Montelukast does not affect exercise performance at subfreezing temperature in highly trained non-asthmatic endurance athletes

Anti-leukotriene therapy represents a new principle in asthma treatment. As elite athletes can have asthma, this double-blind, placebo-controlled, randomised cross-over study investigated the effect of 10 mg oral montelukast, a specific and potent cysteinyl leukotriene receptor antagonist, on physiological responses to submaximal and maximal aerobic exercise at -15 degrees C in 14 non-asthmatic highly trained endurance male athletes (maximal oxygen uptake [VO2 max] > 70 ml x kg(-1) x min(-1)). Heart rate, capillary blood lactate, minute ventilation with tidal volume and breathing frequency, respiratory exchange ratio and oxygen uptake were measured during the warm-up run of 10 min at 50%, runs of 10 min at 90% and 5 min at 80% VO2max, and a timed run to exhaustion. Spirometry was performed at baseline, at four hours after tablet ingestion, after warm-up and exercise at 80% VO2max, and in the post exercise period. Compared to placebo, montelukast did not increase baseline FEV1, have a beneficial effect on physiological performance variables, or increase the mean (SD) running time to exhaustion (montelukast: 332.3 [45.8] s, placebo: 340.1 [53.3] s, P = 0.22). These findings do not suggest the need for disallowing the use of this drug by asthmatic athletes.     

Prolonged exercise in highly trained female endurance runners

The effects of prolonged exercise in a 21 degree C dry bulb and 15 degree C wet bulb environment at 65%-70% VO2max were examined in seven highly trained females. The subjects, aged 22-35 years, underwent an initial incremental treadmill test to exhaustion, with assessment of VO2max and related cardiorespiratory variables. One week later, under similar environmental conditions, subjects ran at approximately 65% VO2max for 80 min on a motor-driven treadmill. Approximately 10 ml of venous blood was withdrawn 10 min prior and immediately prior to the onset of prolonged exercise, and at 20, 40, 60, and 80 min, and 20 min post-exercise. Venous blood was analyzed for glucose, lactate, osmolality, Na+, K+, protein, and hemoglobin (Hb). Hematocrit was measured and changes in plasma volume calculated. VO2, VE, respiratory exchange ratio, and heart rate were recorded at 17, 37, and 77 min. The percent body fat estimated from skinfold thicknesses was 19 +/- 1%. The mean VO2max was 59.3 +/- 1.0 ml . kg-1 . min-1, with a mean max VE STPD and heart rate of 78.75 +/- 3.10 1 . min-1 and 175 +/- 4 beats . min-1, respectively. No significant changes occurred in VO2, VE, % VO2max, heart rate, venous lactate, plasma glucose, or plasma protein during the prolonged exercise. A significant decrease in respiratory exchange ratio was noted. Significant changes also occurred in hematocrit, Hb, Na+, K+, and osmolality. An interesting finding was the pre-exercise expansion of the plasma volume.     

Hemoglobin desaturation in highly trained athletes during heavy exercise

It has been generally accepted that during exercise at sea level, the pulmonary system of normal, healthy individuals is capable of maintaining arterial oxygen tension at near resting levels. However, recent evidence questions whether this generalization applies to the highly trained endurance athlete who is capable of achieving very high levels of metabolic demand. Hence, the purpose of these experiments was to examine the relationship between maximal oxygen consumption (VO2max) and arterial oxygen-hemoglobin saturation (%SaO2) during short-term heavy exercise in trained athletes and untrained individuals. Ten trained distance runners and 7 untrained males exercised at 95% of VO2max for 3 min. Minute-by-minute measurement of %SaO2 was obtained via ear oximetry. The correlation coefficients between %SaO2 and VO2max during exercise were r = -0.68, r = -0.74, and r = -0.72 (P less than 0.05) for minutes 1 through 3, respectively. In general those individuals with the highest VO2max showed the greatest decrease in %SaO2. By comparison there was no difference (P greater than 0.05) in resting %SaO2 between the trained (96.3 +/- 0.2% [SE]) and the untrained (96.3 +/- 0.4%) subjects. However, at minute 3 of exercise, %SaO2 was significantly lower (P less than 0.05) in the trained subjects (87.0 +/- 0.7%) than in the untrained subjects (92.6 +/- 0.7%). These data demonstrate that arterial desaturation occurs in healthy, highly trained endurance athletes during heavy exercise and that the level of the arterial desaturation is inversely related to VO2max.     

Effect of prolonged exercise on arterial oxygen saturation in athletes susceptible to exercise-induced hypoxemia

This study examined the effect of prolonged endurance exercise on the development of exercise-induced hypoxemia (EIH) in athletes who had previously displayed EIH during an incremental maximal exercise test. Five male and three female endurance-trained athletes participated. Susceptibility to EIH was confirmed through a maximal incremental exercise test and defined as a reduction in the saturation of arterial oxygen (SpO(2)) of >/=4% from rest. Sixty minutes of running was conducted, on a separate day, at an oxygen consumption corresponding to 95% of ventilatory threshold. Immediately following the 60 min exercise bout, athletes commenced a time trial to exhaustion at 95% maximal oxygen consumption (VO(2max)). The reduction in SpO(2) was significantly greater during the maximal incremental test, than during the 60 min, or time trial to exhaustion (-8.8+/-1.4%, -3.3+/-1.1%, and -4.1+/-2.3%, P<0.05, respectively). The degree of desaturation during the 60 min was significantly related to the relative intensity of exercise at 95% ventilatory threshold (adjusted r(2)=0.54, P=0.02). In conclusion, athletes who did not exercise at greater than 73% VO(2max) during 60 min of endurance exercise did not display EIH, despite being previously susceptible during an incremental maximal test.     

Effects of inhaled bronchodilators and corticosteroids on exercise induced arterial hypoxaemia in trained male athletes

Objectives: To determine the effect of prophylactic treatment with an inhaled bronchodilator and anti-inflammatory on arterial saturation (SaO₂) in trained non-asthmatic male athletes with exercise induced arterial hypoxaemia (EIAH). Methods: Nine male athletes (mean (SD) age 26.3 (6.7) years, height 182.6 (7.9) cm, weight 79.3 (10.5) kg, VO₂MAX 62.3 (6.3) ml/kg/min, SaO₂MIN 92.5 (1.1)%) with no history of asthma were tested in two experimental conditions. A combination of a therapeutic dose of salbutamol and fluticasone or an inert placebo was administered in a randomised crossover design for seven days before maximal cycling exercise. Oxygen consumption (VO₂), ventilation (VE), heart rate (HR), power output, and SaO₂ were monitored during the exercise tests. Results: There were no significant differences between the drug (D) and placebo (P) conditions for minimal SaO₂ (D = 93.6 (1.4), P = 93.0 (1.1)%; p = 0.93) VO₂MAX (D = 61.5 (7.2), P = 61.9 (6.3) ml/kg/min; p = 0.91), peak power (D = 444.4 (48.3), P = 449.4 (43.9) W; p = 0.90), peak VE (D = 147.8 (19.1), P = 149.2 (15.5) litres/min; p = 0.82), or peak heart rate (D = 182.3 (10.0), P = 180.8 (5.5) beats/min; p = 0.76). Conclusions: A therapeutic dose of salbutamol and fluticasone did not attenuate EIAH during maximal cycling in a group of trained male non-asthmatic athletes.     

The scientific basis for high-intensity interval training: optimising training programmes and maximising performance in highly trained endurance athletes.

While the physiological adaptations that occur following endurance training in previously sedentary and recreationally active individuals are relatively well understood, the adaptations to training in already highly trained endurance athletes remain unclear. While significant improvements in endurance performance and corresponding physiological markers are evident following submaximal endurance training in sedentary and recreationally active groups, an additional increase in submaximal training (i.e. volume) in highly trained individuals does not appear to further enhance either endurance performance or associated physiological variables [e.g. peak oxygen uptake (VO2peak), oxidative enzyme activity]. It seems that, for athletes who are already trained, improvements in endurance performance can be achieved only through high-intensity interval training (HIT). The limited research which has examined changes in muscle enzyme activity in highly trained athletes, following HIT, has revealed no change in oxidative or glycolytic enzyme activity, despite significant improvements in endurance performance (p < 0.05). Instead, an increase in skeletal muscle buffering capacity may be one mechanism responsible for an improvement in endurance performance. Changes in plasma volume, stroke volume, as well as muscle cation pumps, myoglobin, capillary density and fibre type characteristics have yet to be investigated in response to HIT with the highly trained athlete. Information relating to HIT programme optimisation in endurance athletes is also very sparse. Preliminary work using the velocity at which VO2max is achieved (V(max)) as the interval intensity, and fractions (50 to 75%) of the time to exhaustion at V(max) (T(max)) as the interval duration has been successful in eliciting improvements in performance in long-distance runners. However, V(max) and T(max) have not been used with cyclists. Instead, HIT programme optimisation research in cyclists has revealed that repeated supramaximal sprinting may be equally effective as more traditional HIT programmes for eliciting improvements in endurance performance. Further examination of the biochemical and physiological adaptations which accompany different HIT programmes, as well as investigation into the optimal HIT programme for eliciting performance enhancements in highly trained athletes is required.     

Between 21 and 34 years of age, aging alters the catecholamine responses to supramaximal exercise in endurance trained athletes.

The purpose of this study was to determine the effect of aging and training on the adrenaline (A) and noradrenaline (NA) responses during the Wingate-test in three age groups of subjects: 21 year old untrained subjects (21U), 21 year old endurance trained (21T) (national elite runners), 34 year old endurance trained (34T) (national elite runners). Performances during the test were judged using the usual parameters of peak power (Wmax) and mean power (W) expressed in absolute or relative values. A and NA responses were measured at rest (A0 and NA0) immediately at the end of the exercise (Amax and NAmax) and after 5 minutes recovery (A5 and NA5). Plasma maximal lactate (La(max)) was determined 3 minutes after the end of the exercise. Wmax, W and La(max) were always significantly lower in 34T compared to 21T and 21U. The catecholamine responses were similar in 21T and 21U. Inversely, a significantly lower value of Amax was observed in 34T (2.01 +/- 0.5 nmol x l(-1)) compared to 21U (3.62 +/- 0.3 nmol x l(-1)) associated with a significantly higher value of NA(max) in 34T versus 21T and 21U. Thus, the Amax/NA(max) ratio was found to be significantly lower in the older subjects versus both 21T and 21U. All these findings indicated that endurance training did not affect the sympathoadrenergic responses to a supramaximal exercise and suggested that only one decade may reduce the capacity of the medulla to secrete adrenaline and therefore the adrenal medulla responsiveness to the sympathetic nervous activity.     

Incremental exercise test design and analysis: implications for performance diagnostics in endurance athletes

Physiological variables, such as maximum work rate or maximal oxygen uptake (VO2max), together with other submaximal metabolic inflection points (e.g. the lactate threshold [LT], the onset of blood lactate accumulation and the pulmonary ventilation threshold [VT]), are regularly quantified by sports scientists during an incremental exercise test to exhaustion. These variables have been shown to correlate with endurance performance, have been used to prescribe exercise training loads and are useful to monitor adaptation to training. However, an incremental exercise test can be modified in terms of starting and subsequent work rates, increments and duration of each stage. At the same time, the analysis of the blood lactate/ventilatory response to incremental exercise may vary due to the medium of blood analysed and the treatment (or mathematical modelling) of data following the test to model the metabolic inflection points. Modification of the stage duration during an incremental exercise test may influence the submaximal and maximal physiological variables. In particular, the peak power output is reduced in incremental exercise tests that have stages of longer duration. Furthermore, the VT or LT may also occur at higher absolute exercise work rate in incremental tests comprising shorter stages. These effects may influence the relationship of the variables to endurance performance or potentially influence the sensitivity of these results to endurance training. A difference in maximum work rate with modification of incremental exercise test design may change the validity of using these results for predicting performance, and prescribing or monitoring training. Sports scientists and coaches should consider these factors when conducting incremental exercise testing for the purposes of performance diagnostics.     

Effects of formoterol on endurance performance in athletes at an ambient temperature of -20 degrees C

The use of inhaled beta2-agonists is restricted in sports. No benefit of inhaled formoterol upon performance was found in healthy athletes under normal climatic conditions, but it has not been investigated whether formoterol improves performance in athletes during exposure to cold. To investigate the effect of inhaled formoterol vs placebo upon performance and lung function at -20 degrees C in 20 healthy male athletes. We used a randomized double-blind, placebo-controlled, cross-over design. The subjects performed a run until exhaustion after inhaled study drug. The speed was 95% of the predetermined maximal oxygen uptake (VO2 max) the first minute and increased to 107% of VO2 max for the remaining part of the test. Time until exhaustion, ventilation (VE), VO2, respiratory rate (RR), tidal volume (VT), heart rate (HR) and arterial oxyhemoglobin saturation (SPO2) were recorded during exercise. Lung function was measured before inhaling, after inhaling the study drug and after the treadmill run. Inhaled formoterol did not improve endurance performance in cold environments compared with placebo, although formoterol significantly improved lung function (FEV1, FEF50 and PEF) and HR 4 min after the start of the exercise. Inhaled formoterol did not improve endurance performance in healthy, well-trained athletes exposed to cold.     

Evidence of major genes for exercise heart rate and blood pressure at baseline and in response to 20 weeks of endurance training: the HERITAGE family study

Major gene effects on exercise heart rate (HR) and blood pressure (BP) measured at 50 W and 80 % maximal oxygen uptake (VO (2)max) were assessed in 99 White families in the HERITAGE Family Study. Exercise HR and BP were measured both before and after 20 weeks of endurance training. The baseline phenotypes were adjusted for the effects of age and BMI, whereas the training responses (post-training minus baseline) were adjusted for the effects of age, BMI and the corresponding baseline values, within four sex-by-generation groups. Baseline exercise HR at 50 W was under the influence of a major recessive gene and a multifactorial component, which accounted for 30 % and 27 % of the variance, respectively. The training response was found to be under the influence of a major dominant gene, which accounted for 27 % of the variance. These significant major gene effects were independent of the effects of cigarette smoking, baseline VO (2)max, and the resting HR levels. No significant interactions were found between genotype and age, sex, or BMI. No major gene effect was found for exercise BP. Instead, we found the baseline exercise BP at 50 W and 80 % VO (2)max and the training response at 50 W were solely influenced by multifactorial effects, which accounted for about 50 %, 40 % and 20 % of the variance, respectively. No familial resemblance was found for training responses in exercise HR or BP at 80 % VO (2)max. Segregation analysis also was carried out for exercise HR in Whites pooled with a small sample of Blacks in HERITAGE. Similar major effects were found, but the transmission from parents to offspring did not follow Mendelian expectations, suggesting sample heterogeneity. In conclusion, submaximal exercise HR at baseline and in response to endurance training was influenced by putative major genes, with no evidence of interactions with sex, age or BMI, in contrast to a multifactorial etiology for exercise BP.     

Evidence for exercise therapy in the treatment of chronic disease based on at least three randomized controlled trials--summary of published systematic reviews

Final evidence for the overall benefits of exercise therapy in the treatment/rehabilitation of specific chronic disease comes from randomized controlled trials (RCTs). This paper summarizes current evidence that is based on a systematic review including data from at least three RCTs with contrast for exercise only. The quality of specific RCTs as well as the quality of systematic reviews varies, the newest ones usually being of higher quality than the older ones. The most consistent finding of the studies is that aerobic capacity and muscular strength of patients can be improved without causing detrimental effects on disease progression. Severe complications during these carefully tailored programs were rare. The treatment periods and follow-up times of the majority of the RCTs are of a too short duration to document group differences in disease progression. However, exercise reduces disease-related symptoms in many diseases, such as osteoarthritis, asthma and chronic obstructive pulmonary disorder. Also, RCTs studying patients with coronary heart disease as well as patients with heart failure show that all-cause mortality is lower in exercisers than in controls.     

Evidence for an exercise induced increase of TNF‐α and IL‐6 in marathon runners

Regular physical activity of moderate intensity improves cardiovascular risk factors including low‐grade inflammation. However, acute vigorous exercise such as marathon running results in marked increases of circulating pro‐inflammatory markers. Up to now, the origin of this pro‐inflammatory boost is still debated equivocally. We analyzed the change of interleukin‐6 (IL‐6), tumor necrosis factor‐alpha (TNF‐α), and leptin from pre‐ to immediately post‐race in 15 male runners (age 43 ± 10.9 years and body mass index 24.5 ± 2.7 kg/m²) both on the protein level in the plasma and on the messenger ribonucleic acid (mRNA) level in blood mononuclear cells (BMNC). We observed a significant increase of IL‐6 (prerace 2.08 ± 0.10 ng/L and postrace 40.14 ± 24.85 ng/L, P < 0.001) and TNF‐α (prerace 8.14 ± 1.38 ng/L and postrace 12.40 ± 3.15 ng/L, P < 0.001) and a decrease of leptin (prerace 1.64 ± 2.64 μg/L and postrace 0.80 ± 1.70 μg/L, P = 0.04) serum levels after the marathon race. Furthermore, TNF‐α, IL‐6, and leptin were expressed (mRNA level) in BMNC. However no significant differences in mRNA levels were seen before and after the run in these cells. We found an up‐regulation of TNF‐α and IL‐6 in the plasma during vigorous exercise. This increase is not attributable to BMNC. We assume a local production in, or release from, exercised tissues.     

Evidence of major genes for plasma HDL, LDL cholesterol and triglyceride levels at baseline and in response to 20 weeks of endurance training: the HERITAGE Family Study

This study assessed major gene effects for baseline HDL-C, LDL-C, TG, and their training responses (post-training minus baseline) in 527 individuals from 99 White families and 326 individuals from 113 Black families in the HERITAGE Family Study. The baseline phenotypes were adjusted for the effects of age and BMI, and the training response phenotypes were adjusted for the effects of age, BMI, and their respective baseline values, within each of the sex-by-generation-by-race groups, prior to genetic analyses. In Whites, we found that LDL-C at baseline and HDL-C training response were under influence of major recessive genes (accounting for 2--30 % of the variance) and multifactorial (polygenic and familial environmental) effects. Interactions of these major genes with sex, age, and BMI were tested, and found to be nonsignificant. In Blacks, we found that baseline HDL-C was influenced by a major dominant gene without a multifactorial component. This major gene effect accounted for 45 % of the variance, and exhibited no significant genotype-specific interactions with age, sex, and BMI. Evidence of major genes for the remaining phenotypes at baseline and in response to endurance training were not found in both races, though some were influenced by major effects that did not follow Mendelian expectations or were with ambiguous transmission from parents to offspring. In summary, major gene effects that influence baseline plasma HDL-C and LDL-C levels as well as changes in HDL-C levels in response to regular exercise were detected in the current study.