Acute immune-inflammatory responses to a single bout of aerobic exercise in smokers; The effect of smoking history and status

© 2015 Kastelein, Duffield and Marino. This study examined the acute immune and inflammatory responses to exercise in smokers compared to non-smokers, and further, the effect of smoking history on these immune-inflammatory responses. Fifty-four recreationally active males who were either smokers (SM; n = 27) or non-smokers (NS; n = 27) were allocated into either young (YSM, YNS) or middle-aged groups (MSM, MNS) based on smoking status. Participants were matched for fitness and smoking habits and following familiarization and baseline testing, undertook an exercise protocol that involved 40 min of cycle ergometry at 50% of VO2peak. Venous blood was obtained pre- and post- (0 min, 1, and 4 h) exercise to measure circulating leukocytes and inflammatory markers interleukin (IL)-6, IL-1β, IL-1ra, and monocyte chemoattractant protein-1 (MCP-1). Compared to MNS, MSM showed elevated basal concentrations of MCP-1, which were increased with a longer smoking history (P < 0.05). In response to exercise, YSM demonstrated an amplified IL-6 response from immediately- to 1 h-post compared to YNS. Furthermore, IL-1ra in YSM was elevated above that of YNS across all time points (P < 0.05). The MSM group had higher IL-1β at baseline when compared to YSM, although IL-1ra was greater for YSM at baseline (P < 0.05). Finally, the post-exercise leukocyte response was greater in MSM compared to YSM and non-smokers (P < 0.05). In conclusion, smoker's exhibit elevated MCP-1 and IL-1β that seem to be evident with a longer smoking history (~15 years). Furthermore, the differences in exercise-induced inflammatory responses noted in YSM may be indicative tobacco smoke exposure priming circulating leukocytes to amplify inflammatory responses

The effect of high-intensity aerobic interval training on markers of systemic inflammation in sedentary populations

© 2017, Springer-Verlag Berlin Heidelberg. Purpose: This study examined the effects of high-intensity interval training (HIIT; 30 s sprint, 4–5 min passive recovery) and prolonged intermittent sprint training (PIST; 10 s sprint, 2–3 min moderate exercise) on the systemic inflammatory markers C-reactive protein (CRP) and tumor necrosis factor-α (TNF-α), aerobic capacity, and anthropometry in a middle-aged, sedentary population. Methods: Fifty-five sedentary adults (age 49.2 ± 6.1 years) were randomised into HIIT (n = 20), PIST (n = 21), or a sedentary control group (CTRL n = 14). HIIT and PIST performed three training sessions per week for 9 weeks on a cycle ergometer, matched for total high-intensity time, while CTRL continued normal sedentary behaviours. Pre- and post-intervention testing involved measures of anthropometry, peak oxygen consumption (VO2peak), and venous blood collection for analyses of CRP and TNF-α. Results: HIIT and PIST increased VO2peak compared to CTRL (+3.66 ± 2.23 and 3.74 ± 2.62 mL kg min−1). A group × time interaction (p = 0.042) and main effect of time (p = 0.026) were evident for waist girth, with only HIIT showing a significant reduction compared to CTRL (−2.1 ± 2.8 cm). TNF-α and CRP showed no group × time interaction or time effect (p > 0.05). Conclusions: In sedentary individuals, 9 weeks of HIIT or PIST were effective to improve aerobic capacity; however, only HIIT significantly reduced waist girth and WHR compared to CTRL. Markers of systemic inflammation remained unchanged across all groups. Accordingly, for inflammation and VO2peak, the distribution of sprints and the active or passive recovery periods are inconsequential provided that total duration of high-intensity efforts is similar

Cerebral oxygenation and sympathetic responses to smoking in young and middle-aged smokers

© The Author(s) 2016. This study examined the effects of acute tobacco smoking on cerebral oxygenation and autonomic function in 28 male, habitual smokers of shorter young smokers (YSM) or longer middle-aged smokers (MSM) smoking history. Following baseline testing, participants undertook a smoking protocol involving the consumption of two cigarettes within 15 min. Measures of cerebral oxygenation and autonomic function were collected before, during, and 0 min, 30 min, 1 h, and 4 h post-smoking. Tissue saturation index (TSI) for MSM was greater than YSM during cigarette consumption (p < 0.05). Moreover, MSM observed significant within-group changes for TSI during and post-cigarette consumption (p < 0.05). Further, MSM observed an increase in low frequency (LF) band from 30 min to 1 h post-consumption, followed by a decline, whereas elevations above MSM were observed in YSM at 4 h (p < 0.05). Both MSM and YSM showed a decrease in high-frequency (HF) band post-cigarette, while increased LF/HF ratio post-consumption was observed in YSM. A decline in the standard deviation of RR intervals, post-cigarette consumption was evident in MSM (p < 0.05). Moreover, the root mean square of RR interval in both groups similarly decreased following cigarette consumption (p < 0.05). Acute smoking affects heart rate variability, suggestive of vagal withdrawal, and maybe indicate an effect of smoking history. Additionally, prolonged smoking history alters cerebral microcirculatory responses to acute tobacco exposure in MSM

Analysis of arterial intimal hyperplasia: review and hypothesis

which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Background: Despite a prodigious investment of funds, we cannot treat or prevent arteriosclerosis and restenosis, particularly its major pathology, arterial intimal hyperplasia. A cornerstone question lies behind all approaches to the disease: what causes the pathology? Hypothesis: I argue that the question itself is misplaced because it implies that intimal hyperplasia is a novel pathological phenomenon caused by new mechanisms. A simple inquiry into arterial morphology shows the opposite is true. The normal multi-layer cellular organization of the tunica intima is identical to that of diseased hyperplasia; it is the standard arterial system design in all placentals at least as large as rabbits, including humans. Formed initially as one-layer endothelium lining, this phenotype can either be maintained or differentiate into a normal multi-layer cellular lining, so striking in its resemblance to diseased hyperplasia that we have to name it &quot;benign intimal hyperplasia&quot;. However, normal or &quot;benign &quot; intimal hyperplasia, although microscopically identical to pathology, is a controllable phenotype that rarely compromises blood supply. It is remarkable that each human heart has coronary arteries in which a single-layer endothelium differentiates earl

The Acute Exercise-Induced Inflammatory Response: A Comparison of Young-Adult Smokers and Nonsmokers

© 2017 SHAPE America. Purpose: This study examined postexercise inflammatory and leukocyte responses in smokers and nonsmokers, as well as the effects of cigarette smoking on the acute postexercise inflammatory and leukocyte response in habitual smokers. Method: Eleven recreationally active male smokers and 11 nonsmokers matched for age and aerobic fitness were familiarized and underwent baseline fitness testing. Participants then completed 40 min of cycling at 50% peak aerobic workload. Smokers performed 2 randomized exercise sessions, including an acute postexercise smoking condition (2 cigarettes in 15 min of 12 mg tar and 1 mg nicotine) and a no-smoking condition, while nonsmokers performed 1 exercise session without smoking. Venous blood was obtained preexercise and postexercise for analysis of interleukin (IL)-6, IL-1 receptor antagonist (ra), tumor necrosis factor-alpha (TNF-α), and c-reactive protein (CRP). Results: No differences existed between groups for resting CRP (d = 0.25–0.46; p =.374–.617). Despite no baseline difference (d = 0.03–0.07; p =.141–.70), exercise-induced increases were observed for IL-1 ra in smokers (d = 0.50; p =.024–.033), which was not observed in the never-smoker group. No between-group difference was observed for IL-6 across all points (d = 0.09–0.5; p =.102–.728); however, all groups observed significant within-group change (d = 0.27–1.09; p =.001–.042). Further, TNF-α for smokers smoking was elevated above both smokers not smoking and nonsmokers at baseline and across the protocol (d = 1.20–1.80; d = 0.20–1.0; p =.001–.035). Additionally, a marked postexercise increase in leukocyte and neutrophil concentrations was evident in smokers smoking compared with nonsmokers and smokers not smoking as indicated by a moderate-to-large effect size (d = 0.72; d = 0.78). Conclusion: Consequently, male smokers exhibit an altered postexercise proinflammatory profile compared with age- and fitness-matched nonsmokers

Interleukin 10 (IL-10) and viral IL-10 strongly reduce antigen-specific human T cell proliferation by diminishing the antigen-presenting capacity of monocytes via downregulation of class II major histocompatibility complex expression

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