Markers of Chronic Inflammation With Short-Term Changes in Physical Activity
Markers of Chronic Inflammation With Short-Term Changes in Physical Activity
Purpose: Regular exercise is inversely related to markers of chronic inflammation, but we do not know to what extent these changes are the product of recent exercise behavior. The aim of the present investigation was to examine the stability of markers of chronic inflammation in the face of short-term positive and negative changes in physical activity in middle-aged men.
Methods: Two studies were conducted using a randomized counterbalanced design. In the first study (Study 1), eight highly active men (age = 56 ± 5 yr, body mass index (BMI) = 23.3 ± 3.2 kg·m, VO2max = 50.7 ± 7.0 mL·kg·min) undertook two trials; withdrawal of exercise for 1 wk versus control (normal exercise behavior). In the second study (Study 2), 10 sedentary men (age = 57 ± 2 yr, BMI = 27.9 ± 3.6 kg·m, VO2max = 30.4 ± 4.6 mL·kg·min) undertook 30 min of daily walking at 60% VO2max for 1 wk versus control (normal sedentary behavior).
Results: The withdrawal of exercise for 1 wk in highly active men (Study 1) and the imposition of 1 wk of daily exercise in sedentary men (Study 2) did not elicit any substantial changes in the inflammatory proteins C-reactive protein (CRP), IL-6, and TNF-α and circulating leukocyte concentration. The differences in inflammatory proteins between active (Study 1) and sedentary (Study 2) men were marked; for example, baseline CRP was 0.85 ± 0.79 and 3.02 ± 2.30 mg·L, respectively.
Conclusions: The inflammatory markers CRP, IL-6, and TNF-α are stable and not affected by large short-term positive or negative alterations in exercise behavior. This stability strengthens the use of these markers in clinical and research settings because differences and changes are not simply the product of recent exercise behavior.
Cardiovascular disease (CVD) is the number one cause of premature mortality in the United Kingdom. It is a slow-progressing disease with incidence rates increasing dramatically after the age of 45 in men. The process underlying most cases of CVD-atherosclerosis-is a chronic inflammatory condition, and prospective epidemiological studies have linked systemic inflammatory markers to risk of future cardiovascular problems.
Regular physical activity reduces the risk of developing CVD. Some of the beneficial effects are reflected by the attenuation of classic risk factors for the disease. However, prospective studies show that regular physical activity is also associated with reduced inflammation, and this has been postulated as another mechanism that explains why regular physical activity is protective against CVD.
The relationship between risk factors for CVD and physical activity is complex. One key consideration is the extent to which changes in a given risk factor are influenced by recent physical activity or exercise. Some health-related, exercise-induced benefits are gained and/or lost during a relatively short period. For example, Hardman et al. showed that plasma triacylglycerol and the ratio of total cholesterol to high-density cholesterol increased after only 60 h and 6.5 d of exercise withdrawal in endurance-trained individuals, respectively. In contrast, in response to a positive change in exercise behavior (i.e., training), Angelopoulos et al. showed a significant decrease in fasting plasma glucose and insulin concentrations after only 10 d of exercise in obese sedentary males. Indeed, significant improvements in some health-related outcomes have been shown after only a single bout of exercise.
It is very important to understand whether commonly used markers of chronic inflammation are affected by recent changes in exercise/physical activity during the preceding few days. In principle, a change in response to a long-term exercise intervention could reflect changes induced by just the last few bouts of exercise. Conversely, if a short-term absence of exercise exerted a powerful effect on markers of chronic inflammation, then even years of regular exercise training could be ostensibly "undone" with just a few days of exercise abstinence. To our knowledge, no study has investigated the effects of short-term training on inflammatory markers, and only two studies have investigated the effects of short-term detraining on selected inflammatory markers. Notably, both of these studies were in young participants, and one did not use a control group. In one of these studies, there was no mention of when the last bout of acute exercise was performed. The young age group (and very low markers of inflammation) and limitations in study design restrict the conclusions that can be drawn from these detraining investigations. It is noteworthy that many studies that have shown that exercise training reduces markers of inflammation do not include a time course (e.g.,). Therefore, in principle, it is possible that the reported changes in inflammatory markers occurred in the first few days or weeks of the exercise intervention. Consequently, as is the case for many other risk factors for CVD, it is clearly important to understand whether short-term changes in exercise and physical activity affect markers of inflammation. If markers of inflammation do respond to short-term changes in exercise or physical activity, then this would confound clinical interpretation using these markers. Therefore, the aim of the present study was to examine whether markers of chronic inflammation are stable in the face of short-term positive and negative changes in exercise behavior in middle-aged men.
Abstract and Introduction
Abstract
Purpose: Regular exercise is inversely related to markers of chronic inflammation, but we do not know to what extent these changes are the product of recent exercise behavior. The aim of the present investigation was to examine the stability of markers of chronic inflammation in the face of short-term positive and negative changes in physical activity in middle-aged men.
Methods: Two studies were conducted using a randomized counterbalanced design. In the first study (Study 1), eight highly active men (age = 56 ± 5 yr, body mass index (BMI) = 23.3 ± 3.2 kg·m, VO2max = 50.7 ± 7.0 mL·kg·min) undertook two trials; withdrawal of exercise for 1 wk versus control (normal exercise behavior). In the second study (Study 2), 10 sedentary men (age = 57 ± 2 yr, BMI = 27.9 ± 3.6 kg·m, VO2max = 30.4 ± 4.6 mL·kg·min) undertook 30 min of daily walking at 60% VO2max for 1 wk versus control (normal sedentary behavior).
Results: The withdrawal of exercise for 1 wk in highly active men (Study 1) and the imposition of 1 wk of daily exercise in sedentary men (Study 2) did not elicit any substantial changes in the inflammatory proteins C-reactive protein (CRP), IL-6, and TNF-α and circulating leukocyte concentration. The differences in inflammatory proteins between active (Study 1) and sedentary (Study 2) men were marked; for example, baseline CRP was 0.85 ± 0.79 and 3.02 ± 2.30 mg·L, respectively.
Conclusions: The inflammatory markers CRP, IL-6, and TNF-α are stable and not affected by large short-term positive or negative alterations in exercise behavior. This stability strengthens the use of these markers in clinical and research settings because differences and changes are not simply the product of recent exercise behavior.
Introduction
Cardiovascular disease (CVD) is the number one cause of premature mortality in the United Kingdom. It is a slow-progressing disease with incidence rates increasing dramatically after the age of 45 in men. The process underlying most cases of CVD-atherosclerosis-is a chronic inflammatory condition, and prospective epidemiological studies have linked systemic inflammatory markers to risk of future cardiovascular problems.
Regular physical activity reduces the risk of developing CVD. Some of the beneficial effects are reflected by the attenuation of classic risk factors for the disease. However, prospective studies show that regular physical activity is also associated with reduced inflammation, and this has been postulated as another mechanism that explains why regular physical activity is protective against CVD.
The relationship between risk factors for CVD and physical activity is complex. One key consideration is the extent to which changes in a given risk factor are influenced by recent physical activity or exercise. Some health-related, exercise-induced benefits are gained and/or lost during a relatively short period. For example, Hardman et al. showed that plasma triacylglycerol and the ratio of total cholesterol to high-density cholesterol increased after only 60 h and 6.5 d of exercise withdrawal in endurance-trained individuals, respectively. In contrast, in response to a positive change in exercise behavior (i.e., training), Angelopoulos et al. showed a significant decrease in fasting plasma glucose and insulin concentrations after only 10 d of exercise in obese sedentary males. Indeed, significant improvements in some health-related outcomes have been shown after only a single bout of exercise.
It is very important to understand whether commonly used markers of chronic inflammation are affected by recent changes in exercise/physical activity during the preceding few days. In principle, a change in response to a long-term exercise intervention could reflect changes induced by just the last few bouts of exercise. Conversely, if a short-term absence of exercise exerted a powerful effect on markers of chronic inflammation, then even years of regular exercise training could be ostensibly "undone" with just a few days of exercise abstinence. To our knowledge, no study has investigated the effects of short-term training on inflammatory markers, and only two studies have investigated the effects of short-term detraining on selected inflammatory markers. Notably, both of these studies were in young participants, and one did not use a control group. In one of these studies, there was no mention of when the last bout of acute exercise was performed. The young age group (and very low markers of inflammation) and limitations in study design restrict the conclusions that can be drawn from these detraining investigations. It is noteworthy that many studies that have shown that exercise training reduces markers of inflammation do not include a time course (e.g.,). Therefore, in principle, it is possible that the reported changes in inflammatory markers occurred in the first few days or weeks of the exercise intervention. Consequently, as is the case for many other risk factors for CVD, it is clearly important to understand whether short-term changes in exercise and physical activity affect markers of inflammation. If markers of inflammation do respond to short-term changes in exercise or physical activity, then this would confound clinical interpretation using these markers. Therefore, the aim of the present study was to examine whether markers of chronic inflammation are stable in the face of short-term positive and negative changes in exercise behavior in middle-aged men.
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