Is Training to Failure a Safe and Effective Method for Improving Athletic Performance?

TRAINING TO FAILURE IS A POPULAR TRAINING METHOD USED TO IMPROVE MUSCULAR STRENGTH, SIZE, AND ENDURANCE. AT THIS TIME, THE VALUE OF THIS TRAINING STRATEGY FOR IMPROVING ATHLETIC PERFORMANCE IS A TOPIC OF CONSIDERABLE DEBATE. IN THIS COLUMN, THE POTENTIAL BENEFITS AND DETRIMENTS OF THIS TRAINING METHOD WILL BE PRESENTED

Resistance training modulates reticulum endoplasmic stress, independent of oxidative and inflammatory responses, in elderly people

[EN] Aging is related to changes in the redox status, low-grade inflammation, and decreased endoplasmic reticulum unfolded protein response (UPR). Exercise has been shown to regulate the inflammatory response, balance redox homeostasis, and ameliorate the UPR. This work aimed to investigate the effects of resistance training on changes in the UPR, oxidative status, and inflammatory responses in peripheral blood mononuclear cells of elderly subjects. Thirty elderly subjects volunteered to participate in an 8-week resistance training program, and 11 youth subjects were included for basal assessments. Klotho, heat shock protein 60 (HSP60), oxidative marker expression (catalase, glutathione, lipid peroxidation, nuclear factor erythroid 2-related factor 2, protein carbonyls, reactive oxygen species, and superoxide dismutase 1 and 2), the IRE1 arm of UPR, and TLR4/TRAF6/pIRAK1 pathway activation were evaluated before and following training. No changes in the HSP60 and Klotho protein content, oxidative status markers, and TLR4/TRAF6/pIRAK1 pathway activation were found with exercise. However, an attenuation of the reduced pIRE1/IRE1 ratio was observed following training. Systems biology analysis showed that a low number of proteins (RPS27A, SYVN1, HSPA5, and XBP1) are associated with IRE1, where XBP1 and RPS27A are essential nodes according to the centrality analysis. Additionally, a gene ontology analysis confirms that endoplasmic reticulum stress is a key mechanism modulated by IRE1. These findings might partially support the modulatory effect of resistance training on the endoplasmic reticulum in the elderly.SI: Funding for this project was provided by the Department of Exercise Science and Health Promotion at Florida Atlantic University. B. Estébanez was supported by a fellowship from the Ministry of Science, Innovation and Universities, Government of Spain (FPU fellowship, reference FPU15/05051; EST18/0025

Hepatic proteome analysis reveals altered mitochondrial metabolism and suppressed acyl-CoA synthetase-1 in colon-26 tumor-induced cachexia

Cachexia is a life-threatening complication of cancer traditionally characterized by weight loss and muscle dysfunction. Cachexia, however, is a systemic disease that also involves remodeling of nonmuscle organs. The liver exerts major control over systemic metabolism, yet its role in cancer cachexia is not well understood. To advance the understanding of how the liver contributes to cancer cachexia, we used quantitative proteomics and bioinformatics to identify hepatic pathways and cellular processes dysregulated in mice with moderate and severe colon-26 tumor-induced cachexia; ~300 differentially expressed proteins identified during the induction of moderate cachexia were also differentially regulated in the transition to severe cachexia. KEGG pathway enrichment revealed representation by oxidative phosphorylation, indicating altered hepatic mitochondrial function as a common feature across cachexia severity. Glycogen catabolism was also observed in cachexic livers along with decreased pyruvate dehydrogenase protein X component (Pdhx), increased lactate dehydrogenase A chain (Ldha), and increased lactate transporter Mct1. Together this suggests altered lactate metabolism and transport in cachexic livers, which may contribute to energetically inefficient interorgan lactate cycling. Acyl-CoA synthetase-1 (ACSL1), known for activating long-chain fatty acids, was decreased in moderate and severe cachexia based on LC-MS/MS analysis and immunoblotting. ACSL1 showed strong linear relationships with percent body weight change and muscle fiber size (R2 = 0.73–0.76, P < 0.01). Mitochondrial coupling efficiency, which is compromised in cachexic livers to potentially increase energy expenditure and weight loss, also showed a linear relationship with ACSL1. Findings suggest altered mitochondrial and substrate metabolism of the liver in cancer cachexia, and possible hepatic targets for intervention

Tissue-specific dysregulation of mitochondrial respiratory capacity and coupling control in colon-26 tumor-induced cachexia

In addition to skeletal muscle dysfunction, cancer cachexia is a systemic disease involving remodeling of non-muscle organs such as adipose and liver. Impairment of mitochondrial function is associated with multiple chronic diseases. The tissue-specific control of mitochondrial function in cancer cachexia is not well-defined. This study determined mitochondrial respiratory capacity and coupling control of skeletal muscle, white adipose tissue (WAT), and liver in colon-26 (C26) tumor-induced cachexia. Tissues were collected from PBS-injected weight-stable mice, C26 weight-stable mice, and C26 mice with moderate (10% weight loss) and severe cachexia (20% weight loss). The respiratory control ratio (RCR, an index of OXPHOS coupling efficiency) was low in WAT during the induction of cachexia, due to high non-phosphorylating LEAK respiration. Liver RCR was low in C26 weight-stable and moderately cachexic mice due to reduced OXPHOS. Liver RCR was further reduced with severe cachexia, where Ant2 but not Ucp2 expression was increased. Ant2 was inversely correlated with RCR in the liver (r=-0.547, p<0.01). Liver cardiolipin increased in moderate and severe cachexia, suggesting this early event may also contribute to mitochondrial uncoupling. Impaired skeletal muscle mitochondrial respiration occurred predominantly in severe cachexia, at complex I. These findings suggest that mitochondrial function is subject to tissue-specific control during cancer cachexia, whereby remodeling in WAT and liver arise early and may contribute to altered energy balance, followed by impaired skeletal muscle respiration. We highlight an under-recognized role of liver and WAT mitochondrial function in cancer cachexia, and suggest mitochondrial function of multiple tissues to be therapeutic targets

Effect of sampling frequency on isometric midthigh-pull kinetics

Purpose: Skeletal-muscle function can be evaluated using force-times curves generated via the isometric midthigh pull (IMTP). Various sampling frequencies (500–1000 Hz) have been used for IMTP assessments; however, no research has investigated the influence of sampling frequency on IMTP kinetics. Therefore, the purpose of this study was to investigate the influence of sampling frequency on kinetic variables during the IMTP, including peak force, time-specific force values (100, 150, and 200 ms), and rate of force development (RFD) at 3 time bands (0–100, 0–150, 0–200 ms). Methods: Academy rugby league players (n = 30, age 17.5 ± 1.1 y, height 1.80 ± 0.06 m, mass 85.4 ± 10.3 kg) performed 3 IMTP trials on a force platform sampling at 2000 Hz, which was subsequently down-sampled to 1500, 1000, and 500 Hz for analysis. Results: Intraclass correlation coefficients (ICC) and coefficients of variation (CV) demonstrated high within-session reliability for all force and RFD variables across all sampling frequencies (ICC ≥ .80, CV ≤ 14.4%) except RFD 0–100 and 0–150, which demonstrated slightly greater levels of variance (CV = 18.0–24.1%). Repeated-measures analysis of variance revealed no significant differences (P > .05, Cohen d ≤ 0.0171) in kinetic variables between sampling frequencies. Overall, high reliability was observed across all sampling frequencies for peak force, time-specific force, and RFD 0- to 200-ms variables, with no significant differences (P > .05) for each kinetic variable across sampling frequencies. Conclusions: Practitioners and scientists may consider sampling as low as 500 Hz when measuring peak force, time-specific force values, and RFD at predetermined time bands during the IMTP for accurate and reliable data

Mitochondrial physiology

As the knowledge base and importance of mitochondrial physiology to evolution, health and disease expands, the necessity for harmonizing the terminology concerning mitochondrial respiratory states and rates has become increasingly apparent. The chemiosmotic theory establishes the mechanism of energy transformation and coupling in oxidative phosphorylation. The unifying concept of the protonmotive force provides the framework for developing a consistent theoretical foundation of mitochondrial physiology and bioenergetics. We follow the latest SI guidelines and those of the International Union of Pure and Applied Chemistry (IUPAC) on terminology in physical chemistry, extended by considerations of open systems and thermodynamics of irreversible processes. The concept-driven constructive terminology incorporates the meaning of each quantity and aligns concepts and symbols with the nomenclature of classical bioenergetics. We endeavour to provide a balanced view of mitochondrial respiratory control and a critical discussion on reporting data of mitochondrial respiration in terms of metabolic flows and fluxes. Uniform standards for evaluation of respiratory states and rates will ultimately contribute to reproducibility between laboratories and thus support the development of data repositories of mitochondrial respiratory function in species, tissues, and cells. Clarity of concept and consistency of nomenclature facilitate effective transdisciplinary communication, education, and ultimately further discovery

Mitochondrial physiology

As the knowledge base and importance of mitochondrial physiology to evolution, health and disease expands, the necessity for harmonizing the terminology concerning mitochondrial respiratory states and rates has become increasingly apparent. The chemiosmotic theory establishes the mechanism of energy transformation and coupling in oxidative phosphorylation. The unifying concept of the protonmotive force provides the framework for developing a consistent theoretical foundation of mitochondrial physiology and bioenergetics. We follow the latest SI guidelines and those of the International Union of Pure and Applied Chemistry (IUPAC) on terminology in physical chemistry, extended by considerations of open systems and thermodynamics of irreversible processes. The concept-driven constructive terminology incorporates the meaning of each quantity and aligns concepts and symbols with the nomenclature of classical bioenergetics. We endeavour to provide a balanced view of mitochondrial respiratory control and a critical discussion on reporting data of mitochondrial respiration in terms of metabolic flows and fluxes. Uniform standards for evaluation of respiratory states and rates will ultimately contribute to reproducibility between laboratories and thus support the development of data repositories of mitochondrial respiratory function in species, tissues, and cells. Clarity of concept and consistency of nomenclature facilitate effective transdisciplinary communication, education, and ultimately further discovery

An economic feasibility analysis of woodchip production on the Island of Hawaii for export to Japan

Thesis (Ph. D.)--University of Hawaii at Manoa, 1981.Bibliography: leaves 181-189.Microfiche.xv, 189 leaves, bound ill., maps 28 c