Eccentric training is a potent stimulus for enhancements in muscle mechanical function, and muscle-tendon unit (MTU) morphological and architectural adaptations. The inclusion of eccentric loads not constrained by concentric strength appears to be superior to traditional resistance training in improving variables associated with strength, power and speed performance.

An eccentric contraction involves the active lengthening of muscle under an external load. The molecular and neural mechanisms underpinning eccentric contractions differ from those of concentric and isometric contractions and remain less understood. A number of molecular theories have been put forth to explain the unexplained observations during eccentric contractions that deviate from the predictions of the established theories of muscle contraction. Postulated mechanisms include a strain-induced modulation of actin-myosin interactions at the level of the cross-bridge, the activation of the structural protein titin, and the winding of titin on actin. Accordingly, neural strategies controlling eccentric contractions also differ with a greater, and possibly distinct, cortical activation observed despite an apparently lower activation at the level of the motor unit. The characteristics of eccentric contractions are associated with several acute physiological responses to eccentrically-emphasised exercise. Differences in neuromuscular, metabolic, hormonal and anabolic signalling responses during, and following, an eccentric exercise bout have frequently been observed in comparison to concentric exercise. Subsequently, the high levels of muscular strain with such exercise can induce muscle damage which is rarely observed with other contraction types. The net result of these eccentric contraction characteristics and responses appears to be a novel adaptive signal within the neuromuscular system.

The adaptations of muscle to sprint training can be separated into metabolic and morphological changes. Enzyme adaptations represent a major metabolic adaptation to sprint training, with the enzymes of all three energy systems showing signs of adaptation to training and some evidence of a return to baseline levels with detraining. Myokinase and creatine phosphokinase have shown small increases as a result of short-sprint training in some studies and elite sprinters appear better able to rapidly breakdown phosphocreatine (PCr) than the sub-elite. No changes in these enzyme levels have been reported as a result of detraining. Similarly, glycolytic enzyme activity (notably lactate dehydrogenase, phosphofructokinase and glycogen phosphorylase) has been shown to increase after training consisting of either long (>10-second) or short (<10-second) sprints. Evidence suggests that these enzymes return to pre-training levels after somewhere between 7 weeks and 6 months of detraining. Mitochondrial enzyme activity also increases after sprint training, particularly when long sprints or short recovery between short sprints are used as the training stimulus. Morphological adaptations to sprint training include changes in muscle fibre type, sarcoplasmic reticulum, and fibre cross-sectional area. An appropriate sprint training programme could be expected to induce a shift toward type IIa muscle, increase muscle cross-sectional area and increase the sarcoplasmic reticulum volume to aid release of Ca(2+). Training volume and/or frequency of sprint training in excess of what is optimal for an individual, however, will induce a shift toward slower muscle contractile characteristics. In contrast, detraining appears to shift the contractile characteristics towards type IIb, although muscle atrophy is also likely to occur. Muscle conduction velocity appears to be a potential non-invasive method of monitoring contractile changes in response to sprint training and detraining. In summary, adaptation to sprint training is clearly dependent on the duration of sprinting, recovery between repetitions, total volume and frequency of training bouts. These variables have profound effects on the metabolic, structural and performance adaptations from a sprint-training programme and these changes take a considerable period of time to return to baseline after a period of detraining. However, the complexity of the interaction between the aforementioned variables and training adaptation combined with individual differences is clearly disruptive to the transfer of knowledge and advice from laboratory to coach to athlete.

Performance in sprint exercise is determined by the ability to accelerate, the magnitude of maximal velocity and the ability to maintain velocity against the onset of fatigue. These factors are strongly influenced by metabolic and anthropometric components. Improved temporal sequencing of muscle activation and/or improved fast twitch fibre recruitment may contribute to superior sprint performance. Speed of impulse transmission along the motor axon may also have implications on sprint performance. Nerve conduction velocity (NCV) has been shown to increase in response to a period of sprint training. However, it is difficult to determine if increased NCV is likely to contribute to improved sprint performance. An increase in motoneuron excitability, as measured by the Hoffman reflex (H-reflex), has been reported to produce a more powerful muscular contraction, hence maximising motoneuron excitability would be expected to benefit sprint performance. Motoneuron excitability can be raised acutely by an appropriate stimulus with obvious implications for sprint performance. However, at rest H-reflex has been reported to be lower in athletes trained for explosive events compared with endurance-trained athletes. This may be caused by the relatively high, fast twitch fibre percentage and the consequent high activation thresholds of such motor units in power-trained populations. In contrast, stretch reflexes appear to be enhanced in sprint athletes possibly because of increased muscle spindle sensitivity as a result of sprint training. With muscle in a contracted state, however, there is evidence to suggest greater reflex potentiation among both sprint and resistance-trained populations compared with controls. Again this may be indicative of the predominant types of motor units in these populations, but may also mean an enhanced reflex contribution to force production during running in sprint-trained athletes. Fatigue of neural origin both during and following sprint exercise has implications with respect to optimising training frequency and volume. Research suggests athletes are unable to maintain maximal firing frequencies for the full duration of, for example, a 100m sprint. Fatigue after a single training session may also have a neural manifestation with some athletes unable to voluntarily fully activate muscle or experiencing stretch reflex inhibition after heavy training. This may occur in conjunction with muscle damage. Research investigating the neural influences on sprint performance is limited. Further longitudinal research is necessary to improve our understanding of neural factors that contribute to training-induced improvements in sprint performance.

The winter sliding sport known as skeleton requires athletes to produce a maximal sprint followed by high speed sliding down a bobsled track. Athletes are required to complete the course twice in 1 hour and total time for the 2 runs determines overall ranking. The purpose of this investigation was to examine the effect of whole-body vibration (WBV) on lower body power to explore the utility of WBV as an ergogenic aid for skeleton competition. Elite skeleton athletes (1 male and 6 females) completed an unloaded squat jump (SQJ) immediately followed by 2 countermovement jumps (CMJs) and a maximal 30-m sprint before and after WBV or no vibration (CON) using a crossover design. The second 30-m sprint was slower following both CON (1.4% decrement; p = 0.05) and WBV (0.7% decrement; p = 0.03). Mean vertical velocity was maintained following WBV in the SQJ but decreased following CON (p = 0.03). There was a trend for athletes to commence the SQJ from a higher starting stance post-WBV compared to CON (p = 0.08). WBV decreased total vertical distance traveled compared to CON in the SQJ (p = 0.006). WBV had little effect on peak velocity, jump height, dip, and peak acceleration or any CMJ parameters. When sprint athletes' warm up and perform maximal jumps and a 30-m sprint with 15-20 minutes of recovery before repeating the sequence, the second series of performances tend to be compromised. However, when WBV is used before the second series of efforts, some aspects of maximal jumping and sprinting appear to be influenced in a beneficial manner. Further research is required to explore whether WBV can improve the second sprint for athletes in actual competition and/or what sort of WBV protocol is optimal for these populations.

The aims of this study were to talent transfer, rapidly develop, and qualify an Australian female athlete in the skeleton event at the 2006 Torino Winter Olympic Games and quantify the volume of skeleton-specific training and competition that would enable this to be achieved. Initially, 26 athletes were recruited through a talent identification programme based on their 30-m sprint time. After attending a selection camp, 10 athletes were invited to undertake an intensified skeleton training programme. Four of these athletes were then selected to compete for Australia on the World Cup circuit. All completed runs and simulated push starts were documented over a 14-month period. The athlete who eventually represented Australia at the Torino Winter Olympic Games did so following approximately 300 start simulations and about 220 training/competition runs over a period of 14 months. Using a deliberate programming model, these findings provide a guide to the minimum exposure required for a novice skeleton athlete to reach Olympic representative standard following intensified sport-specific training. The findings of this study are discussed in the context of the deliberate practice theory and offer the term "deliberate programming" as an alternative way of incorporating all aspects of expert development.

Very little is currently known about the effects of acute hamstring injury on over-ground sprinting mechanics. The aim of this research was to describe changes in power-force-velocity properties of sprinting in two injury case studies related to hamstring strain management: Case 1: during a repeated sprint task (10 sprints of 40 m) when an injury occurred (5th sprint) in a professional rugby player; and Case 2: prior to (8 days) and after (33 days) an acute hamstring injury in a professional soccer player. A sports radar system was used to measure instantaneous velocity-time data, from which individual mechanical profiles were derived using a recently validated method based on a macroscopic biomechanical model. Variables of interest included: maximum theoretical velocity (V0) and horizontal force (F(H0)), slope of the force-velocity (F-v) relationship, maximal power, and split times over 5 and 20 m. For Case 1, during the injury sprint (sprint 5), there was a clear change in the F-v profile with a 14% greater value of F(H0) (7.6-8.7 N/kg) and a 6% decrease in V0 (10.1 to 9.5 m/s). For Case 2, at return to sport, the F-v profile clearly changed with a 20.5% lower value of F(H0) (8.3 vs. 6.6 N/kg) and no change in V0. The results suggest that the capability to produce horizontal force at low speed (F(H0)) (i.e. first metres of the acceleration phase) is altered both before and after return to sport from a hamstring injury in these two elite athletes with little or no change of maximal velocity capabilities (V0), as evidenced in on-field conditions. Practitioners should consider regularly monitoring horizontal force production during sprint running both from a performance and injury prevention perspective.

Objective: To quantify the impact of eastward long haul travel on diurnal variations in cortisol, psychological sensations and daily measurements of physical performance. Methods: Five elite Australian skeleton athletes undertook a long haul eastward flight from Australia to Canada (LH travel ), while seven elite Canadian skeleton athletes did not travel (NO travel ). Salivary cortisol was measured on awakening, 60 min and 120 min after awakening. Psychological sensations were measured with a questionnaire, and maximal 30 m sprints were performed once a day between 09:30 and 11:00 h local time. Results: Compared with baseline, average (SD) resting salivary cortisol decreased by 67% immediately after long haul travel (23.43 (5.71) nMol/l) (mean¡90% confidence interval) in the LH travel group (p = 0.03), while no changes were found in the NO travel group (p = 0.74). There were no significant differences in 30 m sprint time between baseline and post-flight tests in the LH travel group (p.0.05).