If you are not by this time on a fitness kick, you’re being foolish.
Why? One hyphenated word: COVID-19.
Study after study after study is pointing to cardiometabolic fitness as your best, long-term defense against the disease caused by the SARS-CoV-2 virus.
Not to mention the protection against a host of other diseases aided by fitness.
Yes, any of the various COVID-19 vaccines now widely available offer short-term protection against SARS-CoV-2. But at the rate the virus continues to evolve, none of them can be counted on to offer much in the way of a long-term guarantee.
Israeli researchers posting on MedRxiv, a preprint website for scientific studies yet to be peer-reviewed, on Friday reported early evidence that a SARS-Co-V2 variant originating in South Africa can break through the Pfizer-BioNTech vaccine.
SARS-CoV-2 is increasingly looking like influenza, and the success with annually recooked flu vaccines has been highly variable.
The average over the past 11 flu seasons is 43 percent.
Meanwhile, there is a similarity between the flu and COVID-19 that cannot be ignored:
“Hospitalization and death (for flu) occur mainly among high-risk groups,” according to the World Health Organization (WHO), and this is only proving more true of COVID-19.
“High-risk groups” are those already struggling with chronic health problems, including obesity, before they get “sick.” Because of their pre-existing conditions, their cardiometabolic fitness suffers.
The latest data on the extent to which boosting cardiometabolic fitness can protect you against COVID-19 comes from a study of more than 9,000 people with medical records on file in the United Kingdom’s Biobank.
After studying that data, a team of researchers from the University of Maryland School of Medicine suggested exercise-link blood levels of high-density lipoprotein cholesterol (HDL-C) could be useful in judging the threat COVID-19 poses on an individual basis.
The peer-reviewed study published at PLOS One at the start of the month concluded “that baseline HDL-C level may be useful for stratifying SARS-CoV-2 infection risk and corroborates the emerging picture that HDL-C may confer protection against sepsis in general and SARS-CoV-2 in particular.”
HDL-C is what has come to be called “good cholesterol.” Blood level increases in HDL-C have been directly linked to exercise.
Fat or thin, male or female, diet-conscious or not, “results show that 24 weeks of endurance exercise training induced favorable changes in plasma lipoprotein and lipid profiles,” researchers reported in a peer-reviewed study in the journal Metabolism more than a decade ago.
Research since has only underlined that conclusion. A 2020 meta-analysis of 23 studies on the subject reported that “all the analyses found an improvement in HDL-C levels…in comparison with the control group (no exercise).”
But this has been pretty obvious for a long time. A study of the eight members of the Steger International Polar Expedition was conducted 35 years ago when they decided to launch an unsupported march to the North Pole.
“Unsupported” meant they had to haul enough supplies for themselves and the 42 dogs who would help them get there. The supply issue pretty much forced them to rely on a diet high in fat for both themselves and the dogs – fat being the most calorie-packed of nutrients.
There are approximately 1,800 calories in a pound of sugar. There are about 90 percent more – 3437 calories – in a pound of butter.
That practical reality drove the expedition’s diet toward fat, and Steger – a world-class marketer – saw a financial opportunity.
With research comes research funding, and in the 1980s, the never-ending dietary arguments in the U.S. might have been near their peak of “fat is bad; carbohydrates are good.”
The high-fat diet of the Steger expedition was expected to cause an unhealthy boost in the cholesterol levels of team members. But their overall cholesterol numbers didn’t change much at all.
What did change, and significantly, was the ratio of HDL-C to HDL-L, the bad cholesterol linked to heart disease.
“Before they went to the North Pole, for example, Steger and his team-mates underwent blood fat studies in the expectation that the rations they took with them – including a lot of fat-rich foods like butter, peanut butter and pemmican (beef jerky and suet) – would cause harmful low-density lipid cholesterol (HDL-L) levels in their blood to rise significantly,” the Washington Post reported two years later in the wake of the expedition’s success. “Yet when, within a week of their return from the expedition, they were retested, it was found that this had not occurred.
“Apparently, Steger and (Paul) Schurke report in their book, it had been forestalled by the physical exertion demanded by the harsh polar environment and it was, instead, their blood levels of protective high-density lipoprotein cholesterol (HDL-C) that had climbed.”
Eight people, it must be noted, is a tiny sample size for any study, making the Steger study pretty much worthless for drawing broad conclusions. And the study members were burning an estimated 7,000 calories per day to keep moving and stay alive. Few burn that many calories.
But better studies in the years since have documented the benefits of exercise in increasing HDL-C along with generally enhancing the ability of the human immune system to fight disease.
The health benefits of exercise are now so well recognized that the debate in recent times has shifted to what kind of exercise best achieves those benefits.
Or maybe, Americans being Americans, the debate is more about which exercise makes it “easier” to achieve those benefits. The extremes here generally seem to be defined by long, slow exercise and short, intense exercise.
And which is best might well be individual specific as is indicated by a long-running debate among physiologists about people who don’t appear to respond to exercise; they exercise, but their fitness scores don’t improve.
A pair of Swiss researchers jumped into that debate in a big way in 2017 with a peer-reviewed paper they titled “Refuting the myth of non-response to exercise training: ‘non-responders’ do respond to higher dose of training.”
In that study published in the Journal of Physiology, David Montero and Carsten Lundby from the University of Zurich presented evidence that the “non-response to exercise training is abolished by increasing the dose of exercise.”
Their study, they noted, was driven by earlier conclusions that “one in five adults following physical activity guidelines are reported to not demonstrate any improvement in cardiorespiratory fitness.”
To find out whether that was true, they took 78 “healthy adults,” divided them into five groups and started them on identical exercise programs of 60 minutes per day for one to five days per week for six weeks.
At the end of that time, they reported, they did find some non-responders, who then “completed a successive six-week, endurance-training (ET) period including two additional exercise sessions per week.
“After the second ET period, non-response was eliminated in all individuals.”
How this dovetails with exercise-related changes in immunity has not been well studied, but immunity, in general, has been shown to rise with aerobic fitness.
“Moderate exercise training causes favorable perturbations in immunity and a reduction in incidence of upper-respiratory illness,” a peer-reviewed study in the American Journal of Lifestyle Medicine noted a decade ago. “During each bout of moderate exercise, an enhanced recirculation of immunoglobulins, neutrophils, and natural killer cells occurs that persists for up to three hours postexercise.”
The study reported that this immunity boost subsided after three hours, but added that a cumulative effect followed:
“As moderate exercise continues on a near-daily basis for 12 to 15 weeks, the number of symptom days with upper respiratory illness (URI) is decreased 25 percent to 50 percent compared with randomized sedentary controls. Epidemiological and animal studies support this inverse relationship between URI risk and increased physical activity. Recent evidence indicates that maintaining leanness and a physically active lifestyle during adulthood reduces systemic inflammation, an underlying factor in multiple chronic diseases.”
Few paid attention, and now many are dying from COVID-linked respiratory illnesses.
Fitness is not, of course, a guarantee you won’t catch COVID-19, maybe even die from it. There are no guarantees in life.
Outliers are a norm that shows up in all research. Every year, there are a reported 20,000 to 40,000 cases of lung cancer reported among non-smokers, according to the CDC. Exposure to radon or secondhand smoke is thought to contribute to about a quarter of those cases, but that still leaves a lot of people who suffer lung cancer primarily because they are genetically predisposed or just plain unlucky.
You could be as fit as the healthiest Alaska sled dog and still catch COVID-19. The only absolute way to avoid all risk is to avoid all fellow humans and domestic mink (and maybe cats and dogs exposed to humans), and most people just can’t do this.
And if you think all those masks are going to protect you, think again. The world is now full of people who wore their masks, traveled among the masked, and still caught the disease.
But what is crystal clear in the COVID-19 data to date is that very few wholly healthy people are dying. Estimates on the dead without so-called co-morbidities range from less than 10 percent to about 30 percent.
An examination of U.S. health care records conducted by FAIR Health in cooperation with West Health Institute and Dr.
Marty Makary from Johns Hopkins University School of Medicine reported in November that 16.71 percent of the patient who died of COVID-19 lacked pre-existing health problems.
“About half (51.71 percent) of all patients who were diagnosed with COVID-19 had a preexisting comorbidity. The remainder (48.29 percent) did not” that analysis found. “But although the two groups were roughly evenly divided among patients diagnosed with COVID-19, their division was very different among COVID-19 patients who died. Of deceased COVID-19 patients, 83.29 percent had a preexisting comorbidity.”
More than half of the dead who lacked comorbidities were also over age 70. The frailty that comes with age among those who lack for exercise was not considered to be a comorbidity in the FAIR Health study.
None of this is surprising. It is a fundamental of ecology that death overwhelmingly claims the young, the old and the weak. SARS-CoV-2 is an exception to the rule only in that it has claimed few of the young.
Whether that changes as the disease evolves over time remains to be seen. A trio of authorities on infectious pathogens who offered a SARS-CoV-2 forecast of sorts on the website of Science in early February predicted that such infections are to be expected in future years.
“One year after its emergence, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has become so widespread that there is little hope of elimination,” they wrote. “There are, however, several other human coronaviruses that are endemic and cause multiple reinfections that engender sufficient immunity to protect against severe adult disease.”
Their modeling, they wrote, “that once the endemic phase is reached and primary exposure is in childhood, SARS-CoV-2 may be no more virulent than the common cold.”
“Our analysis of immunological and epidemiological data on endemic human coronaviruses (HCoVs),” the added, “shows that infection-blocking immunity wanes rapidly but that disease-reducing immunity is long-lived.”
That long-lived immunity is built on a foundation of basic natural immunity coupled to the immune system’s ability to recognize and suppress a pathogen.
SARS-CoV-2 has proven so deadly for two reasons, the first being that it’s new and the immune systems of many fail to recognize it. The secondary problem has been that large numbers of people now have weakened immune systems unable to rally to combat the virus.
A peer-reviewed study published in The Lancet on Friday cited the “important defects in immune cells” as one of the reasons obese people appear more than twice as likely to be hospitalized with COVID-19.
“This increased risk of severe disease is linked to higher rates of metabolic and cardiovascular complications,” they wrote. “Another major contributing factor is the presence of substantial immune dysregulation and chronic systemic inflammation.”
Exercise helps strengthen and stabilize the immune system, and reduce inflammation as biomedical engineers at Duke University demonstrated with what is described as “lab-grown, engineered human muscle.”
“When exercising, the muscle cells themselves were directly opposing the pro-inflammatory signal induced by interferon gamma, which we did not expect to happen,” researcher Nenad Bursac, a professor of biomedical engineering at Duke, told a school publication.
It is a little ironic that humans have intellectually evolved to the point where we can now grow human muscle in a test tube while physically devolving to the point where a newly spawned pathogen that focuses mainly on the comorbid has of this date killed almost 3 million around the world.