There is a quiet assumption built into the phrase mitochondria is the powerhouse of the cell. It suggests something steady, reliable, almost automatic. Feed the system, make the energy, move on.

​

Yet biology is rarely that simple.

​

Energy production is not a flat rate. It is dynamic, responsive, and, in some bodies, far more expensive than expected.

​

Imagine again the cell as a city, with mitochondria acting as its factories, converting incoming nutrients into ATP, the currency that funds every action. In most cases, supply and demand stay in balance. Energy is produced at a cost the system can manage, waste is cleared efficiently, and the city runs smoothly.

​

Now shift the lens slightly.

​

In a hypermobile body, the issue is not just how energy is made. It is how much energy is required to maintain normal function in the first place.

​

Connective tissue, especially collagen, provides the structural framework that keeps joints stable with minimal effort. When that framework is more elastic, as seen in hypermobility, stability is no longer passive. It becomes active. Muscles must step in to do the job that connective tissue would normally handle quietly in the background.

​

This changes everything.

​

Posture is no longer a resting state. It is a constant, low-grade muscular contraction. Standing requires micro-adjustments. Sitting upright becomes work. Even lying down does not always fully turn the system off, as the body continues to compensate for laxity in subtle ways.

 

Each of these adjustments costs ATP.

​

This is the beginning of what can be thought of as an energy tax.

​

The mitochondria are no longer simply meeting the demands of movement, exercise, or stress. They are funding the ongoing, invisible labor of keeping the body aligned. The baseline cost of existing rises.

​

At first glance, the system adapts. Mitochondria increase output. Pathways accelerate. Energy is produced to meet demand.

​

Yet increased production is never free.

​

Every round of ATP generation produces byproducts, reactive oxygen species, small, unstable molecules that behave like sparks from an overworked engine. In a balanced system, antioxidant defenses neutralize these molecules efficiently, keeping the internal environment stable.

With chronic demand, the equation shifts.

​

More ATP production leads to more reactive byproducts. More byproducts require more cleanup. If the rate of production begins to outpace the rate of clearance, oxidative stress accumulates. The internal environment becomes less stable, less efficient, and more taxing on the very systems trying to keep up. ¹ ²

​

This is where the concept of cellular fatigue takes shape.

​

It is not simply that energy is low. It is that energy is costly to produce, and the system is paying for it in multiple directions at once.

 

Nutrient processing becomes critical in this context. The body may have adequate intake, yet still struggle at the level of utilization. Variations in the MTHFR gene can influence how folate and related cofactors are processed, affecting methylation pathways that intersect with mitochondrial efficiency and cellular repair. When these pathways are less efficient, the system does not fail outright. It becomes slower, less precise, and more energetically expensive.

​

The factory is still running, but it is burning through resources to maintain output.

​

Now layer this back onto connective tissue.

​

Collagen maintenance and repair depend on a finely tuned biochemical environment. Oxidative stress can disrupt this balance, interfering with the processes that keep connective tissue resilient.³ As that resilience decreases, joint stability may worsen, which in turn increases the muscular demand required to compensate.

​

The energy tax rises again.

​

This creates a feedback loop that is easy to miss when looking at systems in isolation. Structural instability increases energetic demand. Increased energetic demand strains mitochondrial function. Strained mitochondrial function raises oxidative stress. Oxidative stress feeds back into connective tissue vulnerability.

​

The system becomes self-reinforcing.

​

With our floppy friends, this interplay helps explain why fatigue is not just present, but persistent. It is not simply the result of doing too much. It is the result of the body doing more than it appears to, all the time, at a cellular cost that compounds. ³ ⁴

​

So the phrase mitochondria is the powerhouse of the cell remains true, yet incomplete. It tells us where energy is made, but not how hard the system has to work to make it, nor what is sacrificed along the way.

​

In a hypermobile body, the question is not only how much energy is available.

​

It is how much is being spent just to hold everything together.

​

References

1. Filler K, Lyon D, Bennett J, et al. Association of mitochondrial dysfunction and fatigue. Biol Res Nurs. 2021;23(2):163-175.

2. Ngo ST, Steyn FJ, McCombe PA. Mitochondrial dysfunction in neurological disorders and fatigue. Front Neurol. 2022;13:860789.

3. Malfait F, Castori M, Francomano CA, et al. The Ehlers-Danlos syndromes. Nat Rev Dis Primers. 2020;6(1):64.

4. Roma M, Marden CL, De Wandele I, et al. Postural tachycardia syndrome and chronic fatigue in hypermobility disorders. Auton Neurosci. 2021;235:102828.