Muscle Contraction Energy ( Read ) | Biology | CK Foundation
Cellular Respiration Activity – Clothespins and Muscle Fatigue. Purpose: to explore the relationship between cellular respiration and muscle. Recall from the Cellular Respiration concepts that the mitochondria are to the muscle cells fast enough to keep up with the muscles' need for ATP. than it can be removed from the muscle, it can lead to muscle fatigue. In this lesson, the effects of muscle fatigue on task performance are shown by in your body through aerobic (oxygen-requiring) respiration, though a between the experimenter's thumb and forefinger, which should be about 2 cm apart. 3.
Factors that affect muscle contraction and fatigue The production of skeletal muscle force depends on contractile mechanisms, and failure at any of the sites upstream of the cross-bridges can contribute to the development of muscle fatigue, including nervous, ion, vascular and energy systems. Neural contributions Central neurotransmitters, especially 5-HT, DA and NA, play important role during whole-body exercise and fatigue.
However, recent data have shown that drugs influencing the neurotransmitter systems scarcely perturb performance under normal ambient temperatures but significantly improve endurance under high ambient temperatures. However, under heat, reboxetine decreases, whereas bupropion increases performance, thus suggesting that the thermoregulatory system may have an important influence on exercise performance.
The CNS, via a central neurotransmitter, produces various excitatory and inhibitory inputs on the spinal motoneurons, thus ultimately activating motor units MUs to achieve the force output. The strength and timing of contraction are controlled by the firing of the motoneurons.
When first recruited in a healthy system, MUs usually fire at 5—8 Hz. During brief nonfatiguing voluntary contractions in humans, the mean MU firing rates are 50—60 Hz. Motoneuron firing is influenced by intrinsic changes in the motoneuron properties, descending drive and afferent feedback. During fatiguing maximal contractions, motoneuron firing rates decrease because of the following factors: This excitation-contraction coupling process involves the following events: Several possible mechanisms have been proposed: Muscle voluntary contractions increase the mean arterial blood pressure, 22 which consequently decreases the net blood flow to the working muscle and induces fatigue.
However, despite changes in blood flow accompanying the development of muscle fatigue, decreased blood flow does not seem to be a key factor in the development of fatigue. One of the important roles of blood flow is to provide O2 to the working muscles.
Muscle fatigue: general understanding and treatment
It has been well documented that decreased oxygen availability to exercising muscle has profound consequences on muscle fatigue. Breathing hypoxic air can significantly increase muscle fatigue in vivo, 3031 and enhanced O2 delivery to the exercising muscles 32 directly attenuates muscle fatigue and increases muscle efficiency.
However, O2 availability affects the fatigue process at moderate work intensities. During exercise at a very high intensity usually the VO2max is already reachedthe demand for more ATP cannot be met by increases in oxygen delivery, thus resulting in an imbalance of metabolic homeostasis and leading to fatigue.
There are three distinct subcellular localizations of glycogen: Glycolysis leads to the production of pyruvate, which feeds into the TCA cycle for oxidation.
Furthermore, there is a lack of association between changes in pH and MVC throughout fatiguing exercise and in recovery in humans. The concentration of Pi can increase rapidly from approximately 5—30 mM during intense fatigue. Creatine has little effect on contractile function, whereas Pi, rather than acidosis, appears to be the most important cause of fatigue during high-intensity exercise.
As the work intensity increases, ROS production increases. The most convincing evidence that ROS contribute to fatigue comes from experiments showing that pretreatment of intact muscle with a ROS scavenger significantly attenuates the development of fatigue. In skinned fibers, ADP decreases fiber velocity but increases force, presumably because of more cross-bridges in the high force states.
Many fatigue reactants, such as cortisol, catecholamine, IL-6 and HSPs, may have roles in muscle function. Within the family of HSPs, HSP25 protein is abundantly expressed in skeletal muscle and increases with muscle contractile activity. It is predominantly synthesized in the liver, and many extra-hepatic tissues have also been reported to produce ORM under physiological and pathological stress.
Interestingly, exogenous ORM increases muscle glycogen and enhances muscle endurance, whereas ORM deficiency results in decreased muscle endurance, thus indicating that ORM is an endogenous anti-fatigue protein.
Further studies have demonstrated that ORM binds to C—C chemokine receptor type 5 CCR5 on muscle cells and activates AMPK, thus promoting glycogen storage and enhancing muscle endurance, and representing a positive feedback mechanism for resisting fatigue and maintaining homeostasis. Non-invasive techniques of site-specific stimulation can now be used to evaluate the potential sites of the entire system for force production in human studies.
All evoked muscle responses are recorded via electromyography EMG electrodes placed on the muscle.
Transcranial magnetic stimulation Transcranial magnetic stimulation involves applying magnetic stimulation to the motor cortex and is optimized to activate the muscle of interest. MEP is influenced not only by cortical excitability but also by spinal cord motor neuron excitability and muscle factors. MEP depression can occur in the relaxed muscle after a fatiguing exercise, possibly as a result of afferent input from the fatigued muscle. MEP is increased in the upper- and lower-limb muscles during sustained submaximal isometric contractions and is regarded as an augmentation of the central drive to the lower motoneuron pool that allows a constant level of force to be maintained despite the development of peripheral fatigue.
During sustained MVC, MEP has been reported to increase during the first seconds and then to level off, increase linearly or remain stable, depending on the protocol used that is, continuous vs intermittent and the muscle investigated. The signal is then carried along the motor neurons to the muscle, generating a response in the muscle known as the Hoffmann reflex H-reflex. The H-reflex is used to assess spinal excitability and inhibition. Although there are several of an increase 65 or no change, 66 the general consensus is that there is an overall decline in the amplitude of the H-reflex with the development of muscle fatigue, thus indicating a decrease in spinal excitability.
The m-wave is a compound action potential recorded with surface EMG and is used to assess peripheral excitability of the muscle membrane and transmission at the neuromuscular junction.
A change in the twitch force without a change in the m-wave indicates a failure of excitation-contraction coupling. According to the mechanism and metabolic changes during muscle fatigue, three categories of biomarkers have been determined: The best-known biomarkers of muscle fatigue from ATP metabolism include lactate, ammonia, and hypoxanthine.
Hypoxanthine is usually analyzed in the serum or urine. Serum lactate increases with exercise intensity in healthy and diseased subjects. Under the conditions of workload standardization, serum lactate appears to be a promising biomarker of muscle fatigue. Serum ammonia is not associated with age 77 and remains low in physical fitness, but is higher in men than in women.
Oxidative stress biomarkers Reactive oxygen species ROS remain at a low level in resting skeletal muscle but increase in response to contractile activity. ROS products lead to protein, lipid or nucleic acid oxidation accompanied by a marked decrease in the antioxidant capacity, 81 thus ultimately inducing fatigue.
Promising biomarkers to assess oxidative damage in muscle fatigue include lipid peroxidation biomarkers that is, thiobarbituric acid-reactive substances TBARS and isoprostanesand protein oxidation biomarkers that is, protein carbonyls PCs. Isoprostanes are prostaglandin-like compounds derived from the peroxidation of essential fatty acids catalyzed by ROS. PCs are mainly derived from the oxidation of albumin or other serum proteins and are regarded as markers of oxidative protein injury.
GSH is a pseudotripeptide that is present in nearly all cells and plays an important role in ROS scavenging. GPX and catalase are both enzymes that scavenge hydrogen peroxide into water and oxygen. TAC is defined as the sum of the antioxidant activities of the nonspecific pool of antioxidants. Isoprostanes are usually measured in the serum, urine, or other body fluids and blood cells. These changes represent a nonspecific immune response induced by ischemia in a stressed tissue, while there is a lack of a real injury.
IL-6 levels can also be determined in the saliva. With age, the change in T-cells expressing CD8 remains controversial,whereas the change in IL-6 is age independent. Sex differences in T-cell immune responses are particularly evident in graft-versus-host disease, with a stronger effect in females, and IL-6 levels are also markedly lower in females.
At present, there are still no official or semi-official recommendations for the treatment of muscle fatigue. However, some nonspecific treatments, such as synthetic products for example, amphetamine and caffeinenatural products for example, American ginseng and rhodiola rosea and nutritional supplements for example, vitamins and minerals and creatinehave been used clinically or experimentally, and have shown some effects in various studies.
Synthetic products Amphetamine, ephedrine, caffeine, for example, are all synthetic products that excite the central nervous system or sympathetic nervous system and promote resistance to muscle fatigue.
The use of amphetamines, amphetamine derivatives, propanolamine and ephedrine remains illegal in competition. However, caffeine and pseudoephedrine have been accepted at any level since Amphetamine Amphetamine is a phenethylamine-type stimulant and antidepressant that is highly addictive and produces euphoria and an elevated mood.
Amphetamine at low to moderate doses enhances the physical performance of humans and animals. High body temperature is one of the strongest exhaustion signals. Recently, Morozova E has reported that amphetamine may mask or delay fatigue in rats by slowing down the exercise-induced elevation in core body temperature.
Although amphetamine usage is prohibited during competitions, it may be used in some situations, such as in combat, to improve performance by delaying exhaustion. High caffeine dose consumption enhances performance during extended periods of exercise. In addition, taltirelin, a synthetic thyrotropin-releasing hormone TRH analog, effectively improves sports activity. Benzamide derivatives, such as 1- 1, 3-benzodioxolylcarbonyl piperidine 1-BCPsignificantly prolong the time of forced swimming in mice, through an unclear mechanism.
In the past few decades, health scholars and athletic physiologists have been searching for natural products that can improve athletic ability and resist or eliminate fatigue in human beings. Now, more and more natural products and their extracts have been revealed as potentially anti-fatigue agents.
Araliaceae ginseng species American ginseng, panax ginseng C. Meyer and radix notoginseng all belong to the araliaceae ginseng species. American ginseng is the root of panax quinquefolium, which is currently grown in Canada and eastern USA. Chen is cultivated throughout Southwest China, Burma, and Nepal. The root, a commonly used part of this plant, is called radix notoginseng or Sanchi.
All of them contain multiple active components, such as saponins, polysaccharides, flavonoids, vitamins and microelements, which are responsible for the effects in the improvement of physical fatigue in humans and animals. For example, saponins or protein extracted from American ginseng significantly lengthens the swimming time in mice via increasing the levels of liver glycogen and muscle glycogen.
Meyer, have all been reported to have marked anti-fatigue activity in mice swimming or grasping test. Meyer, including enhancing lactate dehydrogenase LDH activity, increasing hepatic glycogen levels, retarding the accumulation of serum urea nitrogen SUN and blood lactic acid BLAinhibiting oxidative stress and improving mitochondrial function in skeletal muscles.
Regarding panax notoginseng, a single dose has been reported to enhance aerobic capacity, endurance and mean blood pressure MAP in young adults. It is also an important resource against fatigue. The ingredients of rhodiola rosea include salidroside and rosavin. Rosavin is the only constituent unique to R. The natural ratio of rosavins to salidrosides in R. Salidroside has been identified as the main anti-fatigue ingredient in Rhodiola rosea.
Garlic was given to soldiers and athletes as a tonic in ancient Rome. Recently, the anti-fatigue effect of garlic has been reported by many researchers. Garlic-processing methods affect the anti-fatigue effects. They have found that raw garlic and AGE prolongs the treadmill running time of mice and enhances the speed of recovery of rectal temperature after immersion in cool water. For contraction to continue beyond that point, ATP must be regenerated for the working muscles.
In other words, the supply of ATP must match its demand. If there is a failure to do so, fatigue develops. While this creates ATP almost instantly, the limited supply of PCr in muscles only lasts for about 15 seconds. Although this may seem like a very limited amount of time, PCr provides the muscles with ATP until other metabolic pathways are activated.
A lack of oxygen in the muscles can occur under short, high-intensity exercise as active, contracting muscles swell and occlude arterial supply. Anoxia may also occur if oxygen delivery is impaired. Glycolysis is relatively quick to start up, and can provide the muscles with energy for up to minutes of strenuous activity. After that time, lactic acid accumulates, which may lead to a point where the muscles cannot function at full capacity.
This occurs as a result of a decrease in intracellular pH. Aerobic respiration requires oxygen and involves a series of chemical reactions that occur in the mitochondria called oxidative phosphorylation. Aerobic respiration can supply the muscles with enough ATP for several hours of activity, provided sufficient glucose and oxygen are available.
Although it can provide ATP for an extended period of time, aerobic respiration is slow to begin, and the muscles must rely on other energy sources such as direct substrate phosphorylation and lactic acid production until aerobic respiration can produce enough ATP to take over production.