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.

No abstract

This investigation examined predictors of compliance with exercise therapy in a clinical trial involving older adults with knee osteoarthritis (OA). The study sample was partitioned into tertiles by level of compliance to determine its effect on several clinical outcome measures in the trial (i.e., knee pain, difficulty with activities of daily living, and performance-related disability). The participants (N = 439) first completed all baseline assessments and were then randomly assigned to one of three treatment conditions: health education control, aerobic exercise, or resistance exercise. The two exercise treatments involved a 3-month center-based phase and a 15-month home-based phase. Variables in five categories (i.e., demographic, fitness, health-related quality of life, performance-related disability, and prior exercise behavior) were entered as predictors of attendance and time spent exercising during each session for three different periods of time across the course of the study. Results of these analyses revealed that it was possible to explain more variance for time spent exercising (approximately 40%) during the first 3 months than for attendance (approximately 10%). Furthermore, once participants completed the first 3 months of their training, prior behavior was the strongest predictor of exercise compliance. In most cases, the regression models accounted anywhere from 26 to 46% of the variance in attendance or time spent exercising (7 of the 8 P values < 0.01). In general, demographic, fitness, psychosocial, and disability-related measures did not predict compliance with any consistency across the various phases of the trial. Analysis of the dose-response data suggest that, in the use of aerobic exercise to deter disability in older people with knee OA, consideration should be given to prescribing frequent bouts of activity (at least 3 times each week) of moderate duration (approximately 35 min).

We tested the hypotheses that the parameters of the power-duration relationship, estimated as the end-test power (EP) and work done above EP (WEP) during a 3-min all-out exercise test (3MT), would be reduced progressively after 40 min, 80 min, and 2 h of heavy-intensity cycling and that carbohydrate (CHO) ingestion would attenuate the reduction in EP and WEP. Sixteen participants completed a 3MT without prior exercise (control), immediately after 40 min, 80 min, and 2 h of heavy-intensity exercise while consuming a placebo beverage, and also after 2 h of heavy-intensity exercise while consuming a CHO supplement (60 g/h CHO). There was no difference in EP measured without prior exercise (260 ± 37 W) compared with EP after 40 min (268 ± 39 W) or 80 min (260 ± 40 W) of heavy-intensity exercise; however, after 2 h EP was 9% lower compared with control (236 ± 47 W; P < 0.05). There was no difference in WEP measured without prior exercise (17.9 ± 3.3 kJ) compared with after 40 min of heavy-intensity exercise (16.1 ± 3.3 kJ), but WEP was lower ( P < 0.05) than control after 80 min (14.7 ± 2.9 kJ) and 2 h (13.8 ± 2.7 kJ). Compared with placebo, CHO ingestion negated the reduction of EP following 2 h of heavy-intensity exercise (254 ± 49 W) but had no effect on WEP (13.5 ± 3.4 kJ). These results reveal a different time course for the deterioration of EP and WEP during prolonged endurance exercise and indicate that EP is sensitive to CHO availability. NEW & NOTEWORTHY The parameters of the power-duration relationship [critical power (CP) and the curvature constant (W′)] have typically been considered to be static. Here we report the time course for reductions in CP and W′, as estimated with the 3-min all-out cycle test, during 2 h of heavy-intensity exercise. We also show that carbohydrate ingestion during exercise preserves CP, but not W′, without altering muscle glycogen depletion. These results provide new mechanistic and practical insight into the power-duration curve and its relationship to exercise-related fatigue development.