Karla van Dyk Biokineticist

08/11/2025

VOmax is one of the strongest predictors of overall health and lifespan-more powerful than blood pressure or cholesterol. Improving it through regular aerobic exercise strengthens every component of the oxygen delivery chain, protecting against disease and functional decline with age.

How much oxygen your body can use is one of the best predictors of long-term health

This figure shows how cardiorespiratory fitness (VO₂max) - the body’s ability to use oxygen during exercise predicts health, longevity, and physical capacity across life. VO₂max reflects how efficiently the lungs, heart, blood, and muscles work together to deliver and use oxygen.

🟡 Panel A: VO₂max levels across populations
Elite endurance athletes reach 70–90 mL/kg/min, while sedentary adults average below 45. Values under 17.5 mark the aerobic frailty threshold, and below 10.5 approach the mortality threshold where daily function and survival are compromised.
➡️ Training can raise VO₂max by 10–20%, while aging lowers it about 7–10% per decade.

🟡 Panel B: Fitness decline and mortality risk
VO₂max steadily declines with age but staying in higher fitness percentiles dramatically reduces all-cause mortality.
➡️ People in the “exceptional” fitness range have about five times lower risk of death compared to those in the lowest fitness group. Even being “above average” lowers mortality by over 40%.

🟡 Panel C: The physiology behind VO₂max
Every system contributes to oxygen delivery and energy use:

Lungs and respiratory muscles draw in oxygen

Red blood cells carry it through the bloodstream

The heart pumps oxygenated blood to tissues

Vessels distribute oxygen efficiently

Muscles extract and convert it into ATP for movement

💡 The bigger picture
VO₂max is one of the strongest predictors of overall health and lifespan—more powerful than blood pressure or cholesterol. Improving it through regular aerobic exercise strengthens every component of the oxygen delivery chain, protecting against disease and functional decline with age.

DOI: 10.1152/physrev.00045.2024

30/10/2025

Stages of Frozen Shoulder

27/10/2025

🧠 Principles for Prescribing Exercise to Improve Cognition in Older Adults

👉The principles for prescribing exercise to improve cognition in older adults are evidence-informed guidelines summarized using the F**T framework (Frequency, Intensity, Time, and Type). These principles are intended to serve as a reference point for practitioners to formulate personalizable prescriptions, which is important given the individual differences in exercise response and heterogeneous health statuses among older adults.

👉The principles emphasize that consistency is key for dementia prevention, and building flexibility into the prescription allows for customization to improve feasibility and enjoyment.

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⚙️ The F**T Framework Principles

🗓️ F: Frequency

▪️ The guiding principle for frequency is as often as feasible.
▪️ The exercise principles for cognition are more flexible regarding frequency than general physical activity guidelines.

💪 I: Intensity

▪️ The recommended intensity is moderate-to-vigorous.
▪️ Rationale:
▫️ This intensity is emphasized because it facilitates muscle-to-brain signaling.
▫️ Moderate-to-vigorous exercise abundantly excretes the myokine l-lactate from contracting muscles, which crosses the blood–brain barrier to the hippocampus where it activates BDNF (brain-derived neurotrophic factor).
▫️ Higher-intensity exercises may increase BDNF and memory more significantly than lower-intensity exercises.
▪️ Measurement – Talk Test:
▫️ During moderate-intensity exercise, it is easy to carry on a steady conversation.
▫️ During vigorous-intensity exercise, only a few words can be uttered.

⏱️ T: Time (Duration/Dose)

▪️ General Principle:
▫️ Some movement is better than no movement.
▫️ There is no minimum threshold for the amount of exercise performed.
▫️ Frequent movement breaks that interrupt prolonged sitting are beneficial and reduce the risk of dementia associated with sedentary behavior.
▪️ Weekly Dose for Clinically Relevant Cognitive Improvements:
▫️ Minimum: 70 minutes of moderate exercise OR 35 minutes of vigorous exercise.
▫️ Optimal: 140 minutes of moderate exercise OR 75 minutes of vigorous exercise.
▪️ Personalization Example:
▫️ The weekly duration can be personalized; for instance, the weekly amounts could be divided into approximately 25–45 minutes of moderate exercise 3 days per week (d·wk⁻¹) or 20–35 minutes of vigorous exercise 2 d·wk⁻¹.

🏃 T: Type

▪️ Older adults are encouraged to engage in a variety of different types of exercises, which suggests the potential for greater cognitive benefits.
▪️ Aerobic Exercise:
▫️ Includes walking, swimming, cycling, hiking, etc.
▫️ Engaging in regular walking or jogging, for example, can increase cardiovascular fitness, hippocampal blood volume, and memory.
▪️ Resistance Exercise:
▫️ Includes strength training utilizing bodyweight, resistance bands, or weights.
▪️ Multicomponent Programs:
▫️ Programs that combine balance, resistance, and aerobic exercise.
▪️ Balance-Enhancing Activities:
▫️ Activities like Tai Chi or yoga.
▫️ These exercises help reduce the risk of falls and help older adults feel safer while exercising.

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🧩 Additional Strategies for Enhancing Cognitive Benefit

▪️ Cognitive Challenge:
▫️ Try new exercise modalities that simultaneously challenge the mind and body.
▫️ Pairing exercise with a cognitively challenging task impacts the brain in synergistic ways, increasing neuroplasticity more than either activity alone.
▫️ Example: Walking or jogging while navigating unfamiliar terrain, as is done in orienteering.
▪️ Enjoyment:
▫️ Engage in activities they enjoy.
▪️ Social Support:
▫️ Exercise in socially supportive environments.
▫️ This helps increase adherence and motivation and combats loneliness, which is a chronic stressor for older adults associated with accelerated hippocampal atrophy, BDNF deficits, and cognitive decline.

Article 👇

17/10/2025

💪 Sarcopenia and Accelerated Aging

▪ Definition: Sarcopenia, defined as the progressive decline in muscle mass, strength, and physical function that accompanies aging, is a hallmark of the aging process. This decline is measurable starting in the fourth-to-fifth decade of life (40-50 years old).

▪ Consequences of Sarcopenia: The reduction in muscle mass places individuals at risk for metabolic disorders such as type 2 diabetes mellitus, as muscle is a metabolically active sink for glucose. Declines in strength (often measured as grip strength) are correlated with reduced health-related quality of life and increased risk of mobility declines and cardiovascular disease.

▪ Role of Inactivity: Muscle disuse or reduced physical activity accelerates sarcopenia significantly. A period of muscle disuse, such as hospitalization, illness, or even reduced daily steps, leads to rapid atrophy, especially in older adults, often having implications equivalent to years of normal aging. Older adults also demonstrate an impaired ability to regain lost muscle and strength following disuse compared to younger persons.

▪ Muscle Protein Balance: Muscle mass is governed by the balance between muscle protein synthesis (MPS) and muscle protein breakdown (MPB). As individuals age, MPS does not increase as robustly in response to protein ingestion, a phenomenon known as anabolic resistance, making it difficult to maintain muscle mass.

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⚙️ Physiological Drivers of Muscle Decline

▪ Muscle Fiber Changes: There is a reduction in both the size and number of muscle fibers, with the most evident decline occurring in Type 2 fibers (which are crucial for force production). Other myofibrillar changes include a loss of motor units (up to 40% loss by age 70), decreased sensitivity to calcium, reduced elasticity (increased stiffness), and compromised force production due to weak cross-bridges formed by post-translational modifications of myosin.

▪ Mitochondrial Dysfunction: Mitochondrial function and structure decline with age, a key theory in aging, and this decline is exacerbated by inactivity and disease. Dysfunction includes increased Reactive Oxygen Species (ROS) production, damaged mitochondrial DNA, and reduced expression of PGC-1a (a regulator of mitochondrial biogenesis). This reduction in mitochondrial function contributes to lower muscular function and higher insulin resistance.

▪ Connective Tissue and ECM Changes: Intramuscular connective tissue, which functions as a supportive force-transferring lattice, shows detrimental changes with age. Aging increases the presence of non-enzymatic crosslinks known as Advanced Glycation End Products (AGEs), causing the extracellular matrix (ECM) to become stiffer and more resistant to turnover (fibrosis).

▪ Muscle Stem Cells and Inflammaging: The muscle satellite cell pool decreases with age, and the capacity for muscle repair/regeneration is reduced. Furthermore, a pro-inflammatory state associated with age, known as inflammaging, involves increased systemic concentrations of markers like IL-6 and CRP, which have detrimental impacts on muscle health and are associated with increased risk of muscle loss and weakness.

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🥗 Mitigation Strategies: Nutrition and Exercise

▪ Protein Intake: Due to anabolic resistance, aging individuals require protein consumption levels significantly higher (at least 50–100% higher) than the current recommended intakes of ~0.8 g protein/kg bodyweight/d to optimally stimulate MPS. A dose of 0.4 g/kg of protein per meal, resulting in a total intake of at least 1.2 g/kg/day, is recommended to maintain muscle mass. Older adults should also focus on distributing protein evenly throughout the day and choosing high-quality sources, such as dairy proteins, which are rich in leucine.

▪ Exercise: Resistance Exercise Training (RET) is highly effective for stimulating MPS and promoting muscle hypertrophy and strength. Lower-load (30–50% 1RM), higher-volume RET may be an alternative training mode that benefits older adults by potentially addressing physiological deficits like improving glycemic control and increasing mitochondrial content. Endurance exercise is effective at stimulating mitochondrial biogenesis and function.

▪ Combined Approach: A regimen combining resistance and aerobic exercise, along with adequate protein, is highly impactful for improving glycemic control, strength, body composition, and function in older adults.

▪ Pre-habilitation: Engaging in physical activity and exercise (pre-habilitation) before predictable periods of disuse (like surgery or illness) is a crucial strategy to attenuate muscle loss and improve recovery outcomes.

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⚠️Disclaimer: Sharing a study or a part of it is NOT an endorsement. Please read the original article and evaluate critically.⚠️

Link to Article 👇

16/10/2025

✅ The Vicious Cycle of Reduced Physical Independence
The vicious cycle of reduced physical independence is a detrimental process observed in aging individuals, schematically represented as the increasing cycle of sedentarism that can eventually lead to dependency.
This cycle is described in the context of declining muscle health (sarcopenia) and mobility loss.

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⚙️ Mechanism of the Vicious Cycle

▪️ Activities of daily living become more difficult
▪️ As a result, these individuals often avoid engaging in these tasks
▪️ This avoidance leads to an increasing cycle of sedentarism
▪️ Ultimately, this sedentarism increases the risk for physical dependence

⏳ Context and Acceleration of the Cycle

▪️ The vulnerability to entering this cycle is linked to age-related decline in muscle function and periods of disuse, which accelerate the process of sarcopenia (the progressive loss of skeletal muscle mass, strength, and function).

💪 Muscle Loss and Function
▪️ Aging is naturally accompanied by a decline in muscle mass, strength, and physical function.
▪️ This decline is termed sarcopenia.
▪️ Muscle strength and power decline at a rate of approximately 3% per year.

🚫 Impact of Disuse
▪️ Muscle disuse, such as that caused by decreased physical activity, illness, or hospitalization, results in a rapid decline in muscle mass in aging individuals and effectively accelerates sarcopenia.

⚠️ Crossing the Threshold
▪️ A period of disuse may cause older individuals to cross the threshold of physical dependence a lot sooner due to mobility loss.
▪️ For instance, older individuals immobilized for two weeks experienced a decline in muscle strength equivalent to roughly 2–3 years of normal aging, highlighting that disuse can resemble accelerated aging.

❤️ Compromised Health States
▪️ The presence of underlying chronic conditions—such as type 2 diabetes, metabolic syndrome, or peripheral arterial disease—could play an additive role in the drastic reduction in muscle mass experienced during hospitalization or periods of disuse, making older adults much more vulnerable to muscle atrophy and the development of sarcopenia.

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🛡️ Mitigating the Cycle

Counteracting this vicious cycle involves interventions focused on maintaining or preserving muscle mass and function.

🏃‍♂️ Exercise and Activity
▪️ Exercise training and increased physical activity in older adults are related to improved mobility and function.
▪️ Engaging in resistance and aerobic exercise will aid in the preservation of muscle mass.

🍗 Nutrition
▪️ Consuming protein at levels above the current recommended intakes (at least 50–100% higher than ~0.8 g protein/kg bodyweight/d) is also critical.

⚙️ Combined Strategy
▪️ A combination of both resistance and aerobic exercise along with adequate protein consumption appears to be a potent strategy to mitigate muscle aging detriments.
▪️ For example, a whey supplement combined with lower-load resistance training attenuated the decline in muscle protein synthesis rates and preserved muscle mass during a two-week step reduction protocol.

🎯 Overall Goal
▪️ The overall goal is to promote mitigation of the decline in muscle mass, which is considered better than having to treat the consequences of low muscle mass and attempting to restore lost muscle.

30/09/2025

The aging journey: The changes in health conditions with aging [being optimal (green line) or suboptimal (orange line)] are related to changes in key physiological functions and can be prevented with diet, sleep and physical activity.

27/09/2025

26/09/2025

🦴✨ Stages of Bone Fracture Healing ✨🦴

After a bone fracture, an inflammatory response occurs that lasts for 2 weeks 🔥. This phase starts an intricate network of proinflammatory signals and growth factors. Polymorphonucleate (PMN) cells and macrophages 🧪 are recruited to endocyte microdebris and micro-organisms derived from the fracture. The damage to the blood vessels results in edema 💧.

📆 After 2–3 weeks from the fracture, endochondral bone formation occurs. During this process, the mesenchymal stem cells (MSCs) are recruited to the injured site and begin to differentiate into chondroblasts (chondrogenesis) 🧬, which proliferate into chondrocytes, resulting in soft calluses 🩹. Chondrocytes synthesize and secrete the cartilage matrix, containing type II collagen and proteoglycans.

🗓️ Between the 3rd and 6th week, the cartilage undergoes hypertrophy and mineralization in a spatially organized way. New MSCs are recruited which differentiate into osteoblasts, leading to the formation of interwoven bone (hard callus) 🪨. Mineralized bone formation is induced by the signaling of factors such as Bone Morphogenetic Proteins (BMP) and TGF-β2/β3 in the cartilaginous callus.

⏳ The last phase of bone remodeling begins 8 weeks after fracture and can last up to 2 years 🕰️. Communication between osteoclasts and osteoblasts mediates the replacement of braided bone with lamellar bone 🧱 through two key activities:

🔹 Removal of bone (resorption) by osteoclasts
🔹 Formation of bone matrix by osteoblasts

💪🦴 Our bones are amazing healers!

Illustration: https://cellregeneration.springeropen.com/articles/10.1186/s13619-025-00225-1

22/09/2025

When you move, you strengthen the muscles, joints, and bones that keep you resilient. But when you stay still, the body begins to weaken and break down. Running isn’t the enemy, it’s a gift that preserves freedom, energy, and mobility.

10/09/2025

In this study (miller et al., 2021), researchers found that elite sprinters had larger hip extensors than sub-elite sprinters.

Glute max size alone explained 43.8% of sprint performance differences, while total hip extensor volume explained 47.5%.

It’s an interesting finding, but correlation ≠ causation. Athletes predisposed to be fast may also be built this way, and a lot more goes into sprint performance than muscle volume alone.

Still, the hip extensors are critical, powerful hip extension drives both acceleration and max velocity.

Sprinting itself is the best way to develop these muscles. Strength and hypertrophy work can support sprinting, but they don’t replace it. Keep the focus where it matters…getting faster on the track or field.

If you want the complete system for how to train speed, how many sprints, rest intervals, strength methods, programming throughout the year, tempo runs, plyos, resisted runs, it’s all broken down inside Speed Kills, my flagship program.

Some of my older programs are also on sale right now as well.

The Art & Science of Sport Preparation - 10-week system for speed, agility, and strength. 51 pages in length.

The Complete Speed System - 16 week program, GPP + focused linear speed development.

Sprint from Scratch - An 8-week beginner sprinting guide focused on technique and progression.

PlayStrong Bundle - A 12-week youth training system for speed, agility, strength, and coordination

30/08/2025

📃Is tendon pathology a continuum? A pathology model to explain the clinical presentation of load-induced tendinopathy

🔎 Existing Tendon Pathology Concepts

-Degenerative tendinopathy: irreversible cell changes, matrix disintegration

-Failed healing: active cells, increased protein production, disorganised matrix, neovascularisation

-Stress-shielding (unloading): induces similar cell/matrix change as overload

📈 New Model of Tendon Pathology (Continuum)

1. Reactive Tendinopathy

Non-inflammatory proliferative response to acute overload

Short-term tendon thickening → reduces stress

Potential to return to normal with load reduction

2. Tendon Dysrepair

Attempt at tendon healing with matrix breakdown

Increased chondrocytic cells, proteoglycans, vascularity

Some reversibility still possible

3. Degenerative Tendinopathy

Cell death, apoptosis, acellularity

Large areas of disordered matrix with vessels, little collagen

Little capacity for reversibility

🧪 Imaging Features

-Reactive: fusiform swelling, intact collagen, diffuse hypoechogenicity

-Dysrepair: focal changes, collagen disorganisation, increased vascularity

-Degenerative: hypoechoic regions, numerous vessels, nodular thickening

👩‍⚕️ Clinical Features

-Reactive: acute overload in young athletes, swelling and pain

-Dysrepair: thick tendon with localised changes, across ages

-Degenerative: older or chronically overloaded tendon, nodular swelling, risk of rupture

📚 Evidence Supporting Continuum

-Histopathology: ground substance change precedes collagen disorganisation

-Imaging: tendons transition between normal, reactive, dysrepair, degenerative

-Clinical: high chronic load → higher incidence of degeneration and rupture

👉Link to article 👇
Nature review update for ttt 👇

23/07/2025

Complete Fitness is a balance.

Becoming a Forever Athlete will take all three.