The physiological determinants of sprint performance: an integrative approach

Abstract

Sprint performance is critical for success in many sports. A high-level sprint performance requires the optimal application of force to produce the highest power output possible. In many athletic events, the time available to generate force is very short (<75 ms), and therefore the capacity to produce high power since the very beginning of contractions is crucial for performance. Neural, muscular and mechanical factors influence the ability to generate outstanding levels of power. Several approaches trying to isolate the role played by each factor have been undertaken. However, there is lack of experimental evidence on how the three components interact to limit performance and how they respond to changes in stimulation (training/detraining) under varying circumstances (duration of contractions, temperature, fatigue, etc.). The force exerted at any given time depends on the number of cross-bridges generating tension. On the other hand, the shortening velocity depends mostly on the speed at which myosin detaches and re-attaches to actin, whose primary determinant is the myosin ATPase activity. The neural component should produce synchronised activation of all motor units at the highest frequency possible during explosive muscle contractions, with timely activation of the agonist and antagonist/synergist muscles. A higher proportion of myosin heavy chain (MCH) IIX is associated with greater force and shortening velocity, a distinctive quality of the faster mammals in nature. The quicker and larger Ca 2+ transients of type II fibers are also contributing factors, which may become more critical as fatigue develops. Calcium transients are sensed by the calcium decoding proteins, namely Ca 2+ /calmodulin-dependent protein kinase II (CaMKII) and calcineurin. Increased CaMKII phosphorylation may induce muscle hypertrophy and reduce muscle breakdown by downregulation of the ubiquitin E3 ligases. Paradoxically, MCH IIX increase with immobilization and decrease with exercise training. Although the most effective strategy to improve muscle power is by loaded contractions performed at the highest speed possible (explosive-type strength training), the level of fatigue reached during each set has a major impact on muscle adaptations. Reducing the level of fatigue allowed during the training session helps to preserve MCH IIX and is associated with greater improvement in jumping and sprinting performance. In vitro experiments indicate that muscle contractions to failure are associated with increased reactive oxygen species production, which reduces Ca 2+ release and Ca 2+ sensitivity, thus hampering peak power output. During prolonged sprints, as well during repeated short sprints, the mechanisms limiting performance become more complex and will be analysed with some detail. The inclusion of ergogenic aids and adequate training may help to overcome some of the limitations.