Johann Els

#Vision is the capacity to believe in what others cannot see, and prepare and plan for it before everyone else see it.

Case study of a 70 year old male patient from @vo2account diagnosed with dilated cardiomyopathy set for LVAD surgery - which was prevented following 18 months (and ongoing) of cardiac rehab using serial CPET evaluations to quantify physiological response to exercise: After 21 months of cardiac rehab…a new pattern is emerging: The heart does not appear to be primary limitation during exercise anymore but rather peripheral oxidative impairment in skeletal muscle clearly shows to be primary limitation as shown by fatmax occrring 5% of peak workload - leading to ventilatory compensation. This leads to maximal glycolytic flux at 97 watts as shown by peak RER of 1.20 and test termination caused by skeletal muscle fatigue while O2 pulse reached 90% of predicted value. This is after 21 months of cardiac rehab data and 6 CPET evaluations to show how peak VO2 increased from 9 ml/kg/min at baseline to 19 ml/kg/min along with basline EF of 27% increasing to 40%. Cardiology confirmed LVAD not required anymore. But this is where the plot thickens…

Working through October’s cardiac rehab data, I could gain further important insight. This is the first month where we have clear objective data confirming that muscle’s oxidative impairment is now preventing the heart to expand in its capacity, as the CPET outcomes are now also confirmed in his cardiac rehab data for October.

• reduction of 4.8% in total exercise volume when October is compared with September
 • reduction of 8.3% in average bubble blowing time (lung protocol) in October when compared with August and September
 • reduction in push ups volume 
• reduction in squats volume

All this correlate with the CPET findings of:

• Peak fitness not improving as expected even though exercise continues to be executed. Peak VO2 only improved 1 ml/kg/min compared to February 2026. Before that every 6 month block of cardiac rehab showed Peak VO2 increasing by 3 ml/kg/min 
• First Ventilatory Threshold improved 48% in 6 months, while Fatmax decreased 58.8% (in 6 months). This is the biggest shift showing a disconnect between ventilatory aerobic metabolism and metabolic aerobic metabolism within skeletal muscle
 • The reliance on glycolytic flux with a significant reduction in oxidative reserve led to the increased peripheral extraction at the expense of fat burning, which led to an increased ventilatory cost and oxygen debt - which is probably linked with insulin resistance - explaining the weight gain even though exercise volume is high.

The month of October has been an important phase of this patient’s recovery. We now have clear evidence that the primary limitation during exercise is not the heart anymore as peak fitness continues to increase, but the muscle seems to prevent to heart to work harder during exercise. We need to restore the metabolic impairment in the muscle in order to allow the heart to pump out more oxygen filled blood at a higher workload. This is further evidenc that Peak VO2 is only the result of skeletal muscle’s oxidative capacity to sustain work.

If this is not addressed in this specific case, I expect the lungs will worsen, the muscle’s inability to burn fat will increase - as I expect insulin resistance might worsen, which might trigger heart failure again due to impairments within the lungs and the muscle, causing strain on the heart. We need to prevent this. This case study shows the importance to treat insulin resistance in cardiac patients. How many similar cases are out there where patients are told they are doomed while they can improve clinical outcomes? @ProfTimNoakes @StefanusSnyman

Interesting how a lot of debate on exercise, mitochondria and reactive oxygen species is circulating yet I have not come across a debate - where the mitochondrial dysfunction and release of reactive oxygen species exposed during low intensity exercise in maximal fat oxidation among individuals with severe mitochondrial dysfunction with ECG monitoring is exposed - are not part of this debate? Is this due to the lack of exercise implementation in populations with chronic conditions combined with a lack of CPET implementation with formal ECG monitoring? Interested to hear if individuals are out there coming across similar findings…because I am seeing quite a lot of it, yet struggling to find individuals debating this phenomenon?

The future of healthcare and finance may depend on understanding human functional capacity before its loss becomes a diagnosis, a disability or a financial claim.

The path less travelled is often where the future is created. Leadership is not always about knowing where you are going. Sometimes, it is about recognising that the direction everyone else is travelling may not lead to the answers the world actually needs. Innovation begins when intuition challenges convention, curiosity questions accepted wisdom, and science provides the discipline to investigate what others have overlooked. The greatest business opportunities are not necessarily found in existing markets. Sometimes, they emerge from problems so deeply embedded in established systems that society has simply accepted them as normal. That is where leadership becomes uncomfortable. You encounter resistance. Established thinking is challenged. The commercial opportunity is not immediately understood because the market has no existing category against which to measure it. But perhaps that is precisely the point. If everyone already understands the opportunity, are you truly creating something new? My journey with the creation of V̇O₂ Human Energy Intelligence has reinforced a powerful lesson: sometimes the most valuable innovation does not come from developing a better solution to an existing problem, but from questioning whether we have been defining the problem correctly in the first place. By combining first-principles thinking, scientific investigation, technology and intuition, entirely new products—and potentially new markets—begin to emerge. The challenges facing the world today, from healthcare and declining human capacity to productivity, insurance and economic sustainability, are enormous. But I increasingly see these challenges differently. Every systemic failure is potentially an undiscovered opportunity. Every unanswered question is an invitation to innovate. Every established assumption deserves to be challenged. The responsibility of leadership is not simply to navigate the world as it exists. It is to recognise what the world could become—and have the conviction, patience and scientific discipline to build towards it. Because the greatest innovations rarely begin with market demand. They begin with someone seeing a possibility that the market does not yet know exists. And perhaps the greatest competitive advantage in business is not having all the answers, but having the courage to ask questions nobody else is asking. The future is not always found by following the market. Sometimes, it is created by fundamentally rethinking it.

Today’s executive assessment 22 October 2026 in South Africa Three developments are material to South Africa’s healthcare-financing outlook. First, Statistics South Africa published September inflation figures yesterday. Headline CPI increased to 4.5%, while medical insurance inflation remained at 8.3%. Second, the 21 October Medium-Term Budget Policy Statement announced temporary fuel-tax relief and additional provincial funding intended partly to address health and education expenditure pressures. Third, newly published option-level analysis confirms that some Medshield members face 2027 contribution increases approaching 10%, despite the scheme’s weighted average of 7.9%. The central finding is that medical insurance costs continue to rise considerably faster than general consumer prices, while household budgets face additional pressure from fuel and transport inflation.

Controlled-work CPET reveals reduced exercise efficiency A matched case-control study published on 6 October compared 18 severely affected post-COVID patients with 18 healthy controls. At the same respiratory exchange ratio—intended to represent comparable metabolic stress—the post-COVID group demonstrated: * 24% lower oxygen uptake: 16.0 vs 21.1 mL/kg/min. * 38% lower power output: 75.6 vs 121.9 W. * Similar heart rate: 139.7 vs 141.9 bpm. * Similar blood lactate: 3.5 vs 3.8 mmol/L. Because mechanical output declined more than oxygen uptake, the authors interpret this as an elevated oxygen cost per unit of external work. Resting lung function and blood pressure were unremarkable, although resting heart rate was higher. A single symptom-limited maximal CPET produced a 16.6% average symptom increase during days 1–3, principally fatigue and joint pain, but group averages returned to baseline during days 4–7. Individual responses varied substantially. The study was small and 83% female, limiting subgroup conclusions. nature.com/articles/s41598-0… This supports making external work produced per unit of physiological cost a central measurement. Heart rate or VO₂ alone may appear proportionate to metabolic stress while the person generates substantially less useful work. However, the study does not prove mitochondrial dysfunction or measure productivity longitudinally. @ProfTimNoakes

When financial markets become unstable, attention turns towards scarce assets that cannot simply be created. But there is another scarce asset underpinning every economy that financial markets barely measure: Human functional capacity. Capital can be raised. Debt can be refinanced. Currency can be created. But the physiological capacity required for people to work, produce, recover and remain economically active cannot simply be printed. Healthcare spends trillions maintaining human beings. Employers spend increasingly more providing healthcare. Governments face ageing populations and growing healthcare liabilities. The question for the future is not simply how much we spend. It is how much measurable Human Energy that expenditure preserves or restores. That is the market we believe still needs to be measured.

A Long COVID rehabilitation case (36 year old male - previously fit) has revealed an important interaction between reduced oxidative reserve, limited stroke-volume response, weakened lumbar stabilisers and nerve pain. During prolonged cycling within the patient’s individually prescribed extended oxidative reserve, the cardiovascular system could not rely on a strong increase in stroke volume to support sustained oxygen delivery. This potentially increased the compensatory burden on heart rate, breathing and the working muscles—even though the external workload remained low. At the same time, the deep lumbar and pelvic muscles had to contract continuously to stabilise a spine with previous pathology (3 surgeries). A narrow saddle may have increased this stabilising demand. As these already weakened muscles fatigued, spinal control may have deteriorated sufficiently to expose an underlying nerve vulnerability, producing sciatic-type pain. The oxidative rehabilitation did not necessarily cause the nerve problem. The prolonged, controlled exposure appears to have revealed a weakness that shorter exercise or a broader, more supportive saddle did not expose. The plausible sequence is: Reduced oxidative reserve + limited stroke-volume augmentation → greater compensation during sustained work → earlier fatigue of weakened lumbar stabilisers → loss of lumbopelvic control → mechanical irritation of a vulnerable nerve → pain and prolonged recovery This remains a clinical hypothesis that must be tested by changing the saddle, reviewing bicycle position and monitoring whether symptoms recur. Rehabilitation should never continue through nerve pain. The immediate priorities are pain-free movement, quality sleep and recovery. Once the nerve irritation has settled, lumbar and pelvic stability can be rebuilt before cycling duration and intensity are progressively restored. This is why Long COVID rehabilitation cannot be prescribed from heart rate or workload alone. Extended oxidative rehabilitation can expose the specific cardiovascular, metabolic, muscular or neurological system that fails first. Exercise should be prescribed according to whole-body physiological stability—not intensity alone. @ProfTimNoakes @StefanusSnyman @TheNoakesF @MyDocFrank

Ramp-defined FatMax does not necessarily identify the sustainable oxidative rehabilitation threshold in chronic disease; prolonged testing may reveal an earlier, patient-specific point at which oxidative supply no longer matches energy demand and compensatory physiology begins.

Exercise is one of the most powerful interventions available for chronic disease. When appropriately prescribed, it can extend life, reduce disability, improve metabolic health, preserve physical function and protect something deeply human: the ability to remain independent. But recognising that exercise is beneficial does not mean every exercise dose is beneficial for every person. Much of the exercise information reaching society is derived from young, healthy or trained participants who already possess sufficient cardiac, pulmonary, vascular, metabolic and muscular reserve to tolerate overload. Their research asks how to improve performance in an already functioning system. Most people exercising for health are not athletes. Many are older, unfit, chronically ill or preparing for or recovering from surgery. For them, the first question should not be how much overload will produce adaptation, but whether sufficient physiological reserve exists to absorb the activity, recover from it and convert it safely into improved capacity. A workload classified as “light” by generic heart-rate zones or population formulas may impose substantial internal metabolic stress when reserve is restricted. The resulting tachycardia, ventilatory compensation, premature carbohydrate dependence, pain, insomnia or delayed fatigue may then be mistaken for ordinary deconditioning. This is not an argument against exercise. It is an argument for prescribing it with the precision expected of medicine. First establish the workload at which oxygen delivery, muscle oxygen utilisation, cardiac output, ventilation and metabolism remain stable. Then confirm recovery over 24–48 hours. Restore sustainable physiological reserve before pursuing conventional overload and performance. Fitness asks: How much stress will stimulate adaptation? Chronic and peri-operative care asks: How much activity can this person absorb, recover from and safely convert into greater physiological reserve? Exercise is medicine—but physiological stability must determine the dose.

FINAL THOUGHT Exercise prescription in fitness is fundamentally different from exercise prescription in chronic and peri-operative care. In a healthy person, the objective is to apply sufficient overload to disrupt homeostasis and stimulate adaptation. Preserved cardiac, pulmonary, vascular, metabolic and muscular reserve allows the individual to recover, supercompensate and progressively perform more work. In chronic and peri-operative care, that reserve may already be severely restricted. Oxygen delivery, muscle oxygen utilisation, substrate regulation, cardiac output, ventilation and recovery can become unstable at workloads that would be considered “light” in fitness. Applying conventional intensity zones may therefore increase physiological compensation, deepen oxygen debt and provoke delayed fatigue, pain or functional decline. The clinical objective is not to maximise workload or simply achieve a target heart rate. It is to identify the workload at which integrated physiology remains stable, confirm that the dose is recoverable for 24–48 hours and then restore reserve without causing decompensation. Fitness exercise asks: How much stress will stimulate adaptation? Chronic and peri-operative exercise asks: How much activity can this individual absorb, recover from and safely convert into greater physiological reserve? That distinction is why exercise in healthcare must be prescribed from individual physiological data—not borrowed from population-based fitness formulas.

11/11 Our real-world case studies suggest that exercise safety requires two thresholds: Acute stability: can the patient tolerate the session? Longitudinal recoverability: can they repeat it for weeks without fatigue, pain, insomnia or functional decline? Exercise should be prescribed by physiological stability—and confirmed by recovery.

10/11 Flu-like symptoms do not automatically prove a new viral infection or viral reactivation. Post-exertional immune signalling can produce body aches, malaise and sore-throat-like symptoms. A genuine infection must be investigated independently rather than inferred from symptoms alone.

9/11 The delayed “acid” sensation is unlikely to be lactate remaining in the muscles for 24–48 hours. It may reflect local metabolic stress and sensitisation of muscle afferents by protons, extracellular ATP, lactate, ion disturbance and inflammatory mediators.

8/11 UNFIT + CHRONIC DISEASE This person has both low capacity and limited physiological reserve. Even a very low external workload may represent a major internal demand. Repeated sessions can progressively exceed recoverability despite apparently acceptable heart rate or fat oxidation.

7/11 FIT + CHRONIC DISEASE This may be the most deceptive phenotype. Peak performance can appear preserved while submaximal oxidative stability, autonomic control or recovery is impaired. Fitness can camouflage disease-related physiological vulnerability.

6/11 UNFIT + NO CHRONIC DISEASE Exercise may initially cause fatigue and ordinary delayed muscle soreness. With appropriate progression, recovery and tolerance should improve. Progressive deterioration after 3+ weeks is not automatically “normal deconditioning” and warrants reassessment.

5/11 FIT + NO CHRONIC DISEASE This person usually has substantial oxidative and recovery reserve. If symptoms emerge after several weeks, consider excessive total training, inadequate sleep or nutrition, biomechanical overload, overreaching—or an unrelated infection.