A Hard, Grinding Workout For Optimal Health?
If HIIT training isn't your thing, no need to worry. Scaling down the intensity to provide something more sustainable might be right up your alley
I wanted to bring to light two separate but very connected subjects: zone 2 training and metabolic syndrome. We live in a world today where the statistics of obesity are at record highs. As we look around, fast food restaurants are increasing in number as well as people's sedentary time. For many who are reading this and have followed the Daily Greens, I’m hopeful that your fast food trips are somewhat infrequent and your sedentary time is minimal. Regardless, the nation's healthcare is taking on some serious water with the increase in chronic health conditions.
Before we dive in, I’d like to define some terms relevant and dispersed throughout the reading today:
Fat Oxidation: The way fat is liberated from adipose tissue is the first step in the process of turning stored lipids into energy sources. Fats are digested and converted into free fatty acids, which are then stored in the adipose tissue as triglycerides. The release of triglycerides from adipose tissue is triggered by a variety of hormones. These triglycerides are broken down into two components: glycerol (which is processed by the liver for further use) and fatty acids, in a process known as lipolysis (fat breakdown), which are released into the bloodstream. The fatty acids are delivered to the mitochondria, which are the parts of the cell that make energy. The enzyme carnitine, which can be found in foods like red meat and chicken, aids in the transfer of fatty acids to the mitochondria. The mitochondria also serve as a repository for deoxyribonucleic acid (DNA) and the enzymes required for cellular formation. Fatty acids are metabolized in the mitochondria, which produces adenosine triphosphate (ATP), the energy-producing fuel for human existence.
Metabolic Syndrome: Insulin resistance, dyslipidemia, high fasting blood glucose levels, and elevated blood pressure are all metabolic disorders that can accompany abdominal obesity and are linked to an increased risk of cardiovascular disease.
Zone 2 Training: An intensity of exercise classically categorized by % of max heart rate that involves the simultaneous use of carbohydrates and fat. It starts at the (bottom end) with fatty acid oxidation being the highest value possible while also being the primary fuel source, and ends at the (top end) with carbohydrate consumption crossing over and becoming the primary fuel source. *Popular fitness wearables will default to give you an average based on demographic norms. Your personal zone 2 will no doubt be close, but slightly different.
Mitochondrial Respiration: Mitochondrial respiration is a collection of oxygen-dependent metabolic activities and processes that occur in mitochondria (the cell's powerhouse) to transform the energy stored in the food we eat and store it as adenosine triphosphate (ATP), the cell's and body's primary energy source.
Maximum Aerobic Capacity: The highest amount of physiological work that an individual can expend, measured by oxygen consumption in Vo2Max.
Fatmax: Exercise at an intensity that brings about a maximal amount of fat oxidation.
Free Fatty Acids: One of the byproducts of the food digestion process is free fatty acids. The term "free" refers to the fact that these acids can go through the bloodstream without the help of any additional carriers. Fat digestion leads to hydrolysis, which produces a number of different fatty acids in the body, each with its own distinct function.
The Crossover Point: The point in exercise where the utilization of carbohydrates takes over as the dominant substrate over fatty acids.
Lipolysis: The breakdown of fats in our systems with the help of enzymes and water. Our adipose tissue stores, which are the fatty tissues that cushion and line our bodies and organs, undergo lipolysis.
White Adipose Tissue (WAT): White adipose tissue, or white fat, is one of the two types of adipose tissue found in mammals. The other kind is brown adipose tissue. It can be either visceral or subcutaneous in the body. A large factor in thermal regulation
To set the context for our discussion, back in 2000-2002, various research groups (1-3) put forth recommendations to categorize exercise based on the substrate (what fuels the activity) used as a source of energy by muscle. Carbohydrates and lipids (fat) are the two main fuels oxidized by the working muscle (4,5), and lipid oxidation reaches a maximum (FATmax) at a highly variable level between 40-50% of maximal aerobic capacity, but could also be much lower of capacity as well. The percentage of energy provided by carbohydrate oxidation grows above this point, and it becomes the primary fuel. The crossover point is what we term it in physiology and how I refer to it in the Cardinal Metabolic & Performance Ramp-exercise testing procedure. What many academics and practitioners still fail to acknowledge is the fact that oxygen is ALWAYS a part of the equation in energy transfer within the body during exercise.
However, the majority of exercise studies over the next 20 years almost always referred to a percentage of maximal aerobic capacity (%Vo2Max) rather than lipid or carbohydrate (CHO) oxidation because this new approach to exercise training through the academic field directed towards those who are overweight or obese (and other metabolic diseases) did not reach a large audience (6,7). However, there has recently been a surge of interest in the concept of undertaking exercise training at this FATmax intensity level (8,9). Well conducted meta-analyses like Chávez-Guevara and colleagues published, have verified this approach's weight-loss benefit. Furthermore, this weight-loss effect was shown to be remarkably long-lasting, lasting several years and resulting in a slow, steady reduction of fat mass (11,12).
The graph above, courtesy of Brooks & colleagues, summarizes the crossover idea, which was introduced to describe the shift in substrate balance that occurs roughly at 40-50% of peak aerobic capacity. The incremental step or ramp test was developed more thoroughly as a result of this experiment and theory. In this type of protocol, you can see gas and substrate exchange at various times throughout the evaluation by having individuals perform at a defined intensity and speed in the chosen modality. This information is then analyzed, and recommendations for current training status and future training recommendations can be made to help an athlete or individual accomplish their intended goal. The graph appears to be at odds with the previously described literature regarding FATmax, which said that it was established at around 40–50% of one's maximum intensity. As you can see in the diagram above, this example shows the FATmax at around 20%, which, as you'll come to realize, isn't unusual. Individual physiological measures don't always fit neatly into a box and can be altered by factors such as training status, intensity, duration, sex variations, and diet when we look at people individually. When Zone 2 training is implemented or discussed, it’s technically categorized as the area in the exercise test where you reach this FATmax value (indicating-bottom end of zone 2) to the point where the “crossover” happens (top end of zone 2).
Benefits of Zone 2 Training
Before focusing more specifically on training for improved lipid oxidation training, it's important to remember that exercise of all types is widely acknowledged as an effective tool for preventing the onset of type 2 diabetes (14,15), improving blood glucose control (16,17), and preventing weight regain in obese people who have already been dieting (18). Exercise is excellent for cardiovascular health, regardless of its impact on body weight, because it lowers blood pressure, blood lipids, inflammation, blood viscosity, mood, and cognitive performance (19). Even just walking (> 150 minutes per week) has been proven to improve blood pressure and plasma insulin levels, as well as changes in muscle proteins that govern mitochondrial biogenesis and metabolism (20).
This idea of losing lean muscle mass as a result of extended, continuous cardio/endurance training is something I’ve mentioned in prior blog posts. Do you notice many bodybuilders running marathons? I realize my thinking is a little reductionist, but I believe the point still comes through. Although resistance training is the most widely acknowledged method of increasing lean mass and fat free mass (21,22), there is some evidence that low-intensity exercise (e.g., a 45-minute walk on a treadmill at 40% Vo2Max) maintains lean mass and prevents muscle protein degradation (23). Because of the low-impact nature of this sort of exercise, it's an effective strategy to maintain or possibly even improve fat-free mass while also growing the bulk of metabolically active muscle. For this reason, I feel this is where zone 2 training really has its benefit- the sedentary community or those new to any exercise regimen.
The most important takeaway from this section about the benefits of low-intensity (Zone 2) training targeted at this FATmax area is that it has significant impacts on whole-body lipid oxidation and mitochondrial respiration, which have been shown in other studies as well (24,25). When the root of the problem, mitochondrial dysfunction, is addressed, all of the other biomarkers mentioned above can begin to normalize in value, assisting in the treatment and alleviation of other physical and even mental disorders.
Lipid (fat) Oxidation vs. Burning Body Fat
This term "FAT Burning" is wildly flung around and asserted, whether it's a conscious marketing ploy or simply taking advantage of the wording (albeit not technically incorrect). I'm hoping to clear some things up in this area. Returning to our earlier definitions, long-term regular exercise can increase fat oxidation at rest, changing the balance of substrate use throughout a 24-hour period toward lipids (26). This is an important topic since a 24-hour increase in the ability to oxidize lipids is a statistically significant predictor of exercise-induced weight loss (27). As a result, exercise programs aimed at improving 24-hour lipid oxidation are likely to be beneficial in the treatment of obesity. According to another study (28), the increase in 24-hour fat oxidation was likely produced by a higher rise in plasma-free fatty acid content and the unsaturated/saturated fat ratio when compared to what occurs when exercise is undertaken postprandial (after a meal). The decrease in glucose after exercise was linked to an increase in plasma-free fatty acids (28). To give an example of a popular supplement, decaffeinated green tea extract with the addition of other compounds [(i.e. quercetin,-lipoic acid (LA), curcumin]] has been reported to significantly increase (+45%) FATmax and shift the point 22.5% further into the exercise test where lipids are no longer oxidized and the individuals were using near 100% carbohydrates (29). Sounds impressive!
So, lipid/fat oxidation vs the “burning” of body fat. As we’ve read so far, the amount and duration of intensity that we can continue to utilize fatty acids as fuel at a high rate compared to carbohydrates can be very beneficial for overall metabolic health. But we’re not burning body fat? Not EXACTLY… An editorial that was published last year (30), I feel, explains this complex topic fairly well regarding its mechanisms of action. Solely restricting the intake of calories alone, however, can result in similar amounts of both fat mass AND lean mass (31,32). Therefore, for people who have a significant amount of weight to lose should focus on reducing body fat rather than body mass. An important thing to remember as people will only look at the scale and assessing change based solely on your number. In fact, being over-fat even when not technically overweight or obese on the BMI scale is more strongly correlated to disease risk than being overweight and lean (33). Research has shown time and time again that a combination approach with caloric restriction grouped with appropriate exercise programming can reduce the fat composition of the body while limiting the loss of lean mass (34,32), although some lean mass will inevitably be lost regardless.
Hang with me here: (35)
Fatty acids (FA) become the predominant source of energy for muscular contraction when exercise is performed at a moderate intensity and for a prolonged period of time.
FA oxidation in muscle depends on the FA supply from multiple sources:
FA is released when triacylglycerols (TG) stored in white adipose tissue (WAT) are broken down by lipolysis.
From very low-density lipoproteins-TG (VLDL-TG) in circulation
From intra-myocellular triacylglycerides
and potentially stored triglycerides within inter/intramuscular adipose tissue.
There are two main groups of fat in the abdominal WAT: subcutaneous WAT (SCAT) on one side and visceral WAT on the other. Exercise mostly turns on lipolysis in the SCAT since only 5–10% of circulating long-chain FA is released from visceral adipose tissue in lean subjects (36). (). White adipose tissue lipolysis also goes up when the intensity is low to moderate and down when the intensity is high (4). Lastly, and this is probably the most important thing to remember, FATmax is a rate of FA oxidation, but the total amount of FA used (or burned) during the day depends on your personal energy expenditure (35)... Your total daily caloric intake.
Zone 2 & Metabolic Syndrome: Tying It Together
Researchers who looked at muscle biopsies found that measurements of lipid and CHO oxidation during exercise are related to the efficiency of mitochondrial function. This was first seen in diabetics (24). Metabolic flexibility is the ability of the mitochondria to switch fuel sources efficiently in response to changing physiological conditions (37). This allows fuel oxidation to adapt to the availability of fuel. Insulin resistance and type 2 diabetes are highlighted in metabolic in-flexibility (38). Changes in how much fat you eat, how active you are, and how much weight you lose may help to fix metabolic stiffness in skeletal muscle and help prevent type 2 diabetes (39). Recently, since metabolic inflexibility in the metabolic syndrome is marked by a decreased ability to oxidize lipids and an early switch from fat to carbohydrate oxidation along with an increase in blood lactate concentration as the intensity of exercise increases, San-Millán and Brooks recently suggested to measure lipid oxidation and blood lactate kinetics during exercise to measure metabolic flexibility.