after the final exercise session. Levels of total and phosphorylated p70S6K, 4E-BP1, rpS6, and p90RSK levels were measured, and phosphorylation of p70S6K, rpS6, and p90RSK was elevated in the 1B group compared with control muscle (CON) after acute resistance exercise, whereas repeated bouts of exercise suppressed those phosphorylation in both 12B and 18B groups. Interestingly, these phosphorylation levels were restored after 12 days of detraining in the DT group. On the contrary, phosphorylation of 4E-BP1 was not altered with chronic training and detraining, indicating that, with chronic resistance training, anabolic signaling becomes less sensitive to resistance exercise stimuli but is restored after a short detraining period.

scholarly journals Changes in muscle size and MHC composition in response to resistance exercise with heavy and light loading intensity

2008 ◽  
Vol 105 (5) ◽  
pp. 1454-1461 ◽  
Author(s):  
L. Holm ◽  
S. Reitelseder ◽  
T. G. Pedersen ◽  
S. Doessing ◽  
S. G. Petersen ◽  
...  
Keyword(s):  
Resistance Training ◽  
Muscle Strength ◽  
Resistance Exercise ◽  
Muscle Hypertrophy ◽  
Vastus Lateralis ◽  
Load Resistance ◽  
Muscle Size ◽  
Heavy Load ◽  
Cross Sectional ◽  
Light Load

Muscle mass accretion is accomplished by heavy-load resistance training. The effect of light-load resistance exercise has been far more sparsely investigated with regard to potential effect on muscle size and contractile strength. We applied a resistance exercise protocol in which the same individual trained one leg at 70% of one-repetition maximum (1RM) (heavy load, HL) while training the other leg at 15.5% 1RM (light load, LL). Eleven sedentary men (age 25 ± 1 yr) trained for 12 wk at three times/week. Before and after the intervention muscle hypertrophy was determined by magnetic resonance imaging, muscle biopsies were obtained bilaterally from vastus lateralis for determination of myosin heavy chain (MHC) composition, and maximal muscle strength was assessed by 1RM testing and in an isokinetic dynamometer at 60°/s. Quadriceps muscle cross-sectional area increased ( P < 0.05) 8 ± 1% and 3 ± 1% in HL and LL legs, respectively, with a greater gain in HL than LL ( P < 0.05). Likewise, 1RM strength increased ( P < 0.001) in both legs (HL: 36 ± 5%, LL: 19 ± 2%), albeit more so with HL ( P < 0.01). Isokinetic 60°/s muscle strength improved by 13 ± 5% ( P < 0.05) in HL but remained unchanged in LL (4 ± 5%, not significant). Finally, MHC IIX protein expression was decreased with HL but not LL, despite identical total workload in HL and LL. Our main finding was that LL resistance training was sufficient to induce a small but significant muscle hypertrophy in healthy young men. However, LL resistance training was inferior to HL training in evoking adaptive changes in muscle size and contractile strength and was insufficient to induce changes in MHC composition.

scholarly journals Combined isometric, concentric, and eccentric resistance exercise prevents unloading-induced muscle atrophy in rats

2007 ◽  
Vol 103 (5) ◽  
pp. 1644-1654 ◽  
Author(s):  
G. R. Adams ◽  
F. Haddad ◽  
P. W. Bodell ◽  
P. D. Tran ◽  
K. M. Baldwin
Keyword(s):  
Resistance Training ◽  
Resistance Exercise ◽  
Muscle Atrophy ◽  
Negative Regulator ◽  
Medial Gastrocnemius ◽  
Muscle Size ◽  
Dynamic Mode ◽  
Resistance Training Program ◽  
Dynamic Components ◽  
Combined Mode

Previously, we reported that an isometric resistance training program that was effective in stimulating muscle hypertrophy in ambulatory rats could not completely prevent muscle atrophy during unloading (Haddad F, Adams GR, Bodell PW, Baldwin KM. J Appl Physiol 100: 433–441, 2006). These results indicated that preventing muscle atrophy does not appear to be simply a function of providing an anabolic stimulus. The present study was undertaken to determine if resistance training, with increased volume (3-s contractions) and incorporating both static and dynamic components, would be effective in preventing unloading-induced muscle atrophy. Rats were exposed to 5 days of muscle unloading via tail suspension. During that time one leg received electrically stimulated resistance exercise (RE) that included an isometric, concentric, and eccentric phase. The results of this study indicate that this combined-mode RE provided an anabolic stimulus sufficient to maintain the mass and myofibril content of the trained but not the contralateral medial gastrocnemius (MG) muscle. Relative to the contralateral MG, the RE stimulus increased the amount of total RNA (indicative of translational capacity) as well as the mRNA for several anabolic/myogenic markers such as insulin-like growth factor-I, myogenin, myoferlin, and procollagen III-α-1 and decreased that of myostatin, a negative regulator of muscle size. The combined-mode RE protocol also increased the activity of anabolic signaling intermediates such as p70S6 kinase. These results indicate that a combination of static- and dynamic-mode RE of sufficient volume provides an effective stimulus to stimulate anabolic/myogenic mechanisms to counter the initial stages of unloading-induced muscle atrophy.

Glioblastoma invasion and NMDA receptors: A novel prospect

2019 ◽  
Vol 106 (3) ◽  
pp. 250-260 ◽  
Author(s):  
DN Nandakumar ◽  
P Ramaswamy ◽  
C Prasad ◽  
D Srinivas ◽  
K Goswami
Keyword(s):  
Glutamate Receptors ◽  
Cell Lines ◽  
Intracellular Signaling ◽  
Transcript Level ◽  
Glioblastoma Cells ◽  
Invasion And Migration ◽  
Matrigel Invasion ◽  
Nmdar Activation ◽  
And Migration

Purpose Glioblastoma cells create glutamate-rich tumor microenvironment, which initiates activation of ion channels and modulates downstream intracellular signaling. N-methyl-D-aspartate receptors (NMDARs; a type of glutamate receptors) have a high affinity for glutamate. The role of NMDAR activation on invasion of glioblastoma cells and the crosstalk with α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors (AMPARs) is yet to be explored. Main methods LN18, U251MG, and patient-derived glioblastoma cells were stimulated with NMDA to activate NMDAR glutamate receptors. The role of NMDAR activation on invasion and migration and its crosstalk with AMPAR were evaluated. Invasion and migration of glioblastoma cells were investigated by in vitro trans-well Matrigel invasion and trans-well migration assays, respectively. Expression of NMDARs and AMPARs at transcript level was evaluated by quantitative real-time polymerase chain reaction. Results We determined that NMDA stimulation leads to enhanced invasion in LN18, U251MG, and patient-derived glioblastoma cells, whereas inhibition of NMDAR using MK-801, a non-competitive antagonist of the NMDAR, significantly decreased the invasive capacity. Concordant with these findings, migration was significantly augmented by NMDAR in both cell lines. Furthermore, NMDA stimulation upregulated the expression of GluN2 and GluA1 subunits at the transcript level. Conclusions This study demonstrated the previously unexplored role of NMDAR in invasion of glioblastoma cells. Furthermore, the expression of the GluN2 subunit of NMDAR and the differential overexpression of the GluA1 subunit of AMPAR in both cell lines provide a plausible rationale of crosstalk between these calcium-permeable subunits in the glutamate-rich microenvironment of glioblastoma.

THE ROLE OF PHOSPHATIDYLINOSITOL-3-KINASE IN CARCINOGENESIS

2017 ◽  
Vol 63 (4) ◽  
pp. 545-556
Author(s):  
Natalya Oskina ◽  
Aleksandr Shcherbakov ◽  
Maksim Filipenko ◽  
Nikolay Kushlinskiy ◽  
L. Ovchinnikova
Keyword(s):  
Genetic Disease ◽  
Intracellular Signaling ◽  
Somatic Mutations ◽  
Pi3k Pathway ◽  
Genetic Alterations ◽  
Phosphatidylinositol 3 Kinase ◽  
Intracellular Signaling Pathway ◽  
Metabolic Activities ◽  
Carcinogenic Process

Currently it is established that cancer is a genetic disease and that somatic mutations are the initiators of the carcinogenic process. The PI3K/AKT/mTOR pathway is an important intracellular signaling pathway regulating the cell growth and metabolic activities. Aberrant activation of the PI3K pathway is commonly observed in many different cancers. In this review we analyze the genetic alterations of PI3K pathway in a variety of human malignancies and discuss their possible implications for diagnosis and therapy.

The Role of DARPP-32, an Intracellular Signaling Molecule, in the Actions of the Nerve Agent Sarin

2005 ◽  
Author(s):  
Tsung-Ming Shih ◽  
Gretchen L. Snyder ◽  
Allen A. Fienberg ◽  
Stacey Galdi ◽  
Minal Rana ◽  
...  
Keyword(s):  
Intracellular Signaling ◽  
Nerve Agent ◽  
Signaling Molecule
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