Okay, you've suffered through the particulars and are sufficiently MRT-educated. Let's get to the good stuff: three tried-and-true MRT strategies guaranteed to help strip away stubborn fat and heighten acid-buffering ability. You can stick with one strategy for a given timeframe or periodize strategies from one week to the next. Regardless of what you decide to do, it's best to insert an "unloading microcycle" (one week of light weight) every fourth week or so to avoid the potential for overtraining. During the unloading cycle, reduce the effort expended so you're not substantially challenging your muscles on the last few reps of each set (aim for about a 7 on an RPE scale of 1-10). As a general rule, limit metabolic training cycles to a maximum of about 8 weeks. Any longer and you risk compromising muscular gains.
In addition to the problems with an increase in insulin resistance, the release of insulin by the pancreas may also be defective and suboptimal. In fact, there is a known steady decline in beta cell production of insulin in type 2 diabetes that contributes to worsening glucose control. (This is a major factor for many patients with type 2 diabetes who ultimately require insulin therapy.) Finally, the liver in these patients continues to produce glucose through a process called gluconeogenesis despite elevated glucose levels. The control of gluconeogenesis becomes compromised.
Optimally, the management approach results in weight loss based on a healthy diet and regular physical activity, which includes a combination of aerobic activity and resistance training, reinforced with behavioral therapy. Metformin, an insulin sensitizer, or a thiazolidinedione (eg, rosiglitazone, pioglitazone) may be useful. Weight loss of ≈ 7% may be sufficient to reverse the syndrome, but if not, each feature of the syndrome should be managed to achieve recommended targets; available drug treatment is very effective.
When you are first diagnosed with hypertension, you can expect a period of time when you will be seeing your doctor more often than usual. You will need some baseline testing to look for an underlying cause for your hypertension, and you will probably need several medical visits to determine whether lifestyle adjustments or medication will be effective in helping you reach your optimal blood pressure.
Research shows that Western diet habits are a factor in development of metabolic syndrome, with high consumption of food that is not biochemically suited to humans.[21] Weight gain is associated with metabolic syndrome. Rather than total adiposity, the core clinical component of the syndrome is visceral and/or ectopic fat (i.e., fat in organs not designed for fat storage) whereas the principal metabolic abnormality is insulin resistance.[22] The continuous provision of energy via dietary carbohydrate, lipid, and protein fuels, unmatched by physical activity/energy demand creates a backlog of the products of mitochondrial oxidation, a process associated with progressive mitochondrial dysfunction and insulin resistance.
Metabolic syndrome is a multiplex risk factor that arises from insulin resistance accompanying abnormal adipose deposition and function. [4] It is a risk factor for coronary heart disease, as well as diabetes, fatty liver, and several cancers. The clinical manifestations of this syndrome may include hypertension, hyperglycemia, hypertriglyceridemia, reduced high-density lipoprotein cholesterol (HDL-C), and abdominal obesity. (See Prognosis, Workup, Treatment, and Medication.)
Because the population of the U.S. is aging, and because metabolic syndrome is more likely the older you are, the American Heart Association (AHA) has estimated that metabolic syndrome soon will become the main risk factor for cardiovascular disease, ahead of cigarette smoking. Experts also think that increasing rates of obesity are related to the increasing rates of metabolic syndrome.

Because metabolic syndrome and insulin resistance are closely tied, many healthcare providers believe that insulin resistance may be a cause of metabolic syndrome. But they have not found a direct link between the two conditions. Others believe that hormone changes caused by chronic stress lead to abdominal obesity, insulin resistance, and higher blood lipids (triglycerides and cholesterol).
Measuring BP takes into account two pressures, measured in millimeters of mercury (mm Hg). The first, systolic pressure, is the force exerted on the blood vessel walls when the heart is pumping blood. Diastolic pressure reflects the force present when the heart relaxes between beats. They are written as systolic over diastolic pressure. For instance, a blood pressure of 120/80 mm Hg or 120 over 80 corresponds to a systolic pressure of 120 and a diastolic pressure of 80.
The fact that the diagnostic criteria for metabolic syndrome vary between ethnic populations is testimony to significant nuances in the manifestation of metabolic syndrome in these groups. The original metabolic syndrome criteria were derived in mostly Caucasian populations, and some have argued for modification of individual criteria for specific ethnic subgroups, as has been done with waist circumference for patients of Asian origin. [39]
Although the first formal definition of metabolic syndrome entered medical textbooks not so long ago (1998), it is as widespread as pimples and the common cold . According to the American Heart Association, 47 million Americans have it. That's almost a staggering one out of every six people. The syndrome runs in families and is more common among African-Americans, Hispanics, Asians, and Native Americans. The risks of developing metabolic syndrome increases as you age.
Insulin is released into the blood by beta cells (β-cells), found in the islets of Langerhans in the pancreas, in response to rising levels of blood glucose, typically after eating. Insulin is used by about two-thirds of the body's cells to absorb glucose from the blood for use as fuel, for conversion to other needed molecules, or for storage. Lower glucose levels result in decreased insulin release from the beta cells and in the breakdown of glycogen to glucose. This process is mainly controlled by the hormone glucagon, which acts in the opposite manner to insulin.[61]

"Secondary" diabetes refers to elevated blood sugar levels from another medical condition. Secondary diabetes may develop when the pancreatic tissue responsible for the production of insulin is destroyed by disease, such as chronic pancreatitis (inflammation of the pancreas by toxins like excessive alcohol), trauma, or surgical removal of the pancreas.
Investigations into the pathophysiology of hypertension, both in animals and humans, have revealed that hypertension may have an immunological basis. Studies have revealed that hypertension is associated with renal infiltration of immune cells and that pharmacologic immunosuppression (such as with the drug mycophenolate mofetil) or pathologic immunosuppression (such as occurs with HIV) results in reduced blood pressure in animals and humans. Evidence suggests that T lymphocytes and T-cell derived cytokines (eg, interleukin 17, tumor necrosis factor alpha) play an important role in hypertension. [14, 15]
Diabetes is a number of diseases that involve problems with the hormone insulin. Normally, the pancreas (an organ behind the stomach) releases insulin to help your body store and use the sugar and fat from the food you eat. Diabetes can occur when the pancreas produces very little or no insulin, or when the body does not respond appropriately to insulin. As yet, there is no cure. People with diabetes need to manage their disease to stay healthy.
Furthermore, of those with high blood pressure (BP), 78% were aware they were hypertensive, 68% were being treated with antihypertensive agents, and only 64% of treated individuals had controlled hypertension. [1] In addition, previous data from NHANES estimated that 52.6% (NHANES 2009-2010) to 55.8% (NHANES 1999-2000) of adults aged 20 years and older have prehypertension, defined as an untreated SBP of 120-139 mm Hg or untreated DBP of 80-89 mmHg. [1] (See Epidemiology.)
^ Saiz, Luis Carlos; Gorricho, Javier; Garjón, Javier; Celaya, Mª Concepción; Muruzábal, Lourdes; Malón, Mª del Mar; Montoya, Rodolfo; López, Antonio (2017-10-11). "Blood pressure targets for the treatment of people with hypertension and cardiovascular disease". Cochrane Database of Systematic Reviews. 10: CD010315. doi:10.1002/14651858.cd010315.pub2. PMID 29020435.
This explains why my attempts at a low fat, high protein, high carb diet left me gaining weight all while eating 1000 calories per day! Those 1000 calories were simply fueling my brain and then getting shuttled into my fat cells. If you are not insulin resistant, then this diet may be just the thing you need to shed some short term pounds (although I never recommend a 1000 calorie diet!- more on that later), but to me it caused metabolic chaos.
Metabolic syndrome is thought to be caused by adipose tissue dysfunction and insulin resistance. Dysfunctional adipose tissue also plays an important role in the pathogenesis of obesity-related insulin resistance. [18] Both adipose cell enlargement and infiltration of macrophages into adipose tissue result in the release of proinflammatory cytokines and promote insulin resistance. [19]

[Guideline] Whelton PK, Carey RM, Aronow WS, et al. 2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA Guideline for the Prevention, Detection, Evaluation, and Management of High Blood Pressure in Adults: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Hypertension. 2018 Jun. 71(6):e13-e115. [Medline]. [Full Text].
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