Effects Of Acute Endurance Exercise Research Articles

Time Course ABCA1 Expression in Response to Acute Endurance Exercise

High density lipoprotein (HDL-C) is inversely correlated with the incidence of coronary artery disease. One of the protective effects of HDL-C against atherosclerosis is via reverse cholesterol transport (RCT) pathway. RCT pathway is critical for the transfer of excess cholesterol from peripheral cells back to liver for subsequent catabolism and exertion. The initial step of RCT is depending on ABCA1 to efflux the cholesterol from cell to lipid-poor Apolipoprotein AI. PURPOSE: To investigate the time course (immediately, after 2 hours and after 24 hours) expressions of ABCA1 in response to acute endurance exercise. Method: All experiments in this study were conducted acoording to the policy of NIH guidelines regarding the use of animals. Twenty male rat (12-14 years old, weighting 200-220 gr) divided into two groups (control n=10 and exercise n=10). Animals were kept in the Central Animal House, School of Medical Sciences of Tarbiat Modares University. Light was controlled using a 12 hour light-dark cycle. Temperature was 22±1.4° C and humidity was 55.6±4.0%. Animals were fed a pellet rodent diet add libitum and had free access to water. Exercise groups were given treadmill running for 2 hours at the intensity of 18 m/min. The first group of rats (control n=3, Exercise n=3) were sacrified immediately after exercise. The second group of rats (control n=3, exercise n=4) sacrified after 2 hours and third group (control n=3, exercise n=4) sacrified 24 hours after the end of exercise. The rat's liver excised immediately and frozen in liquid nitrogen for extraction of mRNA. The liver expression of ABCA1 was determined by semi-quantitative PCR and the levels of ABCA1 mRNA were expressed as a ratio of signal intensity for the Beta actin gene. RESULTS: The results of group 1 didn't show any significant differences between the liver expression of ABCA1 in control and exercise rats (26.74±7.7 vs. 25.9±4.8, P=0.880). But the significant different was observed between the control and exercise rats of group 2 (36.81±2.5 vs. 45.85±3.7, P=0.041) and group 3 (29.81±9.9 vs. 73±4.8, P=0.021) in response to acute endurance exercise. CONCLUSION: This is the first study investigating the effect of acute endurance exercise on the expression of ABCA1. The results clearly show the liver expression of ABCA1 in response to acute endurance exercise after 2 and 24 hours of exercise session but not immediately after exercise. This gene expression suggests that even one exercise session can trigger the reverse cholesterol transport pathway which can lead to prevention of atherosclerosis. This study was supported by Unversity of Tehran.

Improved assessment of the global transcriptional response to endurance exercise in human skeletal muscle

Endurance exercise is a potent stimulus for mitochondrial biogenesis and cellular metabolism. While the molecular events surrounding an acute bout of endurance exercise have been previously evaluated using small‐scale approaches, recent advances in gene microarray technology have substantially improved the number of gene targets available for investigation. Therefore, the purpose of this study was to examine the global mRNA response to a single bout of endurance exercise. Eleven healthy, young men (age 22±1 yrs, VO2peak 46±2 ml·kg−1·min−1) were recruited for this investigation. Muscle samples were acquired prior to and at 30 mins and 3 hours following an exhaustive cycling protocol. At 30 mins post‐exercise 404 genes were differentially expressed from rest (P<0.05), while at 3h 846 genes were significantly altered (P<0.05). When clustered by biological function, the greatest enrichment of genes at 30 mins occurred in those relating to developmental processes, cell differentiation, DNA binding, negative regulation of cellular processes, and primary metabolic processes. At 3h, functional annotation revealed clusters related to developmental processes, signal transduction, anatomical structure development, DNA binding and the regulation of apoptosis. To date, these data provide the most comprehensive transcriptional approach regarding the acute effects of endurance exercise. (Supported by NSERC Canada).

Endurance exercise increases the SIRT1 and peroxisome proliferator-activated receptor γ coactivator-1 α protein expressions in rat skeletal muscle

Peroxisome proliferator-activated receptor γ coactivator-1 α (PGC-1 α) is considered to play a pivotal role in the exercise-induced metabolic adaptation of skeletal muscle. Although the oxidized form of nicotinamide adenine dinucloetide (NAD +)-dependent histone deacetylase SIRT1 has been shown to mediate PGC-1 α–induced metabolic adaptation, the effect of endurance exercise on the SIRT1 protein remains to be elucidated. The purposes of this study were (1) to investigate the distribution of SIRT1 and PGC-1 α proteins in skeletal muscle and (2) to examine the effects of acute endurance exercise and low- or high-intensity exercise training on SIRT1 and PGC-1 α protein expressions and on the metabolic components in rat skeletal muscle. Both the SIRT1 and PGC-1 α proteins preferentially accumulate in red oxidative muscles. Acute endurance exercise on a motor-driven treadmill (20 m/min, 18.5% incline, 45 minutes) increases the PGC-1 α protein expression at 18 hours after exercise and the SIRT1 protein expression at 2 hours after exercise in the soleus muscle. In the training experiment, the rats were divided into control, low-intensity (20 m/min, 18.5% incline, 90 min/d), and high-intensity (30 m/min, 18.5% incline, 60 min/d) training groups. After 14 days of training, the SIRT1 and PGC-1 α proteins, hexokinase activity, mitochondrial proteins and enzyme activities, and glucose transporter 4 protein in the soleus muscle were increased by both trainings. In the plantaris muscle, SIRT1, hexokinase activity, mitochondrial proteins and enzyme activities, and glucose transporter 4 were increased by high-intensity training whereas the PGC-1 α was not. These results suggest that endurance exercise increases the skeletal muscle SIRT1 protein content. In addition, the findings also raise the possibility that the SIRT1 protein expression may play a potentially important role in such adaptations, whereas an increase in the PGC-1 α protein expression is not necessary for such adaptations.

Airway inflammation in nonasthmatic amateur runners

Elite athletes show a high prevalence of symptoms and signs of asthma, but no study has assessed the acute effects of endurance exercise on airway cells in nonasthmatic athletes. We measured exhaled nitric oxide (NO) and collected samples of induced sputum after 3% NaCl aerosol administration for 20 min in nonasthmatic middle-aged amateur runners after the Fourth Palermo International Marathon and 6--9 wk later (habitual training period) at baseline. After the marathon, exhaled NO (n = 9 subjects) was higher [27 +/- 9 parts/billion (ppb)] than at baseline (12 +/- 4 ppb; P < 0.0005). Polymorphonuclear neutrophil (PMN) counts in induced sputum were much higher in runners (91.2 +/- 3.6% of total cells postmarathon and 78.7 +/- 9.1% at baseline) than in sedentary control subjects (9.9 +/- 5.9%; P < 0.001). Expression of L-selectin and CD11b/CD18 in sputum PMNs was lower after the race than at baseline and inversely related to the amount of exhaled NO (r = -0.66 and -0.69, respectively; P < 0.05). Our data indicate that sputum PMNs are increased in nonasthmatic runners both after a marathon and at baseline and suggest that NO may modulate exercise-associated inflammatory airway changes.

Effects of Acute Endurance Exercise and 8 Week Training on the Production of Reactive Oxygen Species from Neutrophils in Untrained Men.

We investigated the effects of acute endurance exercise and habitual physical activity for health maintenance on human neutrophil function in 12 untrained men. The acute exercise condition was a continuous exercise for 90 minutes at the intensity of 50% and 55% of maximal oxygen uptake (VO2max) on an ergometer. The training program was 3 km jogging three times per week for 8 weeks. The capacity of neutrophils to produce reactive oxygen species (ROS) was detected with lucigenin-dependent chemiluminescence (LgCL) and luminol-dependent chemiluminescence (LmCL) on stimulation with opsonized zymosan (OZ) and phorbol myristate acetate (PMA). As for the acute exercise effects, both LgCL and LmCL responses of neutrophils, stimulated using PMA consistently increased after exercise at 50%VO2max, whereas those stimulated with OZ remained unchanged. At 55%VO2max, LgCL responses to both stimulants increase maximally 1 h after exercise, and then decreased 3 h after exercise, whereas LmCL responses to both stimulants increased continuously after exercise at 55%VO2max. These phenomena observed at 55%VO2max compared to 50%VO2max suggests the improved capacity of producing ROS neutrophils after exercise. The number of neutrophils also increased maximally 1 h after exercise, due to the mobilization of band neutrophils (shift to the left), suggesting that functional changes was associated with cell mobilization. The increase in the capacity of neutrophils to produce ROS and marked neutrophilia following the acute endurance exercise suggests that a large quantity of ROS may be produced in vivo. As for the training effects, the LgCL and LmCL responses were maintained in the exercise group as compared to the decreased ones in the control group. The difference between the exercise group and the control group was observed only in LgCL response to OZ. Humoral immune factors (IgG, IgA, IgM, C3, C4) and serum opsonic activity were also unaltered. These phenomena suggest that homeostasis might be kept constant in terms of immunity through regular physical activity.

Differential patterns of the number and proportion of blood leukocytes following endurance exercise of moderate, strenuous and severe conditions

A study was conducted to elucidate the acute effects of endurance exercise on white blood cells by setting three conditions of different intensity and duration; (a) an upper limit of aerobic exercise for health promotion and (b) superior limits within endurance exercise tolerance for untrained persons were prescribed separately for the same healthy untrained male student volunteers (n = 10) at intensities of 85% and 95% of the individual anaerobic threshold (AT) values for 1 h and 1.5 h, respectively, on a bicycle ergometer. In addition, (c) participants in a 100-km marathon race (n = 20) who continued running for 10-13 h were examined. Every condition caused significant leukocytosis due to predominant neutrophilia and, to a minor degree, a significant increase in monocyte number, the magnitude of which depended on the severity of endurance workload and persisted even 1 h after the termination of exercise. Simultaneously, microscopic evaluation of blood smears revealed the occurrence of an increased proportion of band neutrophils and a decreased proportion of hypersegmented neutrophils (shift to the left) following exercise in condition (b) but not in (a), suggesting that neutrophils are mobilized partly from the bone marrow reserve to the circulation. On the other hand, peripheral lymphopenia was observed after the termination of endurance exercise. These phenomena closely mimicked the known effects of exogenous glucocorticoid administration, suggesting an association with endogenous stress hormone (cortisol) secretion following strenuous exercise.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute effects of endurance exercise on human adipose tissue metabolism

In order to study the acute effects of exercise on adipose tissue metabolism, 27 sedentary male subjects, 18 to 27 years of age, performed a prolonged aerobic exercise test. Biopsies of adipose tissue were obtained from the suprailiac fat depot before and immediately after a 90-minute period of exercise on ergocycle at an average intensity of 88% of maximal heart rate. Fat cells, isolated by collagenase digestion, were measured for their glucose conversion into triglycerides and for lipolytic activity. Adipose tissue lipoprotein lipase activity released by heparin was also determined. Mean basal and insulin-stimulated glucose conversion into triglycerides decreased significantly with exercise ( P < .05) while adipose tissue lipoprotein lipase activity increased ( P < .01). Fat cell lipolysis increased during exercise only for its epinephrine-stimulated values ( P < .05). The total amount of work performed during the test was correlated only with changes in lipoprotein lipase activity ( r = .42, P < .05). Finally, the changes induced by exercise in lipoprotein lipase activity ( r = .37, P < .05) and insulin-stimulated glucose conversion into triglycerides ( r = .61, P < .01) were positively correlated with fat cell weight. These results indicate that adipose tissue metabolic activities are selectively influenced by endurance exercise. They also suggest that these metabolic changes are not closely coupled with the amount of work performed in a prolonged exercise bout.

Acute effects of endurance exercise on mitochondrial distribution and skeletal muscle morphology.

Biopsies of vastus lateralis from seven well-trained males were studied 1 month before and 15-30 min after a 100-km race. The distribution of interfibrillar mitochondria was analyzed to determine whether a long bout of exercise induced a redistribution of mitochondria. Capillary densities and mean fiber areas were also estimated. Capillary density and mean interfibrillar mitochondrial volume density were found to be significantly correlated with running time in the race. An earlier study on these biopsies found that the mean volume densities of interfibrillar and subsarcolemmal mitochondria did not change after a race, but the volume densities of lipid droplets and interfibrillar glycogen decreased significantly. In the present study, volume density of interfibrillar mitochondria [Vv(mi,fim)] before the race was highest with a value of 0.098 +/- 0.007 near the fiber border, and decreased progressively with distance to 0.045 +/- 0.004 at the fiber center. After the race, Vv(mi,fim) was unchanged at the fiber border, but was significantly higher (0.062 +/- 0.005) in the center of the fiber. This increase in mitochondrial volume density was attributable to the shrinkage of the fibers from consumption of energy stores, which was relatively greater for interfibrillar glycogen than for subsarcolemmal glycogen. Thus the primary effect of this extended bout of endurance exercise on vastus lateralis was the nearly complete depletion of the interfibrillar glycogen and lipids, but there was no evidence of an acute redistribution of mitochondria.