The rs671 polymorphism is associated with the enzymatic activity of aldehyde dehydrogenase 2 (ALDH2), which is weakened by the A allele in East Asians. We recently reported the association of this polymorphism with the athletic status in athletic cohorts and the muscle strength of non-athletic cohorts. Therefore, we hypothesized the association of ALDH2 rs671 polymorphism with the performance in power/strength athletes. We aimed to clarify the relationship between the ALDH2 rs671 polymorphism and performance in power/strength athletes. Participants comprising 253 power/strength athletes (167 men and 86 women) and 721 healthy controls (303 men and 418 women) were investigated. The power/strength athletes were divided into classic powerlifting (n = 84) and weightlifting (n = 169). No differences in the genotypes and allele frequencies of the ALDH2 rs671 polymorphism and an association between performance and the ALDH2 rs671 genotype were observed in weightlifters. However, the relative values per body weight of the total record were lower in powerlifters with the GA + AA genotype than those with the GG genotype (7.1 ± 1.2 vs. 7.8 ± 1.0; p = 0.010, partial η2 = 0.08). Our results collectively indicate a role of the ALDH2 rs671 polymorphism in strength performance in powerlifters.

/pdf/the-association-between-the-aldh2-rs671-polymorphism-and-deyy1fsu.pdf

The Association between the ALDH2 rs671 Polymorphism and Athletic Performance in Japanese Power and Strength Athletes

The aldehyde dehydrogenase 2 (ALDH2) rs671 polymorphism, which is exclusive to the Asian population, is related to many diseases. A high reactive oxygen species production in mitochondria, and low muscle strength in athletes and non-athletes, has been observed, as our previous study demonstrated. The purpose of this research was to investigate the influence of ALDH2 rs671 on the loss of muscle strength with aging and replicate our previous study in non-athletes.Healthy Japanese individuals (n = 1804) aged 23-94 years were genotyped using DNA extracted from saliva. Muscle strength was assessed using grip strength and chair stand test (CST). The interaction between age and genotypes was analyzed by two-way analysis of covariance (ANCOVA) adjusted for sex, body mass index (BMI), and exercise habit.Individuals aged ≧55 with the AA genotype had a lower performance than those with the GG + GA genotype in the grip strength test (28.1 ± 9.1 kg vs. 29.1 ± 8.3 kg, p = 0.021). There was an interaction between age and genotype, where individuals with ≧55 years old AA genotype had a higher loss of strength compared to GG + GA genotypes in the CST (0.025). No interaction in other models and no sex differences were found.This study replicated previous results of the relationship between the AA genotype with lower muscle strength and as a novelty showed that this genotype is associated with a higher age-related loss of strength. 

/pdf/aldh2-gene-polymorphism-is-associated-with-fitness-in-the-2ayilgyv.pdf

ALDH2 gene polymorphism is associated with fitness in the elderly Japanese population

Aldehyde dehydrogenase 2 (ALDH2) is a mitochondrial enzyme involved in reactive aldehyde detoxification. Approximately 560 million people (about 8% of the world's population) carry a point mutation in the aldehyde dehydrogenase 2 gene (ALDH2), identified as ALDH2*2, which leads to decreased ALDH2 catalytic activity. ALDH2*2 variant is associated with an accumulation of toxic reactive aldehydes and consequent disruption of cellular metabolism, which contributes to the establishment and progression of several degenerative diseases. Consequences of aldehyde accumulation include impaired mitochondrial functional, hindered anabolic signaling in the skeletal muscle, impaired cardiovascular and pulmonary function, and reduced osteoblastogenesis. Considering that aldehydes are endogenously produced through redox processes, it is expected that conditions that have a high energy demand, such as exercise, might be affected by impaired aldehyde clearance in ALDH2*2 individuals. Despite the large body of evidence supporting the importance of ALDH2 to ethanol metabolism, redox homeostasis and overall health, specific research investigating the impact of ALDH2*2 on phenotypes relevant to exercise performance are notoriously scarce. In this commentary, we highlight the consolidated knowledge on the impact of ALDH2*2 on physiological processes that are relevant to exercise. 

Commentary: Aldehyde dehydrogenase, redox balance and exercise physiology: What is missing?

High-intensity exercise stimulates glycolysis, subsequently leading to elevated lactate production within skeletal muscle. While lactate produced within the muscle is predominantly released into the circulation via the monocarboxylate transporter 4 (MCT4), recent research underscores lactate's function as an intercellular and intertissue signalling molecule. However, its specific intracellular roles within muscle cells remains less defined. In this study, our objective was to elucidate the effects of increased intramuscular lactate accumulation on skeletal muscle adaptation to training. To achieve this, we developed MCT4 knockout mice and confirmed that a lack of MCT4 indeed results in pronounced lactate accumulation in skeletal muscle during high-intensity exercise. A key finding was the significant enhancement in endurance exercise capacity at high intensities when MCT4 deficiency was paired with high-intensity interval training (HIIT). Furthermore, metabolic adaptations supportive of this enhanced exercise capacity were evident with the combination of MCT4 deficiency and HIIT. Specifically, we observed a substantial uptick in the activity of glycolytic enzymes, notably hexokinase, glycogen phosphorylase and pyruvate kinase. The mitochondria also exhibited heightened pyruvate oxidation capabilities, as evidenced by an increase in oxygen consumption when pyruvate served as the substrate. This mitochondrial adaptation was further substantiated by elevated pyruvate dehydrogenase activity, increased activity of isocitrate dehydrogenase - the rate-limiting enzyme in the TCA cycle - and enhanced function of cytochrome c oxidase, pivotal to the electron transport chain. Our findings provide new insights into the physiological consequences of lactate accumulation in skeletal muscle during high-intensity exercises, deepening our grasp of the molecular intricacies underpinning exercise adaptation. KEY POINTS: We pioneered a unique line of monocarboxylate transporter 4 (MCT4) knockout mice specifically tailored to the ICR strain, an optimal background for high-intensity exercise studies. A deficiency in MCT4 exacerbates the accumulation of lactate in skeletal muscle during high-intensity exercise. Pairing MCT4 deficiency with high-intensity interval training (HIIT) results in a synergistic boost in high-intensity exercise capacity, observable both at the organismal level (via a treadmill running test) and at the muscle tissue level (through an ex vivo muscle contractile function test). Coordinating MCT4 deficiency with HIIT enhances both the glycolytic enzyme activities and mitochondrial capacity to oxidize pyruvate.

Monocarboxylate transporter 4 deficiency enhances high-intensity interval training-induced metabolic adaptations in skeletal muscle.

The role of telocytes and miR-21-5p in tumorigenicity and metastasis of breast cancer stem cells.

Aldehyde dehydrogenase 2 (ALDH2) detoxifies acetaldehyde produced from ethanol. A missense single nucleotide polymorphism (SNP) rs671 in ALDH2 exhibits a dominant-negative form of the ALDH2 protein. Nearly 40% of people in East Asia carry an inactive ALDH2*2 mutation. Previous studies reported that ALDH2*2 is associated with increased risk of several diseases. In this study, we examined the effect of ALDH2 deficiency on age-related muscle atrophy and its underlying mechanisms. We found that ALDH2 deficiency promotes age-related loss of muscle fiber cross-sectional areas, especially in oxidative fibers. Furthermore, ALDH2 deficiency exacerbated age-related accumulation of 4-hydroxy-2-nonenal (4-HNE), a marker of oxidative stress in the gastrocnemius muscle. Similarly, mitochondrial reactive oxygen species (ROS) production increased in aged ALDH2-knockout mice, indicating that ALDH2 deficiency induced mitochondrial dysfunction. In summary, ALDH2 deficiency promotes age-related muscle loss, especially in oxidative fibers, which may be associated with an increased accumulation of oxidative stress via mitochondrial dysfunction.

Aldehyde dehydrogenase 2 deficiency promotes skeletal muscle atrophy in aged mice.

Aldehyde dehydrogenase (ALDH) is an enzyme that detoxifies aldehydes and is primarily involved in alcohol metabolism. Recently, we have shown that ALDH also plays an important role in skeletal muscle homeostasis. To better understand the role of ALDH in skeletal muscle, it is necessary to clarify the adaptability of ALDH. In this study, we examined the effects of endurance training, compensatory hypertrophy by synergist ablation (SA), and denervation-induced atrophy on gene expression and protein levels of selected ALDH isoforms in skeletal muscle. Ten-week-old C57BL/6J mice were subjected to each intervention, and the plantaris muscle was collected. Gene expression levels of Aldh1a1 were decreased by SA and denervation, but ALDH1A1 protein levels were not affected. Protein levels of ALDH1B1 increased after chronic endurance training, SA, and denervation interventions. However, the increase in Aldh1b1 gene expression was observed only after SA. The gene expression of Aldh2 was decreased after SA, but ALDH2 protein levels remained unchanged. Denervation increased both the Aldh2 gene and ALDH2 protein levels. Taken together, each isoform of ALDH undergoes unique quantitative adaptations in skeletal muscle under different conditions.

Effect of different types of muscle activity on the gene and protein expression of ALDH family members in C57BL/6J mouse skeletal muscle.

PURPOSE: This study aimed to investigate the association between AGTR2 (rs11091046 A>C) gene polymorphism and athletic performance.METHODS: The Korean national team cyclists enrolled in the study performed 30-second Wingate test (peak power, mean power, and power drop), one-repetition maximum (squat and bench press), and isokinetic dynamometer (60° extensor and flexor in both legs) to examine the power/sprint performance between the C and A alleles.RESULTS: The physical characteristics showed no significant difference between the C and A alleles. Comparison of physical fitness tests in cyclists revealed no significant difference between the two alleles in one-repetition maximum and isokinetic dynamometer. However, the C allele had a significantly higher peak power (10.46±0.82 vs. 9.92±0.57, p=.016) and mean power (8.30±0.48 vs. 7.95±0.47, p=.022) than A allele in the Wingate test.CONCLUSIONS: Our results demonstrate that the AGTR2 gene C allele is associated with the power/sprint performance of the Korean national team cyclists.

/pdf/the-agtr2-rs11091046-gene-polymorphism-is-associated-with-3dtqn4c3.pdf

The AGTR2 (RS11091046) Gene Polymorphism is Associated with Cycling Performance in Korean Cyclists

Purpose：Recently ultrasound images has been used to measure the subacromial space with a linear measurement of the acromiohumeral distance. The purpose of this study was to comparison of distance of subacromial space using ultrasonographic measurement on arm positions of shoulder injured patients. Methods：The subjects were 30 shoulder injured patients (19 males and 11 females). Ultrasonography was performed to measure subacromial space during each shoulder resting position, 45° abduction, internal rotation with 45° abduction and external rotation with 45° abduction. Results：Subacromial space was a significantly difference between injured arm and normal arm at shoulder resting position. At 45° abduction, subacromial space was narrowing significantly between injured arm and normal arm. At external rotation with 45° abduction, subacromial space were wider in normal arm than in injured arm but it was not significantly. Intra-observer reliability for ultrasonography measurement of subacromial distance was excellent (.96~.99).Conclusion：These results identified that positions of injured shoulder was related to subacromion space.Key Words：Shoulder Pain, Subacromial space, Ultrasound imaging교신저자：김선엽, E-mail: kimsy@dju.kr논문접수일：2011년08월08일 / 수정접수일：2011년10월18일 / 게재승인일：2011년11월11일

Comparison of Distance of Subacromial Space Using Ultrasonographic Measurement on Arm Positions of Shoulder Injured Patients

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