A Closer Look at Muscle Fatigue in FES Cycling and Spinal Cord Rehabilitation

What we have found in many years of working with spinal cord injured persons using FES Cycling, is that some clients are impatient to see their legs working hard from day one. They are disappointed when their muscles seem to fatigue so quickly when they start training for the first time. To understand why this is the case, we need to look at how muscles behave when contracting with the aid of electrical stimulation. We should also understand how a spinal cord injury produces changes in a person's muscular, skeletal and neural structures.

In this article, we look at skeletal muscles and the energy systems that propel them in some detail. We look at the structure of muscle fibres, how and why they contract and what powers all of this. As you might expect, a spinal cord injury disrupts these processes and structures in complex ways. Ultimately, we should know how to adapt FES Cycling's settings to make exercise more effective and advise clients how to train for best effect; so let's dive in and look at how to do this.

Why commit to exercise?

Claire Lomas is one of our long standing clients and an active advocate for FES Cycling

Exercise is always an important investment to make for our physical and emotional health. For persons with a spinal cord injury and lower limb paralysis, FES Cycling is a way of preserving muscle bulk and muscle quality in the legs, improving circulation, bone health and metabolism and much more. In the past, medical science did not especially focus on preserving the muscular, skeletal and spine structures below the level of a spinal cord injury. This is not the case now, and approaches such as FES Cycling are seen as important advances in rehabilitative treatment and long-term health. Clients often wish to keep as fit as they can to take advantage of any future developments in medical science that could hold out the promise of a cure for their spinal cord injury.

We can all understand the importance of exercising but not everyone is committed to actually doing it. I read an article on LinkedIn by Claire Lomas MBE, who reported that she has ridden the equivalent of 15,000 miles on her RehaMove FES bike since becoming paralysed after a spinal cord injury. That is quite a commitment. Surely, no one would do this level of activity without finding that this was beneficial? Claire talks about her use of a RehaMove FES bike in a short video at this link.

Claire is an exceptional person in many ways and gives so much to help others. At the same time, Claire understands the value of exercise for everyone - whether they are disabled or not. So, her use of FES Cycling is a gift to herself.

What is FES Cycling?

A RehaMove FES cycling system based on the MOTOmed Muvi

As major UK providers of this technology, we have written lots of articles and have hundreds of UK clients working with these products at home. Just in case this idea is not familiar, we should say that FES Cycling holds significant potential in aiding the rehabilitation journey of those with spinal cord injuries, providing a path towards reclaiming their health and independence. There are some providers of this technology in the UK, including ourselves, but fundamentally, the purpose of these systems is the same.

FES Cycling typically involves the major muscle groups of the arms and legs. It stimulates muscle fibres to contract, helping to maintain muscle mass and strength which are often at risk of rapid deterioration following a spinal cord injury. The FES Cycling approach uses carefully controlled electrical energy to trigger muscle contractions that are synchronised with the movement of the bike's pedals. This allows the user to experience active exercise rather than just passive movement.

FES Cycling bolsters circulation, enhancing oxygen and nutrient supply to the muscles, thereby promoting overall health and well-being. As with any exercise, the benefits extend beyond the physical realm into the psychological realm. Users often report a boost in morale and an uplifted spirit, as they witness their resilience and capability in action. As with any new endeavour, initial progress may seem slow, and muscles may fatigue quickly. However, with consistent participation and patience, the benefits become increasingly apparent.

Like any product, FES Cycling systems come with strengths and weaknesses. As a method of exercise for spinal cord injured persons, it has a strong evidence base and is widely recommended by specialist clinicians but it always needs to be fine-tuned to the needs of each individual.

As we will discuss, persons with a spinal cord injury experience changes in muscle physiology and metabolism that influence how such systems are set up. As a modality, using electrical stimulation to make muscles contract is not as efficient as with uninjured individuals engaging in exercise with conscious control of their muscles. We will be exploring why that is the case.

In the Beginning

We need to start with a little exercise and muscle physiology. For most of my life, I have been keen to train and compete in individual sports such as powerlifting, wrestling and karate. I was never going to be a marathon runner, was rubbish at football, and understood that different sports would ideally require different training methods and nutritional demands. We are all limited by our genetic inheritance and must make the best of what is possible for us.

The body operates a "use it or lose it" approach. We want the body to adapt to the exercise or training we carry out and thereby sustain our health, but there are always lots of unknowns about how best to achieve this. Following a spinal cord injury, we hope that by routine stimulation of paralysed muscle, we are able to prevent the abnormal adaptations that we might otherwise expect.

In my personal training history, there seemed to be two opposite approaches (philosophies) that coaches used to encourage training progression.

The first was the "pushing to the limit every rep every set and every session", model; With this High-Intensity approach, you could think of this as relying on the concept of "that which doesn't kill you makes you stronger". The approach here seems to be that constantly nudging the envelope of muscle fatigue and pain would improve your tolerance to it. Anyone who has experienced the onset of lactic acid "burn" has flirted with this concept. I have met lots of people who are addicted to it.

The second approach involved training to avoid, or at least delay, the onset of fatigue and other internal negative conditions, such as lactic acid burn, that would generally limit training progress. As this approach seems less challenging, I guess that's why some people still struggle to believe it can be more effective. This approach can probably be attributed to the 1980s and the glory days of Soviet sports training. The idea of training to produce less lactic acid was born, and since then, it has been refined to be known as Anti-Glycolytic Training (AGT) for reasons we will mention below. There are a number of versions of this but we will leave aside that discussion for another day.

I must admit that once upon a time, those using weights to get bigger and stronger would often be encouraged by coaches to always train a muscle until failure. That is, in each set of an exercise, we had to push or pull that weight until it was impossible to move it even a millimetre. This approach arose from the culture of bodybuilding in the 1970s and 80s and has stuck with many bodybuilders and recreational athletes even today.

However, research in exercise science has shown that this high-intensity training where you often train muscles to failure, can be detrimental to muscle growth and development. This is especially the case for people with disabilities.

Such training to failure is bathing your muscles in acid. There is nothing inherently bad about acid, but in sports, it's usually not helpful if indulged in too often. Such acid equals fatigue in the short term, but can also lead to free-radical-induced health problems in the longer term. For individuals with spinal cord injuries, the effects of this type of intense training can be even more pronounced. Lactic acid robs you of power and strength and inhibits the muscles from contracting properly.

There is another factor at work too that relates to our nervous system. When we train we are engaging our nervous system as well as our physical resources. When we exercise we are not recruiting every muscle fibre in a muscle. We can, however, with skilled practice and greater loads, build our ability to produce a stronger contraction, literally training our nervous system to produce a stronger contraction.

With FES Cycling, we miss out on part of this nervous system skill development as we don't have that natural link to become more consciously aware of how to make muscles contract more strongly. Hence, FES Cycling will always tend to be less efficient in producing muscle contractions.

So is the alternative to high-intensity training, some form of AGT?

We will get to that, but first, let's delve a little deeper into physiology and what powers the work that we do with our muscles. This will help us understand why most people should not routinely train to fail.

The Energy Systems that Power Our Muscles

We all know that we consume food in the form of carbohydrates, proteins and fats and these provide the raw "fuel" to allow our bodies to perform useful work. The body converts the energy from our food into something that can be utilised directly by our muscles and elsewhere by other tissues.

Adenosine Triphosphate (ATP) is a complex compound that plays a crucial role in our body's ability to function. Often described as the 'energy currency' of the body, ATP provides energy storage at the level of the cell that powers various bodily functions, including muscle contraction.

It's formed from a molecule of adenosine and three phosphate groups. The energy stored in the bonds between these groups is released when needed by the body. When ATP is broken down into Adenosine Diphosphate (ADP), energy is released which is then used to power muscular contraction, among other vital biological processes. This process of energy release and ATP conversion is repeated continuously in our bodies, making ATP truly indispensable for life.

Since stored ATP can only power a second or so of intensive activity, this natural process of molecule cycling from ATP to ADP is very important. The body has three main energy systems, and this process is just the first one.

We wrote about these in an earlier article too.

1. The Phosphagen or Alactic ("not lactic") System

The Phosphagen system, also known as the creatine phosphate system, is the quickest way to produce ATP (adenosine triphosphate). It provides energy for short-duration, high-intensity bursts of activity, such as sprints or jumping.

The Phosphagen system stores ATP and creatine phosphate (CP) in the muscle cells. As mentioned above, when a muscle contracts, ATP is broken down into ADP (adenosine diphosphate) and phosphate. This releases energy that is used to power the contraction. CP can then be used to regenerate ATP once more from ADP.

The phosphagen system can only provide energy for a few seconds of intense activity. After that, the muscle will need to switch to another energy system whilst the phosphagen system regenerates.

We can think of the Phosphagen system as having high power for quick deployment but low capacity to sustain that power delivery.

2. The Glycolytic or Lactic System

The glycolytic system is the second fastest way to produce ATP from energy stores in the muscle. It is responsible for providing energy for activities that last between a few seconds and 2 minutes, such as a set of heavy weightlifting exercises or running a 100-meter dash.

The glycolytic system breaks down glycogen, a stored form of glucose, into pyruvate. When we consume food rich in carbohydrates, our body diligently converts that into glucose. But glucose is like a wild horse - energetic, yes, but difficult to manage. Our body, in its "wisdom", has found a way to harness this energy in a more manageable form: this is pyruvate.

Pyruvate can then be broken down into lactate, which can be used to produce ATP in the absence of oxygen. This lack of oxygen means that this is sometimes referred to as an anaerobic process.

The glycolytic system produces lactic acid as a byproduct. This can cause the muscle fatigue and soreness we described above. Most of us will have experienced this at some point.

We can think of the Glycolytic system as having moderate power with moderate capacity to sustain that power.

3. The Oxidative (“Aerobic”) System

The oxidative or aerobic system is the slowest way to produce ATP, but it is also the most efficient. It provides energy for activities that last for more than 2 minutes, such as long-distance running or swimming.

The oxidative system breaks down carbohydrates, fats, and proteins into pyruvate. Pyruvate can then be transported into the mitochondria, the powerhouses of the cell, where it can be broken down into ATP in a process called oxidative phosphorylation.

The oxidative system produces no lactic acid, so it does not cause muscle fatigue and soreness. We can think of the Oxidative system as having relatively low power but a high capacity to sustain it.

The fourth energy system

Can you imagine a scenario where these three energy systems can't meet the demand? Our bodies have that covered too. There is a fourth system that can be called up in emergencies and that is the Myokinase system.

The Myokinase system is a backup energy system that produces ATP quickly but with lower efficiency. It can only provide energy for a short time, perhaps for about 10 to 20 seconds into an all-out effort before switching back to one of the other three systems.

The myokinase system transforms the ADP we mentioned above into something called AMP (where the M stands for Mono). The interesting side effect of AMP is that it is thought to trigger mitochondrial growth.

As we can see, our bodies have evolved to efficiently produce and use energy through these various systems to cope with the demands placed upon us. However, when training or engaging in high-intensity activities, it is important to understand the limitations of these systems and how to properly train and fuel our bodies for optimal performance. By understanding the physiology behind energy production in our muscles, we can make informed decisions about our training and achieve better results.

We should now look at the structure of our muscle fibres and understand how they allow us to perform work.

Muscle Fibre Types

We have seen that the three main energy systems described above deliver different levels of energy that can be sustained for varying periods. Luckily, we have muscle fibre types that are also optimised for different types of work. With normally innervated muscles, the key actors are tiny protein structures known as actin and myosin.

When you decide to move or lift something, your brain sends a signal through your nerves to these muscle fibres. In response, calcium ions flood into the muscle fibre. These ions bind with the actin, unveiling the sites where myosin can attach. Then, powered by ATP (the body's energy currency we described earlier), the myosin heads pull the actin filaments towards each other, causing the muscle fibre to contract.

The traditional classification of skeletal muscle fibres into slow-twitch (Type I) and fast-twitch (Type II) fibres has been refined in recent years to incorporate more nuanced characteristics. The modern designation used to describe muscle fibre types is based on something called the Myosin Heavy Chain isoform composition. Myosin Heavy Chain (MHC) is a protein that is found in the muscle cells of skeletal muscles. Isoform means that there are different versions of the protein that have small variations in their structure. These variations lead to the different properties of the muscle fibres.

MHC Isoform Classification

Skeletal muscle fibres express different isoforms of the MHC, the major structural protein of the myosin filament. These isoforms determine the metabolic and contractile properties of the muscle fibre. MHC isoforms are categorised into three main groups:

1. Type I MHC (MHC I): This isoform is predominantly found in slow-twitch fibres and is associated with oxidative metabolism, fatigue resistance, and high-endurance capacity.

2. Fast-glycolytic MHC (MHC IIa): This isoform is prevalent in fast-twitch glycolytic fibres and is linked to glycolytic metabolism, high power output, and short-term bursts of activity.

3. Fast-oxidative MHC (MHC IIx): This isoform exhibits intermediate properties between MHC I and MHC IIa, combining some characteristics of both. It is found in a small proportion of muscle fibres and is associated with activities that require both endurance and power.

Functional Implications

The distribution of MHC isoforms in a muscle reflects its functional role. For instance, muscles involved in sustained, low-intensity activities, such as postural control, tend to have a higher proportion of MHC I fibres. Conversely, muscles responsible for explosive movements, such as sprinting or jumping, have a greater abundance of MHC IIa and MHC IIx fibres.

Factors Influencing MHC Isoform Expression

Several factors influence the expression of MHC isoforms, including:

1. Genetics: Individual genetic predisposition plays a significant role in determining the MHC isoform profile of a muscle.

2. Exercise Training: Exercise can modify MHC isoform expression, leading to adaptations that enhance the muscle's capacity for specific activities. For example, endurance training promotes the expression of MHC I fibres, while focusing on power training increases the proportion of MHC IIa fibres.

3. Nutrition: A balanced diet rich in essential amino acids is crucial for supporting the synthesis of MHC proteins.

4. Hormonal Status: Hormones, such as testosterone and growth hormone, influence muscle fibre development and MHC isoform expression.

Normally, muscle fibres in humans do not express more than one of the MHC types. However, after a spinal cord injury, the number of hybrid fibres expressing two MHC types increases greatly. (Talmadge RJ. 2000). In fact these muscles tend to exhibit faster muscle fibre types. These muscles therefore become highly fatigable.

In summary, the modern designation for muscle fibre types utilises MHC isoform classification, providing a more detailed and nuanced understanding of the metabolic and contractile properties of individual muscle fibres. This classification has implications for exercise training, rehabilitation, and athletic performance. If the muscles of the spinal cord injured persons tend to become more fatigable, this has consequences for how we should train these muscles.

Generating Strength

The general public might understandably associate the size of a muscle with its strength, but it's not actually as simple as that. The nervous system normally has a very important role in how strength is produced and controlled so let's consider this piece of the puzzle (in a simplified way).

A skeletal muscle typically consists of thousands of muscle fibres that ultimately must generate the force necessary to do useful work. Since a single muscle fibre doesn't generate much force by itself, the body is organised to recruit and coordinate as many fibres as necessary.

How this happens is managed by the nervous system which connects and communicates with a group of muscle fibres through a specialised nerve cell called a motor neuron. This collection of muscle fibres is referred to as a motor unit. Each muscle fibre is either in a contracted state or a relaxed state; there is no such thing as a partially contracted muscle fibre. The nervous system is able to control the force generated by a motor unit by sending "signals" to contract via pulses along the motor nerves. This "firing frequency" turns the motor unit on and off with higher frequencies increasing the muscle's force and power output.

As we have many motor units, the nervous system normally orchestrates how these are involved. By synchronising lots of motor units, the nervous system can increase the total force from the muscle as a whole. Motor units don't fire all the time and in fact, only a small proportion of available motor units are likely to be recruited at any one time. They normally take turns firing to produce a smooth movement.

As we learned above, there are different types of muscle fibres that are classified according to their ability to generate and sustain force. The " faster" types generate high force and move the body part quickly but have very little endurance. In order to recruit such types the nervous system normally needs to send a fairly forceful signal. They have a high firing threshold to be recruited. For everyday activities, we are mostly relying on the slower muscle fibre types that have more endurance.

The nervous system's natural ability to recruit motor units, modulate the firing frequency and synchronise the firing of individual motor units is referred to as intramuscular coordination. For complex and skilled movements, the nervous system is also able to orchestrate the activation of multiple muscle groups to accomplish a movement efficiently. This inter-muscular coordination is refined through training and repeated practice. It's a complex, non-linear system with feedback loops and many complexities.

Spinal cord injury can disrupt the system to varying degrees, and although electrical stimulation can be used to produce useful muscle contractions, it is a relatively inefficient process.

How stimulation frequency influences muscle

When electrical stimulation is used to produce a muscle contraction, changing the stimulation parameters can significantly affect muscle fibre recruitment. The stimulation parameters that can be adjusted include:

The RehaMove FES Cycling system allows fine control of stimulation parameters

1. Stimulation Frequency: The frequency of the electrical pulses delivered to the muscle determines how often the motor neurons are activated. By adjusting the frequency, you can target specific types of muscle fibres based on the desired force output and endurance requirements of the task.

2. Stimulation Intensity: The intensity or amplitude of the electrical stimulus determines the strength of the muscle contraction. Increasing the intensity can recruit more motor units within a muscle, starting with the smaller, weaker ones and progressing to the larger, stronger ones. This is known as the size principle. By adjusting the intensity, you can control the number and size of motor units recruited.

3. Pulse Duration (Pulse Width): The duration of each electrical pulse can also affect muscle fibre recruitment. Short pulses may primarily activate the surface motor neurons and superficial muscle fibres, while longer pulses can penetrate deeper into the muscle and activate a broader range of motor units.

4. Inter-pulse Interval: The time gap between successive electrical pulses can influence the type and number of motor units recruited. A shorter inter-pulse interval may more easily lead to tetanic contractions where motor units are activated repeatedly, resulting in sustained muscle force.

5. Bipolar vs. Monopolar Stimulation: The electrode configuration can impact muscle fiber recruitment. Bipolar stimulation uses two electrodes placed close to each other on the muscle, while monopolar stimulation uses one active electrode with the return electrode farther away. Bipolar stimulation tends to activate a more localized region of the muscle, while monopolar stimulation can activate a larger area. Note that this is not the same thing as "biphasic" which refers to the waveform shape.

6. Stimulation Pattern: Varying the pattern of electrical stimulation, such as a single pulse, continuous train of pulses, or burst stimulation, can also affect recruitment patterns.

By adjusting these parameters, it is possible to target specific motor units or muscle fibres to achieve different outcomes in terms of force production, endurance, and precision of muscle activation. This ability to manipulate muscle fibre recruitment through electrical stimulation is valuable in rehabilitation.

Fatigue in Spinal Cord Injury

We all understand that adaptations to the skeleton, muscles, and nerves take place following a spinal cord injury. Without intervention, for example, bones can become weaker and muscles can and do change their tissue structure. Muscle activity can be a powerful stimulus to the health of the injured person. Limb paralysis that results from a spinal cord injury might leave muscles with intact peripheral nerve innervation, in which case electrical stimulation can be used to make muscles contract strongly (as in FES Cycling). Even denervated muscle can be made to contract with specialised electrical stimulation techniques (the RISE Stimulator). We will only briefly mention denervation here but we have explained this in detail in other articles.

At the start of this article, I mentioned that clients who start using FES cycling often experience a rapid onset of muscle fatigue. We have learned that muscle fibre types tend to transform toward "fast" types following a spinal cord injury, which might explain the rapid onset of fatigue. Also, such users have a reduced ability to consciously recruit muscle fibres and produce a stronger contraction.

Several factors contribute to the rapid onset of muscle fatigue stimulated by electrical stimulation in persons with spinal cord injury. These factors can be broadly categorised into neuromuscular, metabolic, and biomechanical aspects.

Neuromuscular Factors:

1. Denervation: The complete or partial loss of nerve signal transmission to the muscles results in impaired neuromuscular coordination and synchronisation. This can lead to inefficient muscle contractions, increased energy expenditure, and faster fatigue. Over time, denervation produces a loss of muscle fibre and nerve structural integrity.

2. Synaptic Dysfunction: Denervation also causes changes in the neuromuscular junctions, the junctions between nerves and muscles. These changes can affect the release of acetylcholine, the neurotransmitter responsible for muscle contraction. This can lead to further neuromuscular dysfunction and fatigue.

3. Muscle Atrophy: Spinal cord injury can lead to muscle atrophy and decreased quality of the muscle mass. Atrophied muscles have a reduced number of mitochondria, the organelles responsible for energy production. This can limit the muscle's ability to sustain contractions, leading to fatigue.

Metabolic Factors:

1. Impaired Glycogen Metabolism: As we saw above, Glycogen is a primary energy source for muscle contractions. However, denervation and muscle atrophy can impair the muscles' ability to store and utilise glycogen. This can limit the muscle's endurance and contribute to fatigue.

2. Reduced Mitochondrial Function: As mentioned earlier, muscle atrophy can reduce the number of mitochondria, which are essential for oxidative metabolism, the process that generates energy from oxygen. This can further impair the muscle's ability to maintain contractions for extended periods.

3. Increased Acid Production: During muscle contractions, lactic acid is produced as a byproduct of anaerobic metabolism. This can accumulate in denervated muscles, leading to a buildup of acid, which can cause muscle fatigue.

Biomechanical Factors:

1. Inadequate Muscle Activation: Electrical stimulation can activate all muscle fibres, regardless of their fibre type. This can lead to an imbalance between slow-twitch and fast-twitch fibres, which can contribute to fatigue.

2. Muscle Synergy Disruption: Denervation can disrupt the normal pattern of muscle activation, leading to inefficient muscle contractions. This can increase the energy required for a given task, promoting fatigue.

3. Joint Alignment Issues: Spinal cord injuries can affect proprioception, the body's sense of position and movement. This can lead to joint alignment issues, which can increase the load on muscles, promoting fatigue.

In summary, the rapid onset of fatigue in muscles stimulated by electrical stimulation in persons with spinal cord injury is a complex phenomenon with multiple contributing factors. Neuromuscular, metabolic, and biomechanical issues play a role in this phenomenon. Addressing these factors through appropriate therapeutic interventions, such as exercise training and neuromuscular reeducation, can help to improve muscle function and reduce fatigue in individuals with SCI.

Setting FES Cycling Stimulation Parameters

As mentioned above FES Cycling is typically designed to stimulate several muscle groups in sync with the movement of the bike pedals. The type of electrical stimulation uses surface electrodes placed in pairs over each involved muscle group. The intensity and effect of the stimulation on a muscle group is influenced by

• the size and separation of the electrodes.

• the shape of the waveform (typically rectangular, biphasic waveforms are used)

• the frequency of the waveform

• the magnitude of the waveform (often as controlled current)

• the pulse width

A system such as the RehaMove FES Cycling system will use frequencies of between 5 and 50 Hz with a maximum current of 130 mA and a maximum pulse width of 500 microseconds.

As the stimulation frequency increases, from a low value to around 20 Hz, muscle contractions are observed to change from a twitch to a smooth, tetanic contraction. As the frequency increases still further, contractions will typically become stronger but will eventually plateau.

Chronically paralysed muscle will often require higher frequencies to generate a given strength of contraction. However, a difficulty arises if we assume that higher frequencies are necessarily better. If we try to use a frequency higher than that necessary just to reach the "plateau", failure in contractions can occur due to something called "high-frequency fatigue" which is an issue with the neuromuscular transmission system.

This suggests that when starting a programme of FES Cycling, it might be better to use a slightly lower frequency than would first seem optimal. By using a frequency in the 20 to 30 Hz range, we sacrifice some power generation but gain some endurance and avoid high-frequency fatigue.

What about current and pulse width? The intensity of muscle contraction is influenced by the frequency, pulse width and current being used. We have always tried to use pulse width as the major direct variable influencing contraction strength. Although the current in the RehaMove system can be up to 130 mA, we would try to use more moderate levels of current to avoid the possibility of skin irritation.

At the start of this article, I described a typical situation in clients with a spinal cord injury who see their leg muscles fatigue quickly when starting a programme of FES cycling. There seems no doubt that muscles do become more fatigable following a spinal cord injury but that that this can be combated by manipulating the stimulation parameters. Especially in the early stages, using high stimulation frequencies should be avoided. In the early stages of training, imposing 1 or 2-minute breaks in stimulation during a session is a good idea. The RehaMove system facilitates this automatically if desired or manually based on observing when fatigue appears.

Conclusion

Chronic spinal cord injury has a profound impact on the energy systems that power our muscles. These systems, namely the phosphagen, glycolytic, and oxidative phosphorylation systems we described above, work together to provide the adenosine triphosphate (ATP) needed for muscle contraction. However, due to the disruption of neural pathways by the injury, their function and interplay are significantly altered.

Here's how each system is affected:

Phosphagen system: This system provides a rapid burst of ATP but has limited capacity. Following a spinal cord injury, muscle atrophy leads to reduced phosphocreatine stores, limiting the system's contribution to ATP production.

Glycolytic system: This system breaks down glucose for rapid ATP production but produces lactic acid as a byproduct, leading to fatigue. In spinal cord injury, reduced blood flow and oxygen supply to muscles may make the glycolytic system less efficient, further contributing to fatigue.

Oxidative phosphorylation system: This system uses oxygen to efficiently generate ATP from glucose and fatty acids. In spinal cord injury, impaired neural control of blood flow and mitochondrial dysfunction reduce oxygen delivery and oxidative capacity, limiting the system's effectiveness.

Overall, these changes lead to:

Reduced muscle power and endurance: With decreased ATP production, muscles fatigue more quickly and generate less force during contraction.

Here are some additional points to consider:

• The level of injury and the specific muscles affected can influence the degree of energy system disruption.

• Exercise and rehabilitation interventions can help improve muscle function and energy metabolism.

• Research is ongoing to develop new therapies that target the underlying mechanisms of energy system dysfunction in spinal cord injury.

• Increased reliance on glycolysis: This can lead to lactic acid buildup and contribute to muscle fatigue and pain.

• Metabolic imbalances: Changes in energy substrate utilisation can affect body composition and increase the risk of obesity and related health problems.

In the early stages of training, some individuals will demonstrate fairly rapid muscle fatigue due to the changes in muscle fibre type due to the SCI. Persistence is necessary to generate strong and sustainable muscle contractions again.

Muscle activation through FES Cycling exhibits a distinctive muscle fibre recruitment pattern. At lower levels of stimulation, fast-twitch, fatigueable fibres are preferentially engaged, followed by the recruitment of slow-twitch, fatigue-resistant fibres as the stimulation intensity increases. This recruitment pattern is attributed to the association of fast-twitch fibres with large motor units, which are innervated by large-diameter nerve axons that possess a lower firing threshold when externally stimulated. Consequently, electrically stimulated muscles generally experience rapid fatigue and exhibit limited force generation capacity. Additionally, paralysed muscles initially suffer from poor condition due to disuse atrophy and typically display varying degrees of unwanted contractile activity resulting from heightened reflex responses (spasticity).

Further Reading

Sheilds, R.K (2002). Muscular, Skeletal, and Neural Adaptations Following Spinal Cord Injury. Journal of Orthopaedic & Sports Physical Therapy 2002.32:65-74

Talmadge RJ. (2000). Myosin heavy chain isoform expression following reduced neuromuscular activity: Potential regulatory mechanisms. Muscle Nerve. 2000; 23:661–679. [PubMed: 10797389]

Myosin heavy chain isoform expression following reduced neuromuscular activity: potential regulatory mechanisms. Muscle Nerve. 2000; 23:661–679. [PubMed]

Warren, G. et al (2002) What Mechanisms Contribute to the Strength Loss That Occurs During and in the Recovery from Skeletal Muscle Injury? Journal of Orthopaedic & Sports Physical TherapyPublished Online: February 1, 2002, Volume32, Issue2, Pages 58-64

https://www.jospt.org/doi/10.2519/jospt.2002.32.2.58

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Bridging the Gap: The bodies energy systems - https://www.anatomicalconcepts.com/articles/bridging?rq=Bridging%20the%20Gap%3A%20The%20bodies%20energy%20systems
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