193 research outputs found

    EXPLORING DIFFERENCES IN ELECTROMYOGRAPHY AND GROUND REACTION FORCES BETWEEN FRONT AND BACK SQUATS BEFORE AND AFTER A FATIGUING PROTOCOL

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    Limited research has been conducted to explore differences in biomechanical and physiological demands of the front and back squat, especially in response to fatigue where technique may be altered. This study investigated differences in electromyography and ground reaction forces during a 3-repetition maximum back and front squat before and after a fatiguing protocol in 30 males. Mean and peak activation of the semitendinosus was greater in the back squat than the front squat (p \u3c 0.05). There were no differences in quadricep activation between back and front squats. There were no differences in electromyography as a result of fatigue, however, force production decreased for back squats following fatigue (p \u3c 0.01). This research disputed the notion that front squats have a greater quadricep focus, however lends support to the hypothesis that quadricep activation equal to the back squat can be achieved with lighter absolute load in a front squat. The finding of lower ground reaction forces for the back squat following the fatiguing protocol in addition to no differences in electromyography between front and back squats indicates greater effects of the fatiguing protocol on back squat performance

    Exercise metabolism in non-obese patients with type 2 diabetes following the acute restoration of normoglycaemia

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    This study investigated how acute restoration of normoglycaemia affected energy metabolism during exercise in nonobese patients with type 2 diabetes. Six subjects (mean ± SEM) aged 56.2 ± 2.7 years, with a BMI of 24.5 ± 1.5 kg/m2 and a VO2 peak of 28.7 ml/kg/min, attended the lab on two randomised occasions for a four-hour resting infusion of insulin or saline, followed by 30 minutes cycling at 50% VO2 peak. During the 4 h resting infusion, there was a greater (P < 0 0001) reduction in blood glucose in insulin treatment (INS) (from 11.2 ± 0.6 to 5.6 ± 0.1 mmol/l) than in saline treatment/control (CON) (from 11.5 ± 0.7 to 8.5 ± 0.6 mmol/l). This was associated with a lower (P < 0 05) resting metabolic rate in INS (3.87 ± 0.17) than in CON (4.39 ± 0.30 kJ/min). During subsequent exercise, blood glucose increased significantly in INS from 5.6 ± 0.1 at 0 min to 6.3 ± 0.3 mmol/l at 30 min (P < 0 01), which was accompanied by a lower blood lactate response (P < 0 05). Oxygen uptake, rates of substrate utilization, heart rate, and ratings of perceived exertion were not different between trials. Insulin-induced normoglycaemia increased blood glucose during subsequent exercise without altering overall substrate utilization

    Methods to Assess Subcellular Compartments of Muscle in C. elegans

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    Skeletal muscle is essential for locomotion and is the bodies’ main protein store. Muscle health measurements within C. elegans are described. Prospective changes to muscle structure and function are assessed using localized GFP and cationic dyes

    Glutathione reductase gsr-1 is an essential gene required for Caenorhabditis elegans early embryonic development

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    Glutathione is the most abundant thiol in the vast majority of organisms and is maintained in its reduced form by the flavoenzyme glutathione reductase. In this work, we describe the genetic and functional analysis of the Caenorhabditis elegans gsr-1 gene that encodes the only glutathione reductase protein in this model organism. By using green fluorescent protein reporters we demonstrate that gsr-1 produces two GSR-1 isoforms, one located in the cytoplasm and one in the mitochondria. gsr-1 loss of function mutants display a fully penetrant embryonic lethal phenotype characterized by a progressive and robust cell division delay accompanied by an aberrant distribution of interphasic chromatin in the periphery of the cell nucleus. Maternally expressed GSR-1 is sufficient to support embryonic development but these animals are short-lived, sensitized to chemical stress and have increased mitochondrial fragmentation and lower mitochondrial DNA content. Furthermore, the embryonic lethality of gsr-1 worms is prevented by restoring GSR-1 activity in the cytoplasm but not in mitochondria. Given the fact that the thioredoxin redox systems are dispensable in C. elegans, our data support a prominent role of the glutathione reductase/glutathione pathway in maintaining redox homeostasis in the nematode

    Aerobically trained older adults show impaired resting, but preserved exercise-induced circulating progenitor cell count, which was not improved by sprint interval training

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    Older adults exhibit a reduced number and function of CD34 + circulating progenitor cells (CPC), a known risk factor for cardiovascular disease. Exercise promotes the mobilisation of CPCs from bone marrow, so whether ageing per se or physical inactivity in older age reduces CPCs is unknown. Thus, this study examined the effect of age on resting and exercise-induced changes in CPCs in aerobically trained adults and the effect of 8 weeks of sprint interval training (SIT) on resting and exercise-induced CPCs in older adults. Twelve young (22-34 years) and nine older (63-70 years) adults participated in the study. Blood was sampled pre and immediately post a graded exercise test to exhaustion in both groups. Older participants repeated the process after 8 weeks of SIT (3 × 20 s 'all-out' sprints, 2 × a week). Total CPCs (CD34 ) and endothelial progenitor cells (EPCs: CD34 KDR ) were determined by flow cytometry. Older adults exhibited lower basal total CD34 CPCs (828 ± 314 vs. 1186 ± 272 cells·mL , p = 0.0149) and CD34 KDR EPCs (177 ± 128 vs. 335 ± 92 cells·mL , p = 0.007) than younger adults. The maximal exercise test increased CPCs in young (CD34 : p = 0.004; CD34 KDR : p = 0.017) and older adults (CD34 : p  0.232). This study suggests age per se does not impair exercise-induced CPC counts, but does lower resting CPC counts

    Aerobically trained older adults show impaired resting, but preserved exercise-induced circulating progenitor cell count, which was not improved by sprint interval training

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    Older adults exhibit a reduced number and function of CD34 + circulating progenitor cells (CPC), a known risk factor for cardiovascular disease. Exercise promotes the mobilisation of CPCs from bone marrow, so whether ageing per se or physical inactivity in older age reduces CPCs is unknown. Thus, this study examined the effect of age on resting and exercise-induced changes in CPCs in aerobically trained adults and the effect of 8 weeks of sprint interval training (SIT) on resting and exercise-induced CPCs in older adults. Twelve young (22–34 years) and nine older (63–70 years) adults participated in the study. Blood was sampled pre and immediately post a graded exercise test to exhaustion in both groups. Older participants repeated the process after 8 weeks of SIT (3 × 20 s ‘all-out’ sprints, 2 × a week). Total CPCs (CD34+) and endothelial progenitor cells (EPCs: CD34+KDR+) were determined by flow cytometry. Older adults exhibited lower basal total CD34+ CPCs (828 ± 314 vs. 1186 ± 272 cells·mL−1, p = 0.0149) and CD34+KDR+ EPCs (177 ± 128 vs. 335 ± 92 cells·mL−1, p = 0.007) than younger adults. The maximal exercise test increased CPCs in young (CD34+: p = 0.004; CD34+KDR+: p = 0.017) and older adults (CD34+: p  0.232). This study suggests age per se does not impair exercise-induced CPC counts, but does lower resting CPC counts
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