Kevin J. Gries's research while affiliated with Ball State University and other places

... To this end, targeting mitochondrial dynamics and quality control, including optimal functioning of the mitochondrial electron transport chain, which include determining the rate of respiration, ATP production, and ROS production have become important to decipher the pathological consequences of oxidative stress on muscle strength [75,76]. In fact, a growing number of clinical studies support the involvement of mitochondrial dysfunction in muscle wasting and development of sarcopenia. ...

... McClelland and Weyand 16 recently noted a sex difference of ~ 12% for running distances from 800 m to 10 km, attributed to differences in energy supply and demands. Accordingly, Jobe et al. 58 observed that males were 9-13% faster than females in all running events of the United States Olympic trials (from 100 m to marathon). Considering the physiological mechanisms underpinning the decrease of sex difference with the increasing race distance, an explanation might be the different taxing of the energy transfer systems in races varying for distance 58 . ...

... It is, therefore, In 2022, proteomics was performed in 11 studies in the SES field, demonstrating a reduced application to metabolomics which is perhaps due to transient changes in method popularity. These studies were conducted using muscle tissue, 18,96,[112][113][114][115] plasma, 116,117 saliva, 118,119 and urine. 120 Vanderboom et al. 114 indicating a time-differential training adaptation to skeletal muscle lipid availability. ...

... Exercise is a proven strategy to preserve cardiorespiratory fitness and muscle quality in older adults (Cartee et al., 2016;Gries & Trappe, 2022). Increased metabolic rate following acute exercise levels aids in the recovery of substrate stores, as well as stimulating cellular adaptations that, when repeated over time, can lead to phenotypic changes (Egan & Zierath, 2013). ...

... Sources of ROS that have been demonstrated to contribute to unloading-induced muscle atrophy include the mitochondria [7] and NADPH oxidase-2 (Nox2) [8,9]. Indeed, mitochondrial dysfunction has been linked to skeletal muscle wasting with denervation [10,11], unloading [7], and cachexia [12][13][14]. ...

... Among the potential factors, chronic inflammation, inadequate diet and nutrition, and weight and muscle loss may contribute to low bone mineral density in subjects chronically infected with HCV. Taken together, muscle mass and muscle strength stimulate osteogenesis through connections between the bone and skeletal muscle [120]. In addition, skeletal muscle mass is recognised as an independent predictor of bone mineral density in healthy [121] and diseased individuals [122,123]. ...

... We observed no difference in mean fibre CSA in the older trained group compared to the other groups, in contrast to a recent study on lifelong endurance exercisers (Grosicki et al., 2021). This may be explained by the pooling of fibre types, with lifelong endurance exercisers from this cohort having a high distribution of smaller type I fibres (Pollock et al. 2018). ...

... _ VO 2 peak depends on the ability of the respiratory and circulatory systems to transport oxygen and the ability of the skeletal muscle to utilise oxygen, whereas AT largely depends on the oxidative capacity of the skeletal muscle [64]. Several studies showed that respiratory and circulatory capacity steadily declined with ageing [71][72][73][74][75][76], whereas the oxidative capacity of the skeletal muscle was relatively maintained with ageing [77][78][79][80][81][82][83][84]. In summary, the effect of ageing was smaller for AT/kg (mainly dependent on peripheral factors) than for _ VO 2 peak=kg (dependent on central and peripheral factors), suggesting that AT= _ VO 2 peak increases with ageing. ...

... We have shown that expression of nod-like receptor family pyrin domain containing 3 (NLRP3) inflammasome-related cytokines, to some degree, were mirrored in EAT, PAT and SAT [5]. A dysregulated or inflamed AT, often seen in obesity, is infiltrated by pro-inflammatory macrophages (M1mɸ) and other immune cells, resulting in a local production of cytokines [6,7]. If EAT is affected, this could directly affect the myocardium due to its anatomical proximity, potentially changing contractility of the cardiomyocytes and eventually also accelerating the atherosclerotic process in the coronary arteries [8,9]. ...

... In addition, n-3 PUFA lessened cyclooxygenase-2 (COX-2) production via the inhibition of nuclear factor kappa B (NF-κB) [103] through the activation of peroxisome proliferator-activated receptor gamma (PPAR-γ) [104,105] and the stimulation of G-protein coupled receptor GPR120 [22,106]. The consumption of COX inhibitor was previously found to benefit skeletal muscle function [107], lower the risk of sarcopenia [108], and increase muscle fiber size in older adults [109]. However, due to its potential side effects, COX inhibitor was not prescribed for long-term use in the elderly [110]. ...