“The subject of athletics has not been understood until recently; nor has the best method of training been investigated,” Dr. Sargent told a Harvard audience on March 6, 1896. Dr. Sargent seems to be suggesting that everything about athletic training was now settled. 121 years later, however, there is still so much to learn about our amazing bodies, and how to maximize what they can do.
One useful measure is resting heart rate (RHR). A low RHR (along with optimal SpO2) is the hallmark of cardio health. RHR is just what it sounds like, the measure of how many times your heart beats (per minute) when you are at rest. (as opposed to heart rate variability (HRV), which measures the variation between beats.)
You can measure it with wearable tech or kick it old school (2 fingers at the neck) Either way, knowing your baseline RHR will help you monitor progress, and identify problems, before other symptoms emerge.
A normal resting heart rate for adults ranges from 60 to 90. When it comes to RHR, it important to know how to lower resting heart rate. Elite athletes have RHR in the 50s, 40s, even 30s. High RHR is associated with an increase in risk of death. But can you change your RHR? If so, how? And by how much?
The good news? Yes, you can lower your resting heart rate.
The 3 best ways to reduce your RHR?
(Need help remembering? Picture yourself riding a bike. (exercise) Your stress melts away. (relaxation) You’re so stress-free you fall into a deep slumber. (sleep.)
“It is very possible and even common to lower your resting heart rate through exercise,” says Tyler Spraul, a Certified Strength and Conditioning Specialist and Head Trainer at <a href="http://Exercise.com" rel="nofollow">Exercise.com</a>. “The type of exercise is not important, as long as you are challenging your cardiovascular system with your workouts.”
The 4 most Important types of exercise for health include strengthening, stretching, balance, and aerobic exercises. And exercise doesn’t just lower your RHR. Harvard Medical School reminds us that exercise will also ward off depression, enhance your sex life, sharpen your wits, and improve your sleep.
“As you train your cardiovascular system,” Spraul explains, “you will increase its efficiency and capacity. What ends up happening is that your heart is able to do more work with less effort (pump more blood throughout your system while requiring less energy and exertion to do so), so your resting heart rate goes down.“
It’s important to find activities you like, and to mix it up, to avoid boredom and make sure you’re working all parts of your body. Interval training (alternating intensive workouts with periods of rest) is an especially effective way to lower your RHR.
Sleep is emerging as a new frontier of health, with implications for cardio health, cognition, mood and even mortality. That’s right, a good night’s sleep over time can forestall death.
Disturbed sleep negatively impacts heart health and can increase RHR. Sleep has been shown to promote cardiac health and mood, which in turn has a protective function across all aspects of your health and performance. Sleep also protects against weight gain, which can increase your RHR.
Whether we are resting, or stoked with adrenaline during a ‘fight or flight response’, our hearts are in play.
Reduce stress, and your RHR will naturally fall. Increase stress? And it will rise, regardless of sleep and exercise. Stress in teens (measured by parental corporal punishment) was found to increase adolescent resting heart rate variability, while positive parenting helped improve RHR and HRV.
Yet reducing stress is easier said than done.
Some stress is beyond our control. But that makes it even more important to control what we can, and incorporate stress reduction as a daily component of our healthy lifestyle.
These interventions are widely successful to reduce stress.
A recent poster on Researchgate asked, “Is it possible to decrease the heart rate by 20 bpm in 6 months” The consensus? Yes, through exercise, but you need to be healthy to start, and work super hard.
G. Filligoi of Sapienza University of Rome recommends the relaxation route: “You can decrease heart rate by respiration exercises, yoga, meditation. I would suggest some self-consciousness approach in order to reduce the anxiety, nervous stress, and similars.”
Not everyone agrees it’s possible. “In my opinion,” says Oscar Fabregat-Andrés of MED Hospitales, “it is not possible to modulate baseline heart rate in such magnitude, because although exercise is able to regulate autonomic system, "vagal tone" necessary to reach this rate is not performed in 6 months.”
If a low RHR is a sign of health, does that mean lowering your RHR automatically makes you healthy? No, but it’s evidence you’re on the right track. Measuring RHR is a safe, non-intrusive way to track the success of your fitness regime, and spot trouble early.
“A low resting heart rate doesn't necessarily lead to better health in and of itself,” says Spraul, “but it can be used more as an indicator of the effectiveness of your training methods.”
This effectiveness can be positive, or not. “If you are doing workouts that challenge your cardiovascular system and your resting heart rate decreases over time,” he says, “that is a good sign that you are doing the right things.” But it’s important to measure it regularly, even, especially, if you are training hard. An unexpectedly elevated RHR can be a sign of overtraining. “Sometimes the resting heart rate can actually increase,” Spraul cautions, “which is a sign that you have over-stressed your body's systems and may need to focus on better recovery or
Back in 1896, Dr. Sargent wasn’t so far off the mark. “The modern idea of training,” he told his Harvard audience, “is to seek things “which will contribute to health and strength: diet, sleep, bathing, proper clothing and exercise.” “Exercise with energy,” he concluded, “to stimulate the heart and lungs and increase respiration and circulation.” Some things never change.
Exercise stimulates the heart, in a good way. And RHR is a key measure of how well it works.
Stem cells, famous for replenishing the body’s stockpile of other cell types throughout life, may have an additional, unforeseen ability to cache memories of past wounds and inflammation. New studies in the skin, gut and airways suggest that stem cells, often in partnership with the immune system, can use these memories to improve the responses of tissues to later injuries and pathogenic assaults.
“What we are starting to realize is that these cells aren’t just there to make tissue. They actually have other behavioral roles,” said Shruti Naik, an immunologist at New York University who has studied this memory effect in skin and other tissues. Stem cells, she said, “have an exquisite ability to sense their environment and respond.”
But when those responses go wrong, they may cause or contribute to a variety of enduring health problems involving chronic inflammation, such as severe allergies and autoinflammatory disorders.
Most tissues in the body contain small reservoirs of long-lived stem cells that can divide and specialize into myriad cell types as required. A stem cell in the skin, for example, can divide and give rise to lineages of cells that produce pigment or keratin, cells that form the sweat glands, or even the flexible barrier cells that allow the skin to stretch when the body moves. Serving as miniature factories for other cell types seemed to be stem cells’ primary function, and because they need to stay versatile, an underlying assumption has been that they have to be “blank slates,” unchanged by their histories. But now a new picture is starting to emerge.
In August, a Nature paper by Boston-area researchers offered fresh evidence for a kind of memory in stem cells, and some of the first for the phenomenon in humans. The team, led by the single-cell sequencing pioneer Alex Shalek and the immunologist José Ordovas-Montañes, both at the Massachusetts Institute of Technology, and the immunologist Nora Barrett at Brigham and Women’s Hospital, had set out to understand why some people suffer from debilitating chronic allergies to airborne dust, pollen and other substances. Most people experience at most a passing bout of coldlike symptoms from these irritants, but about 12 percent of the population has a severe reaction that persists all year and results in uncomfortable polyps or growths.
The work is the first step in the team’s larger quest to understand chronic inflammatory diseases, such as asthma and inflammatory bowel disease, in which the immune system continues to launch unnecessary attacks even after the initial challenge is over. These types of autoinflammatory disorders have long been blamed on the immune system, which is thought to overreact to a perceived threat. But the Boston team suspected there might be a cause in the tissue itself.
They began by taking cells from the inflamed nasal cavities of people with chronic sinusitis and comparing them to cells from healthy control subjects. After collecting about 60,000 cells from 20 different people, they sequenced RNA molecules taken from individual cells to determine which genes were active in them. In the stem cells from the sinusitis patients, they saw that many of the active genes were associated with allergic inflammation — in particular, the genes were targets of two immune mediators called interleukin 4 (IL-4) and interleukin 13 (IL-13). These are small molecules that immune cells like T and B lymphocytes typically use to communicate with one another.
The fact that the targeted genes were active in stem cells meant that the stem cells were apparently in direct communication with the immune system. A hunch that this communication might have an effect on the chronic nature of the disease led the researchers to a further set of experiments.
They removed cells from the airways of allergy patients, grew them in culture for about five weeks, and then profiled their gene activity. They found that the genes involved in allergic inflammation were still active, even though the allergic threat of dust and pollen was long gone. In addition, the researchers described many of the cells as “stuck” in a less-than-fully-mature state.
For Shalek, this result signals “that stem cells may transfer ‘memories’ to future generations of cells and this can cause near-permanent changes in the tissue they replenish.” This process invites comparisons to the immune system: B cells and T cells draw on their experiences with infections they have previously repelled to fight off new ones more effectively. Similarly, stem cells may retain a record of past assaults to sharpen their responses next time. But in the case of the allergy patients, that memory apparently becomes maladaptive. It may keep stem cells perpetually signaling to the immune system that an attacker is there, creating a feedback cycle that promotes inflammation and polyps.
According to Shalek, an understanding of which cells become “bad actors” and how their response propagates throughout a tissue should lead to more effective interventions. In fact, in their paper they were able to test the effects of an antibody that blocks IL-4 and IL-13 on the stem and secretory cells of an individual with nasal polyps. They noted a substantial restoration of gene expression associated with healthy tissue, a promising step toward the development of future therapies.
“This opens a new paradigm where we don’t only focus on the self-renewal potential of these cells but on their potential interaction with their surroundings,” said Semir Beyaz, an immunologist at Cold Spring Harbor Laboratory. Beyaz was not involved in the study by the Boston group but has made similar findings in the gut: In a paper published in Nature in 2016 he demonstrated that the intestines of mice on a high-fat diet produced a greater number of stemlike cells than did those of mice eating less fat. When dividing, the intestinal stem cells also seemed to add to their own numbers more frequently rather than producing more differentiated cells, a change that has been linked to diseases like cancer.
“Functionally, we are realizing that cells can be tuned,” Naik said. “Immunologists are starting to understand that immune reactions take place in tissues, and the way tissues respond to this is at the level of the stem cell.”
A few years ago, in collaboration with stem cell biologists, Naik looked at the effects of prior injury and inflammation on wound healing in mice, in the hope of understanding whether experience with inflammation affects stem cells. As described in their 2017 paper in Nature, she and her colleagues discovered that if patches of skin on mice were inflamed and allowed to heal, subsequent wounds to that same spot would heal 2.5 times as quickly, an effect that could last as long as six months.
In that experiment, Naik explained, the memory retained in the stem cells was beneficial because it was “tuning cells to be more powerful at healing wounds and regeneration.” But the flip side of this finding, as Shalek, Barrett and Ordovas-Montañes had observed, is that “if you teach [the cells] bad behaviors … they are going to remember those bad behaviors as well,” she said.
How the stem cells are storing these memories is unknown; in both the allergy and the wound healing studies, the mechanism appears to involve some modification of the DNA that makes certain genes more or less accessible to activation. Naik found that the DNA in the skin stem cells of the twice-wounded mice contained many regions that were less tightly packed, which usually indicates gene activity, and some of those open regions were retained long after the inflammation was over.
As Naik and her colleagues discussed recently in a review paper for Cell, stem cells in a wide range of tissues engage in a chemical “dialogue” with the immune system, with both sides — and potentially many other cell types — pooling their information to cope most effectively with changing conditions. Whatever the details of those conversations might be, all the evidence points to stem cells playing a central role in helping to make tissues more adaptable by preserving some record of their history.
“It makes more sense that a tissue would just learn from its experience,” Naik said. “That way it doesn’t have to reinvent the wheel every single time.”
I can say with confidence that I am probably the least popular person in my household this week. While there are likely a few reasons that I would be up for this distinction in any given week, I know for sure that it was my decision to turn on Apple’s new Screen Time function for myself and my kids that earned me the honor this time.
Part of iOS 12, this new Screen Time feature is designed to provide users with detailed information on how long they are on their phone in a given day and for what.
When a company creates a feature that is designed to make you use their product less, it should raise an eyebrow. Apple clearly is aware that our distraction with technology is becoming a serious health issue. In fact, several other technology giants are also starting to acknowledge that technology and social media has both harmful and addictive properties.
There are two main aspects of the Screen Time function: awareness and control. In terms of awareness, it allows you to see your detailed usage stats for the day, including the number of “pickups” – the times when you pick up your phone from the resting position.
In terms of control, you can both limit access to apps and enable “downtime,” which disables the phone overnight except for critical/emergency functions. Screen Time also allows parents to set usage limits and see how kids are using their phones.
I implemented several of the Screen Time features on my phone, including time limits on apps where I know the little red buttons distract me from both the task at hand and conversations in which I should be fully present. I also enabled downtime an hour before bedtime.
When I did the same for my kids, it did not go over as well. They let me know in no uncertain terms how it would impact their life and one of them stated, “Dad, literally no one else does this.” To which I responded, “Great, I don’t want to be like everyone else, nor do I want you to be.”
Here’s the reality. We get better at what we practice. If you practice 100 free throws, chances are that you will get better at free throws. The same goes for driving and studying a subject.
Sadly, what many of us are spending our time practicing these days is being distracted. And we are all getting really good at it. In fact, many of us are probably on our way to becoming distraction masters.
Recent studies have shown that you are actually significantly more distracted just from having your cell phone in the room, even if it’s not turned on. And the distraction gets worse when it’s sitting on a table next to you.
We are training our brains to be distracted in the same way that meditation trains our brains to be focused. And that has a toll. It changes the way our brain develops, hurts our concentration, impacts our relationships and strips us of the ability to be with our own thoughts or appreciate silence and quiet.
We begin to crave technology stimulation like a drug; the dopamine in our brain responds in a similar manner.
A week into our new experiment, I have adjusted to the changes. Even though I can override the controls I set (my kids can’t), it serves as an important reminder for when I am engaged with my phone. This awareness has noticeably reduced my phone use.
While I can’t say that my kids are happy, they too have adjusted. There are no more fights about shutting down at night, they understand the limits and are learning to manage them better and request more time if they really need it.
Hopefully, with less practice at distraction, we will all become worse at it.
Should you need more evidence for why you should use your phone less, watch this incredibly powerful video titled “Look Up.”
Quote of The Week
Daniel Goleman, author of Focus: The Hidden Driver of Excellence
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In a paper published today in the journal Nature, the ALPHA collaboration reports that it has literally taken antimatter to a new level. The researchers have observed the Lyman-alpha electronic transition in the antihydrogen atom, the antimatter counterpart of hydrogen, for the first time. The finding comes hot on the heels of recent measurements by the collaboration of another electronic transition, and demonstrates that ALPHA is quickly and steadily paving the way for precision experiments that could uncover as yet unseen differences between the behaviour of matter and antimatter.
The Lyman-alpha (or 1S-2P) transition is one of several in the Lyman series of electronic transitions that were discovered in atomic hydrogen just over a century ago by physicist Theodore Lyman. The transition occurs when an electron jumps from the lowest-energy (1S) level to a higher-energy (2P) level and then falls back to the 1S level by emitting a photon at a wavelength of 121.6 nanometres.
It is a special transition. In astronomy, it allows researchers to probe the state of the medium that lies between galaxies and test models of the cosmos. In antimatter studies, it could enable precision measurements of how antihydrogen responds to light and gravity. Finding any slight difference between the behaviour of antimatter and matter would rock the foundations of the Standard Model of particle physics and perhaps cast light on why the universe is made up almost entirely of matter, even though equal amounts of antimatter should have been produced in the Big Bang.
The ALPHA team makes antihydrogen atoms by taking antiprotons from CERN’s Antiproton Decelerator (AD) and binding them with positrons from a sodium-22 source. It then confines the resulting antihydrogen atoms in a magnetic trap, which prevents them from coming into contact with matter and annihilating. Laser light is then shone onto the trapped atoms to measure their spectral response. The measurement involves using a range of laser frequencies and counting the number of atoms that drop out of the trap as a result of interactions between the laser and the trapped atoms.
The ALPHA collaboration has previously employed this technique to measure the so-called 1S-2S transition. Using the same approach and a series of laser wavelengths around 121.6 nanometres, ALPHA has now detected the Lyman-alpha transition in antihydrogen and measured its frequency with a precision of a few parts in a hundred million, obtaining good agreement with the equivalent transition in hydrogen.
This precision is not as high as that achieved in hydrogen, but the finding represents a pivotal technological step towards using the Lyman-alpha transition to chill large samples of antihydrogen using a technique known as laser cooling. Such samples would allow researchers to bring the precision of this and other measurements of antihydrogen to a level at which any differences between the behaviour of antihydrogen and hydrogen might emerge.
“We are really excited about this result,” says Jeffrey Hangst, spokesperson for the ALPHA experiment. “The Lyman-alpha transition is notoriously difficult to probe – even in ‘normal’ hydrogen. But by exploiting our ability to trap and hold large numbers of antihydrogen atoms for several hours, and using a pulsed source of Lyman-alpha laser light, we were able to observe this transition. Next up is laser cooling, which will be a game-changer for precision spectroscopy and gravitational measurements.”