During 𝗖𝗵𝗿𝗼𝗻𝗶𝗰 𝗙𝗮𝘁𝗶𝗴𝘂𝗲 𝗦𝘆𝗻𝗱𝗿𝗼𝗺𝗲 (𝗖𝗙𝗦), the body’s mitochondria, which normally produce energy, may not function optimally, contributing to low energy and fatigue.
Mitochondria requires a very specific electrochemical gradient across the inner mitochondrial membrane & this gradient is built by electronic transport chain complexes.
In 2009, Dr. Sarah Myhill demonstrated that patients with Chronic Fatigue Syndrome show dysfunction in Complex I and Complex III of the mitochondrial electron transport chain, impairing ATP production and cellular energy output.
𝗧𝗵𝗮𝘁 𝗺𝗲𝗮𝗻𝘀.
- The electrons aren’t flowing properly through the electron transport chain → Complex I and III are major “handoff points.” When they’re sluggish, the whole chain backs up.
- The proton gradient collapses → Without proper electron flow, the mitochondria can’t pump enough protons into the intermembrane space. → No gradient = no “battery.”
- ATP production tanks → ATP synthase needs that proton gradient to spin and make ATP. → No gradient = no spin = no energy.
𝗕𝘂𝘁, 𝗶𝘁’𝘀 𝗻𝗼𝘁 𝗷𝘂𝘀𝘁 𝘁𝗵𝗮𝘁.
Your cells can’t regenerate the NAD+ they need to keep the process running. This is critical because NAD+ is the electron carrier that keeps everything moving. Without it the the mitochondria just stall out. Generate the result, you can’t generate the ATP required to exist at baseline, let alone everything else.
𝗪𝗵𝗮𝘁’𝘀 𝗮𝗰𝘁𝘂𝗮𝗹𝗹𝘆 𝗵𝗮𝗽𝗽𝗲𝗻𝗶𝗻𝗴 𝘄𝗵𝗲𝗻 𝗡𝗔𝗗⁺ 𝗰𝗮𝗻’𝘁 𝗿𝗲𝗴𝗲𝗻𝗲𝗿𝗮𝘁𝗲?
𝗪𝗵𝗲𝗻 𝗖𝗼𝗺𝗽𝗹𝗲𝘅 𝗜 & 𝗜𝗜𝗜 𝗮𝗿𝗲 𝗱𝘆𝘀𝗳𝘂𝗻𝗰𝘁𝗶𝗼𝗻𝗮𝗹 (𝗹𝗶𝗸𝗲 𝗠𝘆𝗵𝗶𝗹𝗹 𝘀𝗵𝗼𝘄𝗲𝗱 𝗶𝗻 𝗖𝗙𝗦):
- NAD⁺ can’t be regenerated efficiently → NAD⁺ is the electron carrier that hands electrons into the electron transport chain. → If it can’t cycle back to NAD⁺, the whole system chokes.
- Electron flow slows to a crawl → No NAD⁺ = no electrons entering Complex I. → No electrons = no proton pumping.
- The proton gradient collapses → Without that gradient, ATP synthase can’t spin. → No spin = no ATP.
- Mitochondria stall out → You can’t generate the ATP required for baseline survival, let alone movement, cognition, detox, or healing.
𝗛𝗲𝗿𝗲’𝘀 𝗵𝗼𝘄 𝗶𝘁 𝘀𝘁𝗮𝗿𝘁𝘀 𝗳𝗼𝗿 𝗲𝘃𝗲𝗿𝘆𝗯𝗼𝗱𝘆...
After certain viral infections, like 𝗖𝗢𝗩𝗜𝗗‑𝟭𝟵 𝗼𝗿 𝗘𝗽𝘀𝘁𝗲𝗶𝗻–𝗕𝗮𝗿𝗿 𝘃𝗶𝗿𝘂𝘀 (𝗘𝗕𝗩), the body can enter a state of cellular stress and inflammation. For some individuals, this stress can disrupt mitochondrial function, especially the membranes where the 𝗲𝗹𝗲𝗰𝘁𝗿𝗼𝗻 𝘁𝗿𝗮𝗻𝘀𝗽𝗼𝗿𝘁 𝗰𝗵𝗮𝗶𝗻 (𝗘𝗧𝗖) lives.
𝗦𝘁𝗲𝗽 𝟭 — 𝗧𝗵𝗲 𝗘𝗹𝗲𝗰𝘁𝗿𝗼𝗻 𝗧𝗿𝗮𝗻𝘀𝗽𝗼𝗿𝘁 𝗖𝗵𝗮𝗶𝗻 𝗦𝗹𝗼𝘄𝘀 𝗗𝗼𝘄𝗻
When the ETC becomes less efficient:
- Electron flow slows → especially through Complex I & Complex III, the major entry & transfer points.
- Fewer protons are pumped → the proton gradient weakens.
- ATP production drops sharply → ATP synthase can’t generate energy effectively without that gradient.
𝗦𝘁𝗲𝗽 𝟮 — 𝗡𝗔𝗗⁺ 𝗥𝗲𝗰𝘆𝗰𝗹𝗶𝗻𝗴 𝗕𝗲𝗰𝗼𝗺𝗲𝘀 𝗜𝗺𝗽𝗮𝗶𝗿𝗲𝗱
NAD⁺ doesn’t “run out,” but:
- NAD⁺ recycling depends on ATP‑driven processes
- When ATP drops, NAD⁺ turnover slows
- This leads to lower available NAD⁺, which further reduces electron flow into Complex I.
𝗧𝗵𝗶𝘀 𝗰𝗿𝗲𝗮𝘁𝗲𝘀 𝗮 𝗱𝗼𝘄𝗻𝘄𝗮𝗿𝗱 𝘀𝗽𝗶𝗿𝗮𝗹: 𝗟𝗲𝘀𝘀 𝗔𝗧𝗣 → 𝗹𝗲𝘀𝘀 𝗡𝗔𝗗⁺ 𝗿𝗲𝗰𝘆𝗰𝗹𝗶𝗻𝗴 → 𝗳𝗲𝘄𝗲𝗿 𝗲𝗹𝗲𝗰𝘁𝗿𝗼𝗻𝘀 → 𝗲𝘃𝗲𝗻 𝗹𝗲𝘀𝘀 𝗔𝗧𝗣.
𝗦𝘁𝗲𝗽 𝟯 — 𝗖𝗲𝗹𝗹𝘂𝗹𝗮𝗿 𝗘𝗻𝗲𝗿𝗴𝘆 𝗢𝘂𝘁𝗽𝘂𝘁 𝗖𝗼𝗹𝗹𝗮𝗽𝘀𝗲𝘀
This combination: reduced ATP + impaired NAD⁺ recycling, leaves cells struggling to meet even basic energy demands. This is one of the proposed mechanisms behind the fatigue, post‑exertional crashes, and low cellular energy seen in ME*/CFS and some post‑viral syndromes.
*𝗠𝗘: Myalgic Encephalomyelitis - It’s the medical term often paired with CFS, so you’ll see it written as ME/CFS.
𝗪𝗵𝗮𝘁 𝗛𝗮𝗽𝗽𝗲𝗻𝘀 𝗪𝗵𝗲𝗻 𝗔𝗧𝗣 𝗖𝗼𝗹𝗹𝗮𝗽𝘀𝗲𝘀 (𝗮𝗻𝗱 𝗪𝗵𝘆 𝗘𝘃𝗲𝗿𝘆𝘁𝗵𝗶𝗻𝗴 𝗙𝗼𝗹𝗹𝗼𝘄𝘀)
When ATP production drops, like in post‑viral mitochondrial dysfunction, every energy‑dependent system begins to fail in sequence. ATP isn’t just “energy”; it’s the currency required for repair, detox, digestion, immunity, cognition, movement: 𝗲𝘃𝗲𝗿𝘆𝘁𝗵𝗶𝗻𝗴.
𝟭 — 𝗚𝘂𝘁 𝗲𝗽𝗶𝘁𝗵𝗲𝗹𝗶𝗮𝗹 𝗰𝗲𝗹𝗹𝘀 𝗰𝗮𝗻’𝘁 𝗿𝗲𝗯𝘂𝗶𝗹𝗱 𝗽𝗿𝗼𝗽𝗲𝗿𝗹𝘆
The gut lining renews itself every 3–5 days & that process is ATP‑intensive.
𝗪𝗵𝗲𝗻 𝗔𝗧𝗣 𝗶𝘀 𝗹𝗼𝘄:
- The gut barrier can’t repair
- Tight junctions loosen
- Intestinal permeability (“leaky gut”) increases
𝗧𝗵𝗶𝘀 𝗶𝘀𝗻’𝘁 𝗷𝘂𝘀𝘁 𝗮 𝗴𝘂𝘁 𝗽𝗿𝗼𝗯𝗹𝗲𝗺 — 𝗶𝘁 𝗯𝗲𝗰𝗼𝗺𝗲𝘀 𝗮 𝘀𝘆𝘀𝘁𝗲𝗺𝗶𝗰 𝗮𝗺𝗽𝗹𝗶𝗳𝗶𝗲𝗿.
𝟮 — 𝗟𝗲𝗮𝗸𝘆 𝗴𝘂𝘁 𝘁𝗿𝗶𝗴𝗴𝗲𝗿𝘀 𝗶𝗺𝗺𝘂𝗻𝗲 𝗮𝗰𝘁𝗶𝘃𝗮𝘁𝗶𝗼𝗻
When the barrier weakens, the immune system detects more “danger signals.”
𝗧𝗵𝗶𝘀 𝗹𝗮𝘂𝗻𝗰𝗵𝗲𝘀 𝗶𝗻𝗳𝗹𝗮𝗺𝗺𝗮𝘁𝗼𝗿𝘆 𝗽𝗮𝘁𝗵𝘄𝗮𝘆𝘀 𝘁𝗵𝗮𝘁:
- Increase oxidative stress
- Send “danger” signals to the nucleus
- Further impair mitochondrial function
𝗧𝗵𝗶𝘀 𝗰𝗿𝗲𝗮𝘁𝗲𝘀 𝗮 𝗳𝗲𝗲𝗱𝗯𝗮𝗰𝗸 𝗹𝗼𝗼𝗽: 𝗠𝗶𝘁𝗼𝗰𝗵𝗼𝗻𝗱𝗿𝗶𝗮𝗹 𝗱𝘆𝘀𝗳𝘂𝗻𝗰𝘁𝗶𝗼𝗻 → 𝗹𝗲𝗮𝗸𝘆 𝗴𝘂𝘁 → 𝗶𝗻𝗳𝗹𝗮𝗺𝗺𝗮𝘁𝗶𝗼𝗻 → 𝗺𝗼𝗿𝗲 𝗺𝗶𝘁𝗼𝗰𝗵𝗼𝗻𝗱𝗿𝗶𝗮𝗹 𝗱𝘆𝘀𝗳𝘂𝗻𝗰𝘁𝗶𝗼𝗻.
𝟯 — 𝗧𝗵𝗲 𝗲𝗹𝗲𝗰𝘁𝗿𝗼𝗻 𝘁𝗿𝗮𝗻𝘀𝗽𝗼𝗿𝘁 𝗰𝗵𝗮𝗶𝗻 𝘁𝗮𝗸𝗲𝘀 𝗺𝗼𝗿𝗲 𝗱𝗮𝗺𝗮𝗴𝗲
Inflammation and oxidative stress can worsen dysfunction in:
- Complex I
- Complex III
- Mitochondrial membranes
𝗧𝗵𝗶𝘀 𝗿𝗲𝗱𝘂𝗰𝗲𝘀 𝗔𝗧𝗣 𝗲𝘃𝗲𝗻 𝗳𝘂𝗿𝘁𝗵𝗲𝗿 — 𝗮𝗻𝗱 𝘁𝗵𝗲 𝗰𝘆𝗰𝗹𝗲 𝗱𝗲𝗲𝗽𝗲𝗻𝘀.
𝟰 — 𝗧𝗵𝗲 𝗚𝗜 𝘀𝘆𝘀𝘁𝗲𝗺 𝗯𝗲𝗰𝗼𝗺𝗲𝘀 𝘁𝗵𝗲 𝗮𝗺𝗽𝗹𝗶𝗳𝗶𝗲𝗿 𝗼𝗳 𝘁𝗵𝗲 𝗲𝗻𝘁𝗶𝗿𝗲 𝗰𝗼𝗻𝗱𝗶𝘁𝗶𝗼𝗻
This part you’re absolutely right about: The gut isn’t just “affected.”
𝗜𝘁 𝗯𝗲𝗰𝗼𝗺𝗲𝘀 𝗮 𝗱𝗿𝗶𝘃𝗲𝗿 𝗼𝗳 𝗼𝗻𝗴𝗼𝗶𝗻𝗴 𝗱𝘆𝘀𝗳𝘂𝗻𝗰𝘁𝗶𝗼𝗻 𝗯𝗲𝗰𝗮𝘂𝘀𝗲:
- 70% of the immune system sits there
- It’s the largest interface between the outside world and the body
- It’s one of the most ATP‑hungry tissues
𝗪𝗵𝗲𝗻 𝘁𝗵𝗲 𝗴𝘂𝘁 𝗯𝗿𝗲𝗮𝗸𝘀 𝗱𝗼𝘄𝗻, 𝘁𝗵𝗲 𝘄𝗵𝗼𝗹𝗲 𝘀𝘆𝘀𝘁𝗲𝗺 𝗳𝗲𝗲𝗹𝘀 𝗶𝘁.
𝟱 — 𝗪𝗵𝘆 𝗽𝗼𝘀𝘁‑𝗲𝘅𝗲𝗿𝘁𝗶𝗼𝗻𝗮𝗹 𝗺𝗮𝗹𝗮𝗶𝘀𝗲 (𝗣𝗘𝗠) 𝗶𝘀 𝘁𝗵𝗲 𝘀𝗶𝗴𝗻𝗮𝘁𝘂𝗿𝗲 𝗳𝗲𝗮𝘁𝘂𝗿𝗲
In ME/CFS, PEM means:
Any physical or cognitive exertion causes a delayed, disproportionate worsening of symptoms that can last days or weeks.
𝗪𝗵𝘆?
Because exertion demands ATP & when the system is already running on fumes, even small stressors collapse the energy budget. This is why people can feel “okay” during activity but crash hours later: the mitochondria simply can’t keep up.
𝗪𝗵𝘆 𝗣𝗼𝘀𝘁‑𝗘𝘅𝗲𝗿𝘁𝗶𝗼𝗻𝗮𝗹 𝗠𝗮𝗹𝗮𝗶𝘀𝗲 𝗛𝗮𝗽𝗽𝗲𝗻𝘀 (𝗮𝗻𝗱 𝗪𝗵𝘆 𝗜𝘁’𝘀 𝗡𝗢𝗧 𝗣𝘀𝘆𝗰𝗵𝗼𝗹𝗼𝗴𝗶𝗰𝗮𝗹)
In a healthy person, exercise triggers mitochondrial up‑regulation, they have reserve capacity. They can push harder, make more ATP, and then recover because their mitochondria have headroom.
𝗕𝘂𝘁 𝗶𝗻 𝗠𝗘/𝗖𝗙𝗦, 𝘁𝗵𝗲𝗿𝗲 𝗶𝘀 𝗻𝗼 𝗿𝗲𝘀𝗲𝗿𝘃𝗲 𝗰𝗮𝗽𝗮𝗰𝗶𝘁𝘆.
You’re already using all available ATP just to exist to maintain basic cellular function, digestion, immune surveillance, cognition, & repair.
𝗦𝗼 𝘄𝗵𝗲𝗻 𝘆𝗼𝘂 𝗲𝘅𝗲𝗿𝘁 𝘆𝗼𝘂𝗿𝘀𝗲𝗹𝗳:
𝟭 — 𝗬𝗼𝘂 𝗵𝗶𝘁 𝘁𝗵𝗲 𝗰𝗲𝗶𝗹𝗶𝗻𝗴 𝗶𝗺𝗺𝗲𝗱𝗶𝗮𝘁𝗲𝗹𝘆
There’s no extra ATP to pull from. The body shifts into anaerobic metabolism way too early.
Anaerobic metabolism =
- rapid ATP
- but high 𝗿𝗲𝗮𝗰𝘁𝗶𝘃𝗲 𝗼𝘅𝘆𝗴𝗲𝗻 𝘀𝗽𝗲𝗰𝗶𝗲𝘀 (𝗥𝗢𝗦)
- oxidative stress
- membrane damage
Those ROS can damage mitochondrial membranes & further impair the electron transport chain (ETC), especially Complex I and III.
𝟮 — 𝗧𝗵𝗲 𝗰𝗿𝗮𝘀𝗵 𝗵𝗮𝗽𝗽𝗲𝗻𝘀 𝗵𝗼𝘂𝗿𝘀 𝗹𝗮𝘁𝗲𝗿
This is the hallmark of post‑exertional malaise (PEM):
A delayed, disproportionate worsening of symptoms that can last days or weeks.
𝗪𝗵𝘆 𝗱𝗲𝗹𝗮𝘆𝗲𝗱? 𝗕𝗲𝗰𝗮𝘂𝘀𝗲 𝘁𝗵𝗲 𝗱𝗮𝗺𝗮𝗴𝗲 𝗶𝘀𝗻’𝘁 𝗶𝗻𝘀𝘁𝗮𝗻𝘁 — 𝗶𝘁’𝘀 𝘁𝗵𝗲 𝗮𝗳𝘁𝗲𝗿‑𝗲𝗳𝗳𝗲𝗰𝘁𝘀 𝗼𝗳:
- ROS buildup
- mitochondrial membrane stress
- ETC slowdown
- ATP depletion
- immune activation
𝗕𝘆 𝘁𝗵𝗲 𝘁𝗶𝗺𝗲 𝘁𝗵𝗲 𝘀𝘆𝘀𝘁𝗲𝗺 𝗿𝗲𝗮𝗹𝗶𝘇𝗲𝘀 𝗶𝘁 𝗰𝗮𝗻’𝘁 𝗺𝗲𝗲𝘁 𝗲𝗻𝗲𝗿𝗴𝘆 𝗱𝗲𝗺𝗮𝗻𝗱, 𝗶𝘁’𝘀 𝗮𝗹𝗿𝗲𝗮𝗱𝘆 𝘁𝗼𝗼 𝗹𝗮𝘁𝗲. 𝗦𝗶𝘅 𝗵𝗼𝘂𝗿𝘀 𝗹𝗮𝘁𝗲𝗿, 𝘆𝗼𝘂 𝗰𝗿𝗮𝘀𝗵.
𝟯 — 𝗜𝘁’𝘀 𝗻𝗼𝘁 𝗽𝘀𝘆𝗰𝗵𝗼𝗹𝗼𝗴𝗶𝗰𝗮𝗹 — 𝗶𝘁’𝘀 𝗶𝗺𝗺𝘂𝗻𝗼𝗺𝗲𝘁𝗮𝗯𝗼𝗹𝗶𝗰
In ME/CFS, the immune system often detects persistent viral remnants (like EBV) or ongoing danger signals. It refuses to stand down.
𝗖𝗵𝗿𝗼𝗻𝗶𝗰 𝗶𝗺𝗺𝘂𝗻𝗲 𝗮𝗰𝘁𝗶𝘃𝗮𝘁𝗶𝗼𝗻 →
- elevated cytokines
- oxidative stress
- mitochondrial inhibition
- more ETC damage
𝗔𝗻𝗱 𝗵𝗲𝗿𝗲’𝘀 𝘁𝗵𝗲 𝗸𝗶𝗰𝗸𝗲𝗿:
𝗧𝗵𝗲 𝗶𝗺𝗺𝘂𝗻𝗲 𝘀𝘆𝘀𝘁𝗲𝗺 𝗻𝗲𝗲𝗱𝘀 𝗔𝗧𝗣 𝘁𝗼 𝗰𝗹𝗲𝗮𝗿 𝘃𝗶𝗿𝘂𝘀𝗲𝘀.
When ATP is insufficient, it can’t do the job effectively. So inflammation stays high & mitochondria take more damage.
𝟰 — 𝗧𝗵𝗶𝘀 𝗰𝗿𝗲𝗮𝘁𝗲𝘀 𝗮 𝘀𝗲𝗹𝗳‑𝗿𝗲𝗶𝗻𝗳𝗼𝗿𝗰𝗶𝗻𝗴 𝗹𝗼𝗼𝗽
Low ATP → immune activation → mitochondrial damage → lower ATP → more immune activation.
𝗧𝗵𝗶𝘀 𝗶𝘀 𝘄𝗵𝘆 𝗣𝗘𝗠 𝗶𝘀 𝘀𝗼 𝗱𝗲𝘃𝗮𝘀𝘁𝗮𝘁𝗶𝗻𝗴 — 𝗶𝘁’𝘀 𝗻𝗼𝘁 “𝗳𝗮𝘁𝗶𝗴𝘂𝗲.” 𝗜𝘁’𝘀 𝗮 𝘀𝘆𝘀𝘁𝗲𝗺‑𝘄𝗶𝗱𝗲 𝗲𝗻𝗲𝗿𝗴𝘆 𝗰𝗼𝗹𝗹𝗮𝗽𝘀𝗲.
𝟱 — 𝗧𝗵𝗲 𝗵𝗼𝗽𝗲𝗳𝘂𝗹 𝗽𝗮𝗿𝘁
Dr. Trevor Bachmeyer said: “If you provide the biological signals for new healthy mitochondria synthesis you can reverse CFS — I reversed this whole thing.” If you click on the good doc's name 3 lines above under #5, you'll get to hear him break it down on Facebook.
I'm not a doctor and I am definitely not making these claims, but I love to listen to health professional that increase the body's ability to heal itself. Make your own decisions...