Two methods for determining plasma IL-6 in humans at rest and following exercise

We compared two methods to determine IL-6 at rest and following exercise. On two occasions, plasma IL-6 was determined in 10 men and 13 women before and immediately following 90 min of cycling at 65% using a cytometric bead array (CBA) and an ELISA. The CBA detected IL-6 in 63% of pre-exercise samples and 84% of post-exercise samples; the ELISA detected IL-6 in all samples. In samples with detectable IL-6, resting values were comparable between the CBA and ELISA (2.3 ± 1.0 and 2.4 ± 1.2 pg/mL, respectively; p = 0.99); the IL-6 response to exercise was underestimated (p = 0.0003) by the CBA by ~45%, compared with the ELISA. CBA- and ELISA-determined IL-6 values were moderately correlated (r = 0.66, p < 0.0001), but exhibited poor agreement (mean bias ± 1SD = −1.4 ± 2.1 pg/mL). The CBA provided concordant IL-6 concentrations at rest, when detected, but underestimated exercise-induced increases in IL-6 versus the ELISA method.     

Elevated plasma interleukin-6 levels in trained male triathletes following an acute period of intense interval training

The aim of the present study was to investigate possible changes in the plasma IL-6 levels, subjective reporting of sources and symptoms of stress and the innate immune system in response to an acute period of intensified run training in highly trained endurance athletes. Eight healthy endurance trained male subjects (mean ± SD age 23 ± 2 years, VO_2max 64.8 ± 2.6 ml kg⁻¹ min⁻¹, mass 77.1 ± 2.9 kg) completed the study which took place over a 4 week period. In weeks 2 and 3, in addition to their normal endurance training, subjects completed interval-training run sessions on three successive days. Saliva and venous blood samples were taken at the end of each week. Blood samples were analysed for leukocyte counts; neutrophil function; plasma IL-6; creatine kinase activity; and cortisol. Symptoms and sources of stress were assessed by questionnaire. Plasma IL-6 and creatine kinase activity were elevated following intensified training. Neutrophil function was reduced but total leukocyte and neutrophil counts, plasma cortisol and salivary IgA remained unchanged. There was a worsening in symptoms of stress despite there being no significant change in the sources of stress during intensified training. In conclusion, an acute period of intensified training can induce a suppression of the innate immune system and a chronic elevation in IL-6. This was associated with an increase in fatigue and generalised malaise which lends support to the recent cytokine theories of unexplained, underperformance syndrome.     

Plasma IL-6 concentration during ultra-endurance exercise

Interleukin 6 (IL-6) response was studied during two ultra endurance events—one laboratory 24 h protocol (9 men) with exercise intensity set to 60% of VO_2max and one Adventure Race over 6 days (12 men/6 women) with a self-selected race pace, including rests, of about 38% of VO_2max. In the 24-h protocol IL-6 level was elevated from 0.76 ± 0.48 pg mL⁻¹ at rest to 7.16 ± 2.70 pg mL⁻¹ at 6 h, and increased further to 10.58 ± 1.04 pg mL⁻¹ at 12 h, but remained thereafter unchanged at 24 h, (10.89 ± 0.36 pg mL⁻¹). All participants had nearly identical values at 12 and 24 h, supporting intensity as main determinant in the IL-6 response during prolonged exercise since exercise duration did not increase IL-6 level after 12 h. Possible confounding factors do not seem to influence the IL-6 concentration during the longer races (>12 h), but might very well do so during shorter exercise bouts. In the 6-day race IL-6 increased from rest to 24 h, but thereafter there was no change in plasma IL-6 value until the end of the race (mean 143.5 h). There was no elevation of TNF-α in any of the protocols, suggesting that the competitors were free from systemic inflammation. We conclude that during endurance exercise lasting >12 h intensity, and not duration, is the main determinant of the IL-6 response, while during shorter exercise bouts both intensity and duration contribute to the accumulation of IL-6 in plasma.     

Alterations of immunoendocrine responses during the recovery period after acute prolonged cycling

The aim of this study was to determine the timecourse of recovery of immunoendocrine responses following prolonged cycling. With the approval of the Ethics Committee, ten healthy men (age 21.6 ± 0.9 years, height 1.77 ± 0.01 m, body mass 66.9 ± 1.8 kg, VO₂max 54.2 ± 2.0 ml kg⁻¹ min⁻¹; means ± SEM) performed either a 2 h cycling trial at 55% peak aerobic power or a resting control trial in a counterbalanced order, separated by at least 6 days. No food was consumed, though water ingestion was allowed ad libitum, until trials were completed. Venous blood samples were collected at pre-exercise, post-exercise, and at 1, 3, 6 and 9 h post-exercise. Haematological analysis was performed using an automated cell counter. Plasma concentrations of hormones were determined using ELISA kits. Neutrophil degranulation (bacteria-stimulated) and oxidative burst (formyl-methionyl-leucyl-phenylalanine-induced) were measured using an ELISA kit and a chemiluminescence assay, respectively. Results were analyzed using two-factor repeated measures ANOVA with post hoc Tukey tests and paired t tests applied where appropriate. The main findings of this study were that, compared with the resting trial, an acute single bout of prolonged exercise (1) decreased plasma glucose concentrations but increased circulating leukocyte, neutrophil, and monocyte counts for 9 h; (2) increased plasma cortisol concentrations but suppressed neutrophil function on a per cell basis for 6 h. In conclusion, the findings of this study suggest that the impact of a single bout of prolonged cycling on immunoendocrine responses would be recovered around 9 h post-exercise at fasted status.     

Effects of inducing physiological hyperglucagonemia on metabolic responses to exercise

The purpose of the present study was to assess the effects of exogenously increasing the circulating levels of glucagon on the metabolic responses to exercise in rats. A total of six groups of rats were infused (iv) either with glucagon (20 or 50 ng·kg⁻¹·min⁻¹) or saline (0.9% NaCl), either in the resting state or during a bout of running exercise (45 min, 26 m·min⁻¹, 0% grade). Blood samples were taken at the end of the 45-min experiment. Animals infused with glucagon at 50 ng·kg⁻¹·min⁻¹ showed significantly (P<0.01) higher mean plasma glucagon concentrations than animals infused with saline or glucagon at 20 ng·kg⁻¹·min⁻¹. In addition, exercise resulted in significantly (P<0.05) higher mean plasma glucagon concentrations, compared to rest, in all groups. In spite of these differences in glucagon concentrations, there were no significant (P>0.05) effects of exercise and glucagon infusion on mean hepatic glycogen, plasma glucose, insulin, C-peptide, β-hydroxybutyrate, or catecholamine concentrations. Although exercise resulted in a significant (P<0.01) increase in plasma glycerol and free fatty acid concentrations and a significant (P<0.05) decrease in glycogen in the soleus muscle, these responses were not affected by the glucagon infusion. These results suggest that the liver is non-responsive to physiological hyperglucagonemia in a short-term (45 min) exercise situation. Electronic Publication     

Plasma vasopressin,renin activity,and aldosterone responses to maximal exercise in active college females

Summary The effect of maximal treadmill exercise on plasma concentrations of vasopressin (AVP); renin activity (PRA); and aldosterone (ALDO) was studied in nine female college basketball players before and after a 5-month basketball season. Pre-season plasma AVP increased (p<0.05) from a pre-exercise concentration of 3.8±0.5 to 15.8±4.8 pg · ml⁻¹ following exercise. Post-season, the pre-exercise plasma AVP level averaged 1.5±0.5 pg · ml⁻¹ and increased to 16.7±5.9 pg · ml⁻¹ after the exercise test. PRA increased (p<0.05) from a pre-exercise value of 1.6±0.6 to 6.8±1.7 ngAI · ml⁻¹ · hr⁻¹ 5 min after the end of exercise during the pre-season test. In the post-season, the pre-exercise PRA was comparable (2.4±0.6 ngAI · ml⁻¹ · hr⁻¹), as was the elevation found after maximal exercise (8.3±1.9 ngAI · ml⁻¹ · hr⁻¹). Pre-season plasma ALDO increased (p<0.05) from 102.9±30.8 pg · ml⁻¹ in the pre-exercise period to 453.8±54.8 pg · ml⁻¹ after the exercise test. In the post-season the values were 108.9±19.4 and 365.9±64.4 pg · ml⁻¹, respectively. Thus, maximal exercise in females produced significant increases in plasma AVP, renin activity, and ALDO that are comparable to those reported previously for male subjects. Moreover, this response is remarkably reproducible as demonstrated by the results of the two tests performed 5 months apart.     

Changes in markers of muscle damage, inflammation and HSP70 after an Ironman triathlon race

We investigated the effects of an Ironman triathlon race on markers of muscle damage, inflammation and heat shock protein 70 (HSP70). Nine well-trained male triathletes (mean ± SD age 34 ± 5 years; V̇O_2peak 66.4 ml kg⁻¹ min⁻¹) participated in the 2004 Western Australia Ironman triathlon race (3.8 km swim, 180 km cycle, 42.2 km run). We assessed jump height, muscle strength and soreness, and collected venous blood samples 2 days before the race, within 30 min and 14–20 h after the race. Plasma samples were analysed for muscle proteins, acute phase proteins, cytokines, heat shock protein 70 (HSP70), and clinical biochemical variables related to dehydration, haemolysis, liver and renal functions. Muscular strength and jump height decreased significantly (P < 0.05) after the race, whereas muscle soreness and the plasma concentrations of muscle proteins increased. The cytokines interleukin (IL)-1 receptor antagonist, IL-6 and IL-10, and HSP70 increased markedly after the race, while IL-12p40 and granulocyte colony-stimulating factor (G-CSF) were also elevated. IL-4, IL-1β and tumour necrosis factor-α did not change significantly, despite elevated C-reactive protein and serum amyloid protein A on the day after the race. Plasma creatinine, uric acid and total bilirubin concentrations and γ-glutamyl transferase activity also changed after the race. In conclusion, despite evidence of muscle damage and an acute phase response after the race, the pro-inflammatory cytokine response was minimal and anti-inflammatory cytokines were induced. HSP70 is released into the circulation as a function of exercise duration.     

Increased glucagon secretion during hyperthermia in a sauna

Summary Plasma glucagon, adrenaline, noradrenaline, insulin and glucose concentrations were measured in 7 healthy young males during hyperthermia in a sauna bath: plasma glucagon levels increased from baseline values of 127.0±12.9 (SEM) pg · ml⁻¹ to a maximum of 173.6±16.1 (SEM) pg · ml⁻¹ at the 20th min of exposure. No change in plasma insulin and a slight increase in plasma glucose concentration were seen. Since a concomitant moderate increase in plasma catecholamine levels was also present, the adrenergic stimulus is believed to trigger glucagon release during hyperthermia. Diminished visceral blood flow, known to occur in sauna baths, may cause a decrease in the degradation of plasma glucagon and thus contribute to the elevated plasma glucagon levels.     

Muscle sympathetic nerve activity at rest compared to exercise tolerance

Cardiovascular autonomic function is associated with physical performance and exercise training adaptation. The association between physical performance and sympathetic regulation is not well known. We hypothesized that sympathetic nervous system activity is associated with physical performance among male runners. The study population included 26 healthy male club runners [age 33 ± 5 years, body mass index (BMI) 24 ± 1 kg/m², VO_2max 58 ± 5 ml kg⁻¹ min⁻¹; mean ± SD]. Muscle sympathetic nerve activity (MSNA) was assessed from the peroneal nerve by the microneurography technique during 5 min of supine rest. Physical performance was assessed by time to exhaustion during treadmill running. The mean resting MSNA was 20 ± 6 bursts min⁻¹ (range 6–34). The mean time to exhaustion was 1,005 ± 136 s (range 720–1260). When the study group was divided into tertiles according to their running performance (866 ± 69, 994 ± 30 and 1154 ± 71 s in time to exhaustion, P < 0.0001 between the groups), MSNA was lower (P = 0.032) in the group with the best running performance (16 ± 5 bursts min⁻¹) compared to those with the worst running performance (23 ± 7 bursts min⁻¹). In conclusion, baseline sympathetic activity, measured by a microneurography at rest, may be associated with the maximal running performance of healthy subjects.     

Effects of physical exercise and anti-G suit inflation on atrial natriuretic factor plasma level

Summary The purpose of this study was to measure the effect of enhanced venous return on atrial natriuretic factor (ANF) secretion during exercise and upright posture and the consequences on renin angiotensin aldosterone system (RAAS) activity. Six healthy male subjects were submitted to four different procedures. All procedures were performed in the same position, i.e. riding on a support with legs hanging. Two procedures were performed at rest: the subjects were studied after a 25-min rest in this position, with and without the lower limb fitted with an anti-G suit inflated to 60 mmHg. Two procedures were carried out with physical exercise; arm-cranking was performed in the same position with and without the anti-G suit inflated to 60 mmHg. Venous blood was collected before and after each procedure in order to measure plasma ANF, plasma aldosterone concentration (PAC), plasma renin activity (PRA), corticotrophin (ACTH) and catecholamine level. The data mean ±SEM showed that the ANF plasma level decreased significantly (p<0.05) from 32.5±4 to 28±6 pg · ml⁻¹ after a 20-min rest in the upright posture, whereas this effect was absolished with anti-G suit inflation. Physical exercise with and without the anti-G suit increased the ANF level above control values (60±13.6 pg · ml⁻¹ and 53±13 pg · ml⁻¹): anti-G suit inflation had no significant effect. PRA increased after rest in an upright posture and during physical exercise; anti-G suit inflation abolished this increase in both conditions. PAC was not influenced by postural change but significantly increased in all exercise tests. ACTH increased to the same extent in both exercise tests. The plasma catecholamine level increased during upright posture and both physical exercise procedures. These results indiate that enhanced venous return during anti-G suit inflation increases ANF secretion at rest in an upright posture and that physical exercise greatly increases plasma ANF level independently of the anti-G suit inflation. They suggest that ANF release during exercise could be influenced by factors other than haemodynamic stimuli. The comparison between ANF and PRA changes during arm-cranking indicates that PRA is influenced more than ANF by blood volume displacement. The ANF increase during exercise does not inhibit aldosterone secretion.     

Effects of angiotensin II on arterial pressure,renin and aldosterone during exercise

Summary To evaluate the effect of isotonic exercise on the response to angiotensin II, angiotensin II in saline solution was infused intravenously (7.5 ng · kg⁻¹ · min⁻¹) in seven normal sodium replete male volunteers before, during and after a graded uninterrupted exercise test on the bicycle ergometer until exhaustion. The subjects performed a similar exercise test on another day under randomized conditions when saline solution only was infused. At rest in recumbency angiotensin II infusion increased plasma angiotensin II from 17 to 162 pg · ml⁻¹ (P<0.001). When the tests with and without angiotensin II are compared, the difference in plasma angiotensin II throughout the experiment ranged from 86 to 145 pg · ml⁻¹. The difference in mean intra-arterial pressure averaged 17 mmHg at recumbent rest, 12 mmHg in the sitting position, 9 mmHg at 10% of peak work rate and declined progressively throughout the exercise test to become non-significant at the higher levels of activity. Plasma renin activity rose with increasing levels of activity but angiotensin II significantly reduced the increase. Plasma aldosterone, only measured at rest and at peak exercise, was higher during angiotensin II infusion; the difference in plasma aldosterone was significant at rest, but not at peak exercise. In conclusion, the exercise-induced elevation of angiotensin II does not appear to be an important factor in the increase of blood pressure. It is suggested that the vasodilating mechanisms in the working muscles and the vasoconstricting mechanisms in the non-working vascular beds are powerful and dominant during isotonic exercise and attenuate the opposing or additive vasoconstrictor effects of angiotensin II. The negative feedback effect of angiotensin II on renal renin secretion, however, is not inhibited by exercise.     

Effect of short-term endurance training on exercise capacity,haemodynamics and atrial natriuretic peptide secretion in heart transplant recipients

Exercise tolerance of heart transplant patients is often limited. Central and peripheral factors have been proposed to explain such exercise limitation but, to date, the leading factors remain to be determined. We examined how a short-term endurance exercise training programme may improve exercise capacity after heart transplantation, and whether atrial natriuretic peptide (ANP) release may contribute to the beneficial effects of exercise training by minimizing ischaemia and/or cardiac and circulatory congestion through its vasodilatation and haemoconcentration properties. Seven heart transplant recipients performed a square-wave endurance exercise test before and after 6 weeks of supervised training, while monitoring haemodynamic parameters, ANP and catecholamine concentrations. After training, the maximal tolerated power and the total mechanical work load increased from 130.4 (SEM 6.5) to 150.0 (SEM 6.0) W (P < 0.05) and from 2.05 (SEM 0.1) to 3.58 (SEM 0.14) kJ · kg⁻¹ (P < 0.001). Resting heart rate decreased from 100.0 (SEM 3.4) to 92.4 (SEM 3.5) beats · min⁻¹ (P < 0.05) but resting and exercise induced increases in cardiac output, stroke volume, right atrial, pulmonary capillary wedge, systemic and pulmonary artery pressures were not significantly changed by training. Exercise-induced decrease of systemic vascular resistance was similar before and after training. After training arterio-venous differences in oxygen content were similar but maximal lactate concentrations decreased from 6.20 (SEM 0.55) to 4.88 (SEM 0.6) mmol · 1⁻¹ (P < 0.05) during exercise. Similarly, maximal exercise noradrenaline concentration tended to decrease from 2060 (SEM 327) to 1168 (SEM 227) pg · ml⁻¹. A significant correlation was observed between lactate and catecholamines concentrations. The ANP concentration at rest and the exercise-induced ANP concentration did not change throughout the experiment [104.8 (SEM 13.1) pg · ml⁻¹ vs 116.0 (SEM 13.5) pg · ml⁻¹ and 200.0 (SEM 23.0) pg · ml⁻¹ vs 206.5 (SEM 25.9) pg · ml⁻¹ respectively]. The results of this study suggested that the significant improvement in exercise capacity observed after this short-term endurance training period may have arisen mainly through peripheral mechanisms, associated with the possible decrease in plasma catecholamine concentrations and reversal of muscle deconditioning and/or prednisone-induced myopathy.     

Saliva flow and composition in humans exposed to acute altitude hypoxia

Summary The effects of acute hypoxia (2 days at 4350 m) on whole saliva flow and composition were studied on 12 sea-level natives, at rest and following a maximal exercise. Exercise, performed in normoxia and hypoxia, did not induce variations in saliva flow rate, saliva potassium or α-amylase concentrations. In contrast, acute hypoxia did lead to an increase in mean saliva flow rate both at rest (0.63 ml·min⁻¹ to 0.93 ml·min⁻¹,P<0.01) and after exercise (0.56 ml·min⁻¹ to 1.06 ml·min⁻¹,P<0.05) and a decrease in mean saliva potassium concentration at rest (20.8 mmol·1⁻¹ to 14.7 mmol·1⁻¹,P<0.01) as well as after exercise (21.7 mmol·1⁻¹ to 16.5 mmol·1⁻¹,P<0.05). This effect might be the consequence of a hypoxia-induced stimulation of the parasympathetic nervous system.     

Impact of elevated ambient temperatures on the acute immune response to intensive endurance exercise

To date, there has been little research examining how elevated ambient temperatures exert an additional effect on the acute immune response to endurance exercise. Seven endurance-trained, non-heat-acclimated men [mean (95% confidence interval): 29.7 (25.9–33.5) years, V˙O_2max 66.3 (61.3–71.3) ml·kg⁻¹·min⁻¹] performed two 60-min treadmill runs (75% V˙O_2max) in two different environments (EX1: 18°C/50% room temperature/relative humidity and EX2: 28°C/50% room temperature/relative humidity) with a 7-day interval between the runs. Blood samples were drawn at rest and 0, 0.5, 3, 24, and 48 h after exercise. Compared to EX1, exercise-induced increases in core temperature, sweating rate, heart rate, plasma norepinephrine, cortisol, human growth hormone, and neutrophil and monocyte counts were significantly (5% level) more pronounced after EX2. In contrast, responses of plasma epinephrine, myeloperoxidase, interleukin (IL)-6 as well as lymphocyte counts were similar in EX1 and EX2. Plasma concentrations of IL-8 and C-reactive protein were affected by neither exercise nor by additional heat exposure. Our results suggest that the additional impact of elevated ambient temperatures on stress responses to endurance exercise in trained subjects seems to affect primarily the cardiocirculatory and hormonal systems, and resulting changes in neutrophil and monocyte cell-trafficking. In contrast, heat stress does not seem to exert large additional effects on the acute immune response to endurance exercise as performed in the present study. Electronic Publication     

Artificial gravity training reduces bed rest-induced cardiovascular deconditioning

We studied 15 men (8 treatment, 7 control) before and after 21 days of 6o head-down tilt to determine whether daily, 1-h exposures to 1.0 G_z (at the heart) artificial gravity (AG) would prevent bed rest-induced cardiovascular deconditioning. Testing included echocardiographic analysis of cardiac function, plasma volume (PV), aerobic power (VO₂pk) and cardiovascular and neuroendocrine responses to 80o head-up tilt (HUT). Data collected during HUT were ECG, stroke volume (SV), blood pressure (BP) and blood for catecholamines and vasoactive hormones. Heart rate (HR), cardiac output (CO), total peripheral resistance, and spectral power of BP and HR were calculated. Bed rest decreased PV, supine and HUT SV, and indices of cardiac function in both groups. Although PV was decreased in control and AG after bed rest, AG attenuated the decrease in orthostatic tolerance [pre- to post-bed rest change; control: −11.8 ± 2.0, AG: −6.0 ± 2.8 min (p = 0.012)] and VO₂pk [pre- to post-bed rest change; control: −0.39 ± 0.11, AG: −0.17 ± 0.06 L/min (p = 0.041)]. AG prevented increases in pre-tilt levels of plasma renin activity [pre- to post-bed rest change; control: 1.53 ± 0.23, AG: −0.07 ± 0.34 ng/mL/h (p = 0.001)] and angiotensin II [pre- to post-bed rest change; control: 3.00 ± 1.04, AG: −0.63 ± 0.81 pg/mL (p = 0.009)] and increased HUT aldosterone [post-bed rest; control: 107 ± 30 pg/mL, AG: 229 ± 68 pg/mL (p = 0.045)] and norepinephrine [post-bed rest; control: 453 ± 107, AG: 732 ± 131 pg/mL (p = 0.003)]. We conclude that AG can mitigate some aspects of bed rest-induced cardiovascular deconditioning, including orthostatic intolerance and aerobic power. Mechanisms of improvement were not cardiac-mediated, but likely through improved sympathetic responsiveness to orthostatic stress.     

Physical activity and plasma interleukin-6 in humans – effect of intensity of exercise

The present study included data from three marathon races to investigate the hypothesis that a relationship exists between running intensity and elevated concentrations of interleukin (IL)-6 in plasma. The study included a total of 53 subjects whose mean age was 30.6 [95% confidence interval (CI) 1.4] years, mean body mass 77.7 (95%CI 2.0) kg, mean maximal oxygen uptake (V˙O_2max) 59.3 (95%CI 1.4) ml · min⁻¹ · kg⁻¹, and who had participated in the Copenhagen Marathons of 1996, 1997 or 1998, achieving a mean running time of 206 (95%CI 7) min. Running intensity was calculated as running speed divided by V˙O_2max. The concentration of IL-6 in plasma peaked immediately after the run. There was a negative correlation between peak IL-6 concentration and running time (r=−0.30, P < 0.05) and a positive correlation between peak IL-6 concentration and running intensity (r=0.32, P < 0.05). The IL-1 receptor antagonist (IL-1ra) plasma concentration peaked 1.5 h after the run and there was a positive correlation between the peak plasma concentrations of IL-6 and IL-1ra (r=0.39, P < 0.01). Creatine kinase (CK) plasma concentration peaked on the 1st day after the run, but no association was found between peak concentrations of IL-6 and CK. In conclusion, the results confirmed the hypothesized association between plasma IL-6 concentration and running intensity, but did not confirm the previous finding of a connection between IL-6 plasma concentration and muscle damage. Accepted: 6 August 2000     

Effect of brief maximal exercise on circulating levels of interleukin-12

Interleukin-12 (IL-12) is a cytokine that was originally identified as natural killer cell stimulatory factor. It induces the activity of T-helper 1 (Th1) cells and exhibits strong anti-tumor activity. In this study, we studied the effects of brief anaerobic maximal exercise on circulating levels of IL-12. Six healthy males [mean (SD) 25.2 (2.6) years] performed a modified Wingate test exercise (resistance 0.075 kg/kg of body mass). The exercise consisted of five bouts of maximal cycling for 10 s, with rest intervals of 50 s between them. Blood samples were taken before, immediately after, 30 min after, 60 min after and 120 min after the exercise. Plasma concentrations of IL-12 were measured using an enzyme-linked immunosorbent assay. Data were corrected for hemoglobin and hematocrit measurements. Plasma concentrations of IL-12 averaged [mean (SD)] 234.2 (40.9) pg/ml before, 305.2 (62.1) pg/ml immediately after, 202.8 (24.2) pg/ml 30 min after, 239.7 (35.1) pg/ml 60 min after, and 199.6 (49.2) pg/ml 120 min after the exercise. We showed that plasma concentrations of IL-12 increased significantly immediately after brief anaerobic maximal cycle ergometer exercise (P < 0.01). Accepted: 29 October 1999     

Influence of the sample collection method on salivary interleukin–6 levels in resting and post-exercise conditions

Previous studies demonstrated that no significant relationships exist between salivary and serum IL-6 in resting conditions and following exercise and that appropriate saliva collection procedures allow to avoid analytical drawbacks. This investigation aimed to: (a) compare the effects of two methods of saliva collection on IL-6 assay; (b) search for correlation between salivary and serum IL-6 in resting and post-exercise conditions; (c) evaluate the IL-6 response to isometric contractions. Seventeen sedentary subjects and fifteen athletes underwent one blood and two salivary draws: saliva was collected chewing on cotton salivettes and using a plastic straw (SA method and ST method, respectively). Afterwards, the athletes only completed a fatiguing isometric exercise of the knee extensors and blood and saliva were sampled after the exercise. In the entire group (n = 32), ST method produced higher IL-6 levels than SA method and serum sampling. The exercise elicited significant responses of lactate, serum IL-6, salivary IL-6 (by ST method): salivary IL-6 values using the ST collection method were higher at each sampling point than with the SA method. The correlation analyses applied to both resting levels in the entire group and absolute changes above baseline in the athlete group showed that: (1) no significant relationships exist between serum and salivary IL-6 levels; (2) the greater the salivary IL-6 measurement, the higher the resultant inaccuracy of the SA method; (3) significant correlations exist between isometric force and mechanical fatigue during exercise and peaks of lactate and serum IL-6. These data provided demonstration of a cotton-interference effect for the results of salivary IL-6 assay and confirmed the lack of significant correlation between salivary and serum IL-6 in resting and post-exercise conditions.     

Effectiveness of short-term heat acclimation for highly trained athletes

Effectiveness of short-term acclimation has generally been undertaken using untrained and moderately-trained participants. The purpose of this study was to determine the impact of short-term (5-day) heat acclimation on highly trained athletes. Eight males (mean ± SD age 21.8 ± 2.1 years, mass 75.2 ± 4.6 kg, [(V)\dot] \dot{V}O_2peak 4.9 ± 0.2 L min⁻¹ and power output 400 ± 27 W) were heat acclimated under controlled hyperthermia (rectal temperature 38.5°C), for 90-min on five consecutive days (T _a = 39.5°C, 60% relative humidity). Acclimation was undertaken with dehydration (no fluid-intake) during daily bouts. Participants completed a rowing-specific, heat stress test (HST) 1 day before and after acclimation (T _a = 35°C, 60% relative humidity). HST consisted 10-min rowing at 30% peak power output (PPO), 10 min at 60% PPO and 5-min rest before a 2-km performance test, without feedback cues. Participants received 250 mL fluid (4% carbohydrate; osmolality 240–270 mmol kg⁻¹) before the HST. Body mass loss during acclimation bouts was 1.6 ± 0.3 kg (2.1%) on day 1 and 2.3 ± 0.4 kg (3.0%) on day 5. In contrast, resting plasma volume increased by 4.5 ± 4.5% from day 1 to 5 (estimated from [Hb] & Hct). Plasma aldosterone increased at rest (52.6 pg mL⁻¹; p = 0.03) and end-exercise (162.4 pg mL⁻¹; p = 0.00) from day 1 to 5 acclimation. During the HST T _re and f _c were lowered 0.3°C (p = 0.00) and 14 b min⁻¹ (p = 0.00) after 20-min exercise. The 2-km performance time (6.52.7 min) improved by 4 s (p = 0.00). Meaningful physiological and performance improvements occurred for highly trained athletes using a short-term (5-day) heat acclimation under hyperthermia control, with dehydration.     

Potassium kinetics and its relationship with ventilation during repeated bouts of exercise in women

The purpose of this study was to determine the electrolyte concentration changes in arterial plasma from high-intensity repeated bouts of cycling exercise in well-trained females and to determine the relationships between arterial plasma lactate, potassium (K⁺), bicarbonate (HCO₃⁻), and pH with minute ventilation. Fourteen female subjects (mean age = 27 ± 4 years; mean height = 170 ± 7 cm; mean weight = 62 ± 7 kg; maximal oxygen uptake = 50 ± 6 ml/kg/min) were recruited to perform 3 × 5 min bouts of exercise at 236 ± 27 W with 10 min recovery between each set. Minute ventilation, arterial plasma lactate, potassium, calcium, chloride, and sodium ion concentrations were measured a minute 0, 1, 2, 3, 4, 5 of each set and midway through recovery (21 sampling points total per subject). The results showed that the strongest relationship was between arterial plasma K⁺ concentration and minute ventilation (r ² = 0.91), and, that arterial plasma lactate mirrored both arterial plasma HCO₃⁻ and pH. In conclusion, this study demonstrates that women exhibit similar electrolyte responses as reported elsewhere in men, and support the idea that K⁺ may partly contribute to controlling ventilation during high-intensity exercise and recovery.