scholarly journals In Healthy Young Men, a Short Exhaustive Exercise Alters the Oxidative Stress Only Slightly, Independent of the Actual Fitness

2016 ◽  
Vol 2016 ◽  
pp. 1-7 ◽  
Author(s):  
Maya Finkler ◽  
Ayala Hochman ◽  
Ilya Pinchuk ◽  
Dov Lichtenberg

The aim of the present study was to evaluate the apparent disagreement regarding the effect of a typical cycling progressive exercise, commonly used to assessVO2max, on the kinetics ofex vivocopper induced peroxidation of serum lipids. Thirty-two (32) healthy young men, aged 24–30 years, who do not smoke and do not take any food supplements, participated in the study. Blood was withdrawn from each participant at three time points (before the exercise and 5 minutes and one hour after exercise). Copper induced peroxidation of sera made of the blood samples was monitored by spectrophotometry. For comparison, we also assayed TBARS concentration and the activity of oxidation-related enzymes. The physical exercise resulted in a slight and reversible increase of TBARS and slight changes in the activities of the studied antioxidant enzymes and the lag preceding peroxidation did not change substantially. Most altered parameters returned to baseline level one hour after exercise. Notably, the exercise-induced changes in OS did not correlate with the physical fitness of the subjects, as evaluated in this study (VO2max= 30–60 mL/min/kg). We conclude that in healthy young fit men a short exhaustive exercise alters only slightly the OS, independent of the actual physical fitness.

2021 ◽  
Author(s):  
Javier Botella ◽  
Nicholas A. Jamnick ◽  
Cesare Granata ◽  
Amanda J. Genders ◽  
Enrico Perri ◽  
...  

AbstractAutophagy is a key intracellular mechanism by which cells degrade old or dysfunctional proteins and organelles. In skeletal muscle, evidence suggests that exercise increases autophagosome content and autophagy flux. However, the exercise-induced response seems to differ between rodents and humans, and little is known about how different exercise prescription parameters may affect these results. The present study utilised skeletal muscle samples obtained from four different experimental studies using rats and humans. Here we show that following exercise, in the soleus muscle of Wistar rats, there is an increase in LC3B-I protein levels (+ 109%) immediately after exercise, and a subsequent increase in LC3B-II protein levels (+ 97%) 3 hours into the recovery. Conversely, in human skeletal muscle, there is an immediate exercise-induced decrease in LC3B-II protein levels (− 24%), independent of whether exercise is performed below or above the maximal lactate steady state, which returns to baseline 3.5 hours following recovery, while no change in LC3B-I protein levels is observed. p62 protein levels did not change in neither rats nor humans following exercise. By employing an ex vivo autophagy flux assay previously used in rodents we demonstrate that the exercise-induced decrease in LC3B-II protein levels in humans does not reflect a decreased autophagy flux. Instead, effect size analyses suggest a modest-to-large increase in autophagy flux following exercise that lasts up to 24 hours. Our findings suggest that exercise-induced changes in autophagosome content markers differ between rodents and humans, and that exercise-induced decrease in LC3B-II protein levels do not reflect autophagy flux level.


2019 ◽  
Vol 126 (2) ◽  
pp. 305-313
Author(s):  
Naoto Fujii ◽  
Miki Kashihara ◽  
Glen P. Kenny ◽  
Yasushi Honda ◽  
Tomomi Fujimoto ◽  
...  

Hyperthermia causes hyperventilation at rest and during exercise. We previously reported that carotid chemoreceptors partly contribute to the hyperthermia-induced hyperventilation at rest. However, given that a hyperthermia-induced hyperventilation markedly differs between rest and exercise, the results obtained at rest may not be representative of the response in exercise. Therefore, we evaluated whether carotid chemoreceptors contribute to hyperthermia-induced hyperventilation in exercising humans. Eleven healthy young men (23 ± 2 yr) cycled in the heat (37°C) at a fixed submaximal workload equal to ~55% of the individual’s predetermined peak oxygen uptake (moderate intensity). To suppress carotid chemoreceptor activity, 30-s hyperoxia breathing (100% O2) was performed at rest (before exercise) and during exercise at increasing levels of hyperthermia as defined by an increase in esophageal temperature of 0.5°C (low), 1.0°C (moderate), 1.5°C (high), and 2.0°C (severe) above resting levels. Ventilation during exercise gradually increased as esophageal temperature increased (all P ≤ 0.05), indicating that hyperthermia-induced hyperventilation occurred. Hyperoxia breathing suppressed ventilation in a greater manner during exercise (−9 to −13 l/min) than at rest (−2 ± 1 l/min); however, the magnitude of reduction during exercise did not differ at low (0.5°C) to severe (2.0°C) increases in esophageal temperature (all P > 0.05). Similarly, hyperoxia-induced changes in ventilation during exercise as assessed by percent change from prehyperoxic levels were not different at all levels of hyperthermia (~15–20%, all P > 0.05). We show that in young men carotid chemoreceptor contribution to hyperthermia-induced hyperventilation is relatively small at low-to-severe increases in body core temperature induced by moderate-intensity exercise in the heat. NEW & NOTEWORTHY Exercise-induced increases in hyperthermia cause a progressive increase in ventilation in humans. However, the mechanisms underpinning this response remain unresolved. We showed that in young men hyperventilation associated with exercise-induced hyperthermia is not predominantly mediated by carotid chemoreceptors. This study provides important new insights into the mechanism(s) underpinning the regulation of hyperthermia-induced hyperventilation in humans and suggests that factor(s) other than carotid chemoreceptors play a more important role in mediating this response.


Nutrients ◽  
2021 ◽  
Vol 13 (4) ◽  
pp. 1250
Author(s):  
Sarah J. Wherry ◽  
Ryan M. Miller ◽  
Sarah H. Jeong ◽  
Kristen M. Beavers

Despite the adverse metabolic and functional consequences of obesity, caloric restriction- (CR) induced weight loss is often contra-indicated in older adults with obesity due to the accompanying loss of areal bone mineral density (aBMD) and subsequent increased risk of fracture. Several studies show a positive effect of exercise on aBMD among weight-stable older adults; however, data on the ability of exercise to mitigate bone loss secondary to CR are surprisingly equivocal. The purpose of this review is to provide a focused update of the randomized controlled trial literature assessing the efficacy of exercise as a countermeasure to CR-induced bone loss among older adults. Secondarily, we present data demonstrating the occurrence of exercise-induced changes in bone biomarkers, offering insight into why exercise is not more effective than observed in mitigating CR-induced bone loss.


1997 ◽  
Vol 85 (3) ◽  
pp. 1075-1078 ◽  
Author(s):  
D. Craig Huddy ◽  
Robert L. Johnson ◽  
Michael H. Stone ◽  
Christopher M. Proulx ◽  
Katherine A. Pierce

Students (39 men and 27 women) from a southern university, who were enrolled in a 14-wk. introductory weight-training course, were administered a 20-item body-image questionnaire and subsequently underwent skinfold measurements to assess percent body fat. Mean scores were correlated with percent body fat. For men, women, and both sexes combined correlations were significant and inverse ( rs = −.68, −.41, −.66, respectively). Body image as measured was inversely related to percent body fat among these college students. Researchers should examine how dietary and exercise-induced changes in adiposity (pre-post design) influence scores on body image.


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