Amoursibuna: Training for “The COVID-19”

training for COVID-19 Today we welcome guest author Dr. Ronesh Sinha, internal medicine physician and expert on insulin resistance and corporate wellness, author of The South Asian Health Solution. He is a top rated speaker for companies like Google, Oracle, Cisco and more. Check out his media page for lectures, interviews and articles from Dr. Sinha.

Most of us have been sheltering-in-place for a few months now, and we have evolved into an unprecedented state of fear and hyper-vigilance in this pandemic. After a long period of incarceration, we are now gradually released into the wild, which introduces us to a whole new level of anxiety. Public health recommendations appear to be flip-flopping regularly, and we are learning on the fly as the situation evolves.

In today’s post, I’d like to share some thoughts on how we can regain some control of our lives. Rather than duck and cover for several more months, we can face this beast head-on. I don’t mean being careless and reckless and not following social distancing and hygiene protocols. Instead, we can adopt a mindset that we will do what is necessary to minimize our risk of a severe COVID-19 outcome. I titled this post “Training for the COVID-19” to help you reframe this pandemic in your mind, and view it like a warrior approaches an enemy on the battlefield or an athlete faces an opponent in a competition.

Cognitive reframing isn’t just some touchy-feely behavioral technique. Viewing the world through a more positive lens has a beneficial impact on your immune system, which is potentially relevant to COVID-19. One study shows that participants who were cognitive reappraisers, identified by a 10-item Emotion Regulation Questionnaire, and then exposed to an experimental cold virus (rhinovirus not coronavirus) had reduced nasal cytokine release compared to individuals who were emotional suppressors.¹ As you’ll learn in a moment, excessive cytokine release is a crucial mechanism by which COVID-19 imparts significant lung and tissue damage. As with rhinovirus, the nose is a primary portal through which coronavirus accesses our body.

So as you read this post and continue to keep getting bombarded by pandemic news media, remember the lens through which you view this content. Your external world has a direct impact on how your immune system might respond to an infection like COVID-19. Let’s start by summarizing COVID-19’s basic operating system for you.

Fear of the unknown is one of the single most significant stressors to our nervous system. I want you to read this with the attitude that “I will acquire the knowledge I need to understand this virus and defend myself and my loved ones against its effects.” Rather than, “Oh my God, the extra fat around my waistline will be the death of me.”

One way I view our pandemic and its relationship to our individual health is by splitting it into external viral load vs. internal cytokine load. Refer to the image below.

The left side of the image shows how the COVID-19 virus enters a cell by gaining access through the ACE-2 receptor, which hijacks our cell’s reproductive machinery (think 3D printer). Then, it makes copies of itself. This is the external viral load.

The right side of the image illustrates our immune system response. NLRP3 is an alarm sensor in our cells that gets turned on when an infectious pathogen like COVID-19 knocks on the door of our cells, specifically by attaching to the ACE-2 receptor. Once the alarm sounds, a rush of immune system chemical messengers called cytokines comes rushing inside to thwart the attack. NLRP3 is a critical gatekeeper to the cytokine surge. If you want to learn more about how it works and how it’s connected to other common health conditions, watch my 4-minute explainer video here.

The volume of this cytokine response is what I refer to as the internal cytokine load. An optimal cytokine load would be sufficient to thwart an attack by an outside offender. Still, an overzealous cytokine response (aka “cytokine storm” or “fire”) would damage and destroy our cells through a process called pyroptosis, which is literally cellular death by fire.

I want to highlight that cytokines are not the enemy in this process and are an essential part of our innate immune response. It’s excessive cytokine release that inflicts damage and destruction. Fortunately, our cytokine response is something that we can control through targeted lifestyle changes. Just a reminder that these are the same cytokines I mentioned at the beginning of the post, which were released in excess amounts in the noses of emotional suppressors vs. cognitive reappraisers exposed to the cold virus. So what’s the link with obesity?

Obesity is so intimately tied to our risk of a severe COVID-19 outcome that I refer to this association with the term, “Covesity,” which I write about in detail here.² Specifically, it’s the central visceral fat (aka “belly fat”) that is an especially insidious storehouse of proinflammatory cytokines like IL-6 and TNF-alpha, which fuel the cytokine fire.

Another reason fat cells may increase risk is through the ACE-2 receptor shown in the above image. Fat cells have an abundance of these receptors, and their affinity for COVID-19 means they may serve as a viral storehouse. So fat cells not only provide more entry points for COVID-19 but also ready access to an ammunition supply of cytokines.

ACE-2 also puts the brakes on the enzyme angiotensin II, which, if left unrestrained, can contribute to the more severe manifestations of COVID-19 (like acute lung injury, heart damage, etc.). Angiotensin II levels appear to rise in severe COVID-19 infections due to a downregulation in ACE-2 (the “brake pedal” for Angiotensin II). In the case of obesity, angiotensin II increases further by visceral fat cells that secrete angiotensin II in addition to the cytokines we just discussed.

So fat cells provide the fuel to ignite the cytokine fire and release excess amounts of angiotensin II, which can further provoke damage and destruction of vital organs. We also know that obesity increases our risk of chronic health conditions like diabetes and high blood pressure, which are additional risk factors for a more severe COVID-19 infection.

Again, I don’t want this information to set you into a state of panic if you are struggling with extra weight or other COVID-19 health risks. I assure you that this is not a disease where the only people left standing at the end of the pandemic will have single-digit body fat percentages and 6-packs. Fit, lean individuals who are experiencing chronic stress and sleep issues might have a higher risk than slightly more substantial, less fit individuals who are physically active and better manage their sleep and stress. No matter where we are in our health journey, we need to identify our own gaps (physical, mental, social, etc.) and make key changes that will markedly reduce our cytokine load and overall risk.

One common question I get during lectures and in the clinic is, “how do I know if my fat is the inflammatory type?” This is an important distinction. Some of us might be above the recommended BMI (body mass index) cutoff, but not have as much inflammatory adipose tissue. In contrast, others might be underweight but have visceral fat cells packed with proinflammatory cytokines. This is why body weight and BMI can often be a misleading marker. Some clues that you might have more inflammatory adipose tissue are below. Just a reminder that NLRP3 is the alarm sensor that COVID-19 turns on and triggers the cytokine surge.

Increased belly fat: ethnic waistline cutoffs are here and to learn more about body fat and the impact of ethnicity, read my post here.
High triglycerides: aim for triglyceride levels to be closer to 100 mg/dL or below
Low HDL (healthy cholesterol): males should target an HDL>40 mg/dL and for females, HDL>50 mg/dL
High triglyceride/HDL ratio is even better than looking at individual triglyceride and HDL, aiming for a ratio of less than 3.0 (lower the better)
Elevated blood glucose (prediabetes, diabetes)
High blood pressure: More recent research is showing that hypertension may be an inflammatory condition and the NLRP3 inflammasome might be a key switch as discussed in this study.³
Fatty liver: Learn more by reading my post here. ⁴ This mouse study ⁵ is linked to NAFLD (non-alcoholic fatty liver disease) and blockade of this pathway leads to regression of fatty liver.
Elevated hsCRP: this is a test for inflammation that is not indicated in all patients and can give an elevated result for various reasons. Many of my patients with insulin resistance have elevated hs-CRP, and research ⁶ mentions the strong link between CRP and NLRP3, where NLRP3 appears to be predictive of elevated hs-CRP levels.

Some of you might recognize many of the items on this list as being criteria for a condition called metabolic syndrome, ⁷ whose root cause is insulin resistance. Many of us have become disconnected from our health care providers and systems as a result of shelter-in. I strongly encourage you to track the risk numbers applicable to you. For example, I’m putting a growing number of my at-risk patients on continuous glucose monitors (CGMs), especially given studies ⁸ showing a strong correlation between glucose control and COVID-19 severity. I wrote a detailed post on how to get your health care provider to order a CGM here.

I’m seeing many patients losing track of their waistlines since they’ve been living and working in stretchy pants for months. It might be time to dust off those jeans or work pants, so you regain some waistline awareness. Tracking your risk numbers and making appropriate lifestyle changes is a powerful way to regain control of your health.

Lifestyle Changes

So now that you understand COVID-19’s operating system and COVID-specific risk factors more logically and less emotionally, how do you specifically train for the COVID-19? First, we need to understand what type of event we are preparing for. Is this an event based on strength and power, or is it more of an endurance event?

We know major target sites for COVID are the lungs and heart. When you talk to patients that have had a moderate or severe outcome, they report feeling like being dragged underwater or dropped on top of a mountain and asked to run a marathon. There is a distinct sensation of what we call “air hunger,” and this is something we can actually train for without having to live at least 7,000 ft above sea level.

In other words, surviving and even thriving through COVID-19 likely depends on how fast you can walk or run a mile rather than how much you can squat, deadlift, or bench press. We can improve our tolerance to low oxygen (aka hypoxic) stress if we can improve our aerobic fitness through movement and exercise. Tying this back to cytokines and inflammation – hypoxic stress is a powerful trigger for inflammation. It is mediated by several different chemicals referred to as HIFs (Hypoxia-Inducible Factors) as reviewed in this study. ⁹ This makes sense given we can live around three weeks without food, three days without water, but only 3 minutes without air.

Any time our body senses a lack of oxygen, the resulting cytokine surge’s intensity and volume are significant. This is a medical code blue or a five-alarm fire signal to our immune system, and there’s a link to our body fat. This study ¹⁰ shows that hypoxic (low oxygen) stress specifically unlocks cytokines from fat cells. So, if you are carrying extra inches around the waist and are also aerobically deconditioned, then that’s a double whammy for fueling a cytokine storm.

Now that we understand the type of event we are preparing for, let’s turn to our training plan. I have three main principles for COVID-specific training, which I outline as the “ABCs.” “A” is for Activity, “B” is for Breathing and “C” is for cardio. Most of my patients might be doing one or two of these, but rarely is anyone doing all three. I strongly recommend that you do all three of these to improve your resilience to COVID-19.

For activity, I’m referring to regularly staying active throughout your day since interrupting prolonged sitting has been shown in numerous studies to increase the release of proinflammatory cytokines. You might know this already, but our COVID-19 environment takes on a whole new level of significance. Mark refers to these as “microworkouts”, which you can read about in his post here. I refer to it as exercise snacking (not my term). I am teaching my patients to stock their “exercise pantry” with at least 10 different movements they can perform throughout the day. I have 20+ different work positions and mini-exercises that I do while I’m on business calls or doing creative work.

Personalize your pantry to target problem areas. For example, I have struggled with tight hamstrings for many years, so I’m always working in positions like the one below, which has made a huge difference.

Ronesh Sinha MD

Now, after hours of work, when I decide to do something more intense, my legs are limber, warmed up, and ready to go. Work to me is a combination of a light interval workout with flexibility and warm-up drills that have my body prepped and ready to transition to something more intense at any given moment. My patients that do this are more energetic during work hours and less sore after workouts because they are already warmed up.