ACTN3 genotype influences exercise-induced muscle damage during a marathon competition.

PURPOSE: Exercise-induced muscle damage has been identified as one of the main causes of the progressive decrease in running and muscular performance in marathoners. The aim of this investigation was to determine the influence of the ACTN3 genotype on exercise-induced muscle damage produced during a marathon. METHODS: Seventy-one experienced runners competed in a marathon race. Before and after the race, a sample of venous blood was obtained and maximal voluntary leg muscle power was measured during a countermovement jump. In the blood samples, the ACTN3 genotype (R577X) and the changes in serum creatine kinase and myoglobin concentrations were measured. Data from RX heterozygotes and XX mutant homozygotes were grouped as X allele carriers and compared to RR homozygotes. RESULTS: At the end of the race, X allele carriers presented higher serum myoglobin (774 ± 852 vs 487 ± 367 U L-1; P = 0.02) and creatine kinase concentrations (508 ± 346 vs 359 ± 170 ng mL-1; P = 0.04) than RR homozygotes. Pre-to-post-race maximal voluntary leg muscle power reduction was more pronounced in X allele carriers than RR homozygotes (-34.4 ± 16.1 vs -27.3 ± 15.4%; P = 0.05). X allele carriers self-reported higher levels of lower limb muscle pain (7 ± 2 vs 6 ± 2 cm; P = 0.02) than RR homozygotes at the end of the race. CONCLUSIONS: In comparison to RR homozygotes, X allele carriers for the R577X polymorphism of the ACTN3 gene presented higher values for typical markers of exercise-induced muscle damage during a competitive marathon. Thus, the absence of a functional α-actinin-3 produced by the X allele might induce higher levels of muscle breakdown during prolonged running events.

Physiological Demands of Elite Cross-Country Skiing During a Real Competition.

The aim of this study was to assess different physiological variables before and after a 5-km (women) and 10-km (men) cross-country skiing competition to determine potential mechanisms of fatigue. Fourteen elite-level skiers competed in an official cross-country skiing competition using the classical style (9 men and 5 women). Instantaneous skiing velocity was measured during the race by means of 15-Hz global positioning system devices. Before and after the race, a sample of venous blood was obtained to assess changes in blood lactate and serum electrolyte and myoglobin concentrations. Prerace to postrace changes in blood oxygen saturation, forced vital capacity during a spirometry test, jump height during a countermovement jump, and handgrip force were also measured. Mean race speed was 15.8 ± 2.5 and 15.4 ± 1.5 km·h, whereas mean heart rate was 171 ± 6 and 177 ± 3 b·min for men and women, respectively. There were no significant prerace to postrace changes in jump height, handgrip force, and forced vital capacity in men and women. Blood oxygen saturation was reduced from prerace to postrace in men (95.9 ± 2.1% to 93.1 ± 2.3%, p = 0.02) and women (97.8 ± 1.1% to 92.4 ± 2.1%, p < 0.01), whereas blood lactate concentration increased at the end of the race in men (1.4 ± 0.5 to 4.9 ± 2.1 mmol·L, p < 0.01) and women (1.9 ± 0.1 to 6.9 ± 3.2 mmol·L, p < 0.01). After the race, blood markers of muscle damage were at low concentrations, whereas serum electrolytes remained unchanged. Fatigue in 5- and 10-km cross-country skiing competitions was related to a reduced blood oxygen carrying capacity and presumably increased muscle and blood acidosis, whereas the influence of exercise-induced muscle damage on fatigue was minor.

Methodological Approach to Use Fresh and Cryopreserved Vessels as Tools to Analyze Pharmacological Modulation of the Angiogenic Growth.

The sprouting of new vessels is greatly influenced by the procedure chosen. We sought to optimize the experimental conditions of the angiogenic growth of fresh and cryopreserved vessels cultured in Matrigel with the aim to use this system to analyze the pharmacological modulation of the process. Segments of second-order branches of rat mesenteric resistance arteries, thoracic aorta of rat or mouse, and cryopreserved rat aorta and human femoral arteries were cultured in Matrigel for 7-21 days in different mediums, as well as in the absence of endothelial or adventitia layer. Quantification of the angiogenic growth was performed by either direct measurement of the mean length of the neovessels or by calcein AM staining and determination of fluorescence intensity and area. Fresh and cryopreserved arterial rings incubated in Matrigel exhibited a spontaneous angiogenic response that was strongly accelerated by fetal calf serum. Addition of vascular endothelial growth factor, fibroblast growth factor, endothelial growth factor, or recombinant insulin-like growth factor failed to increase aortic sprouting, unless all were added together. Removal of adventitia, but not the endothelial layer, abrogated the angiogenic response of aortic rings. Determination of the mean neovessel length is an easy and accurate method to quantify the angiogenic growth devoid of confounding factors, such as inclusion of other cellular types surrounding the neovessels. Activity of a α1-adrenoceptor agonist (phenylephrine) and its inhibition by a selective antagonist (prazosin) were analyzed to prove the usefulness of the Matrigel system to evaluate the pharmacological modulation of the angiogenic growth.

Influence of endurance running on calcaneal bone stiffness in male and female runners.

PURPOSE: The aim of this investigation was to determine the influence of endurance running on calcaneus bone stiffness in male and female runners. METHODS: A total of 122 marathoners (longer distance runners, men = 101; women = 21) and 81 half-marathon and 10-km runners (shorter distance runners; men = 48; women = 33), competing in an international running event, underwent an ultrasonographic assessment of the right and left calcaneus. Calcaneus bone stiffness was estimated using the measurements of the speed of sound (SOS) and broadband ultrasound attenuation (BUA). Seventy-five age-matched sedentary people served as the control group. RESULTS: Male and female longer distance runners and shorter distance runners presented higher values than sedentary counterparts in SOS (P < 0.05), and calcaneus stiffness (P < 0.05). Although there were no significant differences between longer distance and shorter distance runners in the ultrasonographic variables, longer distance runners presented greater effects size in SOS (1.00 vs. 0.93 males; 1.10 vs. 0.77 females), BUA (0.62 vs. 0.25 males; 0.89 vs. 0.20 females) and calcaneus stiffness (0.88 vs. 0.66 males; 1.20 vs. 0.60 females) than shorter distance endurance runners. CONCLUSION: Calcaneus bone stiffness was higher in all endurance runners compared to a sedentary control population. The volume of ground reaction forces which occur during endurance running might induce the adaptation of the calcaneus bone.

Muscle damage produced during a simulated badminton match in competitive male players.

The purpose of the study was to assess the occurrence of muscle damage after a simulated badminton match and its influence on physical and haematological parameters. Sixteen competitive male badminton players participated in the study. Before and just after a 45-min simulated badminton match, maximal isometric force and badminton-specific running/movement velocity were measured to assess muscle fatigue. Blood samples were also obtained before and after the match. The badminton match did not affect maximal isometric force or badminton-specific velocity. Blood volume and plasma volume were significantly reduced during the match and consequently haematite, leucocyte, and platelet counts significantly increased. Blood myoglobin and creatine kinase concentrations increased from 26.5 ± 11.6 to 197.3 ± 70.2 µg·L(-1) and from 258.6 ± 192.2 to 466.0 ± 296.5 U·L(-1), respectively. In conclusion, a simulated badminton match modified haematological parameters of whole blood and serum blood that indicate the occurrence of muscle fibre damage. However, the level of muscle damage did not produce decreased muscle performance.

ß2- and ß1-Adrenoceptor Expression Exhibits a Common Regulatory Pattern With GRK2 and GRK5 in Human and Animal Models of Cardiovascular Diseases.

To explore if genic expression of ß(1)- or ß(2)-adrenoceptors (ARs) exhibits a common regulatory pattern with G protein-coupled receptor kinase (GRK) 2, GRK3, or GRK5 expression, we determined messenger RNA levels for these genes in different tissues from human and animal models of cardiovascular disease. We measured genic expression by qRT polymerase chain reaction in the left and right ventricles or peripheral blood mononuclear cells from healthy (n = 21), hypertensive (n = 20), heart failure (n = 24), and heart transplanted patients (n = 17) or in left ventricle, peripheral blood mononuclear cells, and kidney from spontaneously hypertensive rats or L-N-methyl-arginine-induced hypertensive rats and their respective controls (n = 4-5). In diseased versus healthy subjects and rats, parallel changes in messenger RNA levels of GRK2 and ß(2)-AR or GRK5 and ß(1)-AR were observed in each territory. Therefore, without excluding other regulatory mechanisms, the parallelism observed suggests a common regulatory pattern for the ß(1)-AR/GRK5 and ß(2)-AR/GRK2 genes, which is independent of cellular type or pathology. This highlights the need to focus not only on GRKs but also on ß(1)- or ß(2)-AR changes to completely understand the involvement of ß-AR/GRK pathways in cardiovascular diseases.

Acute consumption of a caffeinated energy drink enhances aspects of performance in sprint swimmers.

This study investigated the effect of a caffeinated energy drink on various aspects of performance in sprint swimmers. In a randomised and counterbalanced order, fourteen male sprint swimmers performed two acute experimental trials after the ingestion of a caffeinated energy drink (3 mg/kg) or after the ingestion of the same energy drink without caffeine (0 mg/kg; placebo). After 60 min of ingestion of the beverages, the swimmers performed a countermovement jump, a maximal handgrip test, a 50 m simulated competition and a 45 s swim at maximal intensity in a swim ergometer. A blood sample was withdrawn 1 min after the completion of the ergometer test. In comparison with the placebo drink, the intake of the caffeinated energy drink increased the height in the countermovement jump (49.4 (SD 5.3) v. 50.9 (SD 5.2) cm, respectively; P<0.05) and maximal force during the handgrip test with the right hand (481 (SD 49) v. 498 (SD 43) N; P<0.05). Furthermore, the caffeinated energy drink reduced the time needed to complete the 50 m simulated swimming competition (27.8 (SD 3.4) v. 27.5 (SD 3.2) s; P<0.05), and it increased peak power (273 (SD 55) v. 303 (SD 49) W; P <0.05) and blood lactate concentration (11.0 (SD 2.0) v. 11.7 (SD 2.1) mM; P<0.05) during the ergometer test. The caffeinated energy drink did not modify the prevalence of insomnia (7 v. 7%), muscle pain (36 v. 36%) or headache (0 v. 7%) during the hours following its ingestion (P>0.05). A caffeinated energy drink increased some aspects of swimming performance in competitive sprinters, whereas the side effects derived from the intake of this beverage were marginal at this dosage.

The ingestion of a caffeinated energy drink improves jump performance and activity patterns in elite badminton players.

The aim of this study was to investigate the effectiveness of a caffeine-containing energy drink to enhance physical and match performance in elite badminton players. Sixteen male and elite badminton players (25.4 ± 7.3 year; 71.8 ± 7.9 kg) participated in a double-blind, placebo-controlled and randomised experiment. On two different sessions, badminton players ingested 3 mg of caffeine per kg of body mass in the form of an energy drink or the same drink without caffeine (placebo). After 60 min, participants performed the following tests: handgrip maximal force production, smash jump without and with shuttlecock, squat jump, countermovement jump and the agility T-test. Later, a 45-min simulated badminton match was played. Players' number of impacts and heart rate was measured during the match. The ingestion of the caffeinated energy drink increased squat jump height (34.5 ± 4.7 vs. 36.4 ± 4.3 cm; P < 0.05), squat jump peak power (P < 0.05), countermovement jump height (37.7 ± 4.5 vs. 39.5 ± 5.1 cm; P < 0.05) and countermovement jump peak power (P < 0.05). In addition, an increased number of total impacts was found during the badminton match (7395 ± 1594 vs. 7707 ± 2033 impacts; P < 0.05). In conclusion, the results show that the use of caffeine-containing energy drink may be an effective nutritional aid to increase jump performance and activity patterns during game in elite badminton players.

A 7-day oral supplementation with branched-chain amino acids was ineffective to prevent muscle damage during a marathon.

The aim of this study was to determine the effectiveness of a 7-day oral supplementation with branched-chain amino acids (BCAA) to prevent muscle damage during a marathon. Forty-six experienced runners were randomly divided into two groups, one with BCAA supplementation (n = 25, supplemented with 5 g day(-1) of powdered 1:0.5:0.5 leucine:isoleucine:valine, during the 7 days prior to the competition) and the other as a control group (n = 21, supplemented with an isocaloric placebo). Before the marathon race and within 3 min of finishing, leg muscle power was measured with a maximal countermovement jump and a urine sample was obtained. During the race, running pace was measured by means of a time-chip. Myoglobin concentration was determined in the urine samples as an indirect marker of muscle damage. A visual analog scale (0-10 points) was used to assess leg muscle pain during the race. In the BCAA group, the mean running pace during the marathon was similar to the control group (3.3 ± 0.4 vs. 3.3 ± 0.5 m s(-1), respectively, 0.98). The pre- to post-race reduction in muscle power was similar in both BCAA and control groups (-23.0 ± 16.1 vs. -17.3 ± 13.8 %, P = 0.13). Post-race urine myoglobin concentration was similar in both BCAA and control groups (5.4 ± 7.5 vs. 4.5 ± 8.6 µg mL(-1), P = 0.70). Finally, there were no differences between groups in the perceived muscle pain during the race (6 ± 1 vs. 5 ± 1 points, P = 0.80). A 7-day supplementation of BCAA (5 g day(-1)) did not increase the running performance during a marathon. Furthermore, BCAA supplementation was ineffective to prevent muscle power loss, muscle damage or perceived muscle pain during a marathon race.

The use of energy drinks in sport: perceived ergogenicity and side effects in male and female athletes.

The use of caffeine containing energy drinks has dramatically increased in the last few years, especially in the sport context because of its reported ergogenic effect. The ingestion of low to moderate doses of caffeinated energy drinks has been associated with adverse side effects such as insomnia or increased nervousness. The aim of the present study was to assess psycho-physiological changes and the prevalence of side effects resulting from the ingestion of 3 mg caffeine/kg body mass in the form of an energy drink. In a double-blind and placebo controlled experimental design, ninety experienced and low-caffeine-consuming athletes (fifty-three male and thirty-seven female) in two different sessions were provided with an energy drink that contained 3 mg/kg of caffeine or the same decaffeinated energy drink (placebo; 0 mg/kg). At 60 min after the ingestion of the energy drink, participants completed a training session. The effects of ingestion of these beverages on psycho-physiological variables during exercise and the rate of adverse side effects were measured using questionnaires. The caffeinated energy drink increased self-perceived muscle power during exercise compared with the placebo beverage (6·41 (sd 1·7) v. 5·66 (sd 1·51); P= 0·001). Moreover, the energy drink produced a higher prevalence of side effects such as insomnia (31·2 v. 10·4 %; P< 0·001), nervousness (13·2 v. 0 %; P= 0·002) and activeness (16·9 v. 3·9 %; P= 0·007) than the placebo energy drink. There were no sex differences in the incidence of side effects (P>0·05). The ingestion of an energy drink with 3 mg/kg of caffeine increased the prevalence of side effects. The presence of these side effects was similar between male and female participants.

Different expression of adrenoceptors and GRKs in the human myocardium depends on heart failure etiology and correlates to clinical variables.

Downregulation of ß(1)- adrenergic receptors (ß(1)-ARs) and increased expression/function of G-protein-coupled receptor kinase 2 (GRK2) have been observed in human heart failure, but changes in expression of other ARs and GRKs have not been established. Another unresolved question is the incidence of these compensatory mechanisms depending on heart failure etiology and treatment. To analyze these questions, we quantified the mRNA/protein expressions of six ARs (α(1A), α(1B), α(1D), ß(1), ß(2), and ß(3)) and three GRKs (GRK2, GRK3, and GRK5) in left (LV) and right ventricle (RV) from four donors, 10 patients with ischemic cardiomyopathy (IC), 14 patients with dilated cardiomyopathy (DC), and 10 patients with nonischemic, nondilated cardiopathies (NINDC). We correlated the changes in the expressions of ARs and GRKs with clinical variables such as left ventricular ejection fraction (LVEF) and left ventricular end-systolic and left ventricular end-diastolic diameter (LVESD and LVEDD, respectively). The main findings were 1) the expression of the α(1A)-AR in the LV positively correlates with LVEF; 2) the expression of GRK3 and GRK5 inversely correlates with LVESD and LVEDD, supporting previous observations about a protective role for both kinases in failing hearts; and 3) ß(1)-AR expression is downregulated in the LV and RV of IC, in the LV of DC, and in the RV of NINDC. This difference, better than an increased expression of GRK2 (not observed in IC), determines the lower LVEF in IC and DC vs. NINDC.

Myocardial G protein receptor-coupled kinase expression correlates with functional parameters and clinical severity in advanced heart failure.

BACKGROUND: In heart failure (HF), sympathetic hyperactivation induces deleterious effects in myocardial ß-adrenergic signaling, with receptor down-regulation and desensitization mediated by G protein receptor-coupled kinases (GRKs). We hypothesised that changes in GRK isoforms may be associated with clinical status in advanced HF, using the Interagency Registry for Mechanically Assisted Circulatory Support (INTERMACS) scale. METHODS: We included 31 patients with advanced HF undergoing transplantation. According to INTERMACS profiles, mRNA and protein levels of GRK isoforms in left ventricular (LV) myocardium were analyzed and compared with nonfailing LV samples. RESULTS: In failing LV myocardium, GRK2 and GRK5 (but not GRK3) protein was up-regulated compared with control samples. Among HF patients, an increase in GRK2 and GRK5 mRNA and protein abundance was observed in ß-agonist-treated patients (vs ß-blockers: P < .05) and in higher-risk INTERMACS status (profiles 2 and 3 vs 4 and 5: P < .05). A significant negative correlation of GRK2 expression with LV stroke volume supported these findings. CONCLUSIONS: Increased GRK2 correlates with clinical severity using the INTERMACS scale and LV stroke volume, supporting it as a potential target in advanced HF. These changes are paralleled by GRK5 expression in the failing myocardium, suggesting a relevant role in human HF.

Endurance running prevents the age-related decline of calcaneal bone stiffness.

This investigation presents a comparison of calcaneus bone stiffness of endurance runners of different ages and age-matched controls. We found that there was an age-associated decline in calcaneus bone stiffness in the control group while endurance runners prevented this decline, with a higher effect as the participants increased their age. PURPOSE: Previous investigations have found that endurance runners have higher bone mineral density and other bone quality variables in mechanically loaded bones. However, it is unknown if endurance running might counteract the decline in bone stiffness that occurs with age. The purpose of this study was to compare calcaneus bone stiffness of endurance runners of different ages to age-matched controls. METHODS: In a descriptive cross-sectional study, 182 endurance-trained male runners and 116 healthy untrained male controls underwent an ultrasonographic assessment of the calcaneus bone in the right and left heels. Calcaneal bone stiffness was calculated from assessments of the broadband ultrasound attenuation and the speed of sound. RESULTS: The line of best fit for the association between age and calcaneus stiffness was different between marathoners and controls (Z = - 2.1, P = 0.02). A two-way ANCOVA (condition × age) with body mass, and body mass index as covariates, revealed that there were main effects of condition (F = 26.8, P < 0.01) and age (F = 4.2, P < 0.01) for calcaneus stiffness, with a significant interaction between these two factors (F = 2.8, P = 0.03). The post hoc analysis revealed that calcaneus stiffness was significantly higher in marathoners of 40-44 years (121.5 ± 18.2 vs 101.1 ± 21.3 arbitrary units [A.U.], P = 0.01), 45-49 years (121.5 ± 19.7 vs 104.3 ± 13.4 A.U., P = 0.04), and > 50 years (111.2 ± 17.9 vs 92.4 ± 16.0 A.U., P < 0.01) than their untrained counterparts of the same age with no statistically significant differences in the remaining age groups. CONCLUSION: Endurance runners of > 40 years had higher values of calcaneus stiffness than controls, providing evidence to support the potential effect of endurance running to reduce the age-related decline on calcaneus bone stiffness.

Influence of the ACTN3 R577X genotype on the injury epidemiology of marathon runners.

A common single nucleotide polymorphism in the ACTN3 gene might result in the complete deficiency of α-actinin-3 (i.e., XX genotype). It has been found that ACTN3 XX individuals have several traits related to lessened muscle performance. This study aimed to determine the influence, if any, of ACTN3 genotypes on injury incidence of marathoners during the year preceding to participating in a competitive marathon race. Using a cross-sectional experimental design, the type and conditions of sports injuries were documented for one year in a group of 139 marathoners. Injuries were recorded following a consensus statement on injuries in Athletics. Afterward, ACTN3 genotyping was performed, and injury epidemiology was compared among RR, RX, and XX genotypes. The distribution of the RR/RX/XX genotypes was 28.8/42.8/23.5%, respectively. A total of 67 injuries were recorded. The frequency of marathoners that reported any injury during the previous year was not different across the genotypes (55.0/38.8/40.6%, P = 0.241). Although the overall injury incidence was not different among genotypes (2.78/1.65/1.94 injuries/1000 h of running, P = 0.084), the likelihood of suffering an injury was higher in RR than in RX (OR = 1.93: 95%CI = 0.87-4.30), and higher than in XX (OR = 1.79: 0.70-4.58). There was no difference in the conditions, severity, body location, time of year, or leading cause of injury among genotypes. However, XX presented a higher frequency of sudden-onset injuries (P = 0.024), and the OR for muscle-type injuries was 2.0 (0.51-7.79) times higher compared to RR runners. Although XX marathoners did not have a higher overall incidence of injury, the OR in these runners for muscle-type injuries was superior to RR and RX runners. The likelihood of suffering a muscle injury, especially with a sudden-onset, was twice in XX than in RR endurance runners.

Activation of α1A -adrenoceptors desensitizes the rat aorta response to phenylephrine through a neuronal NOS pathway, a mechanism lost with ageing.

BACKGROUND AND PURPOSE: A NO-mediated desensitization of vasoconstrictor responses evoked by stimulation of α1 -adrenoceptors has been reported in different vessels. We investigated the involvement of each α1 -adrenoceptor subtype and constitutive NOS isoforms and the influence of ageing and hypertension on this process. EXPERIMENTAL APPROACH: Wistar and spontaneously hypertensive rats (SHR), 16, 32, 52 and 72 weeks-old, were used to evaluate the desensitization process. Expression of α1 -adrenoceptor subtypes, endothelial NOS (eNOS) and neuronal NOS (nNOS) were determined in rat aorta and left ventricle (LV). Expression levels were also evaluated in LV of a group of heart failure patients with a wide age range. KEY RESULTS: Repeated application of phenylephrine decreased subsequent α1 -adrenoceptor-mediated vasoconstriction by increasing nNOS protein expression in aorta, but not in tail or mesenteric resistance arteries, where mRNA levels of nNOS were undetectable. This desensitization process disappeared in the absence of endothelium or in the presence of L-NAME (100 µM), nNOS inhibitors, SMTC (1 µM) and TRIM (100 µM), and 5-methylurapidil (100 nM, α1A -antagonist), but not BMY7378 (10 nM, α1D -antagonist). The α1A /nNOS-mediated desensitization was absent in aged SHR and Wistar animals, where the expression of α1A -adrenoceptors was reduced in aorta and LV. In human LV, a negative correlation was found between age and α1A -adrenoceptor expression. CONCLUSIONS AND IMPLICATIONS: The α1A -adrenoceptor subtype, through endothelial nNOS-derived NO, may act as a physiological 'brake' against the detrimental effects of excessive α1 -adrenoceptor-mediated vasoconstriction. Reduced α1A -adrenoceptor- and nNOS-mediated desensitization in aged patients could be involved in the age-dependent elevation of adrenergic activity.

Predicting race time in male amateur marathon runners.

BACKGROUND: The aim of the study was to analyze the relationship between anthropometry, training characteristics, muscular strength and effort-related cardiovascular response and marathon race time in male amateur runners. METHODS: A total of 84 male amateur marathon runners aged between 23 and 70 years took part in this study (41.0±9.5 years). All of them competed in the 2013 edition of the Madrid Marathon with a finish time between 169.8 and 316 minutes (226.0±28.5 minutes). Age, running experience, number of marathon races finished, mean kilometers run weekly in the last three months, and previous personal best time in the 10 km, half marathon and marathon were recorded. Moreover, anthropometric characteristics, and the results from the Ruffier Test and a whole-body isometric force test were measured. After the marathon, the race time was registered. RESULTS: Training volume (r=-0.479; P=0.001), previous running milestones (marathon r=0.756; half-marathon r=0.812; 10-km r=0.732; P<0.001), cardiovascular fitness (r=0.371; P=0.001) and anthropometric variables (body mass, Body Mass Index, body fat percentage, skinfolds and lower leg volume) were correlated to marathon performance (P<0.05). Two regression models appeared from the data with r2>0.50. The best, including body fat percentage, heart rate change during the recovery after the Ruffier Test and the half-marathon race time, was strongly correlated with real marathon performance (r=0.77; P<0.001). A second regression model was proposed replacing the half-marathon performance with the 10-km race time, reducing the correlation to 0.73 (P<0.001). CONCLUSIONS: Marathon performance could be partially predicted by two different equations, including body fat percentage, recovery heart rate in the Ruffier Test and a half-marathon or 10-km performance.

CYP1A2 Genotype Variations Do Not Modify the Benefits and Drawbacks of Caffeine during Exercise: A Pilot Study.

Previous investigations have determined that some individuals have minimal or even ergolytic performance effects after caffeine ingestion. The aim of this study was to analyze the influence of the genetic variations of the CYP1A2 gene on the performance enhancement effects of ingesting a moderate dose of caffeine. In a double-blind randomized experimental design, 21 healthy active participants (29.3 ± 7.7 years) ingested 3 mg of caffeine per kg of body mass or a placebo in testing sessions separated by one week. Performance in the 30 s Wingate test, visual attention, and side effects were evaluated. DNA was obtained from whole blood samples and the CYP1A2 polymorphism was analyzed (rs762551). We obtained two groups: AA homozygotes (n = 5) and C-allele carriers (n = 16). Caffeine ingestion increased peak power (682 ± 140 vs. 667 ± 137 W; p = 0.008) and mean power during the Wingate test (527 ± 111 vs. 518 ± 111 W; p < 0.001) with no differences between AA homozygotes and C-allele carriers (p > 0.05). Reaction times were similar between caffeine and placebo conditions (276 ± 31 vs. 269 ± 71 milliseconds; p = 0.681) with no differences between AA homozygotes and C-allele carriers. However, 31.3% of the C-allele carriers reported increased nervousness after caffeine ingestion, while none of the AA homozygotes perceived this side effect. Genetic variations of the CYP1A2 polymorphism did not affect the ergogenic effects and drawbacks derived from the ingestion of a moderate dose of caffeine.

Respiratory function is associated to marathon race time.

BACKGROUND: The purpose of this study was to analyze the relationship between marathon race time and expiratory pulmonary parameters in a heterogeneous group of amateur marathoners. METHODS: A total of 110 marathon runners (age=41.9±9.4 yr, body mass=74.0±9.1 kg, height=175.0±8.0 cm) volunteered to participate in this study. First, they completed a questionnaire about running experience and best performance time in the 10-km, half-marathon and marathon competitions. Then, they performed a maximal spirometry test following guidelines for standardized spirometry. Measurement included peak expiratory flow (PEF), forced expiratory volume in the first second (FEV1) and forced vital capacity (FVC). All these expiratory variables were normalized for the participant's body mass. Within 3 days of the spirometry test, participants competed in an official marathon and race time was measured by a chip-timing. After this, participants were grouped by their marathon race time as follows: <210 min, N.=33; between 210 and 240 min, N.=31; and >240 min, N.=46). RESULTS: Marathon race time correlated to the FVC·kg-1 (r=-0.41; P<0.001), to FEV1·kg-1 (r=-0.40; P<0.001), and PEF·kg-1 (r=-0.50; P=0.005). However, self-reported running experience did not show significant correlations to FVC·kg-1 and PEF·kg-1 (P>0.05). The group of faster marathoners (e.g., <210 min) had greater FEV1·kg-1 (<210 min group: 0.064±0.009; 210-240 min group: 0.058±0.008; >240 min group: 0.057±0.009; P<0.001) and higher FVC·kg-1 (<210 min group: 0.081±0.011; 210-240 min group: 0.075±0.012; >240 min group: 0.072±0.010; P<0.001) than the other two groups of slower runners. CONCLUSIONS: These results suggest a significant relationship between individual pulmonary function and marathon race time. Thus, a higher lung capacity per kg of body mass might be a key variable for marathon performance in amateur runners.

The use of compression stockings during a marathon competition to reduce exercise-induced muscle damage: are they really useful?

STUDY DESIGN: Case-control study; ecological study. OBJECTIVES: To examine the efficacy of wearing compression stockings to prevent muscle damage and to maintain running performance during a marathon competition. BACKGROUND: Exercise-induced muscle damage has been identified as one of the main causes of the progressive decrease in running and muscular performance found during marathon races. METHODS: Thirty-four experienced runners were pair-matched for age, anthropometric data, and best race time in the marathon, and randomly assigned to a control group (n = 17) of runners who wore conventional socks or to a group of runners who wore foot-to-knee graduated compression stockings (n = 17). Before and after the race, a sample of venous blood was obtained, and jump height and leg muscle power were measured during a countermovement jump. Serum myoglobin and creatine kinase concentrations were determined as blood markers of muscle fiber damage. RESULTS: Total race time was not different between the control group and the compression stockings group (210 ± 23 and 214 ± 22 minutes, respectively; P = .58). Between the control group and the compression stockings group, postrace reductions in leg muscle power (-19.8% ± 17.7% versus -24.8% ± 18.4%, respectively; P = .37) and jump height (-25.3% ± 14.1% versus -32.5% . 20.4%, respectively; P = .27) were similar. At the end of the race, there were no differences between the control group and the compression stockings group in serum myoglobin (568 ± 347 ng·mL(-1) versus 573 ± 270 ng·mL(-1), respectively; P = .97) and creatine kinase concentration (390 ± 166 U·L(-1) versus 487 ± 227 U·L(-1), respectively; P = .16). CONCLUSION: The use of compression stockings did not improve running pace and did not prevent exercise-induced muscle damage during the marathon. Wearing compression stockings during long-distance running events is an ineffective strategy to avoid the deleterious effects of muscle damage on running performance. LEVEL OF EVIDENCE: Therapy, level 2b.