The decline of metabolic hormones in ageing is accompanied by a reduced resting metabolic rate (RMR) which is the number of calories the body burns while at rest, and a decrease in the basal metabolic rate (BMR), which is the minimum number of calories required for basic functions at rest in a neutrally temperate environment. Although RMR and BMR may not be dependent on hormonal decline (Meunier et al, 2005), they are highly correlated, frequently observed together in older individuals. Low RMR and BMR lead to weight gain and low-grade inflammation in older age (Welle and Campbell, 1986; Lipsitz 1992). However, an age-related decline in BMR is not observed in individuals who exercise regularly (Pelt et al, 1997).
Historical evidence shows that physical inactivity is detrimental to health and normal organ functional capacities. Physical activity has been proposed as primary prevention against 35 chronic conditions, including accelerated biological ageing and premature deaths, metabolic syndrome, obesity, insulin resistance, type 2 diabetes, non-alcoholic fatty liver disease, coronary heart disease, hypertension, stroke and cognitive dysfunction (Booth et al, 2012).
Lack of exercise and obesity
Increased toxicity is the protagonist in all aspects of physical illness. Lack of exercise leads to increased toxicity and increased vulnerability to one or more chronic physical conditions. Exercise increases lymphatic drainage and detoxification. During exercise, the lymphatic system carries fluid and plasma proteins that have leaked into the interstitial space from tissues back to the cardiovascular system. During steady state exercise in humans, lymph flow has been shown to increase to levels approximately two-to three-fold higher than at rest (Lane et al, 2005). Exercise has been rendered safe and effective for treating many toxicities, including toxicity management in patients with cancer (Kleckner et al, 2018). Toxicity can act as a direct hormone disruptor in the endocrine system and/or an indirect immune system disruptor by disorganising both intercellular and intracellular interactions regulated locally by cytokines and growth factors (Osteen and Sierra-Riviera, 1997). It has been postulated that chemical toxins can explain the global obesity epidemic, because of the exponential production and usage of synthetic organic and inorganic chemicals that may have damaged many of the body's natural weight-control mechanisms (Baillie-Hamilton, 2004).
Toxins
Toxins alter thyroid hormone metabolism, lowering RMR. Hepatic detoxification systems are overloaded by toxicity, which promotes insulin resistance and disorganises hypothalamic satiety modulation of central inhibitors and stimulators of appetite, including leptin that induces satiety and fat burning, and cortisol, which has been strongly related to caloric intake and total consumption, triggering stress eating behaviours (Hyman, 2007; George et al, 2010). Toxicity interferes with all fat-burning hormones, such as insulin (lowers blood sugar by storing glucose in adipocytes), ghrelin (stimulates hunger and fat storage) and adiponectin (lowers blood sugar and burns fat). The resulting hormonal imbalance increases hunger. The vicious circle starts with toxicity triggering hunger increase, which leads to increased fat deposits that store toxins, leading to more hunger and more weight gain. This vicious circle is intensified with age when BMR and RMR decrease, turning weight loss into a losing battle. The reason why both BMR and RMR decrease with age is because the skeletal musculature, the fundamental organ that consumes the largest part of energy in the normal human body, also decreases with age due to hormonal decline in a number of hormones, including IGF-1 and testosterone.
The plateau reached during weight loss by most individuals during dieting is explained by Pettetier et al in their review paper (2003). Individuals with a higher body mass index (BMI) store more toxins because they have more fat. Fat cells release their contents into the bloodstream during weight loss, along with toxins. Toxins interfere with many normal aspects of metabolism, including thyroid hormone levels that slow down the metabolic process, undermining weight loss. The hunger increase during dieting is not due to a genuine need for greater food intake, but because, during dieting, toxins are released into the blood stream, along with stored triglycerides, fatty acids and lipids. Toxins upset central inhibitors and stimulators of appetite, increasing hunger. Accumulated toxicity, including persistent organic pollutants (POPs) resistant to degradation through biological processes, prevents weight loss irrespective of food intake, and in conjunction with the inevitable increase of hunger as a result of toxicity, weight loss becomes an insurmountable project with no easy solution, especially for those who have difficulty or no time to exercise. Research studies on POPs in search of methods other than exercise are hampered by flawed methodologies and small sample sizes (Klein and Kiat, 2015). The alternative to diet is weight gain, and, in that case, blood carrying visceral fat cells stuffed with excess triglycerides take free fatty acids into the liver, pancreas and other organs, leading to fatty liver and fatty pancreas. Over time, free fatty acids cause the organs to dysfunction and, along with the toxicity released from fat cells, they impair the regulation of insulin, blood sugar and cholesterol.
Exercise and safeguarding health
Exercise enhances detoxification and safeguards health. However, it has a downside in older individuals. Exercise is perceived by the body as a form of stress and stimulates the release of cortisol. In younger age, the more your fitness improves, the better the body becomes at dealing with physical stress. This means that less cortisol will be released during exercise, and also in response to emotional or psychological stress. Cortisol has potent anti-inflammatory effects, easing irritation and pain in younger individuals. By raising plasma glucose levels at times of stress, cortisol provides the body with the energy it needs to face bodily attacks from injury, illness or infection. However, cortisol increases with age. Stressing the body with overtraining during an older age results in too much cortisol, which causes tissue breakdown. Cortisol is involved in the conversion of protein to glucose, potentially predisposing older individuals to type 2 diabetes. Cortisol is also related to decreased musculature, which, as stated, leads to decreased RMR, with the inevitable consequence of increased abdominal fat. Cortisol also suppresses growth and sex hormones, thereby reducing libido and fertility. Cortisol's effect on calcium can increase osteoporosis.
Effect of excessive exercise
Excessive exercise is necessary to reduce visceral adipose tissue in older individuals and is associated with increased lactic acid production and a negative relationship between cortisol and testosterone. Lactic acidosis induced by strenuous exercise is also known to upset the body's PH balance. Studies of normal tissue physiology initially considered lactic acid as an indicator of the glycolytic flux. However, more recently, several studies on tumour physiology indicate that lactic acid (i.e. lactate anion and protons) directly contributes to tumour growth and progression. Therefore, although mild to moderate exercise may prove to be useful for oncologists, strenuous exercise can be deleterious to cancer patients as a result of excessive lactic acid production during overtraining (Lucia et al, 2003). The other issue that stands in the way of health and fitness in older individuals is the negative cortisol/testosterone relationship. As cortisol increases, testosterone decreases. Both cortisol increase and testosterone decrease result in weight gain and other complications, which, in older age, are bound to offset the benefits of exercise. In 2008, Hill et al examined the influence of exercise intensity upon the cortisol response of the hypothalamic pituitary adrenal (HPA) axis. Twelve active moderately trained men performed 30 minutes of exercise at intensities of 40, 60 and 80% of their maximal oxygen intake, as well as a 30-minute resting-control session involving no exercise on separate days. Cortisol and ACTH were assessed in blood collected immediately before and after each experimental session. Collectively, the cortisol findings support the view that moderate to high intensity exercise provokes increases in circulating cortisol levels, while low intensity exercise actually results in a reduction in circulating cortisol levels. In 2012, Skoluda et al confirmed that long-term cortisol exposure was significantly higher in endurance athletes. These investigators obtained hair samples from 304 amateur endurance athletes (long distance runners, triathletes and cyclists) and 70 controls. Three different segments of the hair samples were tested for cortisol levels. Endurance athletes exhibited higher cortisol levels in all three hair segments compared to controls at a highly statistically significant level (p<.001).
Research has shown that the administration of cortisol into the circulation at rest will result in reduced total testosterone levels. Brownlee et al (2005) found a negative relationship between cortisol and total testosterone after exercise. In 2006, Handziski et al examined changes in some hormonal parameters in professional football players during a half season competition, and found a significant decrease in testosterone blood levels, with a significant increase in ACTH and cortisol blood levels of more than 30%, at the end of the competition season. This result was accompanied by an absolute and relative muscle mass decrease after the conditioning phase, and an absolute and relative fat mass increase after the competition phase. These studies demonstrate that excessive exercise, necessary to reduce visceral fat deposits that hold large amounts of toxicity, increases cortisol while decreasing testosterone, leading to weight gain despite all the efforts invested in physical activity. Hence the difficulty of reducing visceral adipose tissue at an older age, irrespective of how strenuously and how long you exercise.
In conclusion, although exercise enhances detoxification and safeguards health, excessive exercise, necessary to reduce visceral adipose tissue (which is one of the greatest health dangers encountered in aged individuals), is associated with increased lactic acid production and a negative cortisol/testosterone relationship. Ultimately, this leads to increased weight gain, increased toxicity, increased hunger and the inevitable consequence of greater vulnerability to a number of health complications.
Study
In this study, we adopted a technology originally invented at the University of London by Dr Gerald Pollock and molecular biology professor Dr Donald Gilbert. The technology is designed to offer full musculature 8-second sustained contractions, unlike electrical muscle stimulators that cause topical muscle reflexes. The technology mimics the timing, rhythm and variability of contractions experienced during strenuous physical exercise, ranging from strength and resistance exercises like lifting weights to faster circular movements like swimming.
Unpublished research during the clinical trials of this technology revealed an increase in triiodothyronine (free T3), testosterone and dehydroepiandrosterone (DHEA) concentrations in individuals who exhibited hormonal decline, without ever boosting hormones outside the normal range, while cortisol fluctuations were insignificant. A University of London study by Goldspink et al (1991) used a method developed prior to the completion of Pollock's invention to investigate gene expression, as detected by analysing the RNA to determine fast and slow muscle fibre phenotypes. The resulting rapid hypertrophy of adult skeletal muscle was associated with an increase of up to 250% in RNA content. Gene expression that involved gene switching, associated with the repression of the fast and activation of a slow myosin heavy chain gene, indicated that this stimulation technique induces rapid hypertrophy and myosin isoform gene switching in adult skeletal muscle.
Methodology
The technology emits 24 voltage-driven complex square waveforms that target visceral fat and detox simultaneously. Each of these complex waveforms is composed out of 4 000 sine frequencies, combined on the basis of Dr Pollock's formula that he patented in 1983 at the University of London. There are two waveform controls—one on the left and one on the right—that form 144 combinations, offering different types of 8-second contractions every 2 seconds, designed to give the experience of various effortless exercises. All waveforms are rectangular and have their own specific resultant frequencies that vary from 55 Hz to 888 Hz. The device has a maximum voltage of 25 V at 500 Ω, 100 V at 10K Ω, and a net charge of 0.001 A at 500 Ω, 0.004 A at 2000 Ω and 0.00025 A at 10 000 Ω. The leakage is 0.007μa (10−6 A). The device's voltage-driven complex waveforms are emitted from 16 channels that are isolated by separate transformers. The complex waveforms from these 16 channels reach the skin via silver-plated tour grade microphone cables that are connected to gel pads, which are attached onto the body. The technology has no known side effects. The only contraindication, according to the US Food and Drug Administration (FDA), is having an implanted device like a pacemaker. Furthermore, the main caution is pregnancy. Adverse reactions are limited to temporary skin redness from the pads that happens sporadically. The FDA has cleared earlier versions of this technology with the same hardware design. None of the subjects in the study were pregnant, had a cardiac pacemaker or had any other psychological or medical issues not reported in this study. No risks or burdens were involved in the use of this technology. Every precaution was taken to protect the privacy of research subjects and the confidentiality of their personal information. Other instruments used in the study included a measuring tape and a scale that gives scores on weight, body fat mass, visceral fat, skeletal muscle mass (SMM) and basal metabolic rate (BMR). Blood tests explored the following variables: very low-density lipoprotein (VLDL) cholesterol, high density lipoprotein (HDL), free T3, DHEA, cortisol and testosterone.
Procedure
Eight subjects of Chinese descent (four males and four females), aged 27–45 years, received six effortless exercise 45-minute treatments in a private clinic under the supervision of a consulting physician. Treatments were offered twice weekly, for a total of 3 weeks. Both subjects and operators conducting the study were randomly assigned out of a list of eligible candidates to be subjects or operators. The six device operators received basic training on how to operate the device. Subjects signed a consent form and were given a general health questionnaire to detect conditions like a pacemaker implant or pregnancy. Blood tests and the subjects' measurements, including weight, body fat mass, visceral adipose tissue, SMM, BMR and tape measurements on the waist and abdomen, were obtained before the first treatment. Blood tests were conducted in an independent lab and subjects were instructed to fast for 12 hours prior to getting their blood tests. Measurements were taken in a different room by a technician who did not operate the device. After blood tests and measurements were obtained, the subjects entered the treatment room and lay on a massage table while the gel pads and cables from the 16 channels of the device were being attached onto their bodies. The cables from 10 of the channels were attached onto the gel pads of the waist and abdomen, and the cables from the six remaining channels were attached onto the gel pads placed along the lymphatic system pathways of the legs and arms to enhance lymphatic drainage. During the treatment, the device's controls were facing the operator so that the subject could not see how the operator handled the device. Subjects were given no information as to the treatment results. None of the subjects or device operators had any bias or personal interest in the direction of the results.
The treatment resulted in visible 8-second vigorous full body contractions with 2 seconds rest time that were repeated 1000 times. Contractions were involuntary and painless, and involved the entire body's musculature contracting in a coordinated fashion. These intense, full body, 8-second painless contractions were observed and reported by all operators and all subjects, who described the treatment as a strenuous effortless workout.
Subjects were instructed to fast for 12 hours prior to the sixth treatment and, upon treatment completion, blood tests were administered. One week after the sixth treatment, the subjects' measurements were obtained, including weight, body fat mass, mass of visceral adipose tissue, skeletal muscle mass, BMR and tape measurements on the waist and abdomen. The lab technicians who analysed the subjects' blood tests and the technicians who took the subjects' before and after measurements were not involved in the study in any way and, therefore, they had no bias or personal interest in the direction of the study's results.
Subjects did not receive any specific instructions on adding exercise to their lifestyle or reducing their alcohol and food intake. Overall, subjects did not do anything to change their previous lifestyle during the course of the six treatments, as well as the additional week after treatment completion when the last measurements were taken.
Results
One-tailed T-tests for two dependent variables were performed on each of the subjects before and after measurements and blood test variables. Results yielded statistical significance at the probability level of over 99% (p< 0.01) on all measuring variables that are listed in Table 1. Significance of results can be seen in Table 2.
Table 1. Measurements results raw data
| Subject number | Gender | Measurement | First treatment | 1 week after sixth treatment |
|---|---|---|---|---|
| 1 | Male | Body fat mass | 30.80 | 27.60 |
| Visceral fat | 135.30 | 115.60 | ||
| SMM | 30.30 | 32.20 | ||
| Waist (cm) | 28.50 | 24.20 | ||
| Abdomen (cm) | 102.00 | 98.90 | ||
| 2 | Male | Body fat mass | 22.90 | 19.60 |
| Visceral fat | 95.20 | 83.30 | ||
| SMM | 37.90 | 38.70 | ||
| Waist (cm) | 97.10 | 94.90 | ||
| Abdomen (cm) | 99.00 | 97.00 | ||
| 3 | Female | Body fat mass | 18.50 | 17.00 |
| Visceral fat | 80.50 | 68.00 | ||
| SMM | 19.40 | 20.00 | ||
| Waist (cm) | 27.40 | 26.70 | ||
| Abdomen (cm) | 97.10 | 94.90 | ||
| 4 | Female | Body fat mass | 20.00 | 18.50 |
| Visceral fat | 85.50 | 78.30 | ||
| SMM | 21.00 | 21.80 | ||
| Waist (cm) | 76.20 | 71.50 | ||
| Abdomen (cm) | 86.00 | 79.80 | ||
| 5 | Male | Body fat mass | 55.70 | 54.20 |
| Visceral fat | 17.60 | 13.20 | ||
| SMM | 26.80 | 29.80 | ||
| Waist (cm) | 84.80 | 82.20 | ||
| Abdomen (cm) | 87.00 | 85.70 | ||
| 6 | Male | Body fat mass | 27.50 | 28.90 |
| Visceral fat | 121.50 | 113.30 | ||
| SMM | 37.80 | 38.80 | ||
| Waist (cm) | 99.00 | 98.50 | ||
| Abdomen (cm) | 100.10 | 99.20 | ||
| 7 | Female | Body fat mass | 19.60 | 18.40 |
| Visceral fat | 91.90 | 84.60 | ||
| SMM | 19.40 | 19.30 | ||
| Waist (cm) | 83.00 | 77.40 | ||
| Abdomen (cm) | 89.00 | 85.70 | ||
| 8 | Female | Body fat mass | 26.90 | 23.80 |
| Visceral fat | 72.70 | 69.90 | ||
| SMM | 14.20 | 17.00 | ||
| Waist (cm) | 24.50 | 22.00 | ||
| Abdomen (cm) | 81.30 | 79.90 |
Table 2. Statistical test results on measurement variables
| Mean | S2 =SS/df | S2M=S2/N | SM= √S2M | T Value | Probability | |
|---|---|---|---|---|---|---|
| Body fat mass | -2.02 | 0.99 | 0.12 | 0.35 | 5.75 | P<0.01 |
| Visceral adipose tissue | -9.25 | 28.72 | 3.59 | 1.89 | -4.88 | P<0.01 |
| SMM | 1.54 | 1.14 | 0.14 | 0.38 | 4.07 | P<0.01 |
| BMR | -10.38 | 1469.98 | 183.75 | 13.56 | -0.77 | P=0.23 |
| Waist (cm) | -3.14 | 2.65 | 0.33 | 0.58 | -5.45 | P<0.01 |
| Abdomen (cm) | -2.55 | 2.89 | 0.36 | 0.6 | -4.24 | P<0.01 |
| Weight (kg) | -1.06 | 0.82 | 0.1 | 0.32 | -3.32 | P<0.01 |
Note: Visceral adipose tissue, overall body fat mass, abdomen/waist cm and weight significantly decreased at the probability level p<0.01. SMM increased at the same probability level of p<0.01. Basal metabolic rate (BMR) decreased but did not reach statistical significance
Blood test results
The blood test data analysis yielded a statistically significant decrease of VLDL and triglycerides, and a significant increase in free T3. Cortisol and testosterone fluctuations were statistically insignificant.
The significant decrease in VLDL was accompanied by a moderate to high increase of HDL, which, however, did not reach statistical significance. DHEA showed an increase that did not reach statistical significance at the p<0.05 level. According to the results, HDL increased in 81% of individuals receiving the effortless exercise treatments and DHEA increased in 83% of individuals. Further examination revealed that testosterone increased in most females.
However, the female sample was too small (only four females) to calculate statistical significance.
Discussion
Measurement results indicated a decrease in visceral adipose tissue and overall fat mass, and an increase in skeletal muscle mass (Figure 1). There was also a significant decrease in cm and kgs. Blood tests yielded a statistically significant decrease in VLDL, which was accompanied by a significant decrease in triglycerides (Figure 2), and a significant increase in the metabolite of the thyroid hormone, free T3. HDL increased relatively to VLDL (Figure 3); however, HDL increase did not reach statistical significance. The DHEA increase did not reach statistical significance. There were no significant changes in cortisol, suggesting that effortless exercise does not stress the body. Hormonal increases observed in this study were all within the normal range that is desirable for optimum health, since hormonal spiking outside the normal range indicates hormonal imbalance, and may be suggestive of a medical condition. Testosterone fluctuations were statistically insignificant.
Figure 1. The before and after significant reduction in visceral adipose tissue and the significant increase in SMM 
Figure 2. Very low-density lipoprotein (VLDL) is considered one of the bad forms of cholesterol that can clog your arteries and lead to a heart attack. VLDL particles mainly carry triglycerides to the cells for energy production. Results revealed a statistically significant decrease of both VLDL and triglycerides 
Figure 3. The statistically significant decreases of VLDL plotted against the relative increases of HDL indicated that most subjects showed a decrease in VLDL and an increase of HDL. HDL increases were not consistent among all subjects. One subject showed a moderate increase and one subject showed a decrease in HDL rendering the overall results statistically insignificant
We did not find the inverse cortisol/testosterone correlation (Figure 4) observed after strenuous exercise, where cortisol increase is correlated with testosterone decline, despite the subjects' subjective experience that the treatments had resulted in enhanced fitness as if they had exercised regularly for several months. Testosterone increase was only observed in females (Figure 5), who generally have lower testosterone levels than males. The males in the sample were relatively younger in age, therefore, a testosterone increase in this male population would get testosterone to spike outside the normal range, tipping the scale towards hormonal imbalance.
Figure 4. Two of the male subjects indicated a relative increase in cortisol, unlike all other subjects who mostly showed a decrease of Cortisol or no change. We did not see the inverse cortisol / testosterone relationship observed after strenuous physical exercise 
Figure 5. Interaction between testosterone and cortisol, females only
Cortisol increase during regular exercise enhances eating behaviour which subsequently leads to weight gain. George at al (2009) found that corticotropin-releasing hormone (CRH), which elevates cortisol levels of healthy adults relative to placebo, was strongly related to both caloric intake and total consumption. The subjects in this study reported reduced hunger, but without implying suppressed appetite. We interpreted subjects' subjective reports as a possible effect of optimal cortisol levels combined with a decrease in systemic toxins that disorganise hypothalamic satiety modulation of central inhibitors and stimulators of appetite, generally increasing hunger. However, more research exploring leptin and ghrelin levels is necessary to support this hypothesis. Overall, the results demonstrated that this type of treatment, which is equivalent to effortless exercise, is effective in elevating free T3 at statistically significant levels, as well as reducing VLDL and triglycerides with no significant changes in cortisol. Interestingly, these results were obtained without diet or changes in lifestyle. Additionally, a significant decrease in visceral adipose tissue was found, as well as an increase in SMM, which is what is seen after strenuous exercise, but no other known technology like lasers or radiofrequency.
This double-blind pilot study was based on a small sample of subjects receiving about half the number of treatments usually recommended, which is around 12. Additionally, blood tests were taken immediately after the sixth treatment, which may have been an inadequate interval in showing HDL changes. TSH and T4 were not measured, therefore the metabolic profile was rather incomplete. For diagnostic purposes, a low T3 value accompanied by a high TSH value is considered evidence of hypothyroidism. By contrast, a low TSH value accompanied by a high T3 value is considered evidence of hyperthyroidism. The sample was heterogeneous in terms of age. Subjects' ages ranged from 27–45 years old. Therefore, age and gender-related hormonal variability on certain hormones like testosterone could have interfered with the accuracy of our hormonal profiles, compromising the statistical significance of the results. More research is necessary to test the reliability and validity of the results.