Health, Longevity, Strength and Muscle with Richie Kirwan | Triage Thoughts Ep. 233

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Why muscle and strength keep coming up in longevity research

When you look across the research on exercise and ageing, a pattern keeps appearing: higher levels of muscle mass tend to be protective, and higher levels of strength tend to be protective. Protective of what, exactly? Of both health and length of life.

It helps to separate two ideas here. Lifespan is the number of years you live. Healthspan is the quality of those years. Plenty of interventions move only one of those levers. Some drugs or protocols might improve how you feel without adding years, or add years while making the quality of your life noticeably worse. Exercise, strength and muscle mass are unusual in that they seem to target both at once. That is rare, and it is a big part of why this topic matters.

To dig into it properly, we spoke with Richie Kirwan, who has been on the podcast before. Richie is finishing a PhD at Liverpool John Moores University, and his research looks at the role of muscle mass in reducing the risk of further cardiac events in people who have already had one. That is what is called secondary prevention. So he sits right at the intersection of heart health and the muscle, strength and sarcopenia questions we keep returning to.

Numbers matter, but so does how people actually feel

Most people picture a scientist as someone who measures things. That is quantitative research: muscle mass went up by this much, strength went up by that much, cholesterol dropped by this amount. Clean numbers, clear conclusions.

There is another side that is becoming more common, and for good reason: qualitative research. Instead of measuring, you ask people how they are doing, how something felt, and whether they would keep it up. For people trained on numbers that can feel a bit soft, but it is genuinely important, because the real world is where any of this has to work.

Richie’s team is running a study that actively helps people who have had a cardiac event to build muscle. The qualitative feedback has been striking. The thing everyone has mentioned is that their confidence went up. Think about what a cardiac event does to a person: it is a shock, and it leaves you wondering what your life looks like now, what you can still do, even whether you will be here in six months. The people in the study reported feeling more confident across the board. More confident at work. Getting compliments from friends. Feeling more capable of everyday tasks.

Those everyday tasks matter more than they sound. Getting out of bed easily, standing up from a chair, playing with grandchildren, carrying the shopping and putting it away. Being able to do those things, when before you could not, or could only just about manage, changes how a person feels about their whole life. If someone gains a few kilos of muscle over twelve weeks and their cholesterol improves but they feel awful, what have you really achieved? You might have added to lifespan without doing anything for quality of life.

There is a flip side worth flagging. You can find an intervention that produces brilliant numbers and that nobody will ever repeat. A good example is a VO2 max protocol that alternated days: hard intervals one day, then running flat out as continuous cardio the next, repeated for ten weeks. As far as Richie is aware it produced one of the largest VO2 max improvements on record. When the participants were asked whether they would carry on, the answer was essentially no across the board. It was too draining to sustain.

That is the point. For a short, defined medical course, brutal-but-effective can be the right trade-off. You might want your doctor to say a treatment will be rough but that it is only three months and the best option for the job. For something a person has to do for the rest of their life, the felt experience is not a nice-to-have. If it is miserable, it is useless, because nobody keeps doing it.

This is why Richie designed the study programme to be simple and to be enjoyable. The training was built to be game-like, with a clear way to progress the weights over time, because making something a little more game-like makes it more enjoyable. The diet side was deliberately not strict: a few simple changes rather than a metabolic-ward regime that produces perfect results and that people never want to repeat. So far, everyone who has finished their twelve weeks has said they would keep going, and not a reluctant yes either: a definite yes. They enjoyed getting stronger and watching the weights climb. The team is still measuring the hard outcomes too: muscle size, strength, blood lipids and other markers of cardiometabolic health.

How muscle actually protects the heart and the rest of the body

So why does muscle size and strength contribute to health? There are several threads, and they tie together.

One of the clearer ones is blood sugar control. Larger muscles, and crucially healthier muscles, are much better at taking glucose out of the bloodstream after you eat. Healthier here means muscle that is active, exercised regularly and carrying less fat inside it. So when you get one of those glucose spikes everyone seems terrified of, which are, by the way, perfectly normal, well-trained muscle manages it far more effectively. That is a big reason exercise is so useful for people with type 2 diabetes.

On the cardiac side, there is a strong association between muscle and outcomes. This is where the obesity paradox shows up. In a cardiac population, people with a higher BMI often live longer than those with a lower BMI, up to a point. One likely reason is that higher BMI often comes with more muscle. If you separate people out by muscle and fat, the least healthy group tends to be those with the lowest muscle and the lowest fat, which lines up with frailty. Higher muscle, in general, tracks with surviving and living longer after one of these conditions. We are not fully certain why.

One candidate is signalling molecules released by muscle when it works, sometimes called myokines, some of which appear to be anti-inflammatory. Inflammation is closely tied to heart health, particularly to atherosclerosis, so anything muscle does to dampen it is plausibly relevant.

Richie’s team also ran a Mendelian randomisation study. In plain terms, that is a way of approximating a very large randomised trial using population data, by looking at people’s genes and what those genes are known to do. They looked at how genetically predicted muscle relates to lipoproteins, including LDL and HDL cholesterol. They found no clear association between muscle and the amount of LDL cholesterol, but there was an association with particle size. Larger muscle, and strength specifically (they used grip strength here), tended to go with larger HDL particles and smaller LDL particles. This is still speculative and is mainly giving them mechanisms to chase. The thinking is that larger HDL may be linked to better cholesterol efflux, the process of moving cholesterol out of the tissues and out of the bloodstream, and that smaller LDL particles may be a marker of better metabolic health. So that is one possible route from muscle to heart health.

Beyond the heart, the benefits stack up:

• Bone health. People with more and stronger muscle tend to have better bone density and a lower risk of osteoporosis, because muscle pulls on and loads bone. It is why some strength athletes have exceptionally dense bones.
• Falls and fractures. As people age they tend to lose type 2 muscle fibres, the ones behind quick, reactive movements. Lose those and the fast stabilising response that would normally catch you in a stumble is not there, so you are more likely to hit the ground. Combine that with weaker bones and the chance of a fracture rises. And the stakes are real: someone who fractures a hip has a markedly higher risk of dying within the next six months.
• Cognition. Some aspects of cognitive performance appear better in people with more muscle.
• Mood. There are higher rates of depression in people with lower muscle mass. The honest read is not that low muscle directly causes depression, but that if you are frailer you are less able to do the things you enjoy, less able to get out, meet friends or feel like a productive part of life. Being stuck and limited is not good for mental health.

There are entire bodies of literature behind each of these, and you can disappear down the rabbit hole of individual pathways if you want. The practical message is simpler. Exercise looks like a panacea partly because the act of exercise itself is good for you, especially metabolically and socially, and partly because the adaptations it produces, more strength and more muscle, are also what we are after. You cannot really separate the two, because you have to do the exercise to get the adaptations. People tie themselves in knots trying to find the one perfect protocol. You do not need it. Doing something is associated with benefit in its own right.

The trouble with calf measurements and other proxies

A lot of sarcopenia research seems to lean on a single muscle, the calf, as a stand-in for overall muscle mass. If you have small calves, as plenty of people do, it is fair to ask whether that dooms you.

The honest answer involves understanding why these measures get used at all. Ask why BMI is so common as a health metric, and the answer is that it is quick and easy. A tape measure round the waist, a height, a weight, done. Wrapping a tape round someone’s calf is just as fast. A lot of the sarcopenia work, incidentally, comes out of Japan, which has a rapidly ageing population and saw early that this would be a major problem.

The catch is that focusing on any one muscle is not much use for comparing one individual against another. You cannot line up a person with small calves against a person with large calves and declare one healthier. Where a measure like this earns its keep is over time, within the same person. If someone measured their calf in 2000 and again twenty years later, you can see whether they held it or lost it, and you can look at whether the people losing calf size also show a higher risk of diabetes, heart disease and the rest. On its own, in a single snapshot, it does not tell you much. Like BMI, it is most useful across large populations followed over the years.

So how is muscle measured properly? There is no single universally accepted definition of sarcopenia, but the one most commonly used in Europe, and often in the United States, comes from the European Working Group on Sarcopenia in Older People. Its criteria rest on two things: a measure of muscle function, and a measure of skeletal muscle mass.

For function, that might be a timed up-and-go test or grip strength. Richie’s team uses grip strength. For mass, they use two machines. One is DEXA, often treated as a gold standard, though Richie thinks MRI is better. The other is bioimpedance analysis, BIA, which passes a small electrical current through the body. For tracking an individual over time, a good BIA machine is genuinely fine, even if it is less reliable for comparing people against each other.

What they actually look at is appendicular lean mass, the muscle on the limbs, the arms and legs. The reason is precision. You will hear people talk about fat-free mass, which is everything in the body that is not fat. That includes your organs, and organs can grow and shrink, including in response to protein intake. That is not muscle, but it gets bundled in. Limb muscle is what a resistance programme is actually trying to build, so if someone’s appendicular lean mass goes up by two or three kilos over a few months, that is a clean, meaningful result. A change in fat-free mass is murkier, and something that looks statistically significant there may be clinically meaningless. (For function, grip strength has its limits too. It predicts outcomes well, but a device that measures the force someone produces in something like a deadlift might tell us more. Grip simply wins on being fast and easy, which is how it became a default.)

There is a wider lesson here for anyone reading studies, not just for researchers. We are almost always looking at proxy measures, not the thing we actually care about. People online read research like this and conclude you must train your calves more, then invent elaborate stories about why: the calves work during walking, so they must be a proxy for general activity; calf contraction moves lymph, so maybe it is about lymphatic drainage; and so on. The same happens with grip strength, with people deciding they need to train their grip so they will live longer.

The honest position is that these markers often cannot directly tell us what we want to know, because the only way to truly measure how much muscle or fat changed would be something nobody is volunteering for. So we use proxies, and the discipline is not to start worshipping the proxy. A DEXA scan tells you about lean mass and not a great deal more. Sports nutrition research falls into this trap often: restrict someone’s carbohydrate, then load it back, and their measured mass jumps by a few kilos, which is water, not new muscle. The same caution applies to longevity studies in mice where lean mass changes may actually be organ mass shifting, not muscle. Our tools are imperfect. So do not get too attached to the number itself. What we care about is the functional outcome: more muscle, even measured with blunt instruments, that tracks with better health.

The reassuring part: small calves, on their own, are not a death sentence. If you train regularly and you are fit and healthy in other ways, one lagging muscle group does not matter, unless you happen to be a bodybuilder, which is a small slice of people.

Would you rather be big and weak, or lean and strong?

Here is a useful thought experiment. Picture two people who both train, roughly similarly, but who respond very differently. One is a bit undermuscled by whatever chart you use, but genuinely strong for their size. The other is exceptionally well muscled, near the top of the charts, but relatively weak, middle of the pack on something like a squat. Which is the healthier position to be in?

The honest answer is that you would rather be the genetic outlier who has both. But forced to choose, the research shows stronger correlations between muscle function, meaning strength, and health outcomes than between muscle size and those outcomes.

Part of the reason is muscle quality. Two people can have similarly sized muscle on a DEXA scan yet differ in strength and health, because of what the muscle is made of. A healthy muscle, on an MRI cross-section of the thigh, looks like a solid dark mass with a thin layer of fat around the outside and the bone in the middle. In people with poor metabolic health, type 2 diabetes being a clear example, you see intramuscular fat infiltration: little rivulets of fat running through the muscle itself, so the cross-section is no longer one clean dark block. That fat impairs function. A muscle laced with it cannot contract as powerfully as one that is relatively clean.

A good everyday picture for this is a marbled steak: fat running all the way through the muscle rather than sitting as a cap on the outside. Take it to the extreme and you get Wagyu, which is barely red at all, more a pale pink lace of fat with tiny islands of muscle. It is delicious precisely because of all that fat, but those animals are not healthy. They are deliberately overfed and kept from moving much, more the foie gras of meat than a model of fitness. You would not want your own muscle to look like that. Ideally you want it dense, relatively free of internal fat, and well supplied with blood.

There is the familiar chicken-and-egg loop here too: is the benefit from the exercise, or from the muscle size itself? Training regularly reduces fat infiltration and makes you stronger at the same time, so you cannot cleanly pull them apart. The takeaway is that a strong muscle, large or not, is a good sign of all-round health and of someone who has been training consistently. Strength is probably the better indicator.

One more nuance on the size measure: it is not appendicular lean mass on its own that matters, but appendicular lean mass index, which is muscle mass relative to height squared, the same way BMI relates weight to height. A person who is five foot with three kilos of muscle in their arm and a person who is six foot with 3.2 kilos are not equivalent, because the taller person has far less muscle relative to their frame. You cannot read these raw numbers in isolation. (It is also why taller people can find it harder to look muscular: the same muscle is spread over a longer frame.)

Why we lose muscle as we age, and whether it is inevitable

Sarcopenia is the progressive loss of muscle mass as we get older. To picture it, think of a grandparent over the years: very often they grew a little smaller, a little frailer over time. That is muscle and strength being lost. It was only relatively recently, around 2017, that it became accepted as a properly diagnosable condition.

So is it inevitable? There are several causes, and the main one is reassuringly within reach: inactivity. As people age it becomes almost expected that they will do less. You have worked hard for decades, the thinking goes, so take it easy now. That is poor advice, and we often make things worse with kindness. Insisting on carrying granny’s shopping in for her, because you are a good grandchild, quietly removes the very stimulus that was keeping her muscle. Muscle does not stick around for sentimental reasons. It is only there if you give it a reason to be, and that reason is movement and load. As people age they tend to walk less, lift less and are expected to do less, and they get weaker. It does not have to be that way.

A second cause is what is sometimes called a catabolic crisis. Older people tend to have more hospital stays, and a hospital stay often means a week or so in bed. Even short spells of immobility cause sharp drops in muscle protein synthesis, sharp drops in insulin sensitivity and sudden losses of muscle. The problem is that older people often do not fully regain what they lost once they are out. Then another illness lands them back in hospital, and a bit more goes. This is the grain of truth behind the very common, if anecdotal, observation that someone “was never the same after that stay in hospital”. They take a knock, lose a chunk of muscle, and never get back to where they were.

A third cause is anabolic resistance: a blunted response to the normal signals that build and maintain muscle. The two main signals are exercise and protein. On the protein side, give a young person 20 grams of whey and you get close to maximally stimulating their muscle protein synthesis. Give the same 20 grams to someone in their seventies and you might get roughly half that response. You can partly rescue it with more protein: double the dose to around 40 grams and an older person can get close to the younger person’s response. But it is not only protein. Older people respond less well to exercise too, and may need more intense doses to get the same effect. So building muscle genuinely is harder with age.

There is an important caveat, and it is encouraging. Anabolic resistance seems to be less pronounced in people who have kept exercising throughout life. Lifelong trainers can build or hold muscle with less effort, and can probably get away with slightly less protein, than someone who has never trained. So activity does double duty: it helps you keep muscle, and it keeps the machinery that maintains muscle working better.

Several other things pile on with age, often overlapping. Insulin resistance tends to rise, driven partly by lower activity and partly by fat building up inside the muscle. Pro-inflammatory signalling tends to increase, the mirror image of those anti-inflammatory myokines, raising inflammation and tipping the balance towards breakdown. Sleep often shortens, and sleep matters for maintaining and building muscle and for keeping cortisol in check, since chronically high cortisol eats into muscle. Appetite can fall, so some older people simply eat less protein and cannot stimulate growth.

All of this feeds a self-reinforcing loop, which Richie calls the sarcopenic cycle. Lose a little muscle and strength, and moving becomes harder. Moving less, your activity drops. You may put on a bit of fat, which makes movement harder still, so you do even less, lose more muscle and get weaker again. Round and round it goes: you need to move more to stop getting weaker, but getting weaker makes you move less. When fat is part of the picture it becomes the sarcopenic obese cycle. This is a big reason you see muscle mass start to drop more steeply across the population from around the age of 55. People fall into the cycle and it snowballs.

Is it too late if you have never trained?

So if you train consistently for life, you will likely see a shallower decline. There will still be some drop-off, nobody expects to be as strong at 65 as at 30, but you are in a far better spot. That part is not controversial.

The harder question is what about the person who never exercised and starts at 65, freshly retired and finally with the time? Have they already lost years they cannot get back?

The fair answer leans on an old principle: prevention is better than cure. We simply do not have enough data on people who avoided exercise for decades and then became lifelong exercisers in their sixties to give firm, concrete guidance about that specific path. What we can say with confidence is that people who exercise throughout life are healthier. That is it.

But the absence of that data is not the same as saying you are finished if you start late. From the cardiac populations Richie works with, we know you can get real benefits in the proxies of muscle mass and strength even when people start later. And gains there should bring downstream benefits, in insulin sensitivity and, hopefully as the research matures, in other cardiometabolic markers.

There is, though, a time component to health, and to harm. If your cholesterol has been elevated for years and years, that has an effect, and undoing it can take years, if it is fully possible at all, even with something like statins. The same goes for the wear of years of poor blood glucose control: live with diabetes for a long time without managing it and the body is the worse for it, though it can still improve. A useful analogy: would you rather restore a car that has been thrashed down terrible roads, or drive it carefully and avoid the worst roads in the first place so it never needs the expensive repair? You want to look after it as you go, not damage it actively and fix it later. That is the case for exercising sooner rather than later.

What about the deeper, cellular side, the idea that decades of the “wrong inputs” might leave some lasting mark, through epigenetics or accumulated cellular damage that makes it harder to switch on muscle-building machinery? Honestly, this is fascinating and largely unanswered. We do know exercise causes some epigenetic changes in certain genes, and it could plausibly be part of why lifelong trainers respond better, perhaps by keeping muscle-maintaining genes more active. But it is not being studied heavily yet, and there is no conclusive answer to give. It is an area to watch.

A reasonable mental model, borrowed from how we think about cholesterol, where lower for longer seems better, is that for muscle and strength, more for longer is probably better. There does seem to be an age, often around 75, where people consistently start hitting functional decline, and for some it comes earlier. Past the seventies you see a marked rise in what gets called frailty, although frailty itself still lacks a firm definition.

You do not need to be a bodybuilder

It is worth being clear about scale. None of this research on the health outcomes of muscle is done in bodybuilders or powerlifters. Nobody is saying you need to be at Arnold Schwarzenegger levels to get the benefits. We are talking about a normal population and the value of having slightly above average muscle.

The benefit of added muscle also plateaus. There is a point past which more muscle does not buy you much extra health. Interestingly, muscle is not a U-shaped curve. Body fat is: very low body fat carries a sharply raised risk of death, just as very high body fat does, with a sweet spot in between. Muscle is different. More tends to mean healthier, up to a point, and then it flattens into diminishing returns rather than turning harmful.

This mirrors the dose of exercise. The activity guidelines are best treated as a floor, which is exactly why they are the guidelines. Do them. Roughly double them and you still see benefit. Push much further and the returns get marginal, and at the extremes you simply raise your risk of injury and other problems. More and more is not automatically better.

There is a real return-on-investment point buried in here. Even within natural limits, chasing the last fraction of muscle can demand two or three hours of training a day, when you could have built or held most of it in 45 minutes. Giving up that much of your day for a sliver more is, for most people, not worth it. A language analogy fits well: get to 80 or 90 per cent fluent and you are good to go; nobody is ever truly 100 per cent, even in their native tongue, because there are always words you would have to look up. Muscle is the same. The closer you get to your physiological ceiling, the less each extra effort returns.

And the context most people are actually in makes this easy. The average person does no exercise at all. Get that person into the gym once a week and you are already improving their health. Keep them generally active day to day and train them twice a week, and the strength and muscle benefits are well worth having. Can you do more and gain more? Yes, up to the point of diminishing returns. The practical advice is to find what you enjoy and can sustain. If three days a week is your honest limit and a fourth would make you resent it, three is your sweet spot. Stay there. You do not need to get huge, and you certainly do not need to reach natural bodybuilder levels. Simply having more muscle than the population average puts you in good shape.

That is why it is worth talking about the under-muscled crisis alongside the obesity crisis. Hold everyone’s body fat exactly where it is, whatever the figure, and simply add muscle, and it is very hard to see how health would not improve, given how protective muscle is for the heart and for metabolic health, and given that you have to be active to build it in the first place. You will not find many people who would argue that a population exercising a bit more would be worse off.

What this looks like in practice

So what does someone who knows this material actually do? Richie’s own routine is unfussy. About four days a week, five if time allows, for an hour or a bit more. He favours full-body sessions, partly because they give more frequent chances to stimulate muscle growth and maintenance. He is not actively chasing growth at the moment, mostly trying not to gain fat while spending long hours at a desk. He builds around compound movements and adds some isolation work, and he deliberately includes strength work, cycling between hypertrophy-focused phases and strength-focused phases. The point of the strength work is not powerlifting performance, being able to squat 200 kilos is not a health requirement, but it is enjoyable to chase a bigger bench or squat for a while, until the weights get heavy enough to be sore and the joints start complaining. He changes the routine roughly every six months: long enough to actually see the effects of a programme, with enough novelty to keep it psychologically fresh.

Looking ahead, the main change he plans is more aerobic work to improve aerobic capacity, including a VO2 max test to get a baseline (which he expects to be poor, since his only cardio is currently very steady-state commuting by bike). He also wants to get back into running, on the reasoning that humans are well adapted to an upright gait and to running, that it is a capacity worth having, and that it gets him outside more, with the half-joking bonus of being able to escape quickly if it ever came to that.

On protein, he may increase his intake as he ages, though it is worth noting it is not as high as people assume. He does not think protein needs to be enormous, but it is a sensible lever to pull if he ever notices muscle slipping.

The honest conversation about TRT and assistance

The other thing he keeps an open mind about, specifically for older age, is medical assistance, testosterone replacement therapy being the obvious current example. This came with a lot of caveats and is worth laying out carefully.

The starting point is balance. He is not someone who says steroids are always wrong. For physique athletes who want to get huge, that is their choice, as long as they are open and transparent about it rather than hiding it or, worse, actively denying it. And the medical roots matter: many anabolic steroids were originally developed for medical use, including for people losing large amounts of muscle during long spells in bed. So it is conceivable that for some older people, some form of assistance, testosterone or whatever else exists in years to come, could be warranted.

That is a long way from a recommendation. Going on TRT is a major decision, not something to wave through. The cleaner, first-line intervention is always to fix the lifestyle: most people can get huge benefits from eating well, exercising and sleeping, and those should come first. There is a useful review on lifestyle changes that raise testosterone, and the levers it lists are unsurprising: not eating an overly low-fat or heavily calorie-restricted diet, doing resistance exercise, getting a wide variety of minerals, and getting enough sleep. The honest summary is that if you are already living a genuinely healthy life, you have most of those boxes ticked. These should be the cornerstones, not an afterthought before reaching for a needle.

That also raises a chicken-and-egg question about the decline itself. We tend to see testosterone fall as men age, but it is worth asking how much of that is a foregone conclusion and how much is lifestyle: people moving less, getting less sun and so less vitamin D, and missing the other inputs they should be getting. It mirrors the muscle question. Some of the fall may simply track the habits that slip with age rather than age alone.

There is also a real physiological distinction between natural and exogenous testosterone, beyond just the number on a blood test. As men age, sex hormone binding globulin tends to rise, which changes how much testosterone is actually free and usable. Supplying testosterone from outside shifts that balance, and depending on how it is dosed you can end up with low sex hormone binding globulin and a higher fraction of free testosterone. That state is not necessarily linked to great health outcomes, even if it is linked to good muscle-building outcomes. So two people both reading, say, 500 nanograms per decilitre are not in the same situation if one is producing it naturally and the other is receiving it exogenously. The natural figure is at the mercy of everyday life, a poor night’s sleep, a glass of wine, all of which interact with your own production, whereas an injected dose has already been administered regardless. They are simply different situations.

The part that is genuinely concerning is the rise of TRT clinics, particularly in the United States, where a brief phone or even email consultation can end in a prescription, sometimes for young men in their early twenties. That is a serious problem. This is a major medical decision that warrants a proper conversation, because it is not all upside. There will be downsides too. The right comparison is something like HRT for women around menopause: more socially accepted now, and often very reasonable, but still a real decision that needs a proper case history and a genuine discussion of pros and cons. The same caution applies to putting a young girl on the contraceptive pill almost reflexively, when it carries real risks such as blood clots and deserves an actual conversation.

The underlying principle is the one that runs through everything: there is no biological free lunch. Every intervention has a cost as well as a benefit. Even exercise, for all its upside, costs you free time. None of that is an argument against acting. It is an argument for weighing things honestly, and for having these conversations with a doctor rather than a clinic with a prescription pad.

Move more, full stop

If there is one thing to take from all of this, it is the least controversial statement we can make: if you are doing no exercise, anything is better than nothing. Our bodies are built to move, and getting people moving more is probably one of the most valuable things we can do, for the cardiovascular system and the musculoskeletal system alike. The way we live now works against that. It is easy to spend eight or nine hours at a desk and then another few hours on the couch. So get active, get moving. It really is what we are designed to do.