fitbodyscience

💪 | Your science-based guide to fitness, nutrition, and health. 🧬 Optimize your body, fuel your mind, and live your best life.

[Afshine Emrani MD FACC @afshineemrani]

I'm a cardiologist. A study published today just connected heart failure and Alzheimer's disease in a way that could change how we screen for both — years earlier than we currently do.

Researchers at the Medical University of South Carolina discovered that the same misfolded protein plaques found in Alzheimer's brains are forming in the hearts of patients with idiopathic dilated cardiomyopathy — a condition that silently weakens the heart muscle long before symptoms appear.

Let me explain why this matters so much.

IDCM is a type of heart failure that has no obvious cause. No blocked arteries. No valve disease. The heart just weakens and enlarges — often for years before anyone catches it. We've never fully understood why.
Now we do. The del Monte Lab found that defects in the protein repair system — specifically abnormal post-translational modifications — are pushing heart cells toward self-destruction instead of repair. The same machinery that fails in Alzheimer's is failing in the heart. And the same Alzheimer's-associated genes accelerate the damage.

The lead researcher, Dr. Federica del Monte, said it directly: "We may use the heart as a window to the brain."

Here's why that sentence should stop you. Your heart is easier to image than your brain. An echocardiogram takes fifteen minutes, is non-invasive, widely available, and often covered by insurance. If IDCM shares a protein-misfolding pathway with Alzheimer's, then a routine cardiac ultrasound showing early ventricular enlargement or dysfunction could be one of the earliest signals of neurodegenerative risk — potentially years before any cognitive symptoms appear.

The del Monte Lab has already shown that hearts of Alzheimer's patients contain amyloid-beta deposits and develop diastolic dysfunction — even when the primary diagnosis was neurological, not cardiac. And hearts of IDCM patients contain the same toxic tau fragments found in Alzheimer's brains.

The diseases aren't just related. They may share the same root mechanism — a failing protein quality control system that attacks both organs.

This connects directly to everything I've been writing about on this platform.

Gum bacteria crossing the blood-brain barrier and accelerating Alzheimer's through the same inflammatory pathways that destroy arteries. Insulin resistance starving both the heart and the brain simultaneously. The gut-brain-heart inflammatory highway that links metabolic disease to neurodegeneration.

Your heart, your brain, and your metabolic system are not separate. They never were. We built medicine as if they live in different buildings. Study after study is proving they share the same plumbing — and now, the same protein-misfolding pathology.

What you can do right now: If you're over 50, have a family history of heart disease or Alzheimer's, or experience unexplained fatigue — ask your doctor for an echocardiogram. It's the simplest cardiac screening tool we have, and it can detect early ventricular changes long before symptoms develop.

Get your metabolic foundation tested. Fasting insulin, hsCRP, ApoB, Lp(a), vitamin D, homocysteine. Metabolic dysfunction and inflammation accelerate every protein-misfolding process — in the heart and in the brain.

Protect the protein repair system with what the evidence already supports. Sleep 7-9 hours — protein repair happens primarily during deep sleep. Resistance training plus Zone 2 cardio — both preserve muscle quality and mitochondrial health. Whole-food, high-protein nutrition. Cut ultra-processed food that drives the inflammation feeding these pathways.

This is early research. The study identifies the mechanism — it doesn't yet give us a clinical screening protocol. Targeted therapies are being developed — antibody treatments that remove the toxic protein fragments from heart tissue have already shown promise in preclinical models.

But the paradigm shift is already here: your heart may be the earliest warning system for brain decline. And most doctors aren't looking yet.

Don't wait for symptoms. Symptoms mean the damage has been accumulating for years.

Get the echo. Know your numbers. Protect the foundation. Your heart and your brain are fighting the same war. Now we know it — and we can act on it.

[Daniel Tawfik @dantawfik]

The human proteome just expanded by thousands of proteins—and most of them are sized perfectly for peptide therapeutics.

A new Nature study from the TransCODE Consortium analyzed 95,520 proteomics experiments and found that approximately 25% of 7,264 non-canonical open reading frames encode detectable microproteins in human cells.

These sequences produce peptides ranging from 8 to 100 amino acids. That's the therapeutic window where synthetic peptides can be manufactured, modified for stability, and delivered as drugs.

Peptide therapeutics have been constrained by the need to target biologically active sequences that are small enough to synthesize but specific enough to produce therapeutic effects. The challenge has been identifying which endogenous peptides perform essential cellular functions and which can be modified into pharmacologically stable molecules.

This study systematically maps thousands of naturally occurring peptides that cells translate and use across tissues and disease states. Many were detected in the HLA PeptideAtlas—240 million mass spectrometry spectra from immunopeptidomics datasets showing which peptides cells present on their surface.

That's direct evidence of biological relevance. Cells don't randomly present peptides on HLA molecules. Presentation indicates processing, translation, and integration into cellular signaling or immune surveillance.

The therapeutic implications operate across multiple modalities.

First: peptide replacement therapy. If microproteins perform essential cellular functions but decline with age or disease, synthetic versions could restore activity. This mirrors the logic behind hormone replacement—when endogenous production drops, exogenous supplementation compensates.

The consortium demonstrated that one peptidein from the OLMALINC long non-coding RNA produces a pan-essential cellular phenotype. CRISPR screens showed its loss disrupts fundamental processes. That's a candidate for peptide replacement if expression declines in specific tissues or aging contexts.

Other microproteins may regulate mitochondrial function, proteostasis, or cellular senescence. If age-related decline in these peptides contributes to metabolic dysfunction, peptide-based interventions could target those pathways directly rather than modulating upstream regulatory machinery.

Second: peptide antagonists. Some microproteins may drive pathological processes—inflammatory signaling, oncogenic pathways, or maladaptive stress responses. Designing antagonist peptides that block microprotein activity creates therapeutic options for conditions where microprotein overexpression or dysregulation contributes to disease.

The study found cancer-specific microproteins expressed in malignant cells but not normal tissues. These represent targets for peptide-based inhibitors that disrupt cancer cell signaling without affecting healthy cells. Because these sequences aren't part of the canonical proteome, conventional small molecule screens wouldn't have identified them.

Third: peptide vaccines. The HLA PeptideAtlas detected peptides from 1,785 ncORFs presented on cell surfaces. Cancer cells presenting unique microprotein-derived peptides expose targetable antigens for therapeutic vaccines.

This approach already exists with neoantigens—tumor-specific mutations that generate novel peptides recognized by T cells. Microprotein-derived peptides expand that target space. They're not mutations—they're translation products from sequences that normal cells suppress but cancer cells express.

Peptide vaccines could train the immune system to recognize and eliminate cells presenting these cryptic antigens. Because microproteins are often cancer-restricted, this strategy may produce stronger anti-tumor responses with fewer autoimmune risks than vaccines targeting overexpressed canonical proteins.

Fourth: cell-penetrating peptides and delivery vehicles. Some microproteins may function as endogenous cell-penetrating sequences—naturally occurring peptides that cross membranes or localize to specific organelles. Identifying these sequences could improve drug delivery technology.

Current peptide therapeutics face bioavailability challenges. Oral delivery is difficult due to enzymatic degradation. Systemic delivery requires modifications to extend half-life and prevent renal clearance. Intracellular targeting remains complex because most peptides don't efficiently cross lipid bilayers.

If evolution has already produced microproteins with membrane-crossing or organelle-targeting capabilities, those sequences could be incorporated into therapeutic peptides to improve cellular uptake and subcellular localization.

Fifth: synthetic biology and designed peptides. The study provides a catalog of naturally occurring bioactive peptides that cells translate and tolerate. That catalog becomes a training set for designing synthetic peptides with desired pharmacological properties.

Machine learning models trained on microprotein sequences—combined with data on their tissue expression, HLA presentation, and evolutionary constraint—could predict which synthetic peptide sequences will be stable, non-immunogenic, and biologically active.

This accelerates peptide drug development by narrowing the design space. Rather than screening random sequences, developers can modify known functional microproteins or generate synthetic analogs based on evolutionary patterns.

The manufacturing advantage: peptide synthesis is straightforward. Unlike biologics requiring expression systems and purification pipelines, peptides can be chemically synthesized at scale. Modifications to enhance stability—D-amino acids, cyclization, lipidation—are well-established.

The pharmacokinetic challenge has been specificity and half-life. Endogenous microproteins solve the specificity problem—they're already performing targeted cellular functions. Engineering modifications to extend circulation time becomes the primary optimization.

The evolutionary analysis supports therapeutic viability. The consortium developed ORF relative branch length (ORBL) to measure selective constraint on microproteins. Sequences under purifying selection across mammalian evolution are preserved because they perform functions that natural selection maintains.

That's evidence these peptides matter biologically. Therapeutic interventions modulating microprotein activity aren't targeting random noise—they're engaging functional molecules shaped by millions of years of selection pressure.

The annotation framework enables systematic peptide therapeutic development. By formalizing peptideins as a recognized classification in GENCODE and PeptideAtlas, the consortium creates searchable databases where researchers can identify microproteins relevant to specific diseases, tissues, or cellular processes.

Pharma companies developing peptide therapeutics can now query: which microproteins are dysregulated in this disease? Which are cancer-specific? Which show tissue-restricted expression? Which are presented on HLA in patient samples?

Those queries weren't possible when microproteins remained unannotated. Now they're part of the reference proteome.

The clinical development timeline depends on functional validation. Demonstrating that a microprotein performs a therapeutically relevant function—and that modulating it produces measurable clinical benefits—requires the same rigor as conventional drug development.

But the discovery phase just accelerated. Instead of screening millions of synthetic peptides for activity, researchers can start with endogenous sequences that cells already use.

The study detected 183 ncORFs with high-confidence peptide evidence in conventional samples and 1,785 in HLA immunopeptidomics. That's thousands of potential therapeutic leads—some for replacement, some for antagonism, some for immune targeting.

The immediate research agenda involves characterizing which microproteins show disease-specific expression patterns, which can be chemically synthesized with therapeutic stability, and which produce pharmacological effects when administered exogenously.

The decisions about which microproteins to develop as therapeutics will depend on target validation showing that the peptide performs a function relevant to human disease and that synthetic versions can recapitulate or block that function.

Peptide therapeutics have been limited by the need to find biologically relevant short sequences. This study just mapped thousands of them.

[Daniel Tawfik @dantawfik]

Rapamycin didn't just improve pregnancy rates in the IVF trial. It produced visible structural changes in cells within days—changes that could be measured, imaged, and directly linked to restored cellular recycling.

This is rare in aging research. Most interventions measure biomarkers as proxies for cellular function. Here, researchers watched autophagy reactivate in real-time.

Autophagy—the process by which cells break down and recycle damaged proteins, organelles, and other cellular debris—declines sharply during ovarian aging. By the mid-30s, lysosomal activity drops, protein aggregates accumulate, and the cellular recycling machinery that clears metabolic waste effectively shuts down.

The cell enters a state of chronic overproduction without compensatory clearance.

When researchers treated cultured human cumulus cells with low-dose rapamycin (0.25–0.5 µM), autophagy markers surged within 24–48 hours.

LC3-II, a protein that marks autophagosomes—the vesicles that engulf cellular debris for degradation—increased significantly. p62, a protein that accumulates when autophagy is blocked, decreased sharply.

This shift indicated that the cellular recycling pathway wasn't just partially restored. It was fully operational again.

Imaging confirmed what the biochemical markers suggested. In aging ovarian tissue, nucleoli—the ribosome production centers inside cell nuclei—were visibly enlarged, indicating hyperactive ribosome synthesis.

After rapamycin treatment, nucleoli shrank back to normal size. Ribosomal RNA levels dropped. The cell stopped overproducing ribosomes and shifted resources toward maintenance.

Protein aggregates that had accumulated in the cytoplasm began clearing. Lysosomal activity increased, meaning the organelles responsible for degrading cellular waste were functioning again.

These weren't inferred changes. They were directly observable under microscopy.

In middle-aged female mice (8–10 months), rapamycin treatment for two weeks before superovulation produced similarly visible results.

Eggs from rapamycin-treated mice showed improved meiotic spindle alignment—the structure that segregates chromosomes during cell division. Misaligned spindles are the primary cause of aneuploidy, where eggs carry the wrong number of chromosomes.

Oxidative stress markers declined. Mitochondrial function improved. The number of mature metaphase II eggs—those ready for fertilization—increased.

Again, these weren't subtle molecular changes detectable only through sequencing or mass spectrometry. They were functional improvements observable at the cellular and tissue level.

What makes this particularly compelling is the timeline. Autophagy restoration occurred within days in cultured cells, and within two weeks in living mice.

Most aging interventions require months to show effects. Rapamycin's impact on cellular recycling was detectable almost immediately after mTOR inhibition began.

This speed suggests that autophagy isn't permanently broken during aging—it's actively suppressed by chronic mTOR signaling.

When mTOR is inhibited, even briefly, the autophagy machinery reactivates because the underlying cellular infrastructure remains intact. The blockage is regulatory, not structural.

This distinction matters. If autophagy decline were driven by accumulated damage to lysosomes or degradation of autophagy-related proteins, restoring it would require rebuilding cellular machinery—a slow process.

But if the machinery is simply held offline by mTOR's continuous activity, then inhibiting mTOR removes the brake and autophagy resumes rapidly.

The trial data supports the latter model.

In the human IVF trial, women received 1 mg rapamycin daily for 3–4 weeks. This brief window was sufficient to produce measurable improvements in embryo quality, pregnancy rates, and—based on the preclinical data—autophagy flux.

The intervention didn't need to be sustained indefinitely. A transient metabolic reset was enough to clear accumulated damage and restore cellular homeostasis.

This aligns with emerging concepts in aging biology: periodic autophagy activation, rather than continuous suppression of growth pathways, may be sufficient to prevent the long-term accumulation of cellular debris.

Intermittent rapamycin protocols in mice—one week on, two weeks off—produce similar lifespan and healthspan benefits as continuous dosing, with fewer side effects.

The implication: autophagy doesn't need to be maximally active at all times. It needs to be periodically reactivated to clear the backlog of damage that accumulates during normal metabolic activity.

The ovary provided an ideal tissue to visualize this process because the aging timeline is compressed and the functional readouts are clear.

But the autophagy machinery being restored—LC3 lipidation, p62 degradation, lysosomal activation—is the same across all cell types. Neurons, muscle fibers, hepatocytes, and immune cells all rely on the same core autophagy pathway.

If rapamycin can reactivate autophagy in ovarian tissue within weeks, the principle should extend to other aging tissues where autophagy decline drives dysfunction.

Alzheimer's disease is characterized by accumulation of protein aggregates—amyloid plaques and tau tangles—that autophagy normally clears. Sarcopenia involves buildup of damaged mitochondria and misfolded proteins in muscle. Type 2 diabetes progression correlates with autophagy failure in pancreatic beta cells.

All three conditions share the same upstream problem: chronic mTOR activity suppressing autophagy.

The trial demonstrated that this suppression is reversible—and that reversal produces functional improvements rapidly.

What's less clear is how long the effects persist after rapamycin is discontinued.

In the IVF trial, embryo outcomes were measured immediately after the 3–4 week treatment window. Whether autophagy remains elevated weeks or months later, or whether it gradually declines back to baseline once mTOR becomes active again, wasn't assessed.

Mouse longevity studies suggest that intermittent rapamycin produces sustained benefits even during off-treatment periods, possibly because periodic autophagy activation prevents the accumulation of long-lived damage that would otherwise persist.

But in humans, the durability of autophagy restoration from brief rapamycin courses remains an open question.

Another unanswered question: whether autophagy restoration alone explains the pregnancy rate improvements, or whether other mTOR-dependent processes—mitochondrial quality control, ribosome regulation, DNA repair—contributed equally.

Rapamycin affects multiple downstream pathways simultaneously. Isolating which mechanisms drive which outcomes is difficult without more targeted interventions.

But from a practical standpoint, the convergence may be the point. Aging isn't driven by a single failing pathway. It's the cumulative result of multiple systems—autophagy, mitochondrial function, ribosome regulation, immune surveillance—declining in parallel.

Rapamycin addresses all of them simultaneously by targeting the upstream regulator that coordinates cellular resource allocation between growth and maintenance.

The trial's most important contribution may be methodological: it demonstrated that autophagy restoration can be measured directly in human tissue, not just inferred from animal models or in vitro experiments.

Previous human rapamycin studies measured indirect markers—circulating cytokines, immune cell populations, metabolic parameters. Those are useful, but they don't confirm that the core cellular recycling machinery is actually functioning better.

This trial included preclinical imaging data showing nucleoli shrinkage, protein aggregate clearance, and lysosomal reactivation—direct evidence that rapamycin restored cellular maintenance capacity.

Future aging trials could adopt similar approaches: biopsy tissue before and after intervention, image cellular structures, quantify autophagy flux markers, measure protein aggregate burden.

This would shift aging research from biomarker correlation toward direct observation of cellular aging reversal.

The timeline matters too. If autophagy can be restored within weeks, then trials don't need to run for years to detect effects. Brief interventions with measurable cellular endpoints could accelerate the pace of aging research significantly.

The ovary's compressed aging timeline made it an ideal tissue for this proof of concept. Other tissues age more slowly, but the same principles apply.

If autophagy suppression is regulatory rather than structural—if the machinery remains intact but held offline by chronic mTOR signaling—then transient mTOR inhibition should reactivate it across tissues.

The question isn't whether rapamycin can restore autophagy. The trial demonstrated that it can. The question is how to optimize timing, dosing, and duration to maximize benefit while minimizing risk across different tissues and different aging contexts.

The decisions about when to deploy autophagy-activating interventions—before cellular damage accumulates, or after dysfunction becomes measurable—may shape long-term healthspan trajectories.

Autophagy decline is slow and cumulative. But the trial showed that restoration can be rapid and observable.

In our Healthspan Research Review, we analyze the cellular imaging data, autophagy markers, and mechanistic evidence showing how rapamycin visibly reversed aging-related cellular dysfunction—and what this means for measuring aging interventions directly rather than through proxy biomarkers.

https://t.co/efXV57FWDT

[The Modern Pulse @manavspeakfacts]

Scientists spent decades blaming a single cause for why cells lose energy as you age. A study published in April 2026 found the real cause, and reversed it in two days using a nutrient already in your food.

Mitochondria are the structures inside every cell responsible for producing energy. Their decline is one of the most consistent markers of aging across every organism studied. For decades, the leading explanation was damage accumulating in mitochondrial DNA over a lifetime.

A study published April 18, 2026 in Nature Communications, led by researchers at the Leibniz Institute on Aging in Germany, identified a different and more immediate cause.

The lipid is called phosphatidylcholine. It is one of the primary structural components of mitochondrial membranes, and its flexibility is what allows individual mitochondria to fuse together into networks. These networks let cells share energy molecules, metabolic products, and signalling molecules between mitochondria, replacing damaged components and preventing localised energy shortages.

The researchers found that phosphatidylcholine production declines with age. As it declines, mitochondrial membranes become fragmented and lose the ability to form these networks. When the genes responsible for producing phosphatidylcholine were switched off in young roundworms, their mitochondria rapidly developed the same fragmented appearance normally seen only in old age.

Then the researchers tested the reverse. They fed aged worms phosphatidylcholine, or its precursor molecule choline. Within two days, the worms' mitochondria showed a structure resembling that of young, healthy mitochondria.

The researchers also analysed human data and found the same pattern: phosphatidylcholine synthesis declines with age in humans, correlating with the same markers of mitochondrial dysfunction observed in the worm experiments.

The researchers were explicit about what this does and does not mean. Phosphatidylcholine is present in many common foods, and the study does not establish that supplementation at typical dietary levels would replicate the laboratory effect in humans. What it establishes is a specific, reversible molecular driver of mitochondrial aging that had not been previously identified as a primary cause.

Decades of research pointed to DNA damage as the cause of aging mitochondria. A nutrient already in the food you eat reversed the effect in two days, in a different organism.

Source: Nature Communications, April 18, 2026, Volume 17, Article 3589. DOI 10.1038/s41467-026-71508-7. Leibniz Institute on Aging, Fritz Lipmann Institute. Lead author: Tetiana Poliezhaieva. Senior author: Maria A. Ermolaeva.

[Entrepreneur_cm @entrepreneur_cm]

Research suggests that equal servings of animal protein may pack a much bigger muscle-building punch than their plant-based counterparts. When it comes to protein, the same serving size on paper… https://t.co/yOyBKuuzym #Protein #Nutrition #HealthyEating #Fitness #MuscleBuilding

[fitbodyscience @fitbodyscience_]

The Number That Surprised Researchers:

A meta-analysis found statins raise diabetes risk by 10-12% — even without prior diabetes.

Heart benefits still outweigh the risk. But researchers now recommend regular glucose checks for long-term users.

https://t.co/KZhgAJZ8Us

[Asker Jeukendrup @Jeukendrup]

Don't miss our next webinar! We've launched a "Notify Me" feature. Visit our webinar schedule, select a topic you like, and register your interest to get updates when registration opens. Stay informed on sports nutrition and performance science! Check out upcoming webinars and set your notifications here: https://t.co/ZQQRtbGm9h

[fitbodyscience @fitbodyscience_]

In the latest research on statins, one number stood out:

10-12%.

That's the increase in new-onset diabetes risk over several years. Real — but small enough that the cardiovascular benefits still far outweigh it.

https://t.co/frBJmOiHWH

[fitbodyscience @fitbodyscience_]

Daily low-dose aspirin may extend disability-free years in healthy seniors. Statins linked to small increase in diabetes risk.

https://t.co/frBJmOiHWH

[Narendra Modi @narendramodi]

Thank you President Stubb for your warm wishes.

I fondly recall your recent visit to India and participation as the Chief Guest at this year's Raisina Dialogue. We are committed to further strengthening India-Finland cooperation.

@alexstubb

[fitbodyscience @fitbodyscience_]

Selenium helps Graves eye symptoms short-term but doesnt modify the disease. Magnesium L-threonate boosts sleep & cognition in young adults.

https://t.co/UakeiVVEmR

[Narendra Modi @narendramodi]

कृषि केवल जीविका का साधन नहीं, बल्कि समाज और राष्ट्र के पोषण का मूल आधार है। हमारे किसान भाई-बहनों का पसीना जब मिट्टी में मिलता है तो अन्न बनकर देशवासियों के जीवन को संबल देता है।

ते कृषिं च सस्यं च मनुष्या ��प जीवन्ति।कृष्टराधिरुपजीवनीयो भवति य एवं वेद॥

#12YearsOfKisanSamriddhi

[fitbodyscience @fitbodyscience_]

Evolocumab cuts first CV events by 25% in a 4.6-year trial.

High-protein diets boost satiety but total calorie deficit still drives weight loss.

https://t.co/Gw1tvXDFnq

[Narendra Modi @narendramodi]

2014 में आशा के जिस स���रज का उदय हुआ, वह आज नए आत्मविश्वास के प्रकाशपुंज में बदल चुका है। बीते 12 वर्षों में भारत के लोगों ने पहली बार यह देखा है कि जब सही नीयत से सरकार चलती है तो तेज गति से विकास भी होता है।

[fitbodyscience @fitbodyscience_]

Diet beat liraglutide for visceral fat loss in new research — 9.5% vs 4.8% reduction. Diet also preserved more muscle.

Plus: hamstring growth at long lengths + cable vs barbell for biceps.

https://t.co/9qnlxzcLgp

[Barack Obama @BarackObama]

It was great meeting with the talented folks who’ll be working at the Obama Presidential Center. We're excited to welcome everybody here soon!

[Sama Hoole @SamaHoole]

Nobody tells you that the patty is the victim here.

For fifty years it has been photographed next to the buns, the fries and the Coke. In every study, every documentary, every newspaper feature about the obesity epidemic, there it is: the patty, implicated by proximity.

Nobody isolates the variable. Nobody runs the study on two beef patties and a water. Nobody funds that research because there is nothing in it to patent, no ingredient to reformulate, no supplement to spin off, no product to put in a better-for-you range.

The beef just sits there. Complete protein. B12. Haem iron. Creatine. Zinc. The exact nutrient profile that humans ate almost exclusively for two and a half million years before anyone invented a bun.

Remove the bun. Remove the fries. Remove the Coke.

You have what your ancestors would have considered a proper meal.

You have what a nutritionist will describe as junk food while eating a granola bar containing 28 grams of sugar and a seed oil blend.

The patty knows what it is.

Nobody else seems to.

[fitbodyscience @fitbodyscience_]

New research: giving infants zinc at key intervals cut respiratory infections by up to 79% and diarrhoea by 63%. Supplemented infants also gained 1.4 cm more length and 332 g more weight. A low-cost intervention with outsized impact.

[fitbodyscience @fitbodyscience_]

Why do some people build muscle faster than others? New research suggests it is not just protein and training — molecular and genetic factors drive the difference more than most realize.

[Louisa Nicola @louisanicola_]

"I think the one that stands out probably the most is that you have to train to all-out failure to optimize muscle development. So I came from the old school, either you go all out, or you go home, or the vein in the side of my head wasn't bulging at the end of every set. I wasn't training hard enough. And the research that we have on the topic now really shows you can be a couple reps or three short of failure and still get roughly the same amount of muscle growth."

@BradSchoenfeld