Peer Review reports. Metabolic syndrome is defined as a cluster of at least three out of five clinical risk factors: abdominal visceral obesity, hypertension, elevated serum triglycerides, low serum high-density lipoprotein HDL and insulin resistance [ 1 ]. Of the five clinical risk factors used as diagnostic criteria for metabolic syndrome, abdominal obesity appears to be the most predominant [ 3 , 4 ].

Abdominal visceral obesity, irrespective of other fat deposits, is a major risk factor for systemic inflammation, hyperlipidaemia, insulin resistance and cardiovascular disease for review, see [ 6 ].

The role of abdominal obesity in the development of insulin resistance and the metabolic syndrome was described in [ 7 ]. However, abdominal obesity does not always occur in individuals with an elevated BMI.

It was recognised as early as that normal weight, metabolically obese, individuals existed due to the presence of excessive visceral fat deposits [ 8 ]. Evidence shows that one of the single most important lifestyle changes for the prevention of many chronic diseases is exercise [ 9 ] and as a consequence exercise is now recognised as a medical treatment in its own right [ 6 ].

There is growing evidence that regular and consistent programmes of exercise will reduce abdominal fat deposits significantly, independent of weight loss [ 10 , 11 ]. It is recognised that changes in body composition - particularly a reduction in abdominal fat deposits - are more important than reductions in overall body weight, or BMI, in treating metabolic syndrome.

Reductions in abdominal fat deposits are important because abdominal obesity is a marker of dysfunctional adipose tissue adiposopathy [ 12 ]. Abdominal, or visceral obesity has a central role in the development of a pro-inflammatory state which we now know is associated with metabolic syndrome [ 13 ].

It has been suggested that exercise as a medical intervention should be prescribed in terms of its dose, i. mode, intensity, frequency and duration [ 14 ]. This was the basis of the American College of Sports Medicine Exercise is Medicine® EIM initiative [ 15 ] and their guidance on prescribing exercise [ 16 ].

The aim of this review is to i summarise current evidence on the pathophysiology of dysfunctional adipose tissue adiposopathy , its relationship to metabolic syndrome and how exercise may mediate these processes; and ii evaluate current evidence on the clinical efficacy of exercise in the management of abdominal obesity and to assess the type and dose of exercise needed for optimal improvements in health status.

To understand the significance of abdominal obesity and its contribution to metabolic syndrome, it is necessary to appreciate the link between the diseases associated with this condition.

The accumulation of ectopic fat in tissue surrounding the viscera is directly related to the development of insulin resistance [ 17 ]. Insulin resistance is thought to be the common denominator in the development of metabolic syndrome.

In addition, evidence suggests that systemic inflammation is an important factor in its development, through the development of insulin resistance [ 18 , 19 , 20 , 21 ]. Dysfunctional adipose tissue secretes pro-inflammatory biomarkers including prostaglandins, C-reactive protein CRP , and cytokines such as interleukins e.

interleukin-6 , tumour necrosis factor alpha TNF-α , and leptin [ 22 , 23 ]. With increasing obesity there is also a corresponding decrease in levels of adiponectin, an antiatherosclerotic adipokine [ 24 ].

Inflammatory mediators released by adipose tissue contribute to the development of type II diabetes, hyperlipidaemia and cardiovascular disease [ 25 , 26 ]. If there is a high proportion of fat to muscle this is likely to contribute to this metabolic dysfunction as an increase in circulation of free fatty acids requires greater insulin secretion for control of glucose metabolism.

The resulting hyperinsulinaemia desensitises insulin-sensitive tissues, which predisposes individuals to type II diabetes [ 27 ]. The decrease in adiponectin secretion also inhibits insulin receptor proteins. Moreover, regular consumption of foods rich in carbohydrate results in postprandial hyperglycaemia which causes repetitive acute inflammation which might contribute to a chronic inflammatory state [ 28 ].

Chronic systemic inflammation increases oxidative stress and reduces metabolic flexibility, thus perpetuating metabolic syndrome, leading to a vicious cycle of disease, depression and further inactivity [ 29 , 30 ].

Adipose tissue hypoxia also occurs in the obese state although the mechanisms for this are not fully understood [ 19 ]. It has been suggested that deficient angiogenesis causes decreased blood flow due to reduction in capillary density and excessive growth of adipose tissue. This may also be exacerbated by obstructive sleep apnoea which is common in obese individuals, and results in a reduction of oxygen to the tissues [ 31 ].

Adipose tissue, hypoxia is associated with an increased expression of inflammatory genes and decreased expression of adiponectin, resulting in local and systemic inflammation [ 19 , 32 , 33 ]. The response to adipose tissue hypoxia includes insulin sensitivity and glucose intolerance as adiponectin is associated with normal glucose and lipid metabolism.

Leptin expression has also been shown to increase in obesity and the likely explanation for this is adipose tissue hypoxia [ 34 ].

This is important as leptin expression modulates insulin resistance [ 35 ]. Furthermore, ghrelin regulation in obese individuals is affected and serum ghrelin suppression in response to stomach fullness is impaired which results in a failure to suppress the continued desire to eat, thus compounding the problem [ 35 ].

Hypothlamic-pituitary-adrenal HPA axis hyperactivity is evident in abdominal obesity and is also associated with insulin resistance due to an increase in cortisol levels [ 36 ]. Cortisol, secreted by the adrenal glands, is involved in glucogenesis which increases blood sugar as a response to stress.

Epidemiological data provide evidence for a significant positive association between increased cortisol levels and the risk of developing type II diabetes and atherosclerosis due to a failure to suppress inflammation [ 37 ]. Also, the secretion of low grade inflammatory mediators by adipose tissues may act as an additional chronic stimulus to the activation of the HPA axis which in turn results in increased levels of cortisol secretion, resulting in a positive feedback loop [ 38 ].

At present, there is no explanation for this and it is not known whether these metabolically healthy obese individuals will eventually develop metabolic syndrome and are simply experiencing a delayed-onset of disease [ 24 ]. When BMI is used as a measure of obesity only a modest association with cardiovascular risk factors is found [ 18 ].

However, when abdominal obesity measurements, such as waist circumference or waist:hip ratio are included as a measure of abdominal adiposity a strong association with cardiovascular and metabolic syndrome risk factors is found [ 42 , 43 , 44 , 45 ].

Abdominal adiposity is a reversible condition and its reduction can have excellent effects in diminishing cardiovascular and metabolic syndrome risk. Evidence from a study by Brooks, et al. demonstrated that increased abdominal obesity was associated with systemic inflammation as measured by high-sensitivity C-reactive protein hsCRP [ 18 ].

Given the direct link between abdominal obesity and systemic inflammation it is not surprising that even modest reductions in abdominal adipose tissue are accompanied by improvements in metabolic function and reduced cardiovascular risk.

Several studies show a strong association between obesity and physical inactivity [ 46 , 47 , 48 ] and that metabolic syndrome is associated with sedentary lifestyle and poor cardiorespiratory fitness [ 49 ]. Sedentary behaviour is widely regarded as activity which involves energy expenditure at the level of 1.

Edwardson et al. conducted a meta-analysis that found that individuals who spend more time in sedentary behaviours have greater odds of having metabolic syndrome [ 50 ].

A longitudinal study observing adults found that improvements in cardiometabolic factors occurred in overweight and obese individuals with increased levels of physical activity, although the participants were those participating in a health screening programme and were therefore probably of a higher economic status.

At follow-up, there was a statistically significant decrease in non-HDL concentrations of 5. Of the parameters observed, non-HDL cholesterol and plasma triglycerides were found to have the largest improvement when physical activity was increased.

A study followed 22, participants, aged 30—64 years, comparing metabolic syndrome risk with intensity level of leisure-time exercise and by occupational and commuting activity [ 53 ]. Leisure-time activity was found to be linearly and inversely associated with a risk of developing metabolic syndrome and vigorous-intensity activity alone or a combination of both moderate- and vigorous-intensity activity was associated with a lower risk of metabolic syndrome.

The introduction of increased physical activity into a previously inactive lifestyle might also break the cycle of inflammation-mediated sickness behaviour as described by Nunn, which suppresses the desire to undertake physical activity [ 30 ].

A systematic review and meta-analysis was conducted by Ostman et al. A total of 16 studies participants were included in the review and it was found that aerobic training produced small improvements in fasting blood glucose, triglycerides and low-density lipoproteins. Nevertheless, combined with improvements in maximal oxygen uptake and blood pressure, the overall risk profile for patients was much improved.

The improvements in waist measurement would suggest that the long-term risks associated with metabolic syndrome were reduced. There are a number of studies which have specifically investigated the effect of exercise on abdominal obesity, irrespective of total body weight and these are summarised in a comprehensive review by Pedersen and Saltin [ 56 ].

Amongst their findings they reported that a cross-sectional study of overweight males showed that those with a high level of fitness as measured by activity and maximal oxygen uptake had lower levels of visceral fat than their unfit counterparts when scanned using magnetic resonance imaging [ 39 ].

Lee et al. investigated the effects of exercise without weight loss on total and abdominal adiposity and skeletal muscle mass and composition in previously sedentary, lean men and in obese men with and without type II diabetes [ 11 ]. It was found that, even in the absence of weight loss, moderate-intensity exercise was associated with significant reductions in total and abdominal fat, and there was a reduction in skeletal muscle lipid content independent of group.

Stewart et al. investigated the effects of exercise on cardiovascular and metabolic disease in older adults and found that reductions in total and abdominal fatness and increase in leanness were strongly associated with reductions in risk factors for cardiovascular disease and diabetes, including those that constitute metabolic syndrome [ 57 ].

conducted a longitudinal study of 32, adults who underwent an abdominal computerised tomography scan as part of health screening and found that the ratio of visceral-to-subcutaneous fat was independently associated with all-cause mortality. This suggests that the location of fat deposits in the abdomen viscera is a better indicator of metabolic risk than total body fat, which is unsurprising given the positive association between abdominal adiposity and systemic inflammation [ 58 ].

A number of reviews have shown that exercise training specifically elicits an anti-inflammatory effect, independent of weight loss [ 33 , 59 , 60 , 61 , 62 ]. Other metabolic benefits of exercise were reported in a study on patients with type II diabetes where pedometer-measured exercise was not only associated with reductions in systemic inflammation, but also reductions in abdominal obesity and arterial stiffness [ 63 ].

One of the mechanisms for the anti-inflammatory effect of exercise is a reduction in adipose tissue hypoxia resulting from improved capillary density blood flow. In a review by Golbidi [ 24 ] the inverse relationship between exercise, body mass index BMI , hip-waist ratio, and waist circumference was described.

The anti-inflammatory effect of exercise was also explained as being closely related to oxidative stress. Exercise was shown to improve glucose tolerance, insulin resistance and lipid metabolism and reduce blood pressure in both healthy individuals and those with metabolic disease.

Large population cohort studies observed relationships between plasma CRP and the level of exercise that was independent of obesity as measured by body mass index [ 62 , 64 ].

The effect of exercise training on CRP was investigated in a systematic review which considered a total of 83 studies of different types. It was found that exercise training led to a greater reduction in CRP when accompanied by a decrease in BMI, but that significant reductions in CRP occurred without weight loss [ 65 ].

Furthermore, a Cochrane review provided evidence that exercise improved general health even where no weight was lost because it improved plasma lipoprotein profile [ 66 ]. Not all studies provide evidence that exercise training reduces pro-inflammatory biomarkers.

Melo et al. reviewed 11 studies of patients with type II diabetes and found insufficient evidence to determine whether aerobic or resistance exercise improved systemic levels of inflammatory markers [ 67 ].

However, an earlier review by Hayashino et al. found that both CRP and IL-6 were reduced by exercise training [ 68 ]. It is still unclear whether improvements in inflammatory status are independent of weight loss or entirely dependent upon the changes in body composition that result from exercise training [ 61 ].

Nevertheless, Eaton and Eaton observed that the percentage of lean body mass is critical in avoiding the hyperinsulinaemia which predisposes individuals to type II diabetes because a greater insulin secretion is required for any given glucose load where levels of body fat are disproportionate [ 27 ].

This would suggest that strength training that develops lean tissue is critical in the treatment, or prevention, of metabolic disease. There are no specific guidelines on exercise prescription for systemic inflammation although guidance is available in the form of programmes designed to reduce body fat and improve general health status.

The American College of Sports Medicine ACSM recommends — min of moderate-intensity exercise per week as optimal but other authors have suggested between 30 [ 69 ] and 60 [ 70 ] minutes per day would be required.

A systematic review and meta-analysis by Hayashino et al. They found that exercise training with a longer duration and frequency was more effective in reducing systemic inflammation, suggesting that these effects might be dose-dependent.

More recently, this idea has been challenged and it is now thought that shorter-duration, higher intensity interval training HIIT is beneficial [ 76 ]. Recent findings suggest that HIIT programmes are effective in reducing metabolic syndrome combined with high adherence rates and this is important because incorporating HIIT programmes into daily life is less disruptive.

Gremeaux, et al. studied the effects of HIIT training on a sample of 62 overweight or obese adults who were above the recommended abdominal obesity threshold. It was found that the prevalence of metabolic syndrome was reduced by The metabolic and vascular effects of these three different regimens were studied and improvements were observed in various measures including BMI, waist measurement, glucose metabolism, insulin resistance and lipid profiles.

Zhang et al. also found that high intensity interval training was better than continuous moderate aerobic training in reducing abdominal visceral fat in obese young women [ 78 ].

Similar findings from other studies support the benefit of high-intensity interval training performed in short, high-intensity bursts, involving as little as 10 min of activity at a time, and this might promote better adherence in non-habitual exercisers [ 79 , 80 , 81 ].

A further study of adults found that consistent moderate to vigorous activity was more important than exercise volume in reducing CRP levels associated with systemic inflammation [ 82 ].

A systematic review by Cronin et al. found that greater reductions in inflammatory biomarkers occurred in older healthy inactive participants when higher intensity aerobic exercise was undertaken [ 83 ]. A review by Zdziarski et al. found that largest reductions in systemic inflammation and improvements in well-being, depression and sleep was achieved using multi-modal exercise aerobic and resistance training in individuals with inflammation-related chronic pain [ 84 ].

This is important because it is likely that individuals in a pro-inflammatory state due to abdominal adiposopathy may also be susceptible to chronic pain conditions. Dutheil et al. reported that high resistance-moderate endurance training was efficient in improving visceral fat loss in healthy adults [ 85 ].

If changes in body composition are more important than total body weight loss then resistance training combined with aerobic exercise would produce optimal effects in increasing percentage lean body mass [ 27 ]. One of the major challenges in using programmes of exercise to improve health status is promoting and maintaining adherence in individuals who have often been inactive for many years and who may be overweight or obese [ 86 ].

To promote adherence Clauw and Crofford suggested that additional activity is incorporated very gradually — as little as 5 min daily [ 88 ] although the programme needs to be tailored to the individual whilst aiming to deliver optimal effects [ 84 ].

As discussed above, the recent findings that HIIT programmes are effective in reducing metabolic syndrome combined with high adherence rates is significant because incorporating it into daily life is less disruptive.

Connelly et al. conducted a review to assess the effectiveness of technology to promote physical activity in people with Type 2 diabetes and found that the use of technology-based interventions, such as mobile phone applications, texts and email support, improves compliance [ 89 ].

In summary, evidence suggests that optimal abdominal fat reduction and the development of lean tissue is achieved by combining high-intensity interval training and resistance training with an overall general increase in daily physical activity.

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Eur J Cardiovasc Prev Rehabil epub 30 Nov Download references. No potential conflicts of interest directly relevant to this content of this article were reported. Véronique A. Cornelissen is supported as a Postdoctoral Fellow by Research Foundation Flanders F.

Department of Rehabilitation Sciences, KU Leuven, B , Tervuursevest , , Louvain, Belgium. Nele Pattyn, Véronique A.

Cornelissen, Saeed R. You can also search for this author in PubMed Google Scholar. Correspondence to Nele Pattyn. Open Access This article is distributed under the terms of the Creative Commons Attribution Noncommercial License which permits any noncommercial use, distribution, and reproduction in any medium, provided the original author s and the source are credited.

Reprints and permissions. Pattyn, N. et al. The Effect of Exercise on the Cardiovascular Risk Factors Constituting the Metabolic Syndrome. Sports Med 43 , — Download citation. Published : 19 December Issue Date : February Anyone you share the following link with will be able to read this content:.

Sorry, a shareable link is not currently available for this article. Provided by the Springer Nature SharedIt content-sharing initiative. Download PDF. Abstract Background Numerous meta-analyses have investigated the effect of exercise in different populations and for single cardiovascular risk factors, but none have specifically focused on the metabolic syndrome MetS patients and the concomitant effect of exercise on all associated cardiovascular risk factors.

Objective The aim of this article was to perform a systematic review with a meta-analysis of randomized and clinical controlled trials RCTs, CTs investigating the effect of exercise on cardiovascular risk factors in patients with the MetS.

Results Seven trials were included, involving nine study groups and participants in exercise group and 78 in control group. Conclusions Our results suggest that dynamic endurance training has a favourable effect on most of the cardiovascular risk factors associated with the MetS.

Despite being a flawed measure , BMI is widely used today in the medical community because it is an inexpensive and quick method for analyzing potential health status and outcomes. The magnitude of the beneficial effects was significant but small. This leads to the question as to whether they would make a difference in health outcomes.

Your waistline may shrink, but exercise alone may not be enough to get you to below the threshold of the metabolic syndrome criteria. Your blood tests might look better, but does it mean you have less risk of heart attack or stroke? The researchers note that exercise is just one strategy in managing metabolic syndrome.

Reducing overall sedentary time , improving diet, and getting better sleep are other recommendations to lower risks. Many popular aerobic interval workouts and programs include bursts of higher intensity exercise, such as repeating sprints of a minute followed by walking, or a slower jogging speed for a few minutes.

Whether these types of aerobic workouts are better for metabolic syndrome is still an open question. While there are some studies that show they have more effect than continuous moderate-intensity exercise, these studies have been small and some are not of high quality.

It's too early to say that HIIT is better. But if you enjoy HIIT workouts, they should have at least the same effect as other aerobic workouts.

Treadmills, elliptical trainers, and stationary bikes often have hill or speed interval workouts pre-programmed for you to use. If you enjoy walking or running outdoors, there are many ways to add bursts of higher intensity to your workouts. Speed up, tackle a hill, or use stairs to boost your heart rate.

Looking specifically at the benefits of resistance exercise, a study at the Cooper Clinic in Dallas, Texas analyzed whether over 7, participants in their exercise trials developed metabolic syndrome. They could see that 15 percent of those in their studies developed metabolic syndrome and could look back at their typical amount and type of exercise and whether they met the U.

physical activity guidelines :. These outcome results suggest that you might lower your risk of metabolic syndrome by getting the recommended amount of resistance exercise, in addition to the recommended amount of aerobic exercise. Resistance exercise is muscle-strengthening activity.

You can lift weights , use muscle-targeting exercise machines, use resistance bands, or do bodyweight exercises such as push-ups, crunches, and squats.

Whether you walk, bike, dance, run, or lift weights, you are likely to be reducing your risk of metabolic syndrome. Check with your healthcare provider before you get started and then do what you enjoy most.

Try different forms of exercise to spice things up. If you wear an activity monitor, check your exercise minutes to see if you are reaching the recommended amounts each week. If not, try to steadily increase your exercise time.

Don't skip the resistance exercise and, above all, find activities that are fun so you will continue to do them. National Heart, Lung, and Blood Institute, "Physical Activity". American Heart Association, "Prevention and Treatment of Metabolic Syndrome". By Wendy Bumgardner Wendy Bumgardner is a freelance writer covering walking and other health and fitness topics and has competed in more than 1, walking events.

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