Showing papers in "Exercise and Sport Sciences Reviews in 1992"

Anxiety and sport performance.

Abstract: From the findings summarized in this review, it appears that there is little evidence in support of the inverted-U hypothesis. Available research indicates that there is considerable variability in the optimal precompetition anxiety responses among athletes, which does not conform to the inverted-U hypothesis. Many athletes appear to perform best when experiencing high levels of anxiety and interventions that act to produce quiescence may actually worsen the performance of this group. These findings indicate that there is a need to shift the research paradigm away from theories of anxiety and performance based on task characteristics or group effects and, instead, employ theoretical models that account for individual differences. Hanin's [39, 40] ZOF theory appears to be a good candidate for furthering our knowledge in this area. It was developed on the basis of research with athletes and it explicitly incorporates the concept of individual differences in the anxiety-performance relationship. Most important, because an individual's optimal range of anxiety is precisely defined, the validity of ZOF theory can be directly examined through hypothesis testing, whereas it has been argued that the inverted-U hypothesis is effectively shielded against falsification [84]. Although the findings of ZOF theory indicate that a significant percentage of athletes perform best at high levels of anxiety, Hanin's translated writings do not provide an explanation of why this is so. Further research is clearly indicated, but one explanation for this finding may involve how the athlete interprets or conceptualizes anxiety. For example, Mahoney and Avener [64] found that, although the absolute level of precompetition anxiety was similar between successful and unsuccessful Olympic gymnasts, there were differences in the way the athletes conceptualized the anxiety they were experiencing. The better performers viewed their anxiety as desirable, whereas anxiety was associated with self-doubts and catastrophizing in the unsuccessful gymnasts. Similar differences have been observed in the test anxiety literature where it has been found that poorer test takers perceive their anxiety to be more threatening and debilitating than do better performers [45]. Furthermore, temporal differences in the patterning of anxiety [64], fear responses, or cardiorespiratory measures [28] have been found between successful and unsuccessful performers; this may reflect a difference in the ability to regulate anxiety. It may also be the case that performance is not so much affected by the absolute level of precompetition anxiety as the consistency in the anxiety level across competitions. Athletes may also develop coping strategies that exploit consistent changes in attentional focus that result from elevated anxiety.(ABSTRACT TRUNCATED AT 400 WORDS)

Exercise and the cutaneous circulation.

Abstract: Our understanding of the control of the cutaneous circulation has increased over the past decade, but is still far from complete. There is a cutaneous vasoconstriction at the beginning of exercise that usually effectively competes with concurrent thermoregulatory drives for vasodilation. This cutaneous vasoconstrictor response, however, requires dynamic activity by a significant muscle mass as small muscle groups or isometric exercise are ineffective or nearly so. Also, exercise causes the threshold internal temperature relative to rest such that SKBF is lower during exercise than in resting conditions for a given thermal stimulus. A further influence by exercise on the cutaneous circulation is to limit the degree of cutaneous vasodilation when heat stress and exercise are combined. These three roles for exercise compete with the thermogenic role that promotes vasodilation. The previously described effects act through the adrenergic vasoconstrictor system and the separate active vasodilator system. The increase in SKBF with heat stress represents the combination of withdrawal of vasoconstrictor activity and elevation of active vasodilator activity. The vasoconstrictor effect of the initiation of exercise is accomplished strictly through enhanced vasoconstrictor activity; vasodilator withdrawal does not participate [72]. However, both the exercise-induced elevation in thermoregulatory threshold for raising SKBF and the limitation to cutaneous vasodilation during exercise are strictly functions of the active vasodilator system [69, 73, 78]. In the first case, active vasodilation is delayed until a higher (relative to rest) level of internal temperature is reached. In the second case, the plateau in SKBF during exercise in the heat is due to a similar plateau in active vasodilator activity. Exercise has also served as a tool for the study of other influences on the cutaneous circulation. The influences of alterations in body fluid volumes, osmolarity, acclimatization, hypertension, time of day, menstrual phase, and others on the control of SKBF have been assessed by using exercise as a calorigenic source. The question as to whether the nonthermoregulatory influences of exercise interact with these other influences to give a modification of the pattern of control different from what might be observed at rest is largely unanswered. Future directions for research are numerous, but several fundamental questions are outstanding. The mechanism of active cutaneous vasodilation has been elusive since its discovery and remains an exceptionally important question. Second, the sensory elements associated with exercise giving rise to the alterations in the pattern of control are unclear. This problem is made challenging by the fact that the efferent control by exercise differs between its initiation and events later in exercise.(ABSTRACT TRUNCATED AT 400 WORDS)

Musculoskeletal adaptations and injuries due to overtraining.

Abstract: Overtraining places a demand on the musculoskeletal system that may lead to damage to the musculoskeletal system, as well as to clinical, functional, and biomechanical adaptations that may be detrimental to sport performance. The types of injuries identified range from overt, which are obvious injuries that will usually prevent athletic performance for some period of time, to the subclinical, which decrease performance, but may be seldom recognized. These injuries apparently may be avoided or lessened in severity by a combination of several methods. A thorough preparticipation evaluation is important to detect subtle adaptations in strength and flexibility that can result from overtraining and may increase the athlete's chances of injury. A good sport-specific conditioning program is necessary to give the athlete a strong musculoskeletal base on which to build athletic skills and to decrease the risk of overtraining adaptation. In many sports, prehabilitation exercises can be performed for those musculoskeletal areas that are under high stress in a particular sport. Also, a maintenance conditioning program that extends through the season may be important to maintain fitness throughout the season. Following proper principles of conditioning, including specificity, recovery, and progression, are important. A complete and accurate diagnosis of the injuries that do occur is necessary so that proper treatment may follow. This can be facilitated by understanding the types of clinical presentations of injuries, and the different anatomical and functional alterations that may be acting to cause or to continue the clinical presentation. By following these general guidelines, safe participation in sporting activities as well as performance will be enhanced. The exact point where "training" becomes "overtraining" is difficult to define, especially prospectively. An exciting area of sports medicine research will be to define the anatomic parameters and exercise doses that will cause overtraining, and to devise fitness examinations and training programs that will allow maximal performance with minimal overload risk. At the present time, retrospective studies do indicate that adaptations occur in muscles, tendons, and bones in response to high training loads, and these particular adaptations are not beneficial to performance and may be associated with increased injury risk. Since the optimal exercise dose is not known, provision for evaluation of these adaptations and prehabilitation of all noninjured areas or proper rehabilitation of all injured areas will best prepare the musculoskeletal system for training.

Oxygen transport during exercise at altitude and the lactate paradox: lessons from Operation Everest II and Pikes Peak.

Abstract: It seems unlikely that oxygen-limited metabolism explains the increased lactate concentrations in blood or muscle during exercise at high altitude compared with sea level values because: 1. Even marked hypoxia equivalent to that at the summit of Mt. Everest may not be sufficiently severe to impair function or to impair muscle oxidative metabolism markedly during exercise; 2. At this very high altitude, muscle hypoxemia is probably not the limiting factor for exercise performance; other systems, i.e., the cerebral cortex [24, 33], probably fail before hypoxemia impairs muscle metabolism; 3. The traditional view of oxygen-limited aerobic metabolism during exercise at high altitude does not explain a long-standing dilemma in altitude physiology, the lactate paradox (in which blood lactate accumulation during exercise is increased on arrival at high altitude but falls with acclimatization), because the lactate fall is independent of muscle oxygenation; 4. Net lactate release by the leg during exercise is independent of oxygenation; 5. Kinetic studies show that lactate appearance and disappearance are closely linked and both increase with acute altitude exposure and decrease with acclimatization; 6. Lactate appearance rate is strongly correlated with, and may be influenced by, the extent of beta-adrenergic stimulation; 7. The beta-adrenergic stimulation may be, in part, determined by the degree of arterial oxygenation.

Responses of the cardiac transplant patient to exercise and training.

Abstract: Total denervation persists in the human heart following cardiac transplantation. At rest, there is some increase of heart rate and blood pressure. with a low normal cardiac output. The donor heart remains capable of a satisfactory acute response to exercise, based upon an increase of venous return (acting through the Frank-Starling mechanism) and slower chronotropic and inotropic responses to circulating catecholamines. During submaximal exercise, the stroke volume is greater than normal, but the cardiac output is somewhat reduced, leading to a widening of arteriovenous oxygen difference. Peak heart rate, peak stroke volume, and peak cardiac output are all less than in age-matched normals. Peak power output and peak oxygen intake are also subnormal immediately following cardiac transplantation. The poor ventricular performance reflects, in part, the condition of the transplanted myocardium and, in part, the increased afterloading associated with a loss of lean tissue mass. Although there have, as yet, been no controlled experiments, there is suggestive evidence that an appropriately graded training regimen facilitates restoration of lean tissue and, thus, functional recovery (including the correction of postoperative psychological disturbances). A suitably adapted exercise prescription is thus recommended as a useful component of treatment following cardiac transplantation. There is good evidence that a well-designed training program improves the quality of life for the recipient, although further study is needed to determine the impact of such therapy upon morbidity and mortality.