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Obesidad y sobrepeso
- 2. ¿Puede el ejercicio solo, sin ajuste de dieta, reducir el peso en forma significativa? Algunos estudios muestran significativa pérdida de peso con necesidad de “high levels of exercise” Muchos estudios muestran poco o ningún efecto de modereda cantidad de ejercicio, en el peso corporal.
- 3. ¿Por qué es difícil perder peso haciendo ejercicio solamente? La eficiencia del ejercicio en bajar de peso se altera en la medida que el peso desciende. Varias respuestas metabólicas contribuyen a la resistencia a perder peso. Las respuestas metabólicas son un mecanismo involuntario de protección evolutivo para prevenir la desnutrición y una indefinida pérdida de peso Cuando el peso corporal es reducido debido al ejercicio, en reposo se producen reducciones del gasto metabólico basal En forma colectiva esas respuestas metabólicas intentan resolver el daño potencial en el Balance Energético atenuando el impacto en el GE inducido por el ejercicio.
- 4. Efectos beneficiosos del ejercicio: cambiemos el foco de atención sobre el descenso del peso corporal hacia otros marcadores de salud N A King,M Hopkins, P Caudwell, R J Stubbs, J E Blundell Br J Sports Med 2009;43:924–927
- 5. Otros efectos de la actividad físca independientes del descenso de peso Mejoría del perfil lipídico Mejoría de la HTA leve y moderada y mejoría del tono autonómico Mejoría en la composición física: reducción de peso junto con la dieta, preservación de la masa magra, reducción de la adiposidad abdominal Reducción de la inflamación sistémica Mejoría de la función endotelial Mejoría de la sensación de bienestar y calidad de vida Aumento de la expectativa de vida
- 6. “Un gordo entrenado tiene menos riesgos para la salud que un flaco sedentario”
- 7. Ejercicio y Riesgo Cardiometabólico Global El éxito de la Actividad Física en una persona con sobrepeso/obesidad, no se debe medir solamente según cuánto bajó de peso. El ejercicio mejora todos los componentes del Riesgo Cardiometabólico Global Entrenado y gordito es mejor que flaco y sedentario, pero también entrenado y flaco es mejor que gordito y entrenado. El FCR es un nuevo componente independiente del Riesgo Cardiometabólico Global y es más relevante que la obesidad en predecir riesgo de enfermedad.
- 9. (-) AGL CPT1 Acetil CoA Citrato Malonil CoA + ACC AMPK AMP ATP Sedentarismo y exceso de alimento
- 10. AGL CPT1 Acetil CoA Citrato Malonil CoA + ACC AMPK AMP ATP
- 11. Tejido Muscular consumidor de glucosa y grasa 80 % puede ser incorporado al TM % no despreciable de lípidos oxidados Sedentarios anormal nivel glucemia, Triglicéridos, Colesterol, Alteraciones metabólicas, Riesgo cardiovascular Entrenado no sucede El tejido muscular activo = mantiene los niveles de substratos EL EJERCICIO ESTIMULA LOS MECANISMOS DE ADAPTACIÓN FISIOLÓGICO Y BIOQUÍMICO
- 12. Obesidad Infantil Características Lo ingerido se convierte rápidamente en grasa Incapacidad de abstenerse de comer lo indebido Disminución del movimiento o actividad física Alteración del esquema corporal.
- 13. Los niños obesos tienen Alteración de su imagen corporal (figura, postura, aspecto, dimensiones) Alteración en su sensopercepción del dolor, placer, hambre, saciedad. Insatisfacción de su propio cuerpo.
- 14. Rol del Profesor de Educación Física: Aliado favorecedor de la integración del niño. Detector y derivador. Motivar para realizar actividad física / Incentivar una actitud más activa. Actividades que trabajen el Esquema corporal, la estructuración del espacio – tiempo – objeto el equilibrio estático y dinámico, beneficiarán su condición. Trabajar la autoconfianza. Tener en cuenta que las cargas e impactos del ejercicio Normopeso # Obeso. Contactarse con los padres.
Notas del editor
- Dada la intensidad necesaria para que el ejercicio sea exitoso en bajar de peso, no sorprende que los clínicos tengan pobres resultados y por lo tanto predomine una idea pesimista acerca del ejercicio como modo de controlar el peso
- The mistake is to consider that the benefits of exercise for obesity proceed only from weight loss and to think that if the subject does not lose weight the exercise is unsuccessful ABSTRACT Background: Exercise is widely promoted as a method of weight management, while the other health benefits are often ignored. The purpose of this study was to examine whether exercise-induced improvements in health are influenced by changes in body weight. Methods: Fifty-eight sedentary overweight/obese men and women (BMI 31.8 (SD 4.5) kg/m2) participated in a 12-week supervised aerobic exercise intervention (70% heart rate max, five times a week, 500 kcal per session). Body composition, anthropometric parameters, aerobic capacity, blood pressure and acute psychological response to exercise were measured at weeks 0 and 12. Results: The mean reduction in body weight was -3.3 kg (p,0.01). However, 26 of the 58 participants failed to attain the predicted weight loss estimated from individuals’ exercise-induced energy expenditure. Their mean weight loss was only 0.9 kg (p,0.01). Despite attaining a lower-than-predicted weight reduction, these individuals experienced significant increases in aerobic capacity +6.3 ml/kg/min; p,0.01), and a decreased systolic (-6.00 mm Hg; p,0.05) and diastolic blood pressure (-3.9 mm Hg; p,0.01), waist circumference (-3.7 cm; p,0.01) and resting heart rate (-4.8 bpm, p,0.001). In addition, these individuals experienced an acute exerciseinduced increase in positive mood. Conclusions: These data demonstrate that significant and meaningful health benefits can be achieved even in the presence of lower-than-expected exercise-induced weight loss. A less successful reduction in body weight does not undermine the beneficial effects of aerobic exercise. From a public health perspective, exercise should be encouraged and the emphasis on weight loss reduced. It is difficult to ignore the media attention and public health messages about the current obesity epidemic and the emphasis to reduce body weight. Despite some cynicism about the true status and implications of the obesity epidemic, there is no doubt that preventing weight gain can contribute to improving the health of the nation. The efficacy of exercise as a means of weight reduction is regularly scrutinised and doubted. Body weight loss is commonly regarded as the marker of efficacy by researchers, and more typically the perceived measure of success by lay people. Any lack of weight loss associated with exercise is often attributed to poor compliance and/or compensation for the acute exercise-induced increase in energy expenditure. That is, the net change in exercise-induced energy expenditure is modest and insignificant due to compensatory adjustments in energy intake and a failure to comply fully with the exercise prescription. Clearly, if people do not comply with the exercise prescribed (by themselves or others), the expected weight loss will not occur. The success of exercise in promoting weight loss will vary between individuals; however, those who lose less weight should not be labelled as failures or be perceived negatively. Evidence suggests that individuals have unrealistic weight loss expectations, which is indicative of an inappropriate focus on body weight. Blair and Lamonte suggested that ‘‘a focus on weight loss is often counterproductive and unsuccessful, and sometimes may even be unnecessary.’’ Furthermore, body weight per se might not be the most important risk factor for obesity comorbidities. It is possible that media attention and the persistent barrage of messages to reduce obesity are to blame for the obsession with the capacity of exercise to produce marked and rapid weight loss. Exercise gives rise to a wide range of health benefits, not just weight loss. Disappointment and low-self esteem associated with poor weight loss could lead to low exercise adherence and a general perception that exercise is futile and not beneficial. This viewpoint is potentially damaging—a more transparent and positive attitude to the health benefits of exercise is required. Individuals who drop out of exercise interventions—possibly due to disappointing weight loss—have a history of previous weight loss attempts, and exercise adherence is associated with intrinsic motivation. Unfortunately, focusing on exercise-induced changes in body weight undermines the arguably more important health benefits associated with exercise. Although there is some debate about the direct association between weight loss per se and health benefits, there is evidence to suggest that reductions of 5–10% in body weight improve some health risk markers. For several years Steven Blair has promoted the idea that fitness is more important than fatness, since there are data to demonstrate that a fat but fit person has fewer health risks than a lean but unfit individual. There is a real need to promote physical activity and to prevent it being undervalued by the community and by public health professionals. In fact, when sedentary people undertake exercise, the activity provides a massive stimulus with widespread physiological implications. The effect cannot be readily anticipated, but studies have noted considerable diversity in the responses. In addition, the energy expended in exercise is believed, by some, to stimulate compensation so that energy balance is preserved. We have examined these issues under controlled scientific conditions. MATERIALS AND METHODS Fifty-eight sedentary overweight/obese men (BMI 30.5 (SD 3.3) kg/m2) and women (BMI 32.6 (4.8) kg/m2) completed a 12-week supervised aerobic exercise programme (70% heart rate max) five times a week. Each exercise session was designed to expend approximately 500 kcal. Body composition (air plethysmography), anthropometry, aerobic capacity (submaximal VO2 max test), blood pressure, resting heart rate and the acute affective response (Positive and Negative Affect Scale (PANAS)) to exercise were measured at weeks 0 and 12. Subjects were instructed not to restrict their energy intake during the study. RESULTS When all 58 subjects’ data were pooled, the mean reduction in body weight was -3.3 (3.6) kg (p,0.01)—however there was large interindividual variability. Further examination of the weight-change data revealed that subjects could be categorised into two groups (responders and non-responders) based solely on their actual initial weight relative to the calculated weight change.The non-responders (n=26) lost less weight than predicted based on their individual total exercise-induced energy expenditure. Although statistically significantly lower than baseline (week 0), their mean weight loss was only -0.9 kg (p,0.01), compared with the remaining participants (responders) who experienced an average weight loss of -5.2 kg (p,0.01). Indeed, some of the classified non-responders actually gained weight Therefore, based on body weight alone, exercise could be regarded as ineffective and futile for the nonresponders (and even counterproductive for the weight gainers). However, the effectiveness of exercise should not be exclusively judged on changes in body weight because it undermines the other health benefits that are commonly associated with exercise. Despite the lower-than-expected weight loss, the non-responders did achieve improvements in health markers. They experienced a significant increase in aerobic capacity (6.3) ml/kg/min; p,0.01), reduction in waist circumference (-3.08 cm; p,0.01), and decreases in systolic (-6.0 mm Hg; p,0.05), diastolic blood pressure (-3.9 mm Hg; p,0.01) and resting heart rate (-4.8 bpm; p,0.001). The reduction in both systolic and diastolic blood pressure was more marked when examining the changes in those individuals who were classed as hypertensive (140/90 mm Hg) at baseline. They experienced a significant reduction in systolic (-15 mm Hg p,0.0001) and diastolic (-10 mmHg p,0.0001) blood pressure. In addition to the reduction in health risk markers, the nonresponders experienced an acute improvement in psychological state reflected in the exercise-induced increase in positive mood, which was maintained during the 12 weeks. Interestingly, although the difference in weight loss between the groups was statistically significant, there were no statistically significant differences in the health benefits. Furthermore, when all subjects’ data were pooled, there was no association between weight loss and improvements in health markers. Therefore, the exercise itself, independent of weight loss, made a significant contribution to the health benefits. There were no significant differences between men and women, and the proportion of men in each group was similar Moreover, these results show that, if people fail to lose weight following a recommendation to perform physical activity, it is not necessarily a result of poor compliance. In some individuals, who are resistant to weight loss, it will be due to strong physiological compensatory processes. DISCUSSION These data demonstrate that significant and meaningful health benefits can be achieved even in the presence of lower- than expected exercise-induced weight loss. A novel feature of this study is that the exercise intervention was supervised, and each session was monitored and measured directly. Therefore, unlike most of the other exercise intervention trials, we can guarantee that the lower-than-expected weight loss was not due to poor compliance. Indeed, the degree of adherence and total exercise energy expenditures did not differ between the two groups. Importantly, based on each individual’s predicted weight loss, those who lost less weight than predicted still experienced improvements in other markers of health. It is important to note that these health markers are not overtly accessible to most individuals, whereas other markers such as body weight, perceptions of fitting of clothes and perceived body image are more accessible and transparent. Therefore, most individuals are ‘‘blind’’ to the exercise-induced health improvements. Indeed, these data demonstrate that subjects who lost less than the predicted weight still experienced a mean reduction of approximately 3.7 cm in waist circumference. Waist circumference is promoted as being more important than BMI at predicting risk of obesity-related disease,and a better marker of success than BMI in response to exercise. The reductions in diastolic and systolic blood pressure in the non-responders were similar to other studies. There is a need to increase knowledge and understanding of the health benefits of exercise, and reduce the emphasis on weight loss. This agrees with the evidence that cardiorespiratory fitness is a more powerful predictor of risk than body weight. In addition, evidence from the Finnish Diabetes Preventions study showed that individuals who did not lose weight but who did increase their physical activity maintained a reduction in the risk of diabetes. Among the subjects in the intervention group who did not reach the goal of losing 5 percent of their initial weight, the odds ratio for diabetes in those who had achieved the goal with respect to exercise (more than four hours per week) during the first year was 0.2 (95 percent confidence interval, 0.1 to 0.6) as compared with those in the intervention group who maintained a sedentary lifestyle. Exercise should be promoted as an optimistic method of improving weight management and overall health by highlighting the importance of using othermarkers of success. Weight loss is not the only benefit of exercise; nor is it the most useful and appropriate marker of health. A recent intervention in postmenopausal obese women using low-intensity, low-volume exercise showed improvements in cardiorespiratory fitness with no effect on body weight. Furthermore, partly due to the culture of focusing on obesity and weight loss, individuals will actively seek opportunities which are specifically targeted to promote weight loss—and exercise is one of those. From a public health perspective, exercise should therefore be encouraged; and even though body weight may not change markedly, or match expectations, lean tissue will be increased (or preserved), and body shape will change (waist circumference). There will also be a lowering of risk factors for comorbidity problems and diabetes. In the present study, the reduction in waist circumference—even in the non-responders—is important, since this variable is a proxy measure of visceral fat which is highly associated with cardiometabolic risk factors. It may therefore be important to encourage the replacement of BMI and body weight with waist circumference as a measure of the effectiveness of exercise. thin this framework, there is a key role for physicians and health professionals. These professionals—including dietitians— not only can promote physical activity as a contribution to health but also can be instrumental in improving weight management in non-responders. We have demonstrated that non-responders fail to lose the expected weight because of an increase in appetite reflected in an increased selection of high-fat foods and a decrease in fruit and vegetable consumption and because of an increased orexigenic (hunger) response. Therefore, using dietary behaviour strategies, dietitians and health professionals could help to counter appetite stimulation in the non-responders and therefore help weight management while preserving all of the health benefits of exercise. In conclusion, these data provide support for the belief that poor weight loss associated with exercise should not undermine its capacity to improve health. Health rofessionals, it can be argued, have a responsibility to promote exercise, publicise the health benefits independent of body weight and, more importantly, shift the focus from changes in body weight to changes in overall physical and psychological well-being. Our intervention study has clearly demonstrated that when exercise is carried out, people experience beneficial physiological and psychological effects independent of any effect on body weight. However, the implication of these results for weight management and the obesity epidemic should be interpreted carefully. The results do not mean the exercise is fruitless or ineffective in the battle against obesity. Overall, exercise can help to check weight gain, and in some people it is very effective. Others need additional help to deal with any compensatory response.
- Dyslipidemia The atherogenic lipid profile, consisting of hypertriglyceridemia, low levels of high-density lipoprotein (HDL)-cholesterol, and high levels of low-density lipoprotein (LDL)-cholesterol, in particular small and dense LDL particles, has been tied to abdominal obesity, insulin resistance, and cardiovascular-related morbidity and mortality. Additionally, levels of apolipoprotein-B, the apolipoprotein moiety of the atherogenic lipoproteins (very low–density lipoprotein, intermediate-density lipoprotein, and LDL), have been shown to predict CVD and related events, independent of traditional risk factors. Acute physical activity. Subsequent to the seminal work of Holloszy et al. numerous studies have reinforced the notion that a single bout of aerobic physical activity can lead to significant reductions in TGs and increases in HDLcholesterol levels. These lipid changes are apparent between 24 and 48 h after acute physical activity in both untrained and trained subjects in response to caloric expenditures of 350–500 and 1,000 kcal, respectively. Typical reductions in TG levels range in magnitude from about −10 to −25%, and are greatest among those with the highest baseline TG values. In comparison, increases in HDL-cholesterol after acute activity range from ~7 to 15%. These increases are largely due to the increase in the HDL3-C subfraction amonguntrained subjects, in contrast to the predominant increase in HDL2-C among trained subjects. Although no minimum duration of physical activity appears to exist for inducing improvements in TG or HDL-C, generally, the greater the duration of the physical activity bout, and thus the greater the caloric expenditure, the more pronounced the improvement in lipid levels. On the other hand, the intensity of the acute activity bout has not been shown to have a clear effect on the degree of lipid improvements. Although reductions in LDL-C following extreme feats of physical activity (i.e., following a 42-km marathon) have been reported, more modest sessions of aerobic activity (350–500-kcal expenditures) have failed to note a change in LDL-C levels. Finally, in contrast to the reductions generally reported following chronic physical activity acute aerobic activity (inducing a 350-kcal energy expenditure) in both trained and untrained subjects has been reported to transiently elevate levels of apolipoprotein-B by 4–9%. Chronic physical activity. The evidence for beneficial lipid changes due to chronic physical activity is strongest for HDL-C and TG. A meta-analysis reveals that 30–60 min of aerobic physical activity, 3–5 times per week, at a moderate intensity results in a mean increase in HDL-cholesterol levels of ~4% (0.05 mmol/l), predominantly as a result of increases in the HDL2-C subfraction, and a decrease in TG levels of ~12%. Others have concluded that physical activity, which induces an energy expenditure of 1,200–2,200 kcal/week, may bring about a 4–22% increase in HDL-cholesterol levels, and a 4–37% decrease in TG levels. Considering that every 0.025 mmol/l increase in HDL-C has been shown to reduce risk of CVD by ~5%, these findings suggest that only a modest amount of physical activity is required to produce clinically significant improvements in HDL-cholesterol and TGs. However, a clear dose–response relationship between duration of physical activity and lipid changes has yet to be established. Additionally, it is apparent that the relative intensity of the activity and the extent of the improvement in cardiorespiratory fitness in response to training has little if any appreciable influence on lipid changes. In contrast to the consistent findings for HDL-C and TG, the preponderance of available evidence suggests that chronic physical activity does not significantly alter the levels of LDLcholesterol. However, an elevated proportion of small, dense LDL particles has been shown to predict incidence of CVD independently of total LDL-cholesterol levels. It is thus noteworthy that irrespective of training intensity and clinically significant weight loss, 25 min of daily aerobic activity can increase the mean LDL particle size without altering total LDL-cholesterol levels. Additionally, cross-sectional studies suggest that those who are most active tend to have the lowest apolipoprotein-B levels. A number of exercise intervention studies have also shown physical activity to significantly reduce apolipoprotein-B levels by a magnitude of 7–20%. This reduction appears to be greatest among those with elevated baseline TG concentrations. Although it has previously been suggested that physical activity–induced weight-loss must be achieved in order to bring about significant improvements in lipid status, others have concluded that while improvements in HDL-C and TG are generally greater in those who lose weight, these improvements can be seen even when weight remains virtually unchanged. For example, a number of physical activity interventions that do not significantly alter body weight have documented −5 to −35% reductions in TG levels and/or 3–5% increases in HDL values. Additionally, others have failed to note a correlation betwe en reductions in body weight and changes in TG, HDL-C, and apolipoprotein-B. Finally, significant increases in the average LDL-C particle size have also been noted in response to physical activity consequent to clinically insignificant weight changes (<2% reduction). These lipid improvements independent of significant weight reduction may be mediated by improvements in body composition, such as increases in skeletal muscle mass or reductions in intra-abdominal fat and/or improvements in cardiorespiratory fitness. Indeed, physical activity–induced reductions in visceral fat have been shown to independently predict improvements in lipid status. Additionally, although the improvement in cardiorespiratory fitness in response to training have apparently little influence on TG and HDL-C changes, the reduction in apolipoprotein-B levels have been reported to correlate with improvement in cardiorespiratory fitness, independent of changes in abdominal obesity. Hypertension Inactivity is a major risk factor for high blood pressure, and sedentary individuals have up to a 50% greater likelihood of being hypertensive as compared to more active counterparts. Acute physical activity . Postexercise hypotension is especially pronounced among hypertensive individuals with documented maximal reductions in systolic (SBP) and diastolic blood pressure (DBP) of −11 and −6 mm Hg. The onset of postexercise hypotension is immediate and can persist for up to 22 h after an acute bout of aerobic physical activity. Available evidence suggests that as little as 15 min of low-intensity (40% of maximal oxygen consumption) aerobic physical activity can induce marked postexercise hypotension that persist throughout the day. These encouraging results suggest that independent of any training effects, repeated bouts of aerobic physical activity may be a viable treatment strategy for the treatment of mild hypertension. Chronic physical activity . In fact, chronic physical activity has been shown to reduce both SBP and DBP in lean, obese, hypertensive and normotensive subjects. The results of various reviews and meta-analyses suggest that independent of age and BMI, 40 min of moderate-intensity physical activity performed three times per week reduces SBP by a range of −3 to −11 mm Hg and DBP by −3 to −8 mm Hg. Further, the blood pressure reductions are significantly greater among hypertensive vs. normotensive subjects (−7 and −5 mm Hg vs. −2 and −2 mm Hg reductions in SBP and DBP, respectively). In contrast to the short duration of postexercise hypotension, the blood pressure reductions of chronic physical activity can take up to 2 weeks of inactivity to fully dissipate. Interestingly, the training-induced blood pressure reductions do not appear to be related to alterations in body weight or abdominal obesity. Instead, the blood pressure reductions in response to chronic physical activity are suggested to result from reduced systemic vascular resistance attributable to alterations in autonomic nervous system activity, renin–angiotensin system activity, and/or endothelial function. With regard to ideal physical activity training parameters, most reports have suggested that low-to-moderate intensity is ideal for inducing reductions in blood pressure, but other parameters (duration, frequency) have no clear impact on the level of improvement. Although chronic physical activity will rarely bring about normal blood pressure in previously hypertensive individuals, given that a 2 mm Hg reduction in SBP is associated with a 4–6% lower risk of mortality due to stroke and coronary heart disease, these apparently modest effects may be clinically significant. Thrombosis Acute physical activity. The notion of acute physical activity acting as a trigger for myocardial infarction is well established. Indeed, although physical inactivity is a major risk factor for thrombosis, an acute bout of strenuous physical activity among sedentary and at-risk individuals has been reported to lead to a prothrombotic state, and predispose to cardiovascular events. Interestingly, a single bout of physical activity appears to simultaneously augment both coagulation and fibrinolysis). However, although increased coagulation persists into the recovery period, the enhanced fibrinolysis quickly dissipates, thus providing an ideal environment for clot formation postactivity. Additionally, acute physical activity can also in crease blood platelet adhesiveness and aggregation, changes which may further predispose to a cardiovascular event. Nevertheless, numerous potential factors can influence the effect of acute physical activity on thrombosis such as baseline fitness and intensity of the activity. For example, a number of studies have documented that while acute moderate-intensity (55–65% VO2 max) physical activity can lead to improved fibrinolysis and attenuated platelet adhesiveness and aggregation, high-intensity (80% VO2 max) exercise can induce the opposite effect resulting in a prothrombotic state. Chronic physical activity. Cross-sectional studies regularly document an antithrombotic effect of chronic physical activity. Additionally, intervention studies have documented an enhanced fibrinolytic capacity following physical activity training, as indicated by an increase in tissue plasminogen activator and a decrease in its inhibitor (plasminogen activator inhibitor-1). Chronic aerobic physical activity at a moderate intensity also appears to suppress platelet adhesiveness and aggregation at rest and following acute intense physical activity, and thus may attenuate the cardiovascular risk associated with an acute bout of high- intensity activity. Emerging evidence also suggests that chronic physical activity may increase levels of adiponectin, a cytokine released from adipose tissue that may act to decrease thrombosis and platelet aggregation. Nevertheless, the effects of chronic exercise on these hemostatic factors are reversed to pretraining values within 4 weeks of cessation of regular physical activity, and suggest that regular exercise must be maintained for sustained antithrombotic effects. Lastly, although weight reduction has been shown to lead to improvement in hemostatic factors, the independent effects of chronic physical activity and weight reduction on thrombosis are largely unknown. Systemic inflammation Systemic inflammation is postulated to be the common thread linking various cardiometabolic risk factors including insulin resistance, obesity, and dyslipidemia. Chronic low-grade inflammation, as evidenced by the increased concentration of proinflammatory markers such as C-reactive protein (CRP), tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) among others, may also be a causal factor in the development of atherosclerosis. Acute physical activity. Similar to the evidence for thrombosis, an acute bout of physical activity has been shown to lead to an overall proinflammatory state, as evidenced by significantly elevated (up to 2,000%) levels of CRP postactivity. The magnitudeof the spike in inflammation due to physical activity depends highly on activity intensity, duration, the mass of the musculature recruited, and cardiorespiratory fitness of the participant. An ~100-fold increase of IL-6 is the most immediate and pronounced inflammatory marker response to acute activity (168); an effect that can directly augment CRP levels by promoting its production by the liver. It is thought that the combination of muscle injury and the process of muscle contraction are likely responsible for the rise in IL-6 during acute physical activity Interestingly, acute physical activity is also associated with elevations in numerous anti-inflammatory markers (i.e., IL-10) as well as inhibitors of proinflammatory markers (i.e., IL-1 receptor antagonist). This simultaneous increase in anti-inflammatory mediators may, via counter-regulation, act to limit the extent and duration of the inflammatory response to acute physical activity. Chronic physical activity. Counter to the proinflammatory effect of acute physical activity, numerous cross-sectional studies have documented an inverse relationship between levels of chronic exercise and systemic levels of inflammatory markers. Paradoxically, given that high-intensity acute activity results in the greatest inflammatory response, in reference to chronic physical activity, vigorous intensity appears to be superior to low or moderate intensity for the reduction of inflammation. Additionally, only a limited number of intervention studies have examined the effect of exercise training on systemic inflammation ). Most, but not al exercise interventions ranging in duration from 3 to 9 months reported significant reductions in inflammatory status postintervention. Chronic physical activity also appears to blunt the acute inflammatory response to a single strenuous bout of activity. As is true with other cardiometabolic risk factors, physical activity–induced improvements in inflammatory status may be exclusive to individuals with high levels of inflammatory markers at baseline. The magnitude of reduction in the levels of inflammatory markers postexercise intervention appears to be around 25–48%. In all, the available evidence would support the contention that regular exercise, of sufficient intensity, appears to be anti-inflammatory in nature. A recent systematic review concluded that weight reduction is linearly associated with decrements in CRP, such that for every 1 kg reduction in body weight CRP levels fell by −0.13 mg/l. However, others have shown that increases in physical activity and reductions in body weight are independently predictive of improvements in inflammatory status, suggesting that in the absence of body-weight change chronic physical activity may reduce inflammatory markers. Nonetheless, some have also noted that without significant weight loss, chronic physical activity appears to have no effect on inflammatory status. Thus, it remains unclear whether chronic physical activity independent of significant weight loss has an effect on reducing systemic inflammation. Cardiorespiratory fitness: a novel component of global cardiometabolic risk? Prospective studies from the Aerobics Center Longitudinal Study have consistently reported that cardiorespiratory fitness is a significant predictor of mortality from all-causes and cardiovascular disease, and T2D, independent of obesity status (weight, BMI, or waist circumference). Indeed, it has been shown that cardiorespiratory fitness may be more relevant than obesity in predicting disease risk, as obese individuals with high cardiorespiratory fitness are at lower risk of CVD mortality than lean and unfit individuals. These observations have been confirmed in other cohorts, and remain true independent of visceral fat amount, and levels of other cardiometabolic risk factors such as cholesterol, blood pressure, and blood glucose Importantly, it has been documented that the level of physical activity required to attain moderate or even high levels of cardiorespiratory fitness for most individuals approximates the currently recommended 30 min of moderate-intensity aerobic activity on most days of the week. Given that low cardiorespiratory fitness robustly predicts risk of morbidity and mortality independent of weight status and other cardiometabolic risk factors, it is reasonable to suggest that it be regarded as a genuine cardiometabolic risk factor. Although cardiorespiratory fitness has a significant genetic component, which explains up to 40% of its variance, the level of habitual physical activity is a major determinant of cardiorespiratory fitness and an increase in cardiorespiratory fitness is a well-established outcome in response to properly prescribed aerobic exercise training. In 1998, the American College of Sports Medicine (ACSM) published a position paper with recommendations for the optimal exercise prescription for improving cardiorespiratory. Specifically, the ACSM recommends 20–60 min of continuous or intermittent (minimum of 10-min bouts accumulated throughout the day) aerobic activity performed at a moderate intensity (50–85%of VO2 max) for 3–5 days/week to improve cardiorespiratory fitness. It is estimated that physical activity performed in accordance with these guidelines for a minimum of 6 months would result in a 10–30% increase in cardiorespiratory fitness, depending on genetic background and baseline levels. Indeed, the results of Project Active, performed by colleagues at the Cooper Institute, showed that a structured, 6-month exercise program according to the ACSM guidelines (i.e., 20–60 min of aerobic exercise at 50–85% of VO2 max performed on 3–5 days/week) resulted in a 14% increase in cardiorespiratory fitness among a large group of sedentarymiddle-aged men and women. More recently, Davidson et al. reported that 6 months of either aerobic or the combination of aerobic and resistance exercise training in accordance with ACSM guidelines among sedentary older adults resulted in a 14–18% increase in cardiorespiratory fitness. Additionally, shorter-term (12–14 weeks) physical activity interventions have also been shown to induce significant improvements in cardiorespiratory fitness in men and women. Lastly, it is key to note that cardiorespiratory fitness can improve in response to an exercise stimulus that may fail to induce a significant reduction in body weight. For instance, in the studies of Ross et al. wherein exercising subjects maintained weight by consuming compensatory calories, ~3 months of daily moderate-intensity physical activity resulted in a 19 and 22% increase in cardiorespiratory fitness in obese middle-aged men and women, despite no change in body weight. Thus, by improving an individual’s cardiorespiratory fitness level, the adoption of a physically active lifestyle may reduce the risk of CVD and related mortality without a significant impact on obesity level. Hence, we recommended that cardiorespiratory fitness be considered an important and independent component of global cardiometabolic risk and that it be assessed in clinic as an objective measure of changes in physical activity level. Although the measurement of cardiorespiratory fitness in clinical practice may be difficult for pragmatic reasons, referral of patients to properly trained exercise specialists or kinesiologists working at commercial and/or public health facilities offers a reasonable alternative to practitioners.
- Regulation of fatty acid oxidation by AMPK . The AMPK pathway has profound effects on the regulation of lipid metabolism. Fatty acid oxidation in skeletal muscle involves a rate-controlling step that is regulated by carnitine palmitoyltransferase 1 (CPT1). CPT1 transfers long-chain acyl-CoA into the mitochondria, and this process is inhibited allosterically by malonyl-CoA, synthesized by acetyl CoA carboxylase (ACC). The activity of ACC is regulated by reversible phosphorylation, and AMPK directly phosphorylates and inactivates this downstream target. During exercise and skeletal muscle contraction, activated AMPK inhibits ACC to reduce malonyl-CoA concentration, thereby driving the entry of long-chain acyl-CoA into the mitochondria for β -oxidation to restore energy balance. The ability of AMPK to induce lipid oxidation and thus lower skeletal muscle and liver lipid deposition is considered an important feature for the insulinsensitizing effect of AMPK activation. Indeed, when an activating form of AMPK γ 3(R225Q) subunit is expressed in skeletal muscle via genetic manipulation, the transgenic mice are protected against the development of diet-induced skeletal muscle insulin resistance. This effect is associated with lower skeletal muscle triglyceride stores as a result of increased fatty acid oxidation.
- Regulation of fatty acid oxidation by AMPK . The AMPK pathway has profound effects on the regulation of lipid metabolism. Fatty acid oxidation in skeletal muscle involves a rate-controlling step that is regulated by carnitine palmitoyltransferase 1 (CPT1). CPT1 transfers long-chain acyl-CoA into the mitochondria, and this process is inhibited allosterically by malonyl-CoA, synthesized by acetyl CoA carboxylase (ACC). The activity of ACC is regulated by reversible phosphorylation, and AMPK directly phosphorylates and inactivates this downstream target. During exercise and skeletal muscle contraction, activated AMPK inhibits ACC to reduce malonyl-CoA concentration, thereby driving the entry of long-chain acyl-CoA into the mitochondria for β -oxidation to restore energy balance. The ability of AMPK to induce lipid oxidation and thus lower skeletal muscle and liver lipid deposition is considered an important feature for the insulinsensitizing effect of AMPK activation. Indeed, when an activating form of AMPK γ 3(R225Q) subunit is expressed in skeletal muscle via genetic manipulation, the transgenic mice are protected against the development of diet-induced skeletal muscle insulin resistance. This effect is associated with lower skeletal muscle triglyceride stores as a result of increased fatty acid oxidation.