U.S. government guidelines on exercise are clearly heavily influenced by the notion of “exercise” as a ubiquitously nebulous concept in the collective consciousness of the general public.  On the plus side of this equation, certainly it is true that any amount of exercise, even a paltry 30 minutes 6-7 days a week is better than no exercise at all.  On the negative side, I do not feel that government recommendations go far enough in detailing an actionable definition of what constitutes sufficient frequency, duration and intensity most likely to offer tangible health benefits for the average person.  The terms “exercise” or “moderate physical activity”, as defined by ACSM (American College of Sports Medicine) and government semantics, is at best a useless generalization that is open to broad interpretation by individuals, similar to my Number One pet peeve in nutritional nomenclature: “healthy diet“.

Case in point.  If a person interprets “30 minutes of moderate physical activity” as sluggishly ambling around on a golf course with a caddy in tow or, even worse, driving in a golf cart around the same course, such physical activity is only marginally superior to laying on a sofa vegging out in front of a television with a beer and bag of potato chips in hand.  Studies specifically show that in order to have any significant impact on chronic disease risk factors (e.g. diabetes, obesity, cardiovascular disease, etc.), exercise must raise the heart rate to at least 65-70% of maximum for at least 30 minutes a day a minimum of 5 days/week, a nuance which is tragically missing in FDA guidelines.  Certainly, a person walking on a golf course or around their block at 2 mph is at least burning a few calories, but they are not doing much to benefit their cardiovascular system or to reverse Metabolic Syndrome and insulin resistance that is endemic in sedentary individuals and those not availing themselves of aerobic heart rate zones during exercise, as I previously delineated.

Another crucial consideration in all this is a phenomenon that has only recently come to the forefront of discussion in the halls of academia, a condition informally known as ACPS, i.e. “Active Couch Potato Syndrome“, namely the quandary of a person who exercises diligently 30-60 minutes/day (in many cases, intense exercise), yet spends the remaining 23 hours of their day either sitting on their tush in front of a TV or computer screen, behind the wheel of a car stuck in traffic, or laying in bed sleeping 6-8 hours every night (the only truly requisite down time).  It has been proposed by researchers that no amount of relatively brief daily exercise, 60 minutes or less at any intensity, can fully overcome the detrimental consequences of ACPS.  So don’t think that just because you crushed it in the gym in the morning, that gives you free license to sit around the rest of the day or to eat whatever you want because you’ve “earned it”, but the topic of post-exercise dietary over-indulgences is a huge subject matter on its own, best reserved for a future blog post.  In the meantime, just keep moving, keep walking, keep lifting heavy things, play outdoors with your children, go up the stairs instead of taking the elevator, and NEVER EVER battle for the parking spot closest to the front entrance of your gym (I have seen this with my own two eyes)!



This is indeed a loaded topic.  Before I begin to discuss the science of exercise as a vehicle for “weight loss”, I feel compelled to inject an anecdotally-based observation from my own personal experiences with diet and fat loss, as documented in a bestselling book on evolutionary biology as a foundation for optimizing human health, “The Primal Blueprint” by Mark Sisson, published in 2011.  Here is a link to the digital version of my story:  Both my anecdotal and professional experiences working with clients and patients as a Personal Trainer and Clinical Nutritionist for 10+ years have highlighted the true biochemistry of fat loss, later confirmed by my college studies.  I have repeatedly explained to my clients that “you cannot exercise your way out of a bad diet” and that “80% of weight loss is to be found in the kitchen, not the gym. Granted, you have to have both components in place to achieve meaningful sustained fat loss, and by this I mean loss of body fat, not “weight loss” per say, which could consist from one day to the next of anything from water weight, depletion of intramuscular glycogen stores, or even muscle wasting caused by extreme caloric deficits.  When the number on the scale nudges downward, it is not automatically a cause for celebration because one cannot know for certain how much of that weight decrement is actual loss of body fat.  That said, the impact of exercise on decreasing the size of adipocytes (fat cells) is beyond doubt, but I see this mechanistically as more of a hormonal equation than a caloric one. You can be in a caloric deficit just be eating less and exercising more, but if the macronutrient composition and glycemic load of a diet does not induce lowered insulin and elevated glucagon levels that act upon HSL (hormone sensitive lipase) to cleave triglycerides from adipocytes, the opportunity for lean mass catabolism substituting for a healthy reduction of fat mass is always a danger.  Fat loss is a thorny proposition indeed!

It would behoove us to factor in that the majority of body fat that is burned during even an optimally effective exercise session is in fact derived predominantly from intramuscular fat stores (the marbling we see in a fatty cut of steak), not circulating plasma FFA (Free Fatty Acids) from intra-abdominal or subcutaneous fat stores, i.e. the fat on our bodies that is visible to the naked eye when we walk on a beach in our bathing suits.  Visceral or intra-abdominal fat in particular (the fat around our internal organs, such as our liver) is known to contribute to pathological insulin resistance manifesting as Type II diabetes and the various permutations of a condition known as Metabolic Syndrome, i.e. elevated blood sugar and blood pressure, increased triglycerides and heart disease risk.  An individual who is dieting and exercising to lose weight could get a DEXA (Dual-energy X-ray Absorptiometry) scan done a few weeks after commencing an exercise-based weight loss regimen and they would find that the vast majority of reduction in their body fat stores was in fact attributable to the aforementioned intramuscular fat, not subcutaneous fat, following extensive bouts of aerobic exercise, or even resistance training for that matter, which can certainly elicit frustration in diligent dieters because the change that they see in the mirror is skinnier looking arms and legs due to loss of intramuscular fat while still carrying a significant amount of fat around their abdomen and/or hips (the “pear-shaped” hypothesis), as well as retaining substantial visceral fat stores, e.g. NAFLD (Non-Alcoholic Fatty Liver Disease), which is further exacerbated by standard low-fat high-glycemic weight loss diets.  This is primarily why I am irritated by the meaningless term “weight loss”.  Weight loss consisting of what?  Apparently, many people do not care what their weight loss is comprised of, just as long as the scale shows a lower number than the day before.  On the other hand, physically active people who have dialed in their hormonal health, stress reduction, sleep hygiene, and consume a diet that consists of a high proportion of healthy fats, adequate protein intake, and very low consumption of refined sugars tend to burn more subcutaneous fat while they are asleep, yes, I said asleep, and they wake up in the morning with slightly lower subcutaneous fat than when they went to bed the night before.  Shocking but true!

It is even possible for someone, such as a hard-charging athlete, to lose 5 pounds of subcutaneous and intra-abdominal fat while gaining 5 pounds of muscle, hence they achieve no “weight loss” on the scale, yet look and feel better and have improved health outcomes.  As with all aspects of human physiology, the proverbial “devil is in the details”.  So make sure to be extremely wary of anything that identifies itself as a “weight loss” program.  Oversimplifications are just pure marketing hype directed at emptying the pockets of unsuspecting consumers.  Don’t go to the gym to “lose weight”.  Go there to get stronger and fitter, to improve your flexibility and functional strength, to increase your bone density, to repair your hormones and improve your mood, and you should be skeptical of any Personal Trainer who tells you that they will help you “lose weight” or any book with a tagline such as “Lose 30 pounds in 30 days”.  If you want to lose actual body fat, and do so safely, go home and clean out your pantry and refrigerator.  Get rid of anything containing added sugar, anything that promotes inflammation in the body (such as vegetable oils and margarine), anything that spikes your blood sugar and leaves you feeling drained two hours later.  Then you will finally start to fit into your skinny jeans and recapture your health and vitality, as I myself did 8 years ago, when I switched careers from obese software engineer to health coach and nutritionist.

The physique of the amazing young woman in the picture below is 50% genetics, 40% nutrition, and 10% exercise, but that 10% is just as important as the other 90% of the equation, because when it comes to looking and feeling your best, anything less than 100% amounts to 0%.  We cannot choose our parents (genes), but we can choose what we put into our mouths and how we live our lives!



Get healthy for the sake of getting healthy and you will lose weight as a side effect.  That is the primary message of my blog post today.  Exercise viewed merely as a vehicle for weight loss is a flawed premise.  As the new year is still very young and brimming with resolutions for many people, my initial posts of 2018 will be focused on dispelling the myths underlying common New Years’ resolutions associated with health.  In that spirit, I’m going to talk about exercise and its numerous benefits that do not directly pertain to weight loss.

Let’s start by reverse-engineering exercise as a component in heart health and the etiology of cardiac impairments, since how we look standing naked in front of a mirror is rendered quite irrelevant if we can’t keep our ticker ticking!  A sedentary lifestyle is one of the 5 major cardiac risk factors, along with high blood pressure, abnormal values for blood lipids, smoking, and obesity.  Evidence from numerous clinical and epidemiological studies have clearly shown that reducing the abovementioned risk factors decreases one’s chance of a heart attack or experiencing other cardiac events, such as a stroke, and reduces the possibility of requiring an invasive coronary revascularization procedure, e.g. bypass surgery or coronary angioplasty.  Regular exercise has been found to have a favorable effect on many of the established risk factors for cardiovascular disease.  For example, exercise promotes weight reduction and can help lower blood pressure, lowering the strain on one’s heart.  Exercise can also reduce so-called “bad” cholesterol levels in the blood (LDL in general and VLDL specifically), as well as total cholesterol, although I would posit that reducing systemic inflammation, as identified via a blood marker known as HS-CRP, is an even greater cardiac benefit of exercise, especially aerobic exercise, and can also raise “good” cholesterol (HDL).

Although the isolated effect of an exercise program on reducing any specific risk factor may be relatively small, the cumulative effect of continued moderate exercise on overall cardiovascular disease risk, when combined with other lifestyle modifications such as proper nutrition, smoking cessation and moderating alcohol intake, can be dramatic indeed.  There also exist a number of corollary physiological benefits to regular exercise, e.g. improvements in muscular function and the strength of both muscle and bone, as well as a significant improvement in the body’s ability to take in and use oxygen (maximal oxygen consumption or aerobic capacity, aka VO2 max).  As one’s ability to transport and use oxygen improves, regular daily activities can be performed with less fatigue, improving overall quality of life, tangential to the reduction of cardiovascular disease risk.  This is particularly important for patients with known genetic risk factors and a family history of heart disease whose exercise capacity is markedly lower than that of healthy individuals.  There is also a wealth of clinical evidence that long-term exercise training improves the capacity of the blood vessels to dilate in response to vigorous physical activity, consistent with better vascular function and an increased ability to supply oxygen to working muscles.

Individuals with newly diagnosed heart disease who participate in an exercise program report an earlier return to work and improvements in other measures of quality of life, such as self-confidence, lowered stress, and less anxiety.  Most importantly, as confirmed by meta-analyses of controlled studies, researchers have found that for heart attack patients who participated in a formal exercise program, the death rate is reduced by a whopping 20% to 25%!  This is strong evidence in support of physical activity for patients with heart disease.  Although the clear benefits of exercise are unquestionable, it should also be noted as a caveat that exercise programs alone for patients with advanced heart disease, as an independent variable, have not convincingly shown improvement in the heart’s pumping ability or the diameter of the coronary vessels that supply oxygen to the heart muscle due to confounding variables such as the patient’s extent of atherosclerotic plaque accumulation and arterial blockage concomitant with the narrowing of arteries that deliver oxygenated blood throughout the body.  If the heart itself does not receive adequate amounts of oxygenated blood during exercise, that in itself can be a risk factor for heart attack, thus cardiac patients should check with their cardiologist first before engaging in vigorous aerobic exercise, which might involve a prudent physician-supervised exercise stress test prior to the commencement of a structured exercise program.


The myth of carb loading


Training for a marathon or triathlon?  Thinking of carbing up the night before?  Don’t!  Glycogen “super-compensation” is an outdated archaic myth, a vestigial artifact left over from the 1980’s.  Although it is true that glycogen depletion initiated by an exhaustive fasted aerobic workout of 90-120 minutes at or near anaerobic threshold will deplete approximately 90% of available muscle glycogen stores, doing so will also deplete an athlete’s adrenals and immune function, with little or no benefit on race day compared with simply just going into an event with glycogen stores topped off, achieved healthily via normal carbohydrate consumption just above energy needs in the 2-3 days leading up to competition.  As is, topping off glycogen stores is a risky endeavor for any endurance athlete wishing to optimize their body composition by minimizing their body fat.  Excess carbs consumed over the maximum amount that can be stored in the liver and muscles will upregulate lipogenesis, i.e. triglycerides stored as body fat.

It is also noteworthy that glycogen stores can never truly be “depleted”, as the body will never allow glycogen to get too low, preserving precious glucose for that most important organ of all, the brain.  An additional consideration is that the glycogen depletion that is needed to stimulate the so-called ‘super-compensation’ effect may also result in the catabolism of lean muscle mass in the athlete, which is yet another highly undesirable scenario impacting performance.  If you lose weight by losing muscle, you’re not going to go any faster, nor will you delay the dreaded “bonk” or “wall” that sends shivers through the spine of any endurance athlete!

Carb-loading also brings into question the critical issue of fuel partitioning.  A highly conditioned endurance athlete such as a distance runner or road cyclist should ideally be burning mostly fat stores as their body’s preferred fuel source for activities involving aerobic respiration.  As numerous studies have illuminated over the years, even a very lean athlete has somewhere between 50,000-100,000 calories available to burn as stored body fat, compared with a mere 1500-2000 calories stored as muscle glycogen.  In accordance with the “Central Governor Theory” of fatigue proposed by the brilliant Dr. Timothy Noakes a few years back, as long as your brain does not run low on glucose and/or ketones, there is absolutely no physiologically-justifiable need for excessive consumption of glucose during any endurance event lasting longer than 20 minutes, even when one occasionally dips into the glycolytic (sugar burning) realm, such as during sudden surges in a bike race or while drowning in lactic acid on intense hill climbs.

One final consideration that I always bring up to the athletes that I counsel is that aerobic training fueled with sugary gels and high-glycemic carbs generates a tremendous amount of Reactive Oxygen Species (ROS) that can prematurely age you and expose you to a higher danger of cancer cell proliferation, since cancer cells cannot fuel themselves on ketones, i.e. betahydroxybutyrate, nor free fatty acids.  Cancer cells thrive on glucose.  Virtually anyone can train like a world-class endurance athlete and achieve high levels of aerobic fitness relative to their genetic potential, but can they do so without aging themselves and creating a “cancer-friendly” environment in their body? Yes, they can.

So here’s the practical takeaway.  If you want to perform well in an endurance event, train smart, eat smart, avoid extreme low-carb diets, and train fasted at least 2-3 times/week to turn yourself into a fat-burning machine that will never run out of fuel!

Lack of motivation to exercise?

As a cyclist and former elite runner, my two favorite words in the English language are “mitochondrial biogenesis“.  My least favorite are “mitochondrial myopathy“, the thought of which fills me with horror, as well as great compassion for those afflicted with one of the rare diseases that fall into this category.  Mitochondria is energy.  Energy is life.  Matter without energy is a state of lifelessness.  Your mitochondria are the microscopic “steam engines” of your body.  Imagine an enormous cruise ship whose engine isn’t working.  It would sit in dry dock and never go anywhere.  The most common symptom of mitochondrial myopathy is exercise intolerance.  You can have a perfect nutrition plan, eat all the right foods in the right amounts, get enough calories and carbs, take nutritional supplements religiously, get enough sleep and rest, but if you have a breakdown in the electron transport chain and ATP production, you will be stuck in that “dry dock”.  In other words, the calories from foods that you consume will not be converted into energy.  Nobody wants to be stuck on a cruise ship that is permanently grounded, no matter how grand or magnificent it is!

Let’s expand this discussion of mitochondrial myopathy and exercise intolerance as it relates to exercise physiology specifically.  A genetic link in the etiology of mitochondrial myopathy has been identified by researchers as a mutation in the cytochrome b gene, which appears to be somatic, i.e. a spontaneous event that occurs in muscle and does not affect other types of cells.  The apparent restriction of these mutations to skeletal muscle is interesting but apparently not unique.  A similar restriction has been reported with other mutations of mtDNA that affect both tRNA and protein-coding genes.  It has been posited that this relatively rare syndrome has probably been under-diagnosed in the past, due to reports of exercise intolerance as quite common and highly subjective, not to mention problematic to document objectively.  Hence exercise intolerance is often dismissed as psychogenic in nature.  The finding of lactic acidosis in individuals with exercise intolerance should alert clinicians to the very real possibility of a legitimate cytochrome b gene mutation in an individual.  Confirmation of the diagnosis requires muscle biopsy to document a biochemical deficiency and identify the specific molecular defect.

As a whole, exercise intolerance is just as frustrating for clinicians, who frequently have trouble finding a satisfactory diagnosis, as it is for their patients.  Numerous studies have now identified cytochrome b gene mutations as a valid mitochondrial etiology underlying exercise intolerance, thus somatic mutations in this mitochondrial gene may be more common than previously believed and may need to be included in the differential diagnosis when patients present with often elusive symptoms such as aches, pain, cramps, and just plain lack of motivation to exercise.

As with most disease states, symptoms of mitochondrial myopathy may be extreme or subtle, but the reality of a mitochondrial defect represents a significant compromise in the quality of life for any person who is limited in their ability to lead a healthy physically active lifestyle.  Studies are currently under way to try and develop treatments and pharmacological interventions for those suffering with mitochondrial myopathy.  A nutraceutical “cheat” that I have been experimenting with in my own nutrition plan to support my training as a competitive cyclist is a compound known as “quercetin”, admittedly controversial and inconclusive at this point, but studies appear promising.  The current literature appears to support quercetin’s efficacy in promoting mitochondrial biogenesis, in regard to both skeletal muscle and other cellular energy pathways, such as the brain and heart.


There is also some intriguing evidence that other nutraceuticals related to mitochondrial biogenesis may be helpful for those of us wishing to optimize our mitochondria, even if we do not suffer from an acute mitochondrial myopathy.  These include nicotinamide riboside, creatine monohydrate, alpha-lipoic acid, Co-enzyme Q10, and polyphenols.  However, the jury’s still out on whether or not these compounds can promote mitochondrial biogenesis when taken in supra-physiological doses or whether it is simply a matter of an intracellular deficiency of those compounds that diminishes biogenesis and ATP production.  For example, we know that ribose is important to the Krebs cycle, but can we conclusively posit that supplementation with D-Ribose powder purchased at our local vitamin shop will definitely boost production of ATP via the electron transport chain?  That is unknown at this time.  For those of us on the fringe of cutting-edge nutrition science, it always comes down to the laboratory of our own body, the biohacker’s classic N = 1 experiment.  If you’re low on energy and unmotivated to exercise, talk to your doctor about getting tested for mitochondrial myopathy and try some of the nutraceutical hacks that I discussed in this article.  If you have tried something that works for you, please leave a comment on this blog.  I always welcome feedback from my followers!