Terry Mclaren Functional Physio

14/06/2026

Interesting 🧐

Your muscle rebuilds in about three months. Your tendons and cartilage take roughly a year and a half. Your bone, up to two years. Adding 40 grams of whey daily for two weeks doesn't change any of those timelines.

That's the finding from a study published this month in the American Journal of Clinical Nutrition. The team measured rebuild rates across more than a dozen knee tissues in living older adults using a safe heavy-water tracer. Tissues sampled during routine knee replacement surgery. Half the participants kept their habitual diet. Half added 40 grams of whey daily for 14 days. At the end, the rebuild rates of every tissue were the same in both groups.

The hierarchy was dramatic.
Muscle rebuilt at about 1.2 percent per day. At that rate, your quadriceps theoretically turn over in roughly three months. Synovium, the membrane that lines the joint capsule, rebuilt at 0.8 percent per day. The fat pad behind your kneecap, about 0.5 percent. The cruciate ligaments deep in the knee, about 0.45 percent. The patellar tendon, the femoral cartilage, and the menisci all rebuilt at 0.18 to 0.21 percent per day, putting their full-pool turnover at roughly 1.3 to 1.5 years. Bone rebuilt at 0.12 to 0.21 percent per day across five sites, with the slowest taking up to 2.3 years for a complete cycle.

What this does and does not say.
It does not say protein doesn't build connective tissue. It does. Every tissue in your body depends on dietary amino acids as substrate, and the synthesis rates measured here confirm that all of these tissues are actively turning over. Bone is a living tissue that constantly remodels. Cartilage maintains itself, slowly. Tendons repair from training and from daily mechanical load, slowly.
What the study shows is that for these older adults on their normal diets, adding 40 grams of whey on top for two weeks did not accelerate the rebuild rate of any tissue measured. It is one trial. It is small and short. It cannot rule out effects in people with inadequate baseline intake, or effects that might appear with longer supplementation. What it does establish is that connective tissue synthesis rates are dramatically slower than muscle, and a two-week protein bump does not compress those rates.

That has direct implications for what protein supplementation is and isn't doing.
Protein supplementation is a tool for closing intake gaps and for hitting the per-meal threshold that maximizes muscle protein synthesis after training. It's effective at those goals. People who are not eating enough total protein, or who are not getting enough per meal to drive muscle protein synthesis in older muscle that has lost some sensitivity to amino acids, benefit from supplementation. That's well established and not in dispute.

Protein supplementation is not a connective tissue repair accelerator. Cartilage damage from running mileage, tendon overuse injuries, bone density loss in postmenopausal women, ACL rehabilitation timelines: none of these can be hurried with whey. The biology runs at its own clock speed regardless of how much you put in.

What this means in practice.
For training and recovery, the protein protocol that has actually been shown to work is unchanged. Roughly 1.6 grams per kilogram of body weight per day, spread across three or four meals, each meal hitting at least 0.4 grams per kilogram. Training stimulus and adequate sleep do the heavy lifting on muscle adaptation. Supplemental protein at the meal level helps people hit those thresholds, especially for older adults, vegetarians, and anyone with a small appetite.

For connective tissue, the levers are different. Mechanical load through progressive training is the dominant signal for tendon and ligament adaptation. Resistance training drives bone density gains. Cartilage health responds to weight management and joint loading more than to nutrition. Collagen and vitamin C combined before training has interesting data for tendon collagen synthesis, but the effect sizes are modest. None of these tissues respond meaningfully to a protein bolus in a two-week window the way muscle does after a single training session.

The bigger reframe.
We have been treating tissue protein synthesis like a single dial. The reality is that your body runs many tissue clocks at very different speeds. Muscle is the fast one. Most of what we call "tissue building" outside of muscle takes 1 to 2 years per cycle, not days. When you injure a tendon at 55, the rehab timeline is set by how fast that tendon can lay down new collagen. Mechanical load and time do the work. Adequate protein supports it but doesn't compress the timeline.

Muscle responds to protein on a short timescale. Everything else responds on a long one. The two are not interchangeable.

Houtvast et al., Am J Clin Nutr, 2026
Moore et al., J Gerontol A, 2015
Morton et al., Br J Sports Med, 2018
Bauer et al., J Am Med Dir Assoc, 2013
Shaw et al., Am J Clin Nutr, 2017

12/06/2026

Interesting 🧐

We all slow down as we age—quite literally. When we get older, our walking pace tends to decline, which can even be an indicator of an increased risk of death. According to new research published in the journal Gait & Posture, scientists may finally know what’s going on.

Analyzing movement data from 107 adults aged 26 to 86, aging experts from Australia’s Flinders University discovered some interesting differences in how our ankles work as we age. When taking a step, older people tend to activate ankle muscles in opposition to one another at the same time. Known as “co-contraction,” this stiffens the joint, improving balance, but it comes at the cost of reduced push-off power, shorter strides, and slower walking speeds. Instead of a confident stride, it’s more of a hesitant shuffle.

The study marks the first time the inner workings of the ankle have been investigated in aging adults in this way, but it’s not just mechanical. According to the researchers, this subtle change reflects broader trends in how our nervous system controls our aging bodies and weakening muscles.

“The nervous system adopts a safety-first approach, compensating for age-related changes by favoring stability over performance,” study author Maarten A. Immink explained in a statement. “These changes can also increase fatigue and make walking longer distances more challenging, while reducing the ability to recover from trips or slips—a key factor in falls among older adults.”

The good news is that our stiffened gaits aren’t entirely an inevitable consequence of age-related muscular deterioration. Per the team, exercises that emphasize balance and coordination while targeting muscles that work together could help forestall a stilted stride.

Yoga, anyone?

https://nautil.us/heres-why-our-walking-gets-slower-as-we-age-1281837

03/06/2026

True 🙏

31/05/2026

Excellent variation 👍

24/05/2026

Time needed 😲

21/05/2026

Get huffing and puffing

"Aerobic exercise grows your hippocampus" is a true claim that hides a more interesting one. The hippocampus isn't one structure. It's five connected regions that handle different memory functions and age differently. The IGNITE trial just published a paper that pulls them apart and shows which ones track with fitness, which don't, and why that matters.

The setup: 601 cognitively unimpaired older adults, ages 65 to 80. Aerobic fitness was measured by a graded VO2peak test, the gold-standard for aerobic capacity. The hippocampus was imaged with high-resolution MRI and broken down into its five anatomical regions.

Higher fitness was associated with a bigger hippocampus on both sides of the brain. That part fits the headline. The new information sits one level deeper.

Some regions tracked with fitness. Others didn't. The regions that did move are the same ones most damaged in early Alzheimer's. The regions that didn't move handle a different kind of memory function, and they're relatively spared by Alzheimer's. So the fitness signal in this paper concentrates exactly where the disease hits first. That's not how the headline version usually reads.

The single region that didn't budge handles pattern completion, the brain process that lets you walk into a familiar room and pull up the memories tied to it. That ability declines with normal aging, and this paper suggests aerobic fitness alone may not protect it. Whether anything else does is an open question.

The mediation analysis is the part most coverage will miss. The authors tested whether the fitness-to-memory relationship actually ran through the hippocampus, or whether fitness was just correlated with both. It ran through the hippocampus. Specifically, total left hippocampal volume and the right subiculum (one of the regions that did move with fitness) statistically explained the link between fitness and episodic memory performance. The volume isn't decoration. It's the pathway.

Two limits worth holding in mind.

First, this is cross-sectional. IGNITE is a randomized 12-month aerobic exercise trial with 639 adults assigned to one of two aerobic doses (150 or 225 minutes per week) or a light-intensity control. This paper analyzed the baseline scan, not the training response. You can't conclude from this paper that aerobic training will cause these regions to grow. You can conclude that the fittest people in this cohort had bigger versions of the memory-relevant regions, and those regions explained part of their memory performance.

Second, VO2peak is aerobic capacity, not aerobic effort. Genetics, age, s*x, body composition, and cardiopulmonary health all contribute. Two people with identical exercise habits can have meaningfully different VO2peak values. What this paper measures is the trait, not the training.

Conflict of interest: the senior author is a paid scientific advisor for two companies (NeoAuvra and MedRhythms). Another author is on the advisory board of a third (Wondr Health). The methodology stands. The relationships are worth noting.

The practical takeaway is sharper than the usual version. Higher cardiorespiratory fitness lines up with bigger versions of the specific hippocampal regions most vulnerable to Alzheimer's pathology, and those are the same regions that explain better memory performance. One region that handles a separate memory function didn't show that pattern. The intervention results from IGNITE will publish in the next year or two and will answer the question this paper raised but couldn't settle: whether 12 months of structured aerobic training can do for these regions what natural variation in fitness already appears to.

Ripperger et al., Front Aging Neurosci, 2024 IGNITE NCT02875301, PMID 39749255 Erickson et al., Contemp Clin Trials, 2019 (IGNITE protocol)

20/05/2026

Get going, there’s few excuses

After 50, your hippocampus shrinks by 1 to 2% per year. A 12-month aerobic exercise trial in older adults reversed that. The exercise group gained 2% in hippocampal volume. The stretching controls lost 1.4%. That 3.4-percentage-point gap reverses roughly one to two years of typical age-related decline. Spatial memory improved, and the gains correlated with hippocampal volume changes.

That trial, run by Kirk Erickson's team at Pittsburgh and published in PNAS in 2011, remains one of the strongest single pieces of cognitive-aging intervention evidence we have in healthy older adults. It hasn't been overturned. It's been extended and validated in larger meta-analyses since.

A paper published this month in the Journals of Gerontology adds the mechanism we can't directly measure in humans. The team took 18-month-old mice (roughly equivalent to a person in their 50s or 60s, depending on the conversion table), induced neuroinflammation, and gave them eight weeks of moderate aerobic exercise. Hippocampal mitochondrial homeostasis recovered. Inflammation, oxidative stress, and apoptosis all fell. Memory impairment reversed.

Mouse to human translation isn't automatic. We can't measure mitochondrial dynamics in living human hippocampus, because no one is biopsying living human brain. The mechanism is inferred in humans, not proven. But the human imaging outcomes are real, replicated, and unambiguous.

This is what gets lost in cognitive aging marketing.

Brain health products line shelves. Nootropics, mushroom blends, lion's mane, NAD precursors, methylene blue. Every one is sold with mechanism claims (often plausible) and weak or absent cognitive outcome data. The single intervention with replicated structural brain outcomes in healthy older adults is exercise. It's free, requires no bottle, and takes 150 minutes a week.

Sleep is the other real competitor. The cognitive evidence for sleep quality is solid, and the structural brain effects of chronic poor sleep are well documented. Treat sleep and exercise as the two foundations, not as alternatives.

What the data actually supports:

150 minutes of moderate aerobic exercise per week, split into 3 to 4 sessions of 30 to 45 minutes. Moderate means you can hold a conversation but not sing. Heart rate around 60 to 70 percent of your maximum. Brisk walking on an incline, light jogging, cycling at a sustainable pace, swimming, rowing. The Erickson protocol used progressive walking, ramping up duration over the first weeks until participants were sustaining roughly 40-minute sessions at moderate intensity.

Vigorous exercise produces similar benefits in roughly half the time, though the evidence base is smaller in older adults specifically.

Resistance training has growing evidence for cognitive aging. The SMART trial in Sydney showed it slowed brain atrophy in adults with mild cognitive impairment. It's worth doing for several reasons, including independent mobility, bone density, and fall prevention. But the cognitive-specific evidence stack is thinner than for aerobic exercise.

What the data does not support:

That compounds or cognitive training apps substitute for exercise. Nothing in those categories has reached the structural brain outcomes Erickson demonstrated.

That casual walking counts as the trial dose. The intervention used elevated heart rate, sustained for 30 or more minutes, multiple sessions per week. Walking your dog around the block is good for you. It's not what was tested.

The bottom line:

If you're over 50 and not currently doing 150 minutes a week of moderate aerobic exercise, this is the single highest-confidence intervention with replicated structural brain outcomes for the second half of life. Sleep is the other foundation. Everything else, every compound and app and stack, sits below those two on the evidence ladder.

Start with 10 minutes of brisk walking three times this week. Build to 30 minutes. Get to 150 minutes a week by month two. That's the kind of progression that produced 2% hippocampal growth in 12 months.

Li et al., J Gerontol A, 2026
Erickson et al., PNAS, 2011
Colcombe et al., J Gerontol A, 2003
Northey et al., Br J Sports Med, 2018
Suo et al., Mol Psychiatry, 2016

17/05/2026

Do it

We often hear people worry about the "wear and tear" of running on older joints. But we rarely talk about the wear and tear of staying still

We’re so afraid of a sore knee that we forget to fear a weak heart. We’re so afraid of a trip or a stumble that we forget to fear the loss of our independence.
The "downside" of running is a little sweat and a bit of fatigue. The downside of not running is watching the world go by from a window.

Run (or walk briskly) while you can, so that you always can. You aren't just burning calories; you are burning away the limits. Every step is a victory

17/05/2026

Can you?

The five most powerful predictors of how long you'll live don't require a lab, a doctor, or a needle.

They require your living room.

Walk 10 feet and time yourself. In a study of over 34,000 adults, every tiny increase in walking speed reduced mortality risk by 12 percent. Walking speed integrates your brain, nerves, heart, lungs, muscles, and balance into a single number. It's your body's Wi-Fi signal. A slow connection means systems are disconnecting.

Sit in a chair, cross your arms, and stand up five times as fast as you can. Under 12 seconds is good. Struggle or needing your hands is a red flag linked to higher death risk within 10 years.

Wrap a tape measure around your waist and hips. Divide waist by hips. That ratio predicts heart disease and diabetes better than BMI. The Lancet confirmed it in 2022.

Open the tightest jar in your kitchen. Grip strength has been called the new blood pressure. A UK Biobank study of 500,000 people found that every 5 kg decrease in grip strength raised death risk by 16 percent.

Walk a mile as fast as you can without jogging. Record your time and heart rate. Plug them into a free online calculator. Cardiorespiratory fitness is the strongest predictor of all-cause mortality ever measured. Up to 80 percent lower risk in the most fit.

Five tests. No appointment. No copay. And they tell you more about your future than most bloodwork.

I wrote a full article on each test with target ranges, what they reveal, and how to improve every one, plus a Longevity Scorecard Worksheet.

Read it below 👇️

14/05/2026

👍

Pain is not fixed – and neither are we.
Part 3 explores how yoga may support learning, adaptation and change through the lens of modern pain science.

Inside:
• neuroplasticity (and ‘bioplasticity’)
• attention, breath and self-regulation
• pain as a homeostatic emotion – not just a sensation

Rather than acting as a specific ‘treatment’, yoga may create the conditions for change.
And that shift – from fixing to facilitating – matters.

👉 Read Part 3: https://www.noigroup.com/noijam/yoga-philosophy-and-pain-science-part-3/

This is part 3 of a 4-part series.