The clustering of cardiovascular disease (CVD) risk factors and their impact on metabolic health is far from novel. In the early 20th century, a Swedish physician named Kylin (66) reported elevated blood pressure, elevated blood sugar, and elevated uric acid levels (known today as hyperuricemia or gout) occurring simultaneously in patients and referred to this as a syndrome. A little more than a decade later, Himsworth (50) demonstrated insulin sensitivity and insulin insensitivity in those with diabetes, suggesting that insulin resistance may play a role in the development of many human diseases, particularly coronary artery disease and hypertension (HTN). Adiposity was not considered a part of the syndrome until Vague (96) reported on the relationship between upper body obesity and diabetes, with Avogaro (6) later strengthening this relationship between central adiposity and CVD risk factor clustering.Metabolic syndrome is the clustering of multiple CVD risk factors presenting in an individual more often than by chance alone. What we know today as metabolic syndrome has had many names and differing components. Some of the terminology reported in a review by Ford (36) to describe the various clustering of CVD risk factors have been beer-belly syndrome, special metabolic syndrome, insulin resistance syndrome, deadly quartet, plurimetabolic syndrome, syndrome X, and dysmetabolic syndrome. The term metabolic syndrome as a sole entity was first employed by Haller et al. (46) to describe the aggregation of obesity, diabetes, hyperproteinemia, hyperuricemia, and hepatic steatosis (fatty liver). The World Health Organization (WHO) proposed the first definition for metabolic syndrome in 1998 (4). Subsequently, several medical societies proposed diverging definitions, which have resulted in various prevalence and risk estimates from population studies (17,38).Recently, a unified definition for metabolic syndrome has been proposed. This joint statement defines metabolic syndrome as an individual possessing three or more of the following five CVD risk factors: 1) augmented fasting glucose or pharmacological treatment for elevated blood sugar; 2) augmented blood pressure or pharmacological treatment for elevated blood pressure; 3) augmented waist circumference; 4) augmented triglycerides or pharmacological treatment for elevated triglycerides; and 5) attenuated high-density lipoprotein cholesterol (HDL-C) or pharmacological treatment for this form of dyslipidemia (see Table 1).Metabolic syndrome is a highly prevalent condition in North America (17,36,82) and around the world (8) and has consistently been shown to be associated with increased cardiovascular morbidity and mortality (37,56). A review by Ford (37) illustrates that a metabolic syndrome diagnosis carries a twofold increased risk for coronary heart disease (CHD) and a three- to fivefold increased risk for developing type 2 diabetes (T2D). Isomaa et al. (56) reported a threefold increase risk for CHD and stroke in subjects aged 35 to 70 yr with T2D or poor glucose control who participated in the Botnia study. In addition, following adjustment for potential confounders, the Botnia study participants with metabolic syndrome were found to be 81% (relative risk [RR] 1.81; 95% confidence interval [CI] 1.24, 2.65) more likely to die from CVD compared with participants without the syndrome. In this study, the only factor that carried a greater risk for mortality independent of any other metabolic syndrome criteria was microalbuminuria (RR 2.80; 95% CI 1.62, 4.83).In the Atherosclerosis Risk in Communities study (ARIC) (72), men and women with metabolic syndrome were found to be 46% (hazard ratio [HR] 1.46; 95% CI 1.23, 2.64) and 105% (HR 2.05; 95% CI 1.59, 2.64) more likely, respectively, to develop CHD compared with subjects without metabolic syndrome. In the San Antonio Heart Study (53), similar to what was seen in ARIC, cardiovascular mortality among participants aged 25 to 64 yr with metabolic syndrome as defined by the National Cholesterol Education Program (NCEP) (90) and the WHO (4) was reported to be significantly higher in women (NCEP definition: HR 4.65; 95% CI 2.35, 9.21) (WHO definition: HR 2.83; 95% CI 1.55, 5.17) compared with men (NCEP: HR 1.82; 95% CI 1.14, 2.91) (WHO: HR 1.15; 95% CI 0.72, 1.86). This gender disparity was only significant when the participants possessed metabolic syndrome and T2D. However, findings from other studies (39,74) do not support this gender disparity; thus, more work in this area is warranted.When examining race/ethnicity, a cross-sectional analysis utilizing the American Heart Association/National Heart, Lung, and Blood Institute (AHA/NHLBI) definition for metabolic syndrome and data from the 1999–2004 National Health and Nutrition Examination Survey (NHANES) showed that among adults living in the United States, non-Hispanic blacks have a lower prevalence (30.8%) for metabolic syndrome compared with non-Hispanic whites (36.7%) and Mexican Americans (41.2%) (17). Additionally, non-Hispanic blacks were found to be 31% (odds ratio [OR] 0.69; 95% CI 0.55, 0.85) less likely to have the metabolic syndrome. A more recent analysis of the 2003–2006 NHANES continues to illustrate significantly lower prevalence estimates for metabolic syndrome in non-Hispanic blacks (25.3%) compared with non-Hispanic whites (37.2%) and Hispanics (33.2%) (32). Findings from the HERITAGE family study (24) showed blacks to have more favorable HDL-C levels compared with whites with similar levels of adiposity. Greater levels of HDL-C have been shown to be cardioprotective, with a 2% to 3% reduction in CHD risk for each 1 mg·dL−1 (0.03 mmol·L−1) increase in HDL-C (42). Several studies (20,49) have illustrated that non-Hispanic blacks carry lower proportions of visceral fat compared with other populations. This may impact lipid profiles; thus, this warrants further investigation.Several other demographic variables have also been shown to be associated with metabolic syndrome. Data from the 1999–2004 NHANES (17) illustrates lower prevalence estimates for metabolic syndrome among US adults with greater than a high school education compared with those who did not finish high school based on four of five definitions for metabolic syndrome that were recommended at that time. This study also clearly showed a strong positive association between age (in deciles) and metabolic syndrome prevalence until the >80 yr age category, where prevalence drops off. Women were found to have significantly lower prevalence estimates for two of the five definitions and significantly lower risk estimates for three of the five definitions compared with men. However, when only looking at the AHA/NHLBI definition, prevalence and risk estimates for men and women were similar. No clear relationship between metabolic syndrome and income was found.Physical activity (PA) and its positive effects on blood sugar control were first observed in 1923 (66). Physical activity has been shown to improve rates of glucose uptake in a similar fashion to insulin. Muscle fiber contraction increases the number and activity of GLUT-4 glucose transport proteins in skeletal muscle (41,52), providing an “insulin like effect” and enhancing glucose uptake in skeletal muscle even when insulin action is diminished. Insulin resistance has been shown to be the core component of metabolic syndrome. It has been found to be present in approximately 25% of Western society (21,79). The etiology of insulin resistance involves diminishing beta-cell function over time and has been estimated to result in impaired glucose tolerance and eventually frank T2D approximately 30% to 40% of the time (97). Saltin et al. (85) demonstrated that a low aerobic capacity, expressed per kilogram of body weight, may manifest itself as an early component of the metabolic syndrome, particularly in individuals likely to go on to develop T2D. Furthermore, histological evidence has demonstrated that insulin resistance/hyperinsulinemic individuals have attenuated mitochondrial and capillary density in skeletal muscle, accompanied by a decreased type I versus type II fiber ratio (71). Therefore, genetic abnormalities in skeletal muscle may limit aerobic capacity, resulting in higher levels of physical inactivity.Several studies have illustrated that individuals reporting high volumes of aerobic exercise on a consistent basis present with lower serum insulin levels in the fasting and postprandial states (31,81). Similar effects have been reported in older adults (87). Therefore, regular PA also appears to protect individuals from the deleterious effects of glucose intolerance associated with the normal aging process. When examining insulin sensitivity and glucose uptake in exercise and PA intervention studies, acute bouts of exercise (11) and lifestyle changes, including regular aerobic (88) and muscular strengthening activities (MSA) (19), have been shown to enhance insulin sensitivity and improve glucose control, respectively, in subjects with various levels of glycemia and body mass index (BMI) (70,94).Essential HTN is a heterogeneous condition, which has been shown to be associated with hyperinsulinemia (21,79). More research has been conducted on HTN than any other metabolic syndrome criteria (15,45,54). Current estimates from the US National Center for Health Statistics show that 29% and 28% of US adults have HTN (systolic blood pressure (SBP) >140 mmHg or a diastolic blood pressure (DBP) >90 mmHg) and pre-HTN (SBP between 120–139 mmHg or a DBP between 80–89 mmHg), respectively. This pre-HTN category carries with it a recommendation for lifestyle changes before introducing pharmacological treatment. In a recent study utilizing the 2007 Behavioral Risk Factor Surveillance System (BRFSS) data, Churilla and Ford (18) reported that US adults with self-reported HTN were 15% (OR 0.85; 95% CI 0.82, 0.88) less likely to meet the U.S. Department of Health & Human Services' (DHHS) PA recommendations compared with their non-HTN counterparts.Exercise training and regular PA have been shown to be associated with more favorable blood pressure values (22,33,45,89). Tanaka et al. (89) found a decrease in sitting and supine SBP in 18 previously sedentary subjects with stage 1 and stage 2 HTN following 10 weeks of supervised swimming. Dengel et al. (22) reported decreases in SBP and DBP following 9 mo of aerobic exercise training (40 min, 3 d per week). Similar findings reported from a meta-analysis conducted by Fagard (33) illustrated decreases in SBP and DBP in normotensive and hypertensive individuals. However, the effect was more pronounced in the HTN group.Ishikawa et al. (55) reported a significant reduction in blood pressure in sedentary men and women aged 30 to 69 yr with stage 1 and 2 HTN following an 8 wk aerobic exercise program. In addition, this study demonstrated no differences in efficacy between genders. However, the older subjects with HTN experienced less of a reduction in blood pressure following the exercise program than their younger counterparts. Similar reductions in SBP and DBP were reported by Swartz et al. (88) following an 8 wk walking program of 10,000 steps per day in overweight women. Overall, regular aerobic exercise and PA has been shown to decrease SBP (~11mm Hg) and DBP (~8 mm Hg) in nearly 75% of people with HTN (45). Findings on the relationship between MSA and HTN are equivocal. However, recent evidence suggests that engaging in at least 2 d per week of MSA may provide protection from developing pre-HTN (19).Atherogenic dyslipidemia commonly associated with the metabolic syndrome is represented by elevated triglycerides and decreased levels of HDL-C, particularly HDL2-C (9,10,80), which is associated with cardioprotection. The Diabetes Prevention Program Research group (25) reported that individuals with either impaired glucose tolerance or T2D showed minimal differences in blood pressure, triglycerides, HDL-C or non-HDL-C, or low-density lipoprotein cholesterol (LDL-C). This suggests that the insulin resistance phenotype, irrespective of the progression to T2D, may be primarily responsible for the dyslipidemia characteristic associated with hyperglycemia.Exercise and regular PA have been shown to demonstrate favorable effects on lipid profiles (29,100,101). Exercise can augment the capacity of muscle tissue to take up and oxidize non-esterified fatty acids (9,29) and increase the activity of lipoprotein lipase in muscle (76). Individuals who engage in regular PA, compared with those who are physically inactive, have been found to have higher levels of HDL-C and HDL2-C, in addition to lower levels of triglycerides. In contrast, limited evidence exists demonstrating that individuals who are physically active possess lower levels of total cholesterol and LDL-C (62,63,67). Hence, some lipids and lipoproteins are more favorably impacted by exercise and PA than others (27).Several studies have examined the dose-response relationship between volume of PA and changes in blood lipid levels (26,62,64,67,100,101). Drygas et al. (26) found HDL-C to be approximately 6 mg·dL−1 (0.16 mmol·L−1) greater in men who expended 1,000–1,499 kcal per week of PA compared with men expending less. In a similar study design, Kokkinos et al. (62) reported an inverse association between miles run per week and triglyceride levels and a positive association with HDL-C in a group of middle-aged men. In women, similar results have been reported. Durstine et al. (30) reported that HDL-C levels were greater in female recreational runners and even greater in female elite runners versus their sedentary counterparts, thus demonstrating a favorable dose-response association. Williams has reported a similar positive association between HDL-C levels and running volume in men and women (100,101).The frequency of favorable changes reported in HDL-C and triglycerides levels following regular PA suggests that these lipid values are more responsive to regular exercise and PA than total cholesterol and LDL-C (28). Although regular exercise or PA does result in minimal changes in total cholesterol and LDL-C in the absence of weight loss (102), the concentrations of LDL-C, particularly small dense LDL-C, has been shown to decrease, while LDL-C particle size is augmented, resulting in a less atherogenic environment (64). Regular PA (10,25,28) including MSA (19) has been shown to have favorable effects on the atherogenic dyslipidemia associated with metabolic syndrome. In addition, several prospective studies (64,91,100,101) have confirmed additional improvements in these lipid values with increases in the volume of PA performed. It is difficult to estimate specific changes in the various components of a lipid profile associated with PA, particularly because of the relationship between body weight and lipids. Moving forward, more research examining the potential impact PA volume and intensity may have on lipids is warranted.In a 2010 study, Flegal et al. (34) estimated the current prevalence of overweight and obesity in the US adult population at 68%. Metabolic syndrome has been shown to be linked with increased levels of abdominal or central adiposity (23,83). Upper body obesity, formerly known as android obesity, carries the highest level of CVD risk (96). Regional fat distribution studies performed with computed topography scanning and dual energy x-ray absorptiometry have demonstrated that higher levels of visceral adiposity are related to greater degrees of insulin resistance and HTN (20,40), thus creating a more atherogenic environment. However, these findings are not consistent across racial groups (7).High prevalence of physical inactivity has been reported to be the seminal etiology in the rapid rise in obesity rates (65,78). Regular bouts of PA have been shown to improve percent body fat and body fat distribution. In a cross-sectional study, Troisi et al. (92) found BMI and waist-to-hip ratio to be inversely associated with regular PA. In NHANES III, women who met or exceeded the Centers for Disease Control and Prevention/American College of Sports Medicine (CDC/ACSM) guidelines for PA (75) were found to have lower BMI, percent body fat, and waist-to-hip ratios compared with those not meeting the guidelines (51).In a study by Folsom et al. (35), reporting expending 2,000 kcals per week in leisure-time physical activity (LTPA) was associated with a significantly lower BMI. Similar results were seen in the Bogalusa Heart Study (44). This study examined self-reported levels of LTPA and physical inactivity and found LTPA to be inversely related with BMI and waist circumference. In contrast, a cross-over design study consisting of 22 healthy, slightly overweight, sedentary men resulted in little change in body weight, percent body fat, BMI, or overall CVD risk profile following 12 weeks of moderate-to-vigorous aerobic exercise (69). One explanation for this may be low levels of non-LTPA (e.g., work and domestic activities), which have been shown to reduce CVD risk at higher levels of non-LTPA (98).Findings from several studies suggest overweight and obesity may be more due to low levels of energy expenditure and not excessive caloric consumption (61,78). However, prospective studies have shown moderate amounts of aerobic and resistance exercise combined with hypocaloric diets result in greater weight loss and reductions in body fat percentage compared with hypocaloric diets alone (48,99). Nonetheless, several recent prospective studies have demonstrated that combining regular PA with a weight loss program in individuals at increased risk for developing metabolic syndrome can have favorable effects on the metabolic profile, thus reducing the risk of metabolic syndrome (25,70). Therefore, adding PA to any prescribed weight loss program would be prudent. Including regular PA as an adjunct to a weight loss program has been shown to result in varying degrees of both visceral and subcutaneous fat loss, which is dependent on age and regional fat distribution (86). Furthermore, PA has been shown to decrease as body weight increases (93). However, maintaining a desirable body weight is recommended for the prevention of the metabolic syndrome (75).Similar benefits from performing regular PA have also been observed in older adults. Favorable effects on body weight, body composition, lean body mass, and intra-abdominal adipose tissue have been observed in male and female masters athletes (77,84) compared with sedentary age-matched controls. With people losing 1 kg of muscle per year after the fifth decade of life, PA programs that include MSA can help attenuate this process while preserving function (73).The association between PA and metabolic syndrome was examined prospectively in the Coronary Artery Risk in Young Adults (CARDIA) study (13). The study population was made up of more than 4,000 black and white males and females without metabolic syndrome. Incidence of metabolic syndrome was observed at 7, 10, and 15 yr after base-line. Regular LTPA and occupational PA were assessed by the validated Minnesota Heart Health Program questionnaire (57). Age-adjusted rates of metabolic syndrome were reported per 1,000 person-years. Subjects who reported PA levels above the background population mean at all examinations were classified as being regularly active; those with inconsistent measures over time were considered moderately active. Over a mean of 13.6 yr of follow-up, metabolic syndrome developed in 575 participants. The age-adjusted rate of developing metabolic syndrome was 10 per 1,000 person-years. This was similar in both genders; however, black women had the highest overall incidence. Following adjustments for age, race, gender, weight gain, and PA over time, participants who remained regularly active were found to be 51% (OR 0.49; 95% CI, 0.34, .070) less likely to have metabolic syndrome compared with their sedentary counterparts. The addition of education, baseline BMI, baseline PA, smoking status, drinking status, and dietary covariates to the model attenuated this association slightly. However, it remained significant with regular PA associated with a 35% (OR 0.65; 95% CI, 0.76, 0.98) reduced risk of developing metabolic syndrome.The cross-sectional association between PA and metabolic syndrome was examined in the Canadian Heart Health Surveys, which is a national representative sample of Canadian adults surveyed between 1986 and 1992 (12). A participant was considered active if he or she reported at least 30 min of PA that induced sweating at least once a week over the last 30 days. If he or she did not meet these criteria, he or she was considered inactive. Men who were physically active were 55% less likely to have metabolic syndrome (OR 0.45; 95% CI, 0.29–0.69). However, the effect was attenuated in women and did not reach statistical significance (OR 0.67; 95% CI, 0.44–1.02). Women have traditionally reported greater amounts of domestic PA, which may be at a light-to-moderate intensity and may not provide the same protection as more vigorous PA reported by men.In a more recent cross-sectional analysis of US adults participating in the 1999–2004 NHANES, the relationship between LTPA and metabolic syndrome using varying definitions was examined (16). A continuous MET·min·wk−1 (i.e., exercise METs multiplied by exercise minutes per week) variable was used to create two categorical PA variables. The first categorical variable was a six-level variable allowing a potential dose-response association to be examined. The first level represented those who reported no LTPA during the past month; the referent group for this study and the remaining five levels were divided into LTPA quintiles by MET·min·wk−1. The second LTPA measure used to examine the potential inverse relationship with metabolic syndrome was a three-level categorical variable based on PA recommendations from the ACSM/AHA (47).Investigators found a significant inverse dose-response between increasing MET·min·wk−1 from LTPA and metabolic syndrome. Interestingly, protection manifested at various doses of LTPA, illustrating differences between the two definitions. Based on the WHO criteria for metabolic syndrome, protection began at the 3rd quintile of LTPA (393–736 MET·min·wk−1) where adults were 30% (OR 0.70; 95% CI 0.51, 0.96) less likely to have metabolic syndrome. On the other hand, using the AHA/NHLBI criteria for metabolic syndrome, significant protection was not observed until the 4th quintile of LTPA (737–1360 MET·min·wk−1) where adults were 35% (OR 0.65; 95% CI 0.48, 0.88) less likely to have metabolic syndrome. Furthermore, participants engaging in a level of LTPA meeting the ACSM/AHA PA recommendations (47) were 46% (OR 0.54; 95% CI 0.44, 0.66) and 39% (0.61; 95% CI 0.48, 0.77), respectively, less likely to have the metabolic syndrome according to the WHO and AHA/NHLBI definitions compared with the referent group (no LTPA). Greater levels of PA can lead to increased levels of fitness (e.g., METs, V˙O2 max), and fitness has been shown to provide protection from metabolic syndrome. The most recent ACSM recommendations for PA (47) in 18 to 64 yr old adults is 450 MET·min·wk−1 to 750 MET·min·wk−1, and these findings fall within this range for the prevention of metabolic syndrome independent of definition.Cardiorespiratory and muscular fitness (59,60,68) have been shown to be protective for metabolic syndrome. However, some evidence suggests cardiorespiratory fitness may play a stronger role (58). Recent evidence suggests, independent of HTN, meeting the current DHHS recommendation of 2 d per week of MSA may provide protection from the remaining metabolic syndrome criteria as well as the risk of pre-HTN (19). LaMonte et al. (68) examined incident metabolic syndrome in 20 to 80 yr old adults (N = 10,498) participating in the Aerobic Center Longitudinal Study (ACLS). Following adjustment for potential confounders, men in the middle and upper tertiles of cardiorespiratory fitness were 26% (HR 0.74; 95% CI 0.65, 0.84) and 53% (0.47; 95% CI 0.40, 0.54) (P for trend <0.001), respectively, less likely to develop metabolic syndrome (mean follow-up 5.7 yr) compared with the lowest fit group. In the same models, women in the middle and upper tertiles of cardiorespiratory fitness were 20% (HR 0.80; 95% CI 0.44, 1.46) and 63% (0.37; 95% CI 0.18, 0.80) (P for trend = 0.01), respectively, less likely to develop metabolic syndrome compared with the lowest fit group.In another ACLS study, Katzmarzyk et al. (60) examined all-cause and CVD mortality in approximately 20,000 men based on overweight/obesity and metabolic syndrome. Obese men with metabolic syndrome were 55% (RR 1.55; 95% CI 1.14, 2.11) more likely to die of all causes compared with normal weight healthy men. Overweight and obese men with metabolic syndrome were 80% (RR 1.80; 95% CI 1.10, 2.97) and 183% (RR 2.83; 95% CI 1.70, 4.72), respectively, more likely to die of CVD compared with normal weight healthy men. Following adjustment for cardiorespiratory fitness, overweight and obese men with metabolic syndrome were no longer at risk for CVD mortality [over-weight (RR 1.19; 95% CI 0.72, 1.99); obese (RR 1.43; 95% CI 0.82, 2.49)]; or all-cause mortality [obese (RR 0.93; 95% CI 0.66, 1.30)]. In addition, for each 1 MET increase in cardiorespiratory fitness (based on treadmill time), men with metabolic syndrome were 19% (RR 0.81; 95% CI 0.77, 0.86) and 26% (RR 0.74; 95% CI 0.67, 0.82) less likely to die from all causes and CVD, respectively.The associations between muscular strength (58,59) and MSA (19) with metabolic syndrome and the individual syndrome criteria have also been reported. In a recent study utilizing data from the 1999–2004 NHANES, Churilla et al. (19) examined the relationship between MSA and metabolic health risk in US adults. Following adjustments for potential confounders, individuals meeting the current DHHS recommendation for MSA (>2 days per week) were 28% (OR 0.72; 95% CI 0.62, 0.83) less likely to have dyslipidemia, 29% (OR 0.71; 95% CI 0.54, 0.93) less likely to have impaired fasting glucose, and 43% (OR 0.57; 95% CI 0.46, 0.72) less likely to have an augmented waist circumference compared with those reporting no MSA. Although an association between HTN and MSA was not observed, individuals meeting the DHHS recommendation for MSA were 19% (OR 0.81; 95% CI 0.65, 0.99) less likely to have pre-HTN.The most recent PA guidelines from the DHHS (95) state that adults 18 to 64 yr old should engage in 150 min a week of moderate aerobic PA, 75 min of vigorous aerobic PA, or an aggregate measure equating to this volume. In addition, adults are also recommended to engage in a minimum of 2 d per week of MSA, as these will provide additional health benefits. The current recommended level of PA for the management of the metabolic syndrome is 30 to 60 min per day of moderate-intensity aerobic PA supplemented by 2 d per week of MSA (43). This recommendation is very similar to the earlier ACSM/AHA PA recommendations (47), with the exception of vigorous-intensity PA not being recommended in those with metabolic syndrome due to the increased risk of untoward events. In addition, this recommendation includes reducing caloric intake by 500 to 1,000 kcals per day. Many tools are readily available to assist the clinical exercise physiologist in developing safe and effective training regimens for high-risk individuals.Devices such as heart rate monitors and accelerometers are now widely available. They are easy to use and provide information on exercise volume and intensity, which are necessary for developing, monitoring, and updating exercise prescriptions. Another tool that has proved useful is the Compendium of Physical Activities, which provides estimated MET levels for many physical activities (1,2). Clinical exercise physiologists can refer to this compendium when prescribing specific activities (aerobic and muscular strengthening) based on METs. Prescribing physical activity based on METs (measured or estimated) may be helpful, as it provides estimates of energy expenditure. However, utilizing METs, especially estimated METs, when prescribing exercise warrants further investigation.Metabolic health risks including but not limited to the aggregation of CVD risk factors known as metabolic syndrome has become ubiquitous, with 30% to 40% of the US population being affected. Research has shown that meeting or exceeding current PA recommendations may be necessary for the prevention and/or management of metabolic syndrome. Evidence shows a dose-response relationship between PA and metabolic syndrome. However, more work is warranted in the area of PA type, volume, and intensity. Clinical exercise physiologists will be exposed to greater challenges as these populations continue to increase. These challenges call for increasing knowledge and skills through continuing education and certification (e.g., ACSM Registered Clinical Exercise Physiologist, ACSM Clinical Exercise Specialist). Competent and confident clinical exercise physiologists are in demand, and the field of clinical exercise physiology will play a vital role in chronic disease management, particularly in the area of metabolic health.

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