Sports Performance In Athletes Research Articles

Biomechanical analyses of the performance of Paralympians

A biomechanical analysis of sports performance provides an objective method of determining performance of a particular sporting technique. In particular, it aims to add to the understanding of the mechanisms influencing performance, characterization of athletes and provide insights into injury predisposition. While the performance in sport of able-bodied athletes is well recognized in the literature, less information and understanding are known on the complexity, constraints and demands placed on the body of an individual with a disability. This article provides a dialogue that outlines scientific issues of the performance analysis of multi-level athletes with a disability, including Paralympians. Four integrated themes are explored, the first of which focuses on how biomechanics can contribute to the understanding of sports performance in athletes with a disability and how it may be used as an evidence-based tool. This latter point questions the potential for a possible cultural shift led by the emergence of user-friendly instruments. The second theme briefly discusses the role of reliability of sports performance and addresses the debate of two-dimensional and three-dimensional analyses. The third theme addresses key biomechanical parameters and provides guidance to clinicians and coaches on the approaches adopted using the biomechanical/sports performance analysis for an athlete with a disability starting out, to the emerging and elite Paralympian. For completeness of this discourse, the final theme is based on the controversial issues on the role of assisted devices, and the inclusion of Paralympians into able-bodied sport. All combined, this dialogue highlights the intricate relationship between biomechanics and training of individuals with a disability. Furthermore, it illustrates the complexity of modern training of athletes, which can only lead to a better appreciation of the performances to be delivered in the London 2012 Paralympic Games.

Cardiovascular determinants of exercise capacity in the Paralympic athlete with spinal cord injury

This report briefly summarizes the cardiovascular factors that influence exercise physiology and, eventually, sports performance of athletes with a spinal cord injury (SCI). The consequences of an SCI are numerous and concern voluntary muscle function, deep and superficial sensitivity, and autonomic function to a degree determined by the level and completeness of the spinal lesion. Athletes with SCI perform with their upper body, which limits their maximal exercise capacity and puts them at a disadvantage compared with leg exercise in terms of mechanical efficiency and physiological adaptations to exercise. Studies generally find that maximal oxygen consumption and mechanical power output are inversely related to spinal lesion level. Athletes with cervical or dorsal lesions down to Th6 have limited maximal heart rates owing to a lack of sympathetic drive to the heart. Blood redistribution from body areas lacking autonomic control is impaired, thus reducing venous return and limiting cardiac stroke volume during exercise. Thermoregulatory function is affected through a lack of afferent neural feedback and limited efferent vasomotor and sudomotor control below the lesion. Strategies to support venous return and to promote body cooling potentially improve physiological responses and athletic performance, especially in individuals with high lesion levels. The latter are subject to autonomic dysreflexia, a generalized sympathetic vasoconstriction below the lesion resulting from nociceptive stimulations in insensate body regions. Acute episodes induce high blood pressure, may enhance exercise performance and must be treated as a clinical emergency. Deliberate triggering of this reflex is prohibited by the International Paralympic Committee.

Slow Component of V˙O2 Kinetics

The V·O₂ slow component, a slowly developing increase in V·O₂ during constant-work-rate exercise performed above the lactate threshold, represents a progressive loss of skeletal muscle contractile efficiency and is associated with the fatigue process. This brief review outlines the current state of knowledge concerning the mechanistic bases of the V·O₂ slow component and describes practical interventions that can attenuate the slow component and thus enhance exercise tolerance. There is strong evidence that, during constant-work-rate exercise, the development of the V·O₂ slow component is associated with the progressive recruitment of additional (type II) muscle fibers that are presumed to have lower efficiency. Recent studies, however, indicate that muscle efficiency is also lowered (resulting in a "mirror-image" V·O₂ slow component) during fatiguing, high-intensity exercise in which additional fiber recruitment is unlikely or impossible. Therefore, it seems that muscle fatigue underpins the V·O₂ slow component, although the greater fatigue sensitivity of recruited type II fibers might still play a crucial role in the loss of muscle efficiency in both situations. Several interventions can reduce the magnitude of the V·O₂ slow component, and these are typically associated with an enhanced exercise tolerance. These include endurance training, inspiratory muscle training, priming exercise, dietary nitrate supplementation, and the inspiration of hyperoxic gas. All of these interventions reduce muscle fatigue development either by improving muscle oxidative capacity and thus metabolic stability or by enhancing bulk muscle O2 delivery or local Q·O₂-to-V·O₂ matching. Future honing of these interventions to maximize their impact on the V·O₂ slow component might improve sports performance in athletes and exercise tolerance in the elderly or in patient populations.

Effects of two training protocols on Angiotensin I-converting enzyme (ACE) activity in horses

Studies in man have shown a correlation between Angiotensin I-converting enzyme (ACE) genetic polymorphisms, ACE activity in the blood and superior athletic performance in sports requiring endurance. It has been hypothesised that the same correlation occurs in horses. There is no information in the literature concerning the effects of training on ACE activity in equine plasma. Exercise training influences the activity of circulating ACE and the response observed is dependent on the exercise protocol. Thirteen horses of mixed breeds were randomly allocated 2 different training protocols to be carried out for a period of 15 weeks. Blood samples were collected from each horse before the beginning of training to determine baseline values. Subsequent sampling took place every 15 days throughout the training phase and for 8 weeks of paddock rest. Angiotensin I-converting enzyme activity was determined by automated spectrophotometry. Training for 15 weeks significantly increased plasma ACE activity, irrespective of training protocol. Differences observed in ACE activity pattern between the 2 training protocols were not statistically significant. Increase in ACE activity peaked with maximum workload. As soon as training was interrupted, ACE levels significantly decreased. Exercise training affects levels of ACE activity in equine plasma. The mechanism for this is not yet elucidated, but cardiovascular adaptation to exercise and blood pressure changes might be involved in this regulation. Exercise training produced a gradual increase in enzymatic activity and might warrant the use of ACE as a tool for fitness monitoring. Angiotensin I-converting enzyme enzymatic activity in the plasma might be directly correlated to a change in genetic expression and that variability must be taken into account when evaluating results from horses undergoing a physical training programme.

Mitochondrial biogenesis related endurance genotype score and sports performance in athletes

We determined the probability of individuals having the ‘optimal’ mitochondrial biogenesis related endurance polygenic profile, and compared the endurance polygenic profile of Israeli (Caucasian) endurance athletes (n = 74), power athletes (n = 81), and non-athletes (n = 240). We computed a mitochondrial biogenesis related ‘endurance genotype score’ (EGS, scoring from 0 to 100) from the accumulated combination of six polymorphisms in the PPARGC1A-NRF-TFAM pathway. Some of the variant alleles of the polymorphisms studied were so infrequent, that the probability of possessing an ‘optimal’ EGS (= 100) was 0% in the entire study population. However, the EGS was significantly higher (P < 0.001) in endurance athletes (38.9 ± 17.1) compared with controls (30.6 ± 12.4) or power athletes (29.0 ± 11.2). In summary, although the probability of an individual possessing a theoretically ‘optimal’ genetic background for endurance sports is very low, in general endurance athletes have a polygenic profile that is more suitable for mitochondrial biogenesis.

The ropes and challenge course: a quasi-experimental examination.

In answering the call for empirical documentation of the effect of ropes and challenge course participation on the psychosocial function and sport performance of athletes and teams, exploratory studies have identified postcourse changes in group cohesion and approaches to sport competition. The purpose of the current study was to utilize a pretest-posttest comparison group design to expand knowledge in this area. 35 members of a girls' high school tennis team participated. The 16 individuals who participated in a preseason program and the 19 individuals who did not comprised the treatment and comparison groups, respectively. Team members completed the Group Environment Questionnaire and the Sport Orientation Questionnaire four days prior to and two days after the course experience. A series of 2 x 2 analyses of variance, (group x time) run on each of the scales, gave a significant group x time interaction on one social cohesion scale but none for scores on the Sport Orientation Questionnaire. The findings are discussed in relation to research and the implementation of these programs with athletes.

Sweat inhibition by cutaneous cooling in normal sympathectomized and paraplegic man.

ArticleSweat inhibition by cutaneous cooling in normal sympathectomized and paraplegic man.R O Rawson, and J D HardyR O Rawson, and J D HardyPublished Online:01 Feb 1967https://doi.org/10.1152/jappl.1967.22.2.287MoreSectionsPDF (1 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByHuman temperature regulation under heat stress in health, disease, and injuryMatthew N. Cramer, Daniel Gagnon, Orlando Laitano, and Craig G. Crandall19 August 2022 | Physiological Reviews, Vol. 102, No. 4Integrated fan cooling of the lower back for wheelchair users14 September 2022 | Journal of Rehabilitation and Assistive Technologies Engineering, Vol. 9A Primary Care Provider’s Guide to Autonomic Dysfunction Following Spinal Cord InjuryTopics in Spinal Cord Injury Rehabilitation, Vol. 26, No. 2Heat-related issues and practical applications for Paralympic athletes at Tokyo 202027 June 2019 | Temperature, Vol. 7, No. 1Thermoregulation following spinal cord injuryImplications of altered autonomic control on sports performance in athletes with spinal cord injuryAutonomic Neuroscience, Vol. 209Cooling Athletes with a Spinal Cord Injury15 August 2014 | Sports Medicine, Vol. 45, No. 1Disordered cardiovascular control after spinal cord injuryThermoregulation during Exercise in Individuals with Spinal Cord InjuriesSports Medicine, Vol. 36, No. 10Effects of Spinal Cord Lesion Level upon Thermoregulation during Exercise in the HeatMedicine & Science in Sports & Exercise, Vol. 35, No. 7Thermoregulatory set point in patients with spinal cord injuries (spinal man)Spinal Cord, Vol. 21, No. 4COMPARATIVE PHYSIOLOGY OF SWEATING29 July 2006 | British Journal of Dermatology, Vol. 88, No. 4Experimental hyperthermia in traumatic quadriplegiaInternational Journal of Biometeorology, Vol. 15, No. 2-4 More from this issue > Volume 22Issue 2February 1967Pages 287-91 https://doi.org/10.1152/jappl.1967.22.2.287PubMed6017896History Published online 1 February 1967 Published in print 1 February 1967 Metrics