Endurance exercise training results in profound adaptations of the cardiorespiratory and neuromuscular systems that enhance the delivery of oxygen from the atmosphere to the mitochondria and enable a tighter regulation of muscle metabolism. These adaptations effect an improvement in endurance performance that is manifest as a rightward shift in the 'velocity-time curve'. This shift enables athletes to exercise for longer at a given absolute exercise intensity, or to exercise at a higher exercise intensity for a given duration. There are 4 key parameters of aerobic fitness that affect the nature of the velocity-time curve that can be measured in the human athlete. These are the maximal oxygen uptake (VO2max), exercise economy, the lactate/ventilatory threshold and oxygen uptake kinetics. Other parameters that may help determine endurance performance, and that are related to the other 4 parameters, are the velocity at VO2max (V-VO2max) and the maximal lactate steady state or critical power. This review considers the effect of endurance training on the key parameters of aerobic (endurance) fitness and attempts to relate these changes to the adaptations seen in the body's physiological systems with training. The importance of improvements in the aerobic fitness parameters to the enhancement of endurance performance is highlighted, as are the training methods that may be considered optimal for facilitating such improvements.

For high-intensity muscular exercise, the time-to-exhaustion (t) increases as a predictable and hyperbolic function of decreasing power (P) or velocity (V ). This relationship is highly conserved across diverse species and different modes of exercise and is well described by two parameters: the "critical power" (CP or CV), which is the asymptote for power or velocity, and the curvature constant (W') of the relationship such that t = W'/(P - CP). CP represents the highest rate of energy transduction (oxidative ATP production, V˙O2) that can be sustained without continuously drawing on the energy store W' (composed in part of anaerobic energy sources and expressed in kilojoules). The limit of tolerance (time t) occurs when W' is depleted. The CP concept constitutes a practical framework in which to explore mechanisms of fatigue and help resolve crucial questions regarding the plasticity of exercise performance and muscular systems physiology. This brief review presents the practical and theoretical foundations for the CP concept, explores rigorous alternative mathematical approaches, and highlights exciting new evidence regarding its mechanistic bases and its broad applicability to human athletic performance.

Ϫ ] increased in a dose-dependent manner, with the peak changes occurring at approximately 2-3 h. Compared with PL, 70 ml BR did not alter the physiological responses to exercise. However, 140 and 280 ml BR reduced the steady-state oxygen (O2) uptake during moderateintensity exercise by 1.7% (P ϭ 0.06) and 3.0% (P Ͻ 0.05), whereas time-to-task failure was extended by 14% and 12% (both P Ͻ 0.05), respectively, compared with PL. The results indicate that whereas plasma [NO 2 Ϫ ] and the O2 cost of moderate-intensity exercise are altered dose dependently with NO 3 Ϫ -rich BR, there is no additional improvement in exercise tolerance after ingesting BR containing 16.8 compared with 8.4 mmol NO 3 Ϫ . These findings have important implications for the use of BR to enhance cardiovascular health and exercise performance in young adults.nitrate; nitrite; nitric oxide; blood pressure; exercise economy; O2 uptake; exercise tolerance NITRIC OXIDE (NO) IS A GASEOUS signaling molecule that modulates human physiological function via its role in, for example, the regulation of blood flow, neurotransmission, immune function, glucose and calcium homeostasis, muscle contractility, and mitochondrial respiration (9, 36). 1 NO is generated through the oxidation of the amino acid L-arginine Ϫ ] peaked 3 h postingestion, remained close to peak values until 5 h postingestion, and returned to baseline after 24 h (39). The systolic and diastolic BP and the mean arterial pressure (MAP) were reduced significantly, by ϳ10, ϳ8, and ϳ8 mmHg, respectively, at 2.5-3 h after BR intake. The same research group later reported a dose-dependent increase in plasma [ ] was accompanied by significant reductions in both systolic BP (of ϳ2, ϳ6, and ϳ9 mmHg, respectively) and diastolic BP (of ϳ4, ϳ4, and ϳ6 mmHg, respectively). However, since BR contains polyphenols and antioxidants, which can facilitate the synthesis of NO from NO 2 Ϫ in the stomach (30), it is unclear whether BP is similarly impacted when different doses of BR are ingested compared with equivalent doses of NO 3 Ϫ salts. Given the growing interest in dietary NO 3 Ϫ supplementation in the form of BR amongst athletes and the general population, it is important to determine the pharmacokinetic-pharmacodynamic relationship between different volumes of BR consumption and changes in plasma [NO 2 Ϫ ] and BP to establish an optimal dose for beneficial effects.Recent investigations suggest that dietary NO 3 Ϫ supplementation has the potential to influence human physiology beyond 1 This article is the topic of an Invited Editorial by L. Burke (5a).

Muscular exercise requires transitions to and from metabolic rates often exceeding an order of magnitude above resting and places prodigious demands on the oxidative machinery and O2-transport pathway. The science of kinetics seeks to characterize the dynamic profiles of the respiratory, cardiovascular, and muscular systems and their integration to resolve the essential control mechanisms of muscle energetics and oxidative function: a goal not feasible using the steady-state response. Essential features of the O2 uptake (VO2) kinetics response are highly conserved across the animal kingdom. For a given metabolic demand, fast VO2 kinetics mandates a smaller O2 deficit, less substrate-level phosphorylation and high exercise tolerance. By the same token, slow VO2 kinetics incurs a high O2 deficit, presents a greater challenge to homeostasis and presages poor exercise tolerance. Compelling evidence supports that, in healthy individuals walking, running, or cycling upright, VO2 kinetics control resides within the exercising muscle(s) and is therefore not dependent upon, or limited by, upstream O2-transport systems. However, disease, aging, and other imposed constraints may redistribute VO2 kinetics control more proximally within the O2-transport system. Greater understanding of VO2 kinetics control and, in particular, its relation to the plasticity of the O2-transport/utilization system is considered important for improving the human condition, not just in athletic populations, but crucially for patients suffering from pathologically slowed VO2 kinetics as well as the burgeoning elderly population.

We tested the hypothesis that the asymptote of the hyperbolic relationship between work rate and time to exhaustion during muscular exercise, the "critical power" (CP), represents the highest constant work rate that can be sustained without a progressive loss of homeostasis [as assessed using (31)P magnetic resonance spectroscopy (MRS) measurements of muscle metabolites]. Six healthy male subjects initially completed single-leg knee-extension exercise at three to four different constant work rates to the limit of tolerance (range 3-18 min) for estimation of the CP (mean +/- SD, 20 +/- 2 W). Subsequently, the subjects exercised at work rates 10% below CP (CP) for as long as possible, while the metabolic responses in the contracting quadriceps muscle, i.e., phosphorylcreatine concentration ([PCr]), P(i) concentration ([P(i)]), and pH, were estimated using (31)P-MRS. All subjects completed 20 min of CP exercise was 14.7 +/- 7.1 min. During CP exercise, however, [PCr] continued to fall to the point of exhaustion and [P(i)] and pH changed precipitously to values that are typically observed at the termination of high-intensity exhaustive exercise (end-exercise values = 26 +/- 16% of baseline [PCr], 564 +/- 167% of baseline [P(i)], and pH 6.87 +/- 0.10, all P < 0.05 vs.