Information

Why does hypocalcaemia cause increased muscle contraction?

Why does hypocalcaemia cause increased muscle contraction?


We are searching data for your request:

Forums and discussions:
Manuals and reference books:
Data from registers:
Wait the end of the search in all databases.
Upon completion, a link will appear to access the found materials.

Calcium is needed for muscle contraction, so how does hypocalcaemia cause increased sustained contraction?


Consider the pathophysiology of tetany, which is the involuntary contraction of muscles caused by hypocalcemia.

From the tetany wikipedia page:

Low ionized calcium levels in the extracellular fluid increase the permeability of neuronal membranes to sodium ion, causing a progressive depolarization, which increases the possibility of action potentials. This occurs because calcium ions interact with the exterior surface of sodium channels in the plasma membrane of nerve cells and hypocalcemia effectively increases resting potential (rendering the cells more excitable) since less positive charge is present extracellularly. When calcium ions are absent the voltage level required to open voltage gated sodium channels is significantly altered (less excitation is required).

So, when Ca2+ levels are low, action potentials are spontaneously generated, leading to muscle contraction.


6.4: Muscle Contraction

  • Contributed by Suzanne Wakim & Mandeep Grewal
  • Professors (Cell Molecular Biology & Plant Science) at Butte College

A sport like arm-wrestling depends on muscle contractions. Arm wrestlers must contract muscles in their hands and arms and keep them contracted to resist their opponent's opposing force. The wrestler whose muscles can contract with greater force wins the match.

Figure (PageIndex<1>): Arm wrestling


Muscle Cell Anatomy

To understand the calcium cycle, you need to know a bit about muscle cell anatomy. Strands of fibers called myofilaments are the distinguishing feature that separates muscle cells from other types of cells in your body. A muscle contraction represents shortening of the myofilaments with individual cells that comprise the muscle. A tiny tube-like network called the sarcoplasmic reticulum, or SR, surrounds each myofilament. In a relaxed state, the SR contains a high concentration of calcium. The SR controls muscle contraction and relaxation by regulating calcium flow inside your muscle cells.


Discussion

While the majority of calcium in the body is within the skeletal system or bound to albumin in plasma, free calcium is tightly controlled by homeostasis effected by parathyroid hormone (PTH). Transmembrane gradients in calcium concentration drive membrane excitability in muscles, neurones and myocytes.1 Myocardial contraction is dependent on extracellular calcium because the myocardial sarcoplasmic reticulum cannot store sufficient quantities. As such, prolonged and significant hypocalcaemia can result in heart failure.

Among many causes of hypocalcaemia, thyroid surgery, with the inherent risk of parathyroid removal or injury, is a recognised cause of hypoparathyroidism and subsequent hypocalcaemia.2 Patients should undergo long term follow-up to ensure this complication does not present at a later date. Here, it presented 23 years after the initial surgery.

Acute cardiomyopathies have been induced by hypocalcaemia, and calcium replacement and vitamin D supplementation have been shown to reverse the heart failure.3 Furthermore, renal excretion of sodium is partially dependent on intracellular calcium concentrations, and hypocalcaemia may encourage salt and water retention, exacerbating heart failure.3 In our patient, a mild left ventricular hypokinesia was noted with chamber dilatation. However, clinical signs of heart failure did not occur and the ejection fraction remained normal.

Hypocalcaemia is a recognised cause of QT prolongation via prolongation of the plateau phase of the cardiac action potential.4 , 5 This causes calcium ion channels to remain open for a longer period, allowing a late calcium inflow and the formation of early after-depolarisations.6 , 7 If threshold for depolarisation is reached, new action potentials are induced, initiating a tachycardia and re-entry. Ventricular arrhythmias can follow, in particular torsades de pointes (TdP polymorphic ventricular tachycardia) and ventricular fibrillation (VF).8 Therefore, ventricular arrhythmias are a known complication of hypocalcaemia and patients can present with exertional syncope representing TdP and loss of cardiac output.7 – 9

In contrast, hypercalcaemia and calcium infusions have been shown to reduce immediately the QTc with shortening of the ST segment but prolongation of the T wave ventricular ectopics are suppressed but heart block and bradyarrhythmias can occur.1 , 4 , 5

Recent findings suggest that the disordered repolarisation characteristic of subjects with congenital long QT syndrome (LQTS) occurs in the atria as well as the ventricles.10 Electrophysiological studies showed that congenital LQTS patients had altered atrial electrical conduction such that atrial tachyarrhythmias, such as AF, were more easily induced and persisted for longer than in normal or other patients with AF.10 These induced episodes of AF often had a polymorphic undulating appearance, similar to TdP, and have led to the new term of ‘atrial torsades de pointes’.10 Two large studies have shown that early onset of atrial arrhythmias (typically AF) is 10-fold higher in those with genetically proven LQTS than the general population or matched controls.11 This coincides with genetic studies that suggest the genes that predispose to LQTS (KCNQ1, KCNH2 and KCNA5 encoded potassium channels) also predispose to atrial arrhythmia in the general population.11

These new developments raise the possibility that long QTc triggered by acquired causes, as presented here, could create the same electrophysiological state present in congenital LQTS which destabilises atrial rhythms to trigger atrial arrhythmia. It is possible that hypocalcaemia prolongs atrial repolarisation and therefore triggers atrial arrhythmias with ‘atrial torsades de pointes’ being the underlying abnormality. This mechanism may explain the occurrence of atrial arrhythmia in our patient, though the possibility of a genetic LQTS has not formally been excluded. Furthermore, formal electrophysiological testing may be required because a 12 lead ECG is unlikely to visualise ‘atrial torsades de pointes’, with most previous reports relying on electrophysiology studies or atrial traces from automated defibrillators.

Learning points

Hypocalcaemia is a cause of QTc prolongation and this predisposes to ventricular arrhythmias.

Atrial arrhythmias have an increased incidence in those with congenital long QTc syndrome. While a genetic basis may be involved, acquired causes of QTc prolongation may similarly predispose to atrial arrhythmias.

Hypocalcaemia due to hypoparathyroidism is a known late complication of thyroid surgery. In our case, it presented 23 years after initial surgery.


Factors Affecting Excitability & Contractility | Muscles | Humans | Biology

For stimulation to occur, two factors are necessary—a minimum strength and an adequate duration of the stimulus. Chronaxie, which includes both these factors is the measure of excitability of a tissue.

Factor # 2. Effects of Two Successive Stimuli:

If the second stimulus is applied after sufficient intervals both first and second stimuli will cause contraction and two simple muscle curves will be recorded (Fig. 6.4, stage a). The second curve will be slightly higher than the first one due to the beneficial effect of contraction. If the second stimulus is applied in the re­laxation period of the first, more or less two separate curves will be produced and the second curve will be higher (Fig. 6.3, stage b).

If the second stimulus is ap­plied within the contraction period of the first one the second curve will be super­imposed on the first one with a higher height of contraction (Fig. 6.3, Stage c). These are known as summation of effects (contraction). If the second stimulus is applied within the latent period but after refractory period of the first, then their effects are added together giving a simple muscle curve of larger height than either of them produced separately (Fig. 6.3, stage d).

This effect is known as summation of stimuli. By using maximal or submaximal stimuli, these summated effects can be obtained. This is true for either single muscle fibre or a whole muscle bulk. In case of submaximal stimuli, the summated, effects are due to activation of more nerves and muscle fibres, but in case of maximal stimuli, the greater response cannot be due to an increase in numbers of responding nerves and muscle fibres, but due to a difference in contractile mechanisms.

It is claimed that these effects are due to beginning of second twitch before the active state for the first twitch is complete. That is the duration of the active state of the first response makes possible the augmentation of the second response. Thus this effect goes against the law of all-or-none.

Factor # 3. Effects of Repetition of Stimuli:

Following phenomena are observed:

i. Staircase Phenomena:

When a freshly excised muscle is stimulated with a single induction shock of sufficient strength then a contraction of certain amplitude is recorded. If second stimulus of same strength is applied at an interval of about 1 second to the muscle after completion of the effect of first stimulus, then increased amplitude of contraction is recorded.

With a series of such stimuli (5 to 6 stimuli) but under the condition that each contraction is allowed to be completed before the next stimulus is applied, then a gradual increase in amplitude of contraction is obtained. This stair-like rise is called the staircase (treppe) phenomenon. Increased H+ ion concentration and an increase of temperature within the muscle create a favourable condition for more work (beneficial effect). Hence, the contraction becomes stronger.

When repeated stimuli are applied, the type of response will vary according to frequency. When the frequency is such that each successive stimulus falls within the period of relaxation of the previous curve the record will show a series of wavy oscillations. This is called clonus or incomplete tetanus (Fig. 6.4, B-E).

When the frequency is more, so that the stimuli fall within the latent period of the previous curve, the record traces a clear steady line, which rises at first abruptly and then gradually, till maximum contraction takes place. This is called tetanus (Fig. 6.4, F). Here the fusion is complete and the muscle, instead of vibrating, exerts a steady pull.

Due to summation, the height of tetanic contrac­tion is usually higher than that of a single twitch. Frequency of stimulation, required for the induction of tetanus, varies with the na­ture of the muscle. In external eye muscle it is about 350/sec., in gastrocnemius muscle it is about 100/sec.

Clonus may be described as summation of successive contraction, whereas tetanus is summation of successive stim­uli. The mechanical movement in response to voluntary stimuli is neither a twitch nor tetanus. During voluntary movement, the skeletal muscles are stimulated at low frequency, which is less than fusion frequency, and also asynchronously, so that the infrequent contraction of a large number of fibres give the appearance of a smooth response.

When repeatedly stimu­lated, the muscle has lost its irritabil­ity, becomes gradually less excitable and ultimately ceases to respond. This phenomenon is called fatigue (Fig. 6.5, 6.6, 6.8). Muscular fatigue can be defined as the inability of the muscle to do further work. In the fa­tigue curve, all the periods are lengthened. The relaxation period is so much prolonged that the curve fails to reach the base line before the next stimulus arrives, thus leaving a contraction remainder (Fig. 6.5).

The causes of fatigue might be due to:

(a) Exhaustion of sources of energy of the muscle,

(b) Accumulation of the end products of chemical reactions, such as lactic acid, carbon dioxide, ketone bodies, and

(c) Decrease of local synthesis of acetylcholine—like substances during prolonged exer­cise.

Oxygen is required for the removal of these substances and so for recovery. Fatigued muscle left in nitrogen does not recover. In studying fatigue in muscle with circulation and without circulation, the muscle gets fatigue more earlier in case of the latter and does not recover on rest (Fig. 6.6A). But in case of muscle with circulation, fatigue comes later and the muscle recovers on rest (Fig. 6.6B).

This shows that oxygen, which is supplied through blood circulation, is required for recovery of fa­tigue. The seat of fatigue lies in the muscle when it is directly stimulated. But when it is stimulated through the motor nerve, the seat of fatigue is in the neuromuscular junction. In physiological ex­ercise, the seat of fatigue is neither in the muscle nor in the neuromuscular junction but at the syn­apses in the central nervous system (central fa­tigue).

On comparison, it is seen that fatigue after voluntary work first appears in the synapses, then in the neuromuscular junctions and lastly in the muscle itself. In human subjects fatigue can be studied with the help of an instrument called Ergograph (Fig. 6.7).

Fatigue can be experimented by noxious stimulation at the foot of a spinal frog. If a reflex withdrawal of foot is obtained and by continuous stimulation the reflex contraction of the muscle is lost, the foot does not withdraw. At this stage if the flexor nerve is stimulated, then contraction of the muscle again occurs.

This cessation of contraction is due to changes in the spinal cord. This can also be demonstrated in man by protective mechanism. When the arm or leg muscles of a subject are used to contract repeatedly with a weight attached to the part and he is unable to lift weight voluntarily, then electrical stimulation of the motor nerve through the skin produces a powerful contraction.

Factor # 4. All-or-None Law:

It means that if a single muscle fibre contracts at all, it will contract to its maximum, provided the conditions re­main constant. If internal and external conditions are changed, the amount of contraction will vary. This law holds good for a single muscle fibre and does not apply for the whole muscle, which is composed of innumerable mus­cle fibres.

Because, in the latter case, as the strength of the stimulus is increased, more and more muscle fibres will be affected and the degree of contraction will be raised (staircase phenomena) and a stage will be achieved when there will be no further rise (all-or-none law for whole muscle). But modern theory claims that the all-or-none law is applicable in case of development of the action potential but not for the activation of the contractile materials.

Factor # 5. Effects of Temperature:

Moderate warmth (25°C.) increases and cold (5°C.) depresses both excitability and con­tractility. The former shortens and the latter lengthens all the periods of the muscle curve (Fig. 6.9). Temperature above 42°C produces heat rigor due to coagulation of proteins pres­ent in the muscle.

Factor # 6. Effects of Load:

Load lengthens the latent period but reduces the periods of contraction and relaxation. It also reduces the degree of contraction, i.e., the height of the curve (Fig. 6.10). The effect of load on the work done by the muscle depends on the way in which the load is applied.

If the weight is allowed to stretch the muscle prior to its contraction, the muscle is said to be free-loaded but if the lever is supported then the muscle is only stretched when the contraction begins, the muscle is said to be after-loaded. The mechanical efficiency in free-loaded muscle is higher than that in after-loaded muscle. This is mostly related with the increase in initial length of muscle fibres.


Treatment of Hypocalcemia

Calcium supplements, given by mouth, are often all that is needed to treat hypocalcemia. If a cause is identified, treating the disorder causing hypocalcemia or changing drugs may restore the calcium level.

Once symptoms appear, calcium is usually given intravenously. Taking vitamin D supplements helps increase the absorption of calcium from the digestive tract.

Sometimes people with hypoparathyroidism are given a synthetic form of parathyroid hormone.


Depolarization

Circulatory system

…into the cell and cause depolarization, which leads to muscle cell contraction.

Dipole current source

This sequence, called depolarization and repolarization, is accompanied by a flow of substantial current through the active cell membrane, so that a “dipole-current source” exists for a short period. Small currents flow from this source through the aqueous medium containing the cell and are detectable at considerable distances…

Muscle contraction

The channels are opened by depolarization (an increase in membrane potential) of the nerve terminal membrane and selectively allow the passage of calcium ions.

…the resting membrane potential is depolarized to a critical potential (Ecrit), a self-generating action potential follows, leading to muscle contraction. Phase 0, the upstroke, is associated with a sudden increase in membrane permeability to Na + . Phases 1, 2, and 3 result from changes in membrane permeability and conductance to Na + ,…

Nervous system

…it less negative is called depolarization.

Because it varies in amplitude, the local potential is said to be graded. The greater the influx of positive charge—and, consequently, depolarization of the membrane—the higher the grade. Beginning at the resting potential of a neuron (for instance, −75 mV), a local potential can…

…most common potential change is depolarization, caused by a net influx of cations (usually Na + ). Because this infusion of positive charge brings the membrane potential toward the threshold at which the nerve impulse is generated, it is called an excitatory postsynaptic potential (EPSP). Other neurotransmitters stimulate a net efflux of…

Physiological response of photoreceptors

The depolarization is brought about by the entry of sodium and calcium ions that results from the opening of membrane channels. The biochemistry of the transducer pathway is not entirely clear some proposed models envision a somewhat different pathway from that in vertebrates. Rhodopsin isomerization activates…

Postsynaptic potential occurrence

Depolarization—a decrease in negative charge—constitutes an excitatory PSP because, if the neuron reaches the critical threshold potential, it can excite the generation of a nerve impulse (action potential).


Fundamentals of Strength Training

Quick-Release Contractions

This method combines isometric and concentric contractions. At the beginning of exercises there is a 3–5 s isometric contraction to increase muscle tension at a given joint angle contractile elements contract and lengthen elastic elements, thus during contraction the muscle contracts at a high speed. Several motor units are recruited in this way, thus this type of exercise improves neuromuscular coordination. Fast fibers are fatigable, thus this type of exercise prefers low repetitions and enough resting between sets. To carry out these exercises one needs a training partner or a special machine, since isometric contractions need to be executed with maximal intensity or close to it. Thus, it is recommended for professional athletes.


Why do muscles hurt after exercise?

As long as I'm stranded in a snowstorm (thankfully fading right now) and unable to teach my human physiology class this morning, I thought I'd at least put a small part of the story I was going to tell on the web. We're currently talking about muscle physiology, and I've already gone over the sliding filament theory of muscle contraction…oh, you know that one, right?

Muscles contract using interlaced filaments of myosin (in red, above) and actin (blue), and myosin acts as a kind of motor gear, burning ATP to ratchet the actin filaments along their length, shortening the muscle. The ratchet functions whenever the cell has ATP and also is flushed with the release of calcium from internal stores, which is the chemical trigger to initiate a contraction. But you knew that already.

You also knew about basic metabolic biochemistry, the process that breaks down sugars to release energy, which is captured in the form of ATP and various reducing agents.

All you need to remember to follow along is that there is the glycolytic pathway, which snaps a 6-carbon sugar in half to produce two 3-carbon fragments and a little bit of energy, and that there is the rest of the biochemistry shown here, which takes the 3-carbon fragments and burns them down the rest of the way to CO2, producing a lot of energy in the form of ATP. Unfortunately, that second, very efficient part is dependent on the availability of oxygen, so in many cases, where your muscles are working harder than the respiratory/circulatory system can deliver oxygen to them, they are only doing the glycolytic part of the process.

Like I said, though, you already knew all that. I was planning a quick review of these basics this morning, and to discuss factors that influence strength and endurance in muscle activity, and then to answer the one question I'm addressing here: why do my muscles hurt after exercising?

There are actually a couple of reasons. One that you may have heard of before is lactic acid buildup, but this is actually only a short term concern. Lactic acid is a byproduct of glycolysis. If you're working hard, you can't deliver oxygen to the muscles as fast as they need it, so they rely almost entirely on the glycolytic pathway for energy, which in my diagram above has three products: ATP (which the cell wants to use for contractions), and pyruvic acid and the reducing agent NADH2, which the cell is unable to use at that time because of the lack of oxygen. What the cell does to keep the unusable products from accumulating and bringing the glycolytic pathway to a halt is, in short, to use the reducing agent to convert pyruvic to lactate, which then diffuses away into the bloodstream. Later, when you're taking it easy and recovering from your workout, the lactate will be recovered and reprocessed to recover more ATP and also to rebuild some of the glucose that was burned.

(Scratch much of the above paragraph. While many physiology textbooks state that lactic acid accumulation is a problem, the biochemists say otherwise: what builds up is lactate, which doesn't acidify the tissues and can actually act as a buffer. The source of acids that cause the transient ache are the hydrolysis reactions that occur as ATP is used at a rapid rate.)

Anyway, the point here is that one source of that burning ache during exercise is lactic acid accumulation. This does not explain why it hurts the next morning when you get up, though, because the acid will have been cleaned up by then. That's a different problem.

One reason for stiffness and soreness is the long term effect of flushing the muscle cell with calcium. During exercise, each contraction is accompanied by a surge of calcium ions, followed by its removal by pumps in the sarcoplasmic reticulum slurping it back up for storage. So exercise consists of a repeated cycle of surge and slurp of calcium ions, and one of the effects is that the increased levels of ions lead to actual physical swelling of the muscle fibers, which can reduce short-term performance. Another effect is that altering the calcium balance of the cell leads to the activation of enzymes that break down and rebuild proteins in the cell. What that does is promote active remodeling of those actin/myosin filaments, construction of new filaments, and growth of the muscle. It hurts because the muscle is under construction and is being physically remodeled, just like your coach probably told you. No pain, no gain.

There's another reason muscles may hurt a great deal the day after exercise, and that is that you can actually disrupt and damage and even kill muscle fibers, and that certain kinds of exercise are particularly effective at damaging the tissue.

A couple of years ago, I had this brought home personally. Our students have to give a senior seminar in a biology topic of their choice in their last year, before we let them graduate, and one of my students was interested in exercise physiology and knew about this phenomenon of eccentric exercise promoting greater tissue damage. He also knew that it had its most potent effects in naive tissue — muscles can adapt to repeated abuse, and show smaller and smaller responses to this kind of exercise over time. He was an athlete, so it was going to have minimal effect on him, so he looked about for a flabby, lazy, deskbound sort of person to test, and somehow he thought his advisor, me, would be a perfect subject.

Concentric and eccentric exercise are different. Imagine holding a weight in your hand as you sit there, and you contract your biceps to bend your elbow and lift the weight towards your face — imagine drinking a large stein of beer, for instance (it's exercise, really). The muscle filaments are ratcheting along to contract, and they are shortening the muscle: that is concentric exercise. Now, though, you lower your hand to put the stein back on the table. You don't simply relax all your muscles and let your arm flop so the stein falls with a crash to the table — it might spill! — instead, the muscle fibers in your biceps are at a low level of activity, the myosin/actin filaments are ratcheting to generate tension, while the muscle is lengthening, rather than shortening. That's eccentric exercise: some of your muscle fibers are trying to shorten the muscle while the muscle is actually lengthening.

So my student took me to the gym for a relatively easy hour of working out in the weight room, concentrating on eccentric exercise. It wasn't bad at all, and he kept the workout relatively light, so I never strained myself. So we did things like assisted bench presses, where he would help me raise the weight (the concentric part), and then I would ease it down slowly (the eccentric part). It wasn't bad at all, I thought, and we did a series of simple exercise to work out different muscle groups.

Then, the next morning, I tried to get up. Aaaaiaiaiaeeeaaargh. His experiment had been spectacularly successful, and I could barely move. Let me tell you, brushing my teeth that day was the most exquisite agony — just raising my hand to my mouth was bad enough, but wiggling my arm gently once I got it there? Forget about it.

So I got to be a prop at his seminar, standing still at the front of the room and occasionally screaming through gritted teeth when he asked me to move in certain ways, while he explained what was going on in my muscles. I had to give him an A for admiration at his fabulously sadomasochistic technique.

So what had I done to my muscles? Forced lengthening of muscles under tension actually causes small tears in the fibers, disrupting the excitation-contraction coupling mechanism. There are tiny membranous tubes running through the muscle fibers called the t-tubule system, which conducts electrical activity at the membrane deep into the interior, where it activates the sarcoplasmic reticulum to release calcium. Those were being torn. That makes the membrane leaky and sensitive, leading to fluid imbalances, and generally making the muscle less responsive until repaired.

Another factor is damage to the filament structure. The peculiar extension while contracting would lead to errors in the alignment of the overlapping parts of the myosin and actin filaments, leading to tangled, disrupted structures that are no longer able to function efficiently, and further contraction could cause physical injury to the fiber, which triggers a pain and inflammation response.


During an active lengthening, longer, weaker sarcomeres are stretched onto the descending limb of their length-tension relation where they lengthen rapidly, uncontrollably, until they are beyond myofilament overlap and tension in passive structures has halted further lengthening. Repeated overextension of sarcomeres leads to their disruption. Muscle fibres with disrupted sarcomeres in series with still-functioning sarcomeres show a shift in optimum length for tension in the direction of longer muscle lengths. When the region of disruption is large enough it leads to membrane damage. This could be envisaged as a two-stage process, beginning with tearing of t-tubules. Any fall in tension at this point would be reversible with caffeine. It would be followed by damage to the sarcoplasmic reticulum, uncontrolled Ca2+ release from its stores and triggering of a local injury contracture. That, in turn, would raise muscle passive tension. If the damage was extensive enough, parts of the fibre, or the whole fibre, would die. This fall in tension would not be recoverable with caffeine. Breakdown products of dead and dying cells would lead to a local inflammatory response associated with tissue oedema and soreness.

This process actually messes up your muscles. These are electron micrographs of muscle biopsies taken from human subjects who'd been put through the procedure (I drew the line there, and did not let me student stab me with big needles — hadn't he gotten enough pleasure out of this already — so these aren't my muscles).

The control at the top left shows normal, healthy, well-organized muscle fibers the panel just below it as a sample from muscle immediately after eccentric exercise, which is clearly more disorganized. The three panels labeled "1d" all show muscle one day after eccentric exercise, and all show signs of disruption — look at those z discs, the dark bands in the muscle. They've been broken up quite a bit.

If your muscles hurt, though, don't panic: the panel at the top right is of muscle fibers 14 days after exercise, and they are fully recovered and are once again well-ordered.

So why do your muscles hurt after exercise? There are three major reasons. 1) a transient accumulation of acids produced by ATP hydrolysis that can cause some soreness during exercise. 2) Changes in ion concentrations in the muscle that can cause some fluid swelling, and also triggers active remodeling of the proteins for growth. And 3) you broke 'em. You can cause micro-tears and internal disruption of muscle proteins that can actually force your muscles to throw out and reconstruct whole fibers.

What should you do if your muscles are aching after exercise? Personally, I say just stop it altogether, but that's just me. For the more active and sensible among you, a better solution would be to reduce the intensity of exercise to light, submaximal exertion and stretching exercises, which have been found to reduce soreness and promote more rapid recovery of muscle tension. Light massage is also good for reducing pain, but hasn't been found to do much to facilitate actual physical recovery otherwise. I'm all for reducing pain, of course.

As usual, though, if pain worsens or continues for more than a few days, or is particularly intense and localized, get off the internet and SEE A REAL DOCTOR. In the case of my intentionally induced eccentric muscle exercise, the serious pain only lasted for about 3 days, and after a week, felt no after-effects at all.

Proske U, Morgan DL (2001) Muscle damage from eccentric exercise: mechanism, mechanical signs, adaptation, and clinical applications. J Physiol 537(2):333-345.


Management

Therapy should focus on the prevention of ARF and the management of life-threatening metabolic complications such as acute hyperkalaemia. Prompt fluid resuscitation with crystalloids is the most important intervention in the prevention of ARF. Hypovolaemia exacerbates myoglobin-induced renal damage by promoting sluggish urine flow and renal vasoconstriction. Considerable quantities of fluid can be sequestered in damaged muscle, and aggressive fluid resuscitation is often required. Compound sodium lactate (Hartman's solution) should be avoided as it contains potassium. In cases of entrapment, sodium chloride 0.9% should be infused at the scene before extrication and has been shown to decrease the incidence of subsequent renal failure.

In addition to early aggressive fluid resuscitation, the urine should be alkalinized. The solubility of the THP–myoglobin complex increases in an alkaline environment and leads to the washout of casts from the tubules. Alkalinization may also inhibit myoglobin-induced lipid peroxidation. Alkalinization of the urine is usually achieved by the continuous i.v. infusion of sodium bicarbonate 1.26% aiming for a urinary pH of greater than 7. Bicarbonate therapy is also useful in the management of hyperkalaemia and metabolic acidosis. Some advocate the use of diuretics, in particular mannitol, to promote urinary flow and prevent obstructive myoglobin casts. However, this is controversial and has not been shown to be superior to simply giving adequate fluid resuscitation.

Despite optimal management, a number of patients will inevitably develop ARF. Acute severe hyperkalaemia should be treated initially in the conventional manner e.g. dextrose–insulin, bicarbonate therapy. Persistent oliguria/anuria and metabolic disturbance will require renal-replacement therapy. Haemodialysis is highly efficient at rapidly correcting severe electrolyte abnormalities and other metabolic abnormalities such as hyperphosphataemia, hyperuricaemia and hypocalcaemia. When cardiovascular instability exists, continuous renal-replacement techniques may be more appropriate. Haemodiafiltration should be used if hyperkalaemia is a problem.

The prognosis for myoglobin-induced renal failure is excellent. Full recovery of renal function is expected within 3 months in the vast majority of survivors.