1. Normal Versus Chronic Adaptations to Aerobic Exercise - StatPearls - NCBI
May 29, 2023 · Adaptive changes in work capacity, skeletal muscle capillarization and enzyme levels during training and detraining. ... muscle oxidative capacity ...
Effective aerobic exercise has been shown to elicit adaptations at both the molecular and macroscopic levels. These adaptations profoundly impact the cardiovascular and musculoskeletal systems (the two most affected organ systems), enabling more efficient oxygen delivery, endurance capacity, and improved performance. When implemented consistently for prolonged periods of time, aerobic exercise may lead to chronic adaptations with beneficial clinical outcomes.
2. Effect of Aerobic Exercise Training and Deconditioning on ... - NCBI
Sep 26, 2020 · Thus, it seems as the ability to obtain oxidative capacity and increase mitochondrial volume with intensive aerobic training is preserved with ...
Mitochondrial dysfunction is thought to be involved in age-related loss of muscle mass and function (sarcopenia). Since the degree of physical activity is vital for skeletal muscle mitochondrial function and content, the aim of this study was to investigate ...
3. Impact of Aerobic Exercise Training on Age-Related Changes in Insulin ...
Aug 1, 2003 · Insulin resistance increases and muscle oxidative capacity decreases during aging, but lifestyle changes—especially physical activity—may ...
Insulin resistance increases and muscle oxidative capacity decreases during aging, but lifestyle changes—especially physical activity—may reverse these trends.
4. Three Minutes of All-Out Intermittent Exercise per Week Increases ...
We hypothesized that the training intervention would increase skeletal muscle oxidative capacity, as reflected by the maximal activity and protein content ...
We investigated whether a training protocol that involved 3 min of intense intermittent exercise per week — within a total training time commitment of 30 min including warm up and cool down — could increase skeletal muscle oxidative capacity and markers of health status. Overweight/obese but otherwise healthy men and women (n = 7 each; age = 29±9 y; BMI = 29.8±2.7 kg/m2) performed 18 training sessions over 6 wk on a cycle ergometer. Each session began with a 2 min warm-up at 50 W, followed by 3×20 s “all-out” sprints against 5.0% body mass (mean power output: ∼450–500 W) interspersed with 2 min of recovery at 50 W, followed by a 3 min cool-down at 50 W. Peak oxygen uptake increased by 12% after training (32.6±4.5 vs. 29.1±4.2 ml/kg/min) and resting mean arterial pressure decreased by 7% (78±10 vs. 83±10 mmHg), with no difference between groups (both p<0.01, main effects for time). Skeletal muscle biopsy samples obtained before and 72 h after training revealed increased maximal activity of citrate synthase and protein content of cytochrome oxidase 4 (p<0.01, main effect), while the maximal activity of β-hydroxy acyl CoA dehydrogenase increased in men only (p<0.05). Continuous glucose monitoring measured under standard dietary conditions before and 48–72 h following training revealed lower 24 h average blood glucose concentration in men following training (5.4±0.6 vs. 5.9±0.5 mmol/L, p<0.05), but not women (5.5±0.4 vs. 5.5±0.6 mmol/L). This was associated with a greater increase in GLUT4 protein content in men compared to women (138% vs. 23%, p<0.05). Short-term interval training using a 10 min protocol that involved only 1 min of hard exercise, 3x/wk, stimulated physiological changes linked to improved health in overweight adults. Despite the small sample size, potential sex-specific adaptations were apparent that warrant further investigation.
5. Skeletal muscle energy metabolism during exercise - Nature
Aug 3, 2020 · Exercise increases protein turnover during exercise, and although amino acids, notably the branched-chain amino acids, can be oxidized by ...
The continual supply of ATP to the fundamental cellular processes that underpin skeletal muscle contraction during exercise is essential for sports performance in events lasting seconds to several hours. Because the muscle stores of ATP are small, metabolic pathways must be activated to maintain the required rates of ATP resynthesis. These pathways include phosphocreatine and muscle glycogen breakdown, thus enabling substrate-level phosphorylation (‘anaerobic’) and oxidative phosphorylation by using reducing equivalents from carbohydrate and fat metabolism (‘aerobic’). The relative contribution of these metabolic pathways is primarily determined by the intensity and duration of exercise. For most events at the Olympics, carbohydrate is the primary fuel for anaerobic and aerobic metabolism. Here, we provide an overview of exercise metabolism and the key regulatory mechanisms ensuring that ATP resynthesis is closely matched to the ATP demand of exercise. We also summarize various interventions that target muscle metabolism for ergogenic benefit in athletic events. Hargreaves and Spriet review regulatory mechanisms of ATP resynthesis during exercise and summarize nutritional interventions that target muscle metabolism to enhance athletic performance.
6. The Effect of Aerobic Exercise on the Oxidative Capacity of Skeletal ...
This is consistent with our results that aerobic exercise increases the activity of mitochondrial oxidase in skeletal muscle (Figure 3). Mitochondria are ...
Background/Objective. Impaired glucose tolerance (IGT) is an intermediate metabolic state between normal and diabetes and shows insulin resistant (IR) which to be linked with mitochondria dysfunction. This study is aimed at investigating whether aerobic exercise increases Mfn2 to promote mitochondrial function and improve glucose tolerance and insulin sensitivity in mice with high-fat diet. Methods. Male C57BL/6J mice were randomly divided into six different experimental groups (8 animals/group): (1) normal group (NOR), (2) normal control group (NC), (3) normal + exercise group (NE), (4) IGT group (IGT), (5) IGT control group (IC), and (6) IGT+ exercise group (IE).The exercise group received aerobic exercise for 8 weeks. After the intervention, a blood glucose meter was used to detect the level of glucose tolerance in the mouse’s abdominal cavity; a biochemical kit was used to detect serum lipid metabolism indicators, malondialdehyde, and superoxide dismutase levels; the ELISA method was used to detect serum insulin and mouse gastrocnemius homogenate LDH, PDH, SDH, and CCO levels. Western blot method was used to detect the protein expression levels of NOX4, PGC-1α, and Mfn2 in the gastrocnemius muscle of mice. Results. (1) Mice with high-fat diet for 30 weeks showed impaired glucose tolerance, insulin resistance, and lipid metabolism disorders. The level of LDH, PDH, SDH, and CCO in the gastrocnemius homogenate of mice was reduced. The expressions of NOX4 protein were significantly upregulated, while the expressions of PGC-1α and Mfn2 proteins were significantly downregulated. (2) 8-week aerobic exercise improved the disorders of glucose and lipid metabolism in IGT mice and increased homogenized LDH, PDH, SDH, and CCO levels, and the expressions of NOX4, PGC-1α, and Mfn2 proteins in the gastrocnemius muscle of mice were reversed. It is speculated that aerobic exercise can accelerate energy metabolism. Conclusion. (1) C57BL/6 mice were fed high fat for 30 weeks and successfully constructed a mouse model of reduced diabetes; the mice with reduced diabetes have impaired glucose tolerance, insulin resistance, and lipid metabolism disorders; (2) 8 weeks of aerobic exercise improve glucose tolerance, reduce glucose tolerance in mice, reduce insulin resistance, improve lipid metabolism disorders, and reduce oxidative stress; (3) 8-week aerobic exercise reduces skeletal muscle NOX4 expression and increases glucose tolerance; reduces the expression of LDH, PDH, SDH, and CCO in mouse skeletal muscle; increases the expression level of mitochondrial fusion protein 2 and PGC-1α; improves glucose tolerance; reduces energy metabolism of mouse skeletal muscle; reduces oxidative stress; and reduces insulin resistance. It is speculated that aerobic exercise can accelerate energy metabolism. This process may involve two aspects: firstly, increase the expression level of oxidative metabolism enzymes and promote the tricarboxylic acid cycle; secondly, increase the expression of Mfn2 and accelerate mitochondria fission or fusion to regulate energy metabolism, thereby reducing oxidative stress and insulin resistance.
7. The Effect of Aerobic Exercise on Oxidative Stress in Skeletal Muscle ...
Jan 14, 2023 · Performing intense aerobic exercise leads to an increase in the level of reactive oxygen species (ROS) and a decrease in the level of ...
Context: Performing intense aerobic exercise leads to an increase in the level of reactive oxygen species (ROS) and a decrease in the level of antioxidant enzymes in body tissues, especially skeletal muscles, and ultimately oxidative stress. Therefore, it is very important to measure oxidative stress before it causes damage to cells and destroys them. Evidence Acquisition: In this review, 92 articles were studied between 2012 and 2022, of which 54 were used. The search was done in Google Scholar, PubMed, Science Direct, and SID databases. An electronic search of studies was done using the keywords ROS, aerobic training, exercise, oxidative stress, antioxidant defense, skeletal muscle, and nuclear factor-erythroid 2-related factor 2 (NRF2). Results: The review of studies conducted in the field of antioxidant adaptations of skeletal muscle shows that the intensity and duration of activity are the main factors in controlling (creating or preventing) oxidative stress in skeletal muscle tissue. Also, taking antioxidant supplements before ROS levels reach peak physiological performance can reduce the beneficial effects of exercise. On the other hand, antioxidant treatment, after maximal performance related to ROS, can lead to reduced fatigue and/or improved performance. Conclusions: It seems that the increase in oxidative stress caused by aerobic exercise is a function of the amount of ROS production and the internal and external antioxidant defense capacity of the individual. However, different types of aerobic exercise along with various antioxidant supplements need to be performed for a long time in different people in order to achieve better approaches to early prediction of oxidative stress and reducing the destructive effects of skeletal muscle.
8. Skeletal Muscle Insulin Resistance: Roles of Fatty Acid Metabolism and ...
Aerobic exercise training decreases the amounts of these lipid products and increases the lipid oxidative capacity of muscle cells. Thus, aerobic exercise ...
The purpose of this review is to provide information about the role of exercise in the prevention of skeletal muscle insulin resistance, that is, the inability
9. [PDF] chapter 3 physiologic responses and long-term adaptations to exercise
(providing that size and activity level are normal- ized). Relative ... Muscle adaptations to aerobic training. Sports. Science Exchange 1995;8:1–4. Thompson ...
10. Effect of aerobic exercise training and ... - Department of Neuroscience
This evidence was accompanied by a similar training-induced increase in muscle citrate synthase (CS) (31%) and mitochondrial complex I-IV activities (51-163%) ...
The Løland lab focuses on structure-function relationships in membrane transporters with focus on the Neurotransmitter:Sodium Symporter (NSS) class of proteins.
11. Aerobic Exercise - Physiopedia
Maximum aerobic capacity increases with aerobic training. The resting Vo2 is stable, as is the Vo2 at a given workload. The changes are specific to the trained ...
Original Editor - Manisha Shrestha
12. Glycogen availability and skeletal muscle adaptations with endurance ...
Dec 21, 2015 · In short, endurance exercise training mainly results in mitochondrial biogenesis, increases capillary density and enzymes leading to enhanced ...
It is well established that glycogen depletion affects endurance exercise performance negatively. Moreover, numerous studies have demonstrated that post-exercise carbohydrate ingestion improves exercise recovery by increasing glycogen resynthesis. However, recent research into the effects of glycogen availability sheds new light on the role of the widely accepted energy source for adenosine triphosphate (ATP) resynthesis during endurance exercise. Indeed, several studies showed that endurance training with low glycogen availability leads to similar and sometimes even better adaptations and performance compared to performing endurance training sessions with replenished glycogen stores. In the case of resistance exercise, a few studies have been performed on the role of glycogen availability on the early post-exercise anabolic response. However, the effects of low glycogen availability on phenotypic adaptations and performance following prolonged resistance exercise remains unclear to date. This review summarizes the current knowledge about the effects of glycogen availability on skeletal muscle adaptations for both endurance and resistance exercise. Furthermore, it describes the role of glycogen availability when both exercise modes are performed concurrently.
13. Aerobic Exercise Training in Patients With mtDNA-Related Mitochondrial ...
Mar 26, 2020 · From exercise intensity of 50% of VO2max, oxidation of carbohydrate increases linearly with increase in exercise intensity, but from exercise ...
In patients with mitochondrial DNA (mtDNA) mutation, a pathogenic mtDNA mutation is heteroplasmically distributed among tissues. The ratio between wild-type and mutated mtDNA copies determines the mtDNA mutation load of the tissue, which correlates inversively with oxidative capacity of the tissue. In patients with mtDNA mutation, the mutation load is often very high in skeletal muscle compared to other tissues. Additionally, skeletal muscle can increase its oxygen demand up to 100-fold from rest to exercise, which is unmatched by any other tissue. Thus, exercise intolerance is the most common symptom in patients with mtDNA mutation. The impaired oxidative capacity in skeletal muscle in patients with mtDNA mutation results in limitation in physical capacity that interferes with daily activities and impairs quality of life. Additionally, patients with mitochondrial disease due to mtDNA mutation often live a sedentary lifestyle, which further impair oxidative capacity and exercise tolerance. Since aerobic exercise training increase mitochondrial function and volume density in healthy individuals, studies have investigated if aerobic training could be used to counteract the progressive exercise intolerance in patients with mtDNA mutation. Overall studies investigating the effect of aerobic training in patients with mtDNA mutation have shown that aerobic training is an efficient way to improve oxidative capacity in this condition, and aerobic training seems to be safe even for...
14. Whole-body and muscle responses to aerobic exercise training and ...
Muscle MAPR for palmitate increased with training in HO (57%; p=0.041) and HY (56%; p=0.003), and decreased with exercise withdrawal in HO (−45%; p=0.036) and ...
Background Chronic obstructive pulmonary disease (COPD) patients exhibit lower peak oxygen uptake ( V ′O2peak), altered muscle metabolism and impaired exercise tolerance compared with age-matched controls. Whether these traits reflect muscle-level deconditioning (impacted by ventilatory constraints) and/or dysfunction in mitochondrial ATP production capacity is debated. By studying aerobic exercise training (AET) at a matched relative intensity and subsequent exercise withdrawal period we aimed to elucidate the whole-body and muscle mitochondrial responsiveness of healthy young (HY), healthy older (HO) and COPD volunteers to whole-body exercise. Methods HY (n=10), HO (n=10) and COPD (n=20) volunteers were studied before and after 8 weeks of AET (65% V ′O2peak) and after 4 weeks of exercise withdrawal. V ′O2peak, muscle maximal mitochondrial ATP production rate (MAPR), mitochondrial content, mitochondrial DNA (mtDNA) copy number and abundance of 59 targeted fuel metabolism mRNAs were determined at all time-points. Results Muscle MAPR (normalised for mitochondrial content) was not different for any substrate combination in HO, HY and COPD at baseline, but mtDNA copy number relative to a nuclear-encoded housekeeping gene (mean±sd) was greater in HY (804±67) than in HO (631±69; p=0.041). AET increased V ′O2peak in HO (17%; p=0.002) and HY (21%; p<0.001), but not COPD (p=0.603). Muscle MAPR for palmitate increased with training in HO (57%; p=0.041) and HY (56%; p=0.003), and decreased with exercise withdrawal in HO (−45%; p=0.036) and HY (−30%; p=0.016), but was unchanged in COPD (p=0.594). mtDNA copy number increased with AET in HY (66%; p=0.001), but not HO (p=0.081) or COPD (p=0.132). The observed changes in muscle mRNA abundance were similar in all groups after AET and exercise withdrawal. Conclusions Intrinsic mitochondrial function was not impaired by ageing or COPD in the untrained state. Whole-body and muscle mitochondrial responses to AET were robust in HY, evident in HO, but deficient in COPD. All groups showed robust muscle mRNA responses. Higher relative exercise intensities during whole-body training may be needed to maximise whole-body and muscle mitochondrial adaptation in COPD. Muscle mitochondrial function is not impaired in age or COPD. Whole-body and mitochondrial exercise training adaptations are robust in young, evident in older and deficient in COPD. COPD adaptation may require high-intensity exercise training programmes.
15. effects of aerobic exercise training on oxidative stress in the skeletal ...
HFD reduced GSH-Px activity in both muscles, and the MICT protocol prevented this reduction in the soleus muscle, while the HIIT protocol partially prevented ...
ABSTRACT Introduction Obesity is a complex and multifactorial metabolic disorder characterized...
16. Aerobic exercise training induces metabolic benefits in rats ... - Elsevier
Exercise induces rapid increases in GLUT4 expression, glucose transport capacity, and insulin-stimulated glycogen storage in muscle. J Biol Chem, 269 (1994), pp ...
OBJECTIVESWe evaluated the effects of aerobic exercise training without dietary changes on
17. Effects of Treadmill Training on Muscle Oxidative Capacity and ...
Jul 1, 2019 · 11–15 While exercise training has been shown to increase VO2peak in people with MS, measures of whole-body oxygen consumption are influenced by ...
AbstractBackground:. Exercise can improve muscle function and mobility in people with multiple sclerosis (MS). However, the effects of exercise training on skeletal muscle oxidative capacity and endurance in people with MS remain unclear, and few studies have evaluated muscle plasticity in people with MS who have moderate-to-severe disability. The present study evaluated the effects of treadmill training on muscle oxidative capacity and muscle endurance and examined the relationship to walking function in people with MS who have moderate-to-severe disability.Methods:. Six adults (mean ± SD age, 50 ± 4.9 years) with MS (Expanded Disability Status Scale score, 6.0–6.5) performed treadmill training for 24 minutes approximately twice per week for approximately 8 weeks (16 sessions total) using an antigravity treadmill system. The following measures were taken before and after the intervention phase: muscle oxidative capacity in the medial gastrocnemius using near-infrared spectroscopy after 15 to 20 seconds of electrical stimulation; muscle endurance in the medial gastrocnemius using accelerometer-based mechanomyography during 9 minutes of twitch electrical stimulation in three stages (3 minutes per stage) of increasing frequency (2, 4, and 6 Hz); and walking function using the 2-Minute Walk Test.Results:. Mean ± SD muscle oxidative capacity increased from 0.64 ± 0.19 min−1 to 1.08 ± 0.52 min−1 (68.2%). Mean ± SD muscle endurance increased from 80.9% ± 15.2% to 91.5% ± 4.8% at 2 Hz, from 56.3% ± 20.1% to 76.6% ± 15.8% at 4 Hz, and from 29.2% ± 13.1% to 53.9% ± 19.4% at 6 Hz of stimulation in the gastrocnemius. There were no significant improvements in walking function.Conclusions:. Treadmill training can improve muscle oxidative capacity and endurance in people with MS who have moderate-to-severe levels of disability.
FAQs
How Does Regular Aerobic Exercise Training Increase Oxidative Capacity Of Muscle? ›
Aerobic exercise training decreases the amounts of these lipid products and increases the lipid oxidative capacity of muscle cells. Thus, aerobic exercise training may prevent insulin resistance by correcting a mismatch between fatty acid uptake and fatty acid oxidation in skeletal muscle.
How does exercise increase oxidative stress? ›These physiological changes that occur during acute exercise increase free radical production, leading to oxidative damage to biomolecules. Exercise-induced oxidative stress associated with increased free radical production has been studied for 40 years, since it was first reported by Dillard et al., in 1978 [14].
How does aerobic exercise affect your muscles? ›Aerobic exercise keeps your muscles strong, which can help you maintain mobility as you get older. Exercise can also lower the risk of falls and injuries from falls in older adults. And it can improve your quality of life. Aerobic exercise also keeps your mind sharp.
How does aerobic training improve aerobic metabolism? ›Aerobic exercises use large muscle groups to perform the same actions for at least 10 minutes at a time. This raises your heart rate and breath rate as your body delivers the oxygen needed to your muscles for aerobic metabolism. This burns sugars and fats for energy.
How does exercise reduce oxidative stress? ›The exercise-induced ROS generation results in increased activity of enzymatic antioxidants, which then lead to an increased resistance to oxidative challenges, including a wide variety of oxidative stress-related diseases, including cardiovascular diseases, acquired neurodegenerative disorders (Alzheimer's and ...
Does stress increase oxidative stress? ›The chronic stress contributes to the formation of oxidative stress in the parts of the brain involved in the development of depression and AD. The scientific literature reports the significant role of antioxidants, which are highly effective in treating these diseases.
How do you train the oxidative system? ›- Steady state cardio – long duration, low intensity workouts such as jogging, cycling, swimming, or rowing. ...
- Long intervals – using a 1:1 or 1:2 work/rest interval, for example, three minutes fast running, three minutes walking/jogging, repeated five times to total 30 minutes.
Aerobic exercise is cardiovascular conditioning that strengthens both your heart and lungs. The word “aerobic” means “with oxygen,” as this kind of exercise is fueled by the oxygen that you get from breathing. As you exercise, your muscles need more oxygen, which is carried by the blood, to keep going.
What do aerobic exercises improve muscle? ›Regular aerobic exercise can help build stronger bones, improve muscle strength and endurance, and reduce the risk of falling.
Does aerobic exercise increase muscle strength? ›Adding some muscle also improves physical fitness and bone mineral density and reduces the risk of musculoskeletal injury. Running, swimming, playing soccer and other aerobic exercise do a lot for the cardiovascular system — our heart and blood vessels — but they don't do much for overall muscle mass or strength.
What is the aerobic oxidative metabolism? ›
Aerobic metabolism is the oxidative process of the generation of ATP or energy that occurs in the body to provide the body with fuel during both resting and exercise states.
Does aerobic training increase fat oxidation? ›Endurance exercise training increases the capacity skeletal muscle fat oxidation by increasing mitochondrial density, the activity of enzymes involved in β-oxidation, and oxygen delivery to muscle.
How does aerobic exercise increase energy? ›Exercising also boosts oxygen circulation inside your body. This increase in oxygen not only supports the mitochondria's energy production, it allows your body to function better and to use its energy more efficiently.
Does oxidative stress cause muscle loss? ›Oxidative stress is able to produce mitochondrial dysfunction, increase ubiquitin proteasome system activity, increase myonuclear apoptosis, decrease the protein synthesis pathway, and deregulate autophagy, all of which are involved in cachexia-skeletal muscle atrophy.
What is the role of physical exercise and antioxidants in oxidative stress? ›Exercise enhances antioxidant response, decreases age-related oxidative stress and pro-inflammatory signals, and promotes the activation of anabolic and mitochondrial biogenesis pathways in skeletal muscle.
What is the role of oxidative stress in the body? ›Oxidative stress (OS) has the ability to damage different molecules and cellular structures, altering the correct function of organs and systems. OS accumulates in the body by endogenous and exogenous mechanisms.
What factors increase oxidative stress? ›- obesity.
- diets high in fat, sugar, and processed foods.
- exposure to radiation.
- smoking cigarettes or other tobacco products.
- alcohol consumption.
- certain medications.
- pollution.
- exposure to pesticides or industrial chemicals.
Prolonged or high intensity exercise can result in both: (1) oxidative damage in skeletal muscle fibers and (2) accelerated muscle fatigue. Exercise-induced increases in the production of reactive oxygen species in skeletal muscle plays a required role in skeletal muscle adaptation to endurance training.
What causes oxidative stress in athletes? ›Exercise is one such stressor. Simply stated, any situation in which the consumption of oxygen is increased, as during physical exercise, could result in an acute state of oxidative stress.