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Abstract: Objectives: To investigate the frequency of the ACTN3 R577X polymorphism in elite endurance triathletes, and whether ACTN3 R577X is significantly associated with performance time. Design: Cross-sectional study. Methods: Saliva samples, questionnaires, and performance times were collected for 196 elite endurance athletes who participated in the 2008 Kona Ironman championship triathlon. Athletes were of predominantly North American, European, and Australian origin. A one-way analysis of variance was conducted to compare performance times between genotype groups. Multiple linear regression analysis was performed to model the effect of questionnaire variables and genotype on performance time. Genotype and allele frequencies were compared to results from different populations using the chi-square test. Results: Performance time did not significantly differ between genotype groups, and age, sex, and continent of origin were significant predictors of finishing time (age and sex: p <5×10−6; continent: p =0.003) though genotype was not. Genotype and allele frequencies obtained (RR 26.5%, RX 50.0%, XX 23.5%, R 51.5%, X 48.5%) were found to be not significantly different from Australian, Spanish, and Italian endurance athletes (p >0.05), but were significantly different from Kenyan, Ethiopian, and Finnish endurance athletes (p <0.01). Conclusions: Genotype and allele frequencies agreed with those reported for endurance athletes of similar ethnic origin, supporting previous findings for an association between 577X allele and endurance. However, analysis of performance time suggests that ACTN3 does not alone influence endurance performance, or may have a complex effect on endurance performance due to a speed/endurance trade-off. [Copyright &y& Elsevier]

Abstract: Background: Peak exercise capacity (VO2peak) is a measure of the severity of chronic heart failure (CHF); however, few indices of resting cardiopulmonary function have been shown to predict VO2peak. A prolonged circulation time has been suggested as an index of increased severity of CHF. The aim of this study was to investigate the relationship between resting lung-to-lung circulation time (LLCT) and VO2peak in CHF. Methods and Results: Thirty CHF patients (59 ± 13 years, New York Heart Association: 1.9 ± 1.0) undertook the study. Each subject completed resting pulmonary and echocardiography measures and an incremental exercise test. LLCT was measured using the reappearance of end-tidal acetylene (PET,C2H2) after a single inhalation. Univariate and multivariate stepwise linear regression was used to determine the predictors of VO2peak. Univariate correlates of VO2peak (group mean 1.53 ± 0.44 L/min−1) included LLCT (r = −0.75), inspiratory capacity (r = 0.41), ejection fraction (r = 0.33), peak early flow velocity (r = −0.39), and the ratio of early to late flow velocity (r = −0.31). LLCT was the only independent predictor where VO2peak = 3.923–0.045 (LLCT); r2 = 54%. Conclusions: These results suggest that resting LLCT determined using the soluble inert gas technique represents a simple, noninvasive method that provides additional information regarding exercise capacity in CHF. [Copyright &y& Elsevier]

Abstract: We examined the influence of operational lung volumes and mean inspiratory flow on the amplitude of the slow component of O2 uptake () during constant-load cycling performed below and above the respiratory compensation threshold (RCT) in young (24±1yr), healthy individuals (n =10). Subjects demonstrated a significantly greater rise in expiratory reserve volume (ERV) and mean inspiratory flow over the period during exercise performed above compared with below the RCT (P <0.05). Inspiratory reserve volume (IRV) was, on average, smaller for trials performed above relative to below the RCT (P <0.05). The difference in the magnitudes of change in ERV and mean inspiratory flow, but not IRV, were positively correlated with the increase in amplitude between work rates (R 2 =0.86, P <0.01). These findings suggest that dynamic hyperinflation and mean inspiratory flow (by increasing inspiratory resistive work) contribute to the development of the , particularly when exercise is performed above the RCT. [Copyright &y& Elsevier]

Exercise is cardioprotective, though optimal interventions are unclear. We assessed duration dependent effects of exercise on myocardial ischemia-reperfusion (I-R) injury, kinase signaling and gene expression. Responses to brief (2 day; 2EX), intermediate (7 and 14 day; 7EX and 14EX) and extended (28 day; 28EX) voluntary wheel running (VWR) were studied in male C57Bl/6 mice. Cardiac function, I-R tolerance and survival kinase signaling were assessed in perfused hearts. Mice progressively increased running distances and intensity, from 2.4 ± 0.2 km/day (0.55 ± 0.04 m/s) at 2-days to 10.6 ± 0.4 km/day (0.72 ± 0.06 m/s) after 28-days. Myocardial mass and contractility were modified at 14–28 days VWR. Cardioprotection was not 'dose-dependent', with I-R tolerance enhanced within 7 days and not further improved with greater VWR duration, volume or intensity. Protection was associated with AKT, ERK1/2 and GSK3β phosphorylation, with phospho-AMPK selectively enhanced with brief VWR. Gene expression was duration-dependent: 7 day VWR up-regulated glycolytic (Pfkm) and down-regulated maladaptive remodeling (Mmp2) genes; 28 day VWR up-regulated caveolar (Cav3), mitochondrial biogenesis (Ppargc1a , Sirt3) and titin (Ttn) genes. Interestingly, I-R tolerance in 2EX/2SED groups improved vs. groups subjected to longer sedentariness, suggesting transient protection on transition to housing with running wheels. Cardioprotection is induced with as little as 7 days VWR, yet not enhanced with further or faster running. This protection is linked to survival kinase phospho-regulation (particularly AKT and ERK1/2), with glycolytic, mitochondrial, caveolar and myofibrillar gene changes potentially contributing. Intriguingly, environmental enrichment may also protect via similar kinase regulation. [ABSTRACT FROM AUTHOR]