Bout Of Strenuous Exercise Research Articles

Pain Catastrophizing Mediates the Relationship Between Self-Reported Strenuous Exercise Involvement and Pain Ratings: Moderating Role of Anxiety Sensitivity

To investigate the cross-sectional associations among self-reported weekly strenuous exercise bouts, anxiety sensitivity, and their interaction with pain catastrophizing and pain responses to the cold pressor task (CPT) in healthy, ethnically diverse young adults (n = 79). Exercise involvement has been shown to have hypoalgesic effects and cognitive factors may partially explain this effect. Particularly, alterations in pain catastrophizing have been found to mediate the positive pain outcomes of multidisciplinary treatments incorporating exercise. Further, recent evidence suggests that exercise involvement and anxiety sensitivity may act together, as interacting factors, to exert an effect on catastrophizing and pain outcomes; however, further research is needed to clarify the nature of this interaction. Before the CPT, participants were asked to complete the Godin Leisure-Time Exercise Questionnaire, the Beck Depression Inventory, and the Anxiety Sensitivity Index. After the CPT, participants completed a modified version of the Pain Catastrophizing Scale and the Short Form-McGill Pain Questionnaire. At a high level of anxiety sensitivity, controlling for depressive symptoms, CPT immersion time, and sex differences, a bias-corrected (BC), bootstrapped confidence interval revealed that pain catastrophizing significantly mediated the relationship between self-reported weekly strenuous exercise bouts and pain response (95% BC Confidence Interval = -9.558, -0.800 with 1000 resamples). At intermediate and low levels of anxiety sensitivity, no significant mediation effects were found. These findings support that, for pain catastrophizing to mediate the strenuous exercise-pain response relation, individuals must possess a high level of anxiety sensitivity.

Human blood mononuclear cell in vitro cytokine response before and after two different strenuous exercise bouts in the presence of bloodroot and Echinacea extracts

The purpose of this multidisciplinary investigation was to characterize cytokine production by human blood mononuclear cells after 2 contrasting exercise bouts (a maximal graded oxygen consumption [VO 2max] test and 90 min of cycling at 85% of ventilatory threshold [VT]) when stimulated in vitro with extracts from bloodroot ( Sanguinaria canadensis), coneflower ( Echinacea tennesseensis), or solvent vehicle controls. Blood was sampled pre- and post-exercise. Production of TNF, IL-1β, and IL-10 were measured at 24, 48, and 72 h, respectively. In the VO 2max test there was a main effect of exercise such that exercise increased cytokine synthesis and a main effect of stimulant such that bloodroot extracts significantly increased cytokine production compared to other stimulants or controls. In the 90-min bout, there was a main effect of exercise for TNF and IL-1β (but not IL-10) such that exercise decreased cytokine synthesis and a main effect of stimulant such that bloodroot extracts significantly increased cytokine production compared to other stimulants or controls, with exercise × stimulant interactions for both IL-1β and IL-10. A similar though weaker effect was seen with Echinacea extracts; subsequent biochemical analyses suggested this was related to alkamide decay during 3 years undisturbed storage at ultralow (− 80 °C) temperature. In this study, the VO 2max test was associated with enhanced cytokine production whereas the 90-min cycling at 85% VT was associated with suppressed cytokine production. Bloodroot extracts were able to increase cytokine production in both contexts. Herbal extracts purported to offset exercise-associated effects on immune activity warrant continued investigation.

Increased Lipid Peroxidation in Trained Men after 2 Weeks of Antioxidant Supplementation

To assess the effects of an encapsulated antioxidant concentrate (EAC) and exercise on lipid peroxidation (LIPOX) and the plasma antioxidant enzyme glutathione peroxidase (Pl-GPx). Eight trained male cyclists (VO2max > 55 ml x kg(-1) x min(-1)) participated in this randomized, placebo-controlled, double-blinded, crossover study and undertook 4 cycle-ergometer bouts: 2 moderate exercise bouts over 90 min at 45% of individual VO2max and 2 strenuous exercise bouts at 75% of individual VO2max for 30 min. The first 2 exercise tests--1 moderate and 1 strenuous-were conducted after 4 weeks wash-out and after 12 and 14 days of EAC (107 IU vitamin E, 450 mg vitamin C, 36 mg beta-carotene, 100 microg selenium) or placebo treatment. After another 4 weeks wash-out, participants were given the opposite capsule treatment and repeated the 2 exercise tests. Physical exercise training was equal across the whole study period, and nutrition was standardized by a menu plan the week before the tests. Blood was collected before exercise, immediately postexercise, and 30 min and 60 min after each test. Plasma samples were analyzed for LIPOX marker malondialdehyde (MDA) and the antioxidant enzyme pl-GPx. MDA concentrations were significantly increased after EAC supplementation at rest before exercise and after moderate exercise (p < .05). MDA concentrations showed no differences between treatments after strenuous exercise (p > .1). Pl-GPx concentrations decreased at all time points of measurement after EAC treatment (p < .05). The EAC induced an increase of LIPOX as indicated by MDA and decreased pl-GPx concentrations pre- and postexercise.

Single Bout of Strenuous Upper Extremity Exercise and Repeated Blood Pressure Measurement in the Upper Limb of Healthy Women and Breast Cancer Survivors

Single Bout of Strenuous Upper Extremity Exercise and Repeated Blood Pressure Measurement in the Upper Limb of Healthy Women and Breast Cancer Survivors

A single bout of whole-body resistance exercise augments basal VLDL-triacylglycerol removal from plasma in healthy untrained men

A single bout of prolonged aerobic exercise lowers plasma TAG (triacylglycerol) concentrations the next day by increasing the efficiency of VLDL (very-low-density lipoprotein)-TAG removal from the circulation. The effect of resistance exercise on VLDL-TAG metabolism is not known. Therefore we evaluated VLDL-TAG kinetics by using stable isotope-labelled tracers in eight healthy untrained men (age, 25.3+/-0.8 years; body mass index, 24.5+/-0.6 kg/m(2)) in the post-absorptive state in the morning on two separate occasions: once after performing a single 90-min bout of strenuous isokinetic resistance exercise (three sets x ten repetitions, 12 exercises at 80% of maximum peak torque production, with a 2-min rest interval between exercises) on the preceding afternoon and once after an equivalent period of rest. Fasting plasma VLDL-TAG concentrations in the morning after exercise were significantly lower than in the morning after rest (0.23+/-0.04 compared with 0.33+/-0.06 mmol/l respectively; P=0.001). Hepatic VLDL-TAG secretion rate was not different (P=0.31), but plasma clearance rate of VLDL-TAG was significantly higher (by 26+/-8%) after exercise than rest (31+/-3 compared with 25+/-3 ml/min respectively; P=0.004), and the mean residence time of VLDL-TAG in the circulation was significantly shorter (113+/-10 compared with 144+/-18 min respectively; P=0.02). Fasting plasma NEFA (non-esterified fatty acid; 'free' fatty acid) and serum beta-hydroxybutyrate concentrations were both significantly higher after exercise than rest (P<0.05), whereas plasma glucose and serum insulin concentrations were not different (P>0.30). We conclude that, in healthy untrained men, a single bout of whole-body resistance exercise lowers fasting plasma VLDL-TAG concentrations by augmenting VLDL-TAG removal from plasma. The effect appears to be qualitatively and quantitatively similar to that reported previously for aerobic exercise.

Toll-like receptor expression on classic and pro-inflammatory blood monocytes after acute exercise in humans

Monocytes are a heterogeneous group of cells, the relative distribution of which change in peripheral blood following a strenuous bout of aerobic exercise. Monocyte subtypes can be identified in blood based on the cell surface expression of CD14 and CD16: classic (CD14++bright/CD16−negative) and the CD16+dim (CD14++bright/CD16+dim) and CD16++bright (CD14+dim/CD16++bright) pro-inflammatory subtypes. Whole monocyte population changes in TLR2, TLR4 and HLA.DR expression have previously been documented after acute exercise without accounting for relative changes in monocyte subpopulations, therefore, this study examined their expression on classic and pro-inflammatory monocyte subsets following 45min of treadmill running at 75% V˙O2max. Mononuclear cells isolated from the peripheral blood of moderately trained male subjects (n=15) before (PRE), immediately after (POST) and 1h after (1H) exercise were assessed for TLR2, TLR4 and HLA.DR expression on blood monocytes and their subpopulations using three-colour flow cytometry. Compared to PRE, the proportion of CD14+/CD16+ monocytes was 27% greater POST and 49% less at 1H and was associated with changes in the CD16++bright pro-inflammatory subtype (p<0.05). TLR2 expression was 12% lower on CD16+dim monocytes POST (p<0.05), whereas TLR4 and HLA.DR expression on total monocytes was 12% and 22% lower at 1H, respectively, and was attributed to changes in the classic (p<0.05) and not the pro-inflammatory subsets (p>0.05). We conclude that acute exercise causes localised changes in TLR2, TLR4 and HLA.DR expression within specific blood monocyte subpopulations, and could therefore be occurring at the cellular level. Such alterations might have significant implications for modulation of post-exercise immune surveillance.

Changes in vascular and cardiac function after prolonged strenuous exercise in humans

Prolonged exercise has been shown to result in an acute depression in cardiac function. However, little is known about the effect of this type of exercise on vascular function. Therefore, the purpose of the present study was to investigate the impact of an acute bout of prolonged strenuous exercise on vascular and cardiac function and the appearance of biomarkers of cardiomyocyte damage in 15 male (32 +/- 10 yr) nonelite runners. The subjects were tested on two occasions, the day before and within an hour of finishing the London marathon (229 +/- 38 min). Function of the brachial and femoral arteries was determined using flow-mediated dilatation (FMD). Echocardiographic assessment of cardiac strain, strain rate, tissue velocities, and flow velocities during diastole and systole were also obtained. Venous blood samples were taken for later assessment of cardiac troponin I (cTnI), a biomarker of cardiomyocyte damage. Completion of the marathon resulted in a depression in femoral (P = 0.04), but not brachial (P = 0.96), artery FMD. There was no change, pre- vs. postmarathon, in vascular shear, indicating that the impaired femoral artery function was not related to hemodynamic changes. The ratio of peak early to atrial radial strain rate, a measure of left ventricular diastolic function, was reduced postmarathon (P = 0.006). Postrace cTnI was elevated in 12 of 13 runners, with levels above the recognized clinical threshold for damage in 7 of these. In conclusion, when taken together, these data suggest a transient depression in cardiac and leg vascular function following prolonged intensive exercise.

Exercise-Associated Increases in Cardiac Biomarkers

At present, the risk of myocardial damage by endurance exercise is under debate because of reports on exercise-associated increases in cardiac biomarkers troponin and B-type natriuretic peptide (BNP); these markers are typically elevated in patients with acute myocardial infarction and chronic heart failure, respectively. Exercise-associated elevations of cardiac biomarkers can be present in elite and in recreational athletes, especially after prolonged and strenuous endurance exercise bouts (e.g., marathon and ultratriathlon). However, in contrast to cardiac patients, it is still unclear if the exercise-associated appearance or increase in cardiac biomarkers in obviously healthy athletes represents clinically significant cardiac insult or is indeed part of the physiological response to endurance exercise. In addition, elevations in cardiac biomarkers in athletes after exercise may generate difficulties for clinicians in terms of differential diagnosis and may result in inappropriate consequences. Therefore, the aim of this article is to provide an overview of exercise-associated alterations of the cardiac biomarkers troponin T and I, ischemia-modified albumin, BNP, and its cleaved inactive fragment N-terminal pro BNP for the athlete, coach, scientist, and clinician.

Acute exercise-induced changes in basal VLDL-triglyceride kinetics leading to hypotriglyceridemia manifest more readily after resistance than endurance exercise

Resistance training is considered less effective than endurance training in lowering plasma triglyceride (TG) concentrations. Acutely, however, a single bout of strenuous exercise, whether endurance or resistance, increases the efficiency of very low-density lipoprotein (VLDL)-TG removal from the circulation and leads to hypotriglyceridemia. The comparative effects of these two types of exercise on VLDL-TG metabolism are not known. We therefore examined basal VLDL-TG kinetics by using stable isotope-labeled tracers in seven healthy, nonobese, untrained young men in the postabsorptive state, the morning after a single 90-min bout of either low-intensity endurance exercise (approximately 30% of peak oxygen consumption) or high-intensity resistance exercise (3 sets of 10 repetitions for 12 exercises at 80% of peak torque production), matched for total energy expenditure (approximately 400 kcal), or an equivalent period of rest on the preceding afternoon. Compared with rest, resistance exercise lowered fasting plasma VLDL-TG concentration by -28 +/- 10% (P = 0.034), increased VLDL-TG plasma clearance rate by 30 +/- 8% (P = 0.003), and shortened the mean residence time (MRT) of VLDL-TG in the circulation by -36 +/- 11 min (P = 0.016), whereas endurance exercise had no effect (all P > 0.05). Basal VLDL-TG plasma clearance rate was greater (P = 0.003) and VLDL-TG MRT was shorter (P = 0.012) the morning after resistance than endurance exercise. We conclude that, for the same total energy expenditure, resistance exercise is more potent than endurance exercise in eliciting changes in VLDL-TG metabolism that have been linked with hypotriglyceridemia, and it should thus be considered as an alternative to or in addition to endurance exercise for the control of plasma TG concentrations.

High-intensity interval aerobic training reduces hepatic very low-density lipoprotein-triglyceride secretion rate in men

A single bout of strenuous endurance exercise reduces fasting plasma triglyceride (TG) concentrations the next day (12-24 h later) by augmenting the efficiency of very low-density lipoprotein (VLDL)-TG removal from the circulation. Although much of the hypotriglyceridemia associated with training is attributed to the last bout of exercise, the relevant changes in VLDL-TG metabolism have never been investigated. We therefore examined basal VLDL-TG kinetics in a group of sedentary young men (n=7) who underwent 2 mo of supervised high-intensity interval training (3 sessions/wk; running at 60 and 90% of peak oxygen consumption in 4-min intervals for a total of 32 min; gross energy expenditure: 446+/-29 kcal) and a nonexercising control group (n=8). Each subject completed two stable isotope-labeled tracer infusion studies in the postabsorptive state, once before and again after the intervention (approximately 48 h after the last exercise bout in the training group). Peak oxygen consumption increased by approximately 18% after training (P <or= 0.05), whereas body weight and body composition were not altered. Fasting plasma VLDL-TG concentration was reduced after training by approximately 28% (P <or= 0.05), and this was due to reduced hepatic VLDL-TG secretion rate (by approximately 35%, P <or= 0.05) with no changes (<5%, P>0.7) in VLDL-TG plasma clearance rate and the mean residence time of VLDL-TG in the circulation. No significant changes in VLDL-TG concentration and kinetics were observed in the nonexercising control group (all P >or= 0.3). We conclude that a short period of high-intensity interval aerobic training lowers the rate of VLDL-TG secretion by the liver in previously sedentary men. This is different from the mechanism underlying the hypotriglyceridemia of acute exercise; however, it remains to be established whether our finding reflects an effect of the longer time lapse from the last exercise bout, an effect specific to the type of exercise performed, or an effect of aerobic training itself.

Resistance exercise decreases eIF2Bε phosphorylation and potentiates the feeding-induced stimulation of p70S6K1 and rpS6 in young men

We investigated the effect of resistance exercise and feeding on the activation of signaling proteins involved in translation initiation. Nine young men (23.7+/-0.41 yr; BMI=25.5+/-1.0 kg/m2; means+/-SE) were tested twice after they performed a strenuous bout of unilateral resistance exercise, such that their contralateral leg acted as a nonexercised comparator, in either the fasted and fed [1,000 kJ, each 90 min (3 doses): 10 g protein, 41 g carbohydrate, 4 g fat] states. Muscle biopsies were obtained 6 h postexercise from both legs, resulting in four experimental conditions: rest-fasted, rest-fed, exercise-fasted, and exercise-fed. Feeding increased PKB/Akt (Ser473) phosphorylation (P<0.05), while exercise increased the phosphorylation of Akt and the downstream 70 kDa S6 protein kinase (p70S6K1, Thr389) and ribosomal protein S6 (rpS6, Ser235/236, Ser240/244; all P<0.05). The combination of resistance exercise and feeding increased the phosphorylation of p70S6K1 (Thr389) and rpS6 (Ser240/244) above exercise alone (P<0.05). Exercise also reduced phosphorylation of the catalytic epsilon subunit of eukaryotic initiation factor 2B (eIF2Bepsilon, Ser540; P<0.05). Mammalian target of rapamycin (mTOR, Ser2448), glycogen synthase kinase-3beta (GSK-3beta, Ser9), and focal adhesion kinase (FAK, Tyr576/577) phosphorylation were unaffected by either feeding or resistance exercise (all P>0.14). In summary, feeding resulted in phosphorylation of Akt, while resistance exercise stimulated phosphorylation of Akt, p70S6K1, rpS6, and dephosphorylation eIF2Bepsilon with a synergistic effect of feeding and exercise on p70(S6K1) and its downstream target rpS6. We conclude that resistance exercise potentiates the effect of feeding on the phosphorylation and presumably activation of critical proteins involved in the regulation of muscle protein synthesis in young men.

Genetic Variants in MCP1 and MCP1R are Associated with Markers of Muscle Damage

PURPOSE: Understanding the genetic factors that underlie inflammation and muscle repair could have profound effects on improved therapeutics for pain relief. We hypothesized that single nucleotide polymorphisms (SNPs) in the gene MCP1, which is highly expressed in injured skeletal muscle and involved in the repair and functional recovery of the injured muscle, would be associated with markers of muscle damage. METHODS: We genotyped nine different SNPs in MCP1 and three SNPs in MCP1R in a group of 151 individuals who completed a bout of eccentric exercise (50 maximal eccentric contractions). The SNPs were examined with indicators of muscle damage [strength loss, muscle soreness, and increases in circulating levels of creatine kinase (CK) and myoglobin (Mb)] and maximum baseline isometric strength values. RESULTS: In females, two SNPs in MCP1 were associated with baseline CK levels: rs1026411 (AA: N=42; 73.7 ± 5.5 U/l vs. AG/GG: N=34; 99.7 ± 6.1 U/l, p=0.002), rs13900 (CC: N=42; 73.9 ± 5.4 U/L vs. AG/GG: N=35; 98.9 ± 6.0 U/l, p = 0.003), and a SNP in MCP1R rs1799865 (TT: N=36; 94.7 ± 6.1 U/l vs. CT/CC: N=41; 77.0 ± 5.7 U/l, p = 0.03). In addition, females with a copy of the C allele for rs3918358 in MCP1R had higher myoglobin values four days post-exercise (AA: N=33; 237.8 ± 64.7 ng/ml vs. AC/CC: N=43; 165.3 ± 17.0 ng/ml, p = 0.04) and greater maximum strength loss (AA: N=34; −12.2 ± kg vs. AC/CC: N=43; −24.3 ± kg, p = 0.04). In the MCP1R gene, males with a copy of the rare allele for two SNPs had higher values of myoglobin seven days post-exercise for rs3918358 (AA: N=33; 85.0 ± 19.3 ng/ml vs. AC/CC: N=38; 159.8 ± 18.0 ng/ml, p = 0.007) and rs1799865 (TT: N=32; 76.4 ± 19.0 ng/ml vs. TC/CC: N=40; 165.3 ± 17.0 ng/ml, p = 0.001). In addition, males showed a differences in average baseline strength for rs3918358 (AA: N=33; 119.8 ± 4.8 kg vs. AC/CC: N=41; 106.7 ± 4.2 kg, p = 0.001; p = 0.04. CONCLUSIONS: We have discovered variants in the MCP1 and MCP1R genes that affect measures of muscle damage (muscle soreness, isometric strength, myoglobin, and CK) after a bout of strenuous eccentric exercise. Baseline CK and strength were also affected in a sex-dependent manner. These data suggest that these SNPs affect MCP1 RNA or protein levels, which could modify signaling between macrophages and satellite cells, promoting or hindering repair during the recovery period.

Changes of CT-1 and JAK/STAT Expression in Myocardium Induced by Acute Exercise

Cardiotrophin-1 (CT-1) has been reported to activate the Janus kinase (JAK)/signal transducers and activators of transcription (STAT) pathway. This activation induces cardiac hypertrophy in genetically hypertensive and experimental post-myocardial infarction rats, as well as in isolated ventricular myocytes subject to mechanical stretch. However, no reports have documented the activation of CT-1 and the JAK/ STAT pathway in the myocardium following exercise. PURPOSE: To investigate the immediate changes of CT-1 and JAK/STAT expressions in the myocardium following a single bout of strenuous treadmill running exercise. METHODS: Adult male Sprague-Dawley rats (220±5g, n=70) were randomly divided into sedentary (S) and exercise groups (E). Rats in exercise groups ran on a treadmill continuously at 8.5 m/min, 0% grade for 15 min, 15m/min, 5%grade for 15min, then followed by 10% grade at 19.5m/min till fatigue. After exercise, rats were sacrificed 0, 1, 3, 5, 12, and 24 hour (hr) s respectively. CT-1, STAT3, phosphorylated (p)-STAT3 and JAK1 expressions in the myocardium were determined with western immunoblots and immunohistochemistry. RESULTS: Expression of CT-1 tended to gradually increase after running, and but did not show significantly higher at any time points in comparison with the control group baroreflex function curve were lower in older subjects at rest. During exercise G (P>0.05), JAK1 expression significantly increased immediately after running, peaking at 1, 3, and 5 hrs(the percentage of JAK-positive cells was 19.0±2.2%, 20.4 ± 19.4%,21.0 ± 5.6%, respectively, all P<0.01), and remained elevated throughout 24 hrs (S: 9.2 ± 5.1%, vs. E:14.8 ± 2.4%, P<0.01).the percentage of STAT3-positive cells was significantly increased 1, 3, and 5,12 hrs(S: 33.8 ± 6.8%, E:64.4 ± 4.8%, 60.9 ±12.2%, 59.3 ±4.5%, 52.5 ± 2.6%, all P<0.01)after running, while p-STAT3 increased only from 1-5 hrs after running (S: 11.9 ± 9.7% vs. E: 30.7± 5.1%, 35.3 ± 5.4%, 47.7 ± 10.5%, P < 0.01). CONCLUSIONS: A single bout of exercise induces a trend to increase in CT-1 expression in the myocardium. This tendency to increase is linked to a clear activation of the JAK/STAT pathway in the myocardium, and is likely an early trigger for cardiac hypertrophy. Increased JAK1 expression remained elevated throughout 24 hrs post-exercise, whereas phosphorylation of STAT3 was transiently increased after acute exercise.

The Effects of Watkins Antioxidant Supplement on DOMS and Serum Oxidative Damage Biomarkers

Reactive oxygen species (ROS) have been reported to increase following a strenuous bout of eccentric exercise. Supplemented antioxidants were utilized in this study to determine its effectiveness in attenuating oxidative damage caused by ROS that leads to delayed onset muscle soreness (DOMS). Results of the effectiveness of supplemented antioxidants from previous studies are unclear. This study investigated the relationship between ROS activity, antioxidant supplementation, and DOMS. PURPOSE: The purpose of this study is to test the effectiveness of an antioxidant mixture on attenuating ROS activity and DOMS. METHODS: Twenty-four non-aerobically trained college-aged volunteers underwent 30 minutes of eccentric treadmill exercise at −10 % grade at 80 % estimated max heart rate. The subjects began daily supplement (S) and placebo (P) treatments three days prior to the exercise bout and continued three days post. The randomly assigned groups, (S and P), were measured for pain, creatine kinase (CK) levels, and strength measurements prior to exercise, and at 12, 24, 48, and 72 hours post-exercise. Blood draws to measure myoglobin (Mb) and protein carbonyl (PC) levels were taken pre-exercise and at 24 h post-exercise. RESULTS: A time main effect was found for all variables (p<.05) excluding myoglobin (p=.81). No statistically significant group × time differences were reported (p>0.05). CK (p=0.061) and the numerical pain scale (p=0.062) indicated a trend in the supplement having lower values than the placebo. CK levels for S and P groups peaked at 12 h post-exercise (S 273+132, P 320+252 U/L) (mean+SD). Force loss (S 1.67+0.36, P 1.41+0.38 ft lb•kg−1) and the numerical pain scale (S 4.92+2.23, P4.54+1.76) peaked at 24 h post-exercise. CONCLUSIONS: The antioxidative supplementation utilized does not significantly diminish markers of delayed-onset muscle soreness, or biomarkers of tissue or oxidative damage employed in this study. However, results for CK and the numerical pain scale both indicate a strong trend for improvement over the placebo group in samples taken after the 48 hours. Future studies may need a longer preloading supplementation period and greater frequency of sampling times to better determine supplementation effects.

CrossRef Listing of Deleted DOIs

Recreational activity frequently produces large increases in circulating CK activity without consequence. Thus, high CK levels alone do not portend renal failure. Most cases of exertional rhabdomyolysis can, and probably do, resolve on their own without treatment. When taking a blood sample during a routine check, for example in monitoring patients on statin therapy, a high blood CK activity may indicate that strenuous exercise was performed in the previous 10 days. Patients should be queried as to their exercise history during this time. Snow shoveling, dirt shoveling, lifting and lowering heavy boxes, strenuous resistance training, and excessive calisthenics (such as push-ups and pull-ups) are exercises that may dramatically increase circulating CK activity for several days due to forceful eccentric contractions. In addition to elevated CK, factors such as underlying disease, dehydration, environmental heat stress, or genetic predisposition (eg, sickle cell trait) are likely required for exertional rhabdomyolysis to result in acute renal failure [8]. Persons who present to the emergency room with painful, swollen muscles about 2 days after a bout of strenuous exercise should be monitored for kidney function (BUN and creatinine), evidence of myoglobinuria and dehydration, and be queried regarding hydration, heat stress during the exercise, and possible trauma. In cases of exertional rhabdomyolysis, especially in laboratory situations, CK levels up to 100,000 U/L in the absence of nephrotoxic factors have been found to resolve without consequence when no treatment is provided. However, because few data confirm this in a clinical situation in which there may be comorbidities, it remains conservative and prudent in the emergency room to hydrate intravenously and monitor closely to help avoid hyperkalemia and/or acute renal failure in the face of fulminant exertional rhabdomyolysis.

若年健常男性における短期間のビタミンＥサプリメント摂取は長時間の反復運動後の炎症および筋損傷マーカーに影響を及ぼさない

After a single bout of prolonged strenuous exercise, inflammatory and muscle damage markers increase. The present study investigated whether vitamin E supplementation can attenuate inflammatory (C-reactive protein (CRP) and interleukin-6 (IL-6)) and muscle damage (creatine kinase (CK) and lactate dehydrogenese (LDH)) markers after prolonged repeated bouts of cycling in healthy young men. Eight young males (aged 21–30 y) were received both vitamin E supplement (300 mg/day) and placebo (control) for 14 days separated by at least an interval of 1 month in a randomised, counterbalanced design. On day 12 of both trials, subjects cycled at 80% of maximal heart rate in two, 90-min bouts (150 min rest between each). Blood samples were collected on days 1 (baseline), 12 (pre- and post-exercise 1 and pre- and post-exercise 2), 13, 14, and 15. After 14 days of supplementation, serum α-tocopherol concentrations increased in the vitamin E trial (P<0.0005) but not the placebo trial. Serum CRP concentrations did not differ between trials and did not significantly change over the observation period in both trials. Serum IL-6, CK, and LDH concentrations increased (P≤0.024) in response to repeated bouts of exercise in both trials but did not differ between trials. The study demonstrates that short-term vitamin E supplementation appears to have no effect on attenuating markers of inflammatory and muscle damage in response to repeated bouts of prolonged exercise in healthy young men.

운동과 면역반응에 대한 고찰

면역학이 발점함에 따라서 인간의 면역체계에 영향을 미치는 많은 요인들에 대한 수많은 연구들이 진행되고 있다. 연령, 영야상태, 스트레스, 질병, 비만, 고지혈증, 장애 등 무수히 많은 변인들이 면역방응에 직접적인 영향을 주고 있으나 운동 또한 상당한 영향력이 있어, 운동시 나타나는 면역 반응에 대하여 고찰하게 되었다. 규칙적인 운동은 초기면역과 그 이후의 적응면역을 증진시키며 특히 적응면역 중 세포 매개 면역반응과 항체매개 면역반응에 영향을 미치는 것으로 알려져 있다. 하지만 이러한 운동도 몸의 상태가 건강하거나 몸에 맞는 운동을 규칙적으로 실시해야 효과적이며, 운동의 경험이 없거나 스트레스나 질병이 있는 상태에서의 운 동은 오히려 신체에 부담을 주어 면역력을 악화하는 결과를 초래하게 된다. 또한 일회성의 운동도 체력수준에 맞게 수행되어야 하는데, 장시간 너무 무리하게 수행하면 에너지 고갈과 함께 면역력의 감소를 초래하여 상기도 감염과 같은 질환을 야기하게 된다. 따라서 무리한 운동 후 'open window' 시기에 적절한 이온음료의 섭취, 영양분 공급 및 휴식은 건강 관리에 필수적이라 할 수 있다. 또한 수행한 운동이 규칙적이라 할지라도 운동은 운동 환경이나 선천적인 요소에 따라 운동 유발성 천식을 포함하는 운동 유발성 알레르기 질환을 야기하는 환경을 조성할 수 있으므로 본론에서 제시한 지식을 바탕으로 마라톤과 같은 장기간 운동 시 특히 주의해야 할 것으로 여겨진다. Exercise is the strongest stress to which the body is ever exposed. The body responds to this stress through a set of physiological changes in its metabolic, hormonal, and immunological systems. In this study, responses of the immune system to the long-term aerobic and anaerobic exercises have been investigated. Regular moderate exercise is associated with a reduced incidence of infection compared with a sedentary groups. Aerobic training increases the heart rate and enhances the body's intake of oxygen long enough to benefit the condition of the body. In recent years, the importance of exercise in everyday life has been rapidly increasing. Moderate exercise appears to stimulate the immune system. And also, Exercise elicits an increase in the numbers of circulating lymphocytes and lymphocyte subsets (including NK cells) which is followed by a decrease in the numbers of cells during recovery from exercise. However, prolonged bouts of strenuous exercise cause a temporary depression of various aspects of immune functions (e.g. lymphocyte proliferation, monocyte antigen presentation, open window periods, exercise induced asthma, exercise induced anaphylaxis) that usually lasts 2-24 hr after exercise depending on the intensity and duration of the exercise bout. Exercise-induced bronchoconstriction (EIB) was defined as a decrease of at least 15% in pre exercise forced expiratory volume in one second at any time point after exercise. This includes elevation of cortisol and cathecholamines in plasma. On the other hand, highly trained athletes exhibit a chronic mild hypercortisolism at baseline that maybe an adaptive change to chronic exercise. And, Consuming carbohydrate during prolonged strenuous exercise attenuates rises in stress hormones and appears to limit the degree of exercise-induced immune depression. Recent evidence suggests that antioxidant vitamin supplementation may also reduce exercise stress and impairment of leukocyte functions.

Repeated exercise in mice alters expression of IL-10 and TNF-α in intestinal lymphocytes

Intestinal inflammation is characterized by mucosal damage that may arise, in part, to imbalances in pro- and anti-inflammatory cytokines. The purpose of this study was to describe the effects of repeated bouts of strenuous exercise on cytokine expression in mouse intestinal lymphocytes (IL). Thirty-four female C57BL/6 mice were randomly assigned to three groups: three repeated bouts of treadmill running separated by 24 h followed by sacrifice immediately or after a 24 h period or a sedentary (no exercise) control. The pro-inflammatory cytokine, TNF-α, and the anti-inflammatory cytokine, IL-10, were measured in IL by Western blotting. IL-10 concentration increased by 48% ( p < 0.05) in the immediate group compared to the sedentary control. TNF-α levels in mouse IL were significantly lower 24 h after completion of the exercise protocol compared to the immediate group ( p < 0.05). The results suggest a possible physiological compensation in which intestinal lymphocytes increase the expression of IL-10 in response to exercise-induced stress.

Exercise, oxidative stress and hormesis

Physical inactivity leads to increased incidence of a variety of diseases and it can be regarded as one of the end points of the exercise-associated hormesis curve. On the other hand, regular exercise, with moderate intensity and duration, has a wide range of beneficial effects on the body including the fact that it improves cardio-vascular function, partly by a nitric oxide-mediated adaptation, and may reduce the incidence of Alzheimer's disease by enhanced concentration of neurotrophins and by the modulation of redox homeostasis. Mechanical damage-mediated adaptation results in increased muscle mass and increased resistance to stressors. Physical inactivity or strenuous exercise bouts increase the risk of infection, while moderate exercise up-regulates the immune system. Single bouts of exercise increases, and regular exercise decreases the oxidative challenge to the body, whereas excessive exercise and overtraining lead to damaging oxidative stress and thus are an indication of the other end point of the hormetic response. Based upon the genetic setup, regular moderate physical exercise/activity provides systemic beneficial effects, including improved physiological function, decreased incidence of disease and a higher quality of life.

Immune function in sport and exercise

Regular moderate exercise is associated with a reduced incidence of infection compared with a completely sedentary state. However, prolonged bouts of strenuous exercise cause a temporary depression of various aspects of immune function (e.g., neutrophil respiratory burst, lymphocyte proliferation, monocyte antigen presentation) that usually lasts approximately 3-24 h after exercise, depending on the intensity and duration of the exercise bout. Postexercise immune function dysfunction is most pronounced when the exercise is continuous, prolonged (>1.5 h), of moderate to high intensity (55-75% maximum O(2) uptake), and performed without food intake. Periods of intensified training (overreaching) lasting 1 wk or more may result in longer lasting immune dysfunction. Although elite athletes are not clinically immune deficient, it is possible that the combined effects of small changes in several immune parameters may compromise resistance to common minor illnesses, such as upper respiratory tract infection. However, this may be a small price to pay as the anti-inflammatory effects of exercise mediated through cytokines and/or downregulation of toll-like receptor expression are likely mediators of many of the long-term health benefits of regular exercise.