The gas exchange threshold and the critical power demarcate discrete exercise intensity domains. For the first time, we show that the limit of tolerance during whole body exercise within these domains is characterized by distinct metabolic and neuromuscular responses. Fatigue development during exercise greater than critical power is associated with the attainment of consistent “limiting” values of muscle metabolites, whereas substrate availability and limitations to muscle activation may constrain performance at lower intensities.

Key pointsr The power-asymptote (critical power; CP) of the hyperbolic power-time relationship for high-intensity exercise defines a threshold between steady-state and non-steady-state exercise intensities and the curvature constant (W ) indicates a fixed capacity for work >CP that is related to a loss of muscular efficiency.r The present study reports novel evidence on the muscle metabolic underpinnings of CP and W during whole-body exercise and their relationships to muscle fibre type.r We show that the W is not correlated with muscle fibre type distribution and that it represents an elevated energy contribution from both oxidative and glycolytic/glycogenolytic metabolism.r We show that there is a positive correlation between CP and highly oxidative type I muscle fibres and that muscle metabolic steady-state is attainable CP.r Our findings indicate a mechanistic link between the bioenergetic characteristics of muscle fibre types and the power-time relationship for high-intensity exercise.Abstract We hypothesized that: (1) the critical power (CP) will represent a boundary separating steady-state from non-steady-state muscle metabolic responses during whole-body exercise and (2) that the CP and the curvature constant (W ) of the power-time relationship for high-intensity exercise will be correlated with type I and type IIx muscle fibre distributions, respectively. Four men and four women performed a 3 min all-out cycling test for the estimation of CP and constant work rate (CWR) tests slightly >CP until exhaustion (T lim ), slightly CP T lim isotime to test the first hypothesis. Eleven men performed 3 min all-out tests and donated muscle biopsies to test the second hypothesis. Below CP, muscle [PCr] [42.6 ± 7.1 vs. 49.4 ± 6.9 mmol (kg d.w.) −1 ], [La − ] [34.8 ± 12.6 vs. 35.5 ± 13.2 mmol (kg d.w.) −1 ] and pH (7.11 ± 0.08 vs. 7.10 ± 0.11) remained stable between ß12 and 24 min (P > 0.05 for all), whereas these variables changed with time >CP such that they were greater [[La − ] 95.6 ± 14.1 mmol (kg d.w.) −1 ] and lower [[PCr] 24.2 ± 3.9 mmol (kg d.w.) −1 ; pH 6.84 ± 0.06] (P < 0.05) at T lim (740 ± 186 s) than during the

These findings suggest that dietary NO3 (-) enhances repeated sprint performance and may attenuate the decline in cognitive function (and specifically reaction time) that may occur during prolonged intermittent exercise.

Nitric oxide (NO) plays a plethora of important roles in the human body. Insufficient production of NO (for example, during older age and in various disease conditions) can adversely impact health and physical performance. In addition to its endogenous production through the oxidation of l-arginine, NO can be formed nonenzymatically via the reduction of nitrate and nitrite, and the storage of these anions can be augmented by the consumption of nitrate-rich foodstuffs such as green leafy vegetables. Recent studies indicate that dietary nitrate supplementation, administered most commonly in the form of beetroot juice, can ( a) improve muscle efficiency by reducing the O cost of submaximal exercise and thereby improve endurance exercise performance and ( b) enhance skeletal muscle contractile function and thereby improve muscle power and sprint exercise performance. This review describes the physiological mechanisms potentially responsible for these effects, outlines the circumstances in which ergogenic effects are most likely to be evident, and discusses the effects of dietary nitrate supplementation on physical performance in a range of human populations.

Introduction Hospitals are under pressure to provide care that not only shortens hospital length of stay, but reduces subsequent hospital admissions. Hospital readmissions have received increased attention in outcome reporting. We identified survivors of acute respiratory failure who then required subsequent hospitalization. A cohort of acute respiratory failure survivors, who participated in an early ICU-mobility program, was assessed to determine if variables from the index hospitalization predict hospital readmission or death, within 12 months of hospital discharge. Methods Hospital database and responses to letters mailed to 280 ARF survivors. Univariate predictor variables shown to be associated with hospital readmission or death (p<0.1) were included in a multiple logistic regression. A stepwise selection procedure was used to identify significant variables (p<0.05). Results Of the 280 survivors, 132 (47%) had at least one readmission or died within the first year, 126 (45%) were not readmitted, and 22 (8%) were lost to follow-up. Tracheostomy [OR 4.02 (CI 1.72, 9.40)], female gender [OR1.94 (CI 1.13, 3.32)], a higher Charlson Comorbidity Index assessed upon index hospitalization discharge [OR 1.15 (CI 1.01, 1.31)], and lack of early ICU mobility therapy [OR 1.77 CI (1.04, 3.01)] predicted readmission or death in the first year post-Index hospitalization. Conclusions Tracheostomy, female gender, higher Charlson Comorbidity Index and lack of early ICU mobility were associated with readmissions or death during the first year. Although the mechanism(s) of increased hospital readmission are unclear, these findings may provide further support for early ICU mobility for acute respiratory failure patients.