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Showing papers in "Exercise and Sport Sciences Reviews in 1999"



Journal ArticleDOI
TL;DR: 5 Exercise and Pain: The Neurobiology, Measurement, and Laboratory Study of Pain in Relation to Exercise in Humans
Abstract: 5 Exercise and Pain: The Neurobiology, Measurement, and Laboratory Study of Pain in Relation to Exercise in Humans PATRICK O'CONNOR;DANE COOK; Exercise and Sport Sciences Reviews

231 citations


Journal ArticleDOI
TL;DR: Exercise training programs that consist of various modes of exercise, and which require the use of a large muscle mass, such as swimming, power walking, and strength training, may be the most advantageous for the prevention and treatment of insulin resistance and associated diseases.
Abstract: The benefits of exercise training in the prevention and treatment of insulin resistance, impaired glucose homeostasis, and NIDDM are strongly supported by current research. The actual mechanisms involved have not been completely identified but occur at the systemic, tissue, and cellular levels. The adaptations that are responsible for the prophylactic effects of exercise training, however, start to subside rapidly once training ceases and are completely lost within 1 to 2 weeks of detraining [4, 17, 37, 68, 161]. Thus, the benefits of exercise training must be renewed on a regular basis. In addition, many of the systemic and cellular adaptations that are responsible for an improved skeletal muscle insulin action occur in only those muscles involved in the training program [4, 28]. Therefore, exercise training programs that consist of various modes of exercise, and which require the use of a large muscle mass, such as swimming, power walking, and strength training, may be the most advantageous for the prevention and treatment of insulin resistance and associated diseases.

202 citations







Journal ArticleDOI
TL;DR: This review has tried to focus on what is known about four specific physiological challenges--mechanical load, intracellular calcium, hypoxia, and redox state to provide insight into potential mechanisms that govern exercise-induced transcriptional changes.
Abstract: Much progress has been made in recent years into understanding molecular mechanisms by which transcription is regulated following changes in physiological stimuli. This review has tried to focus on what is known about four specific physiological challenges--mechanical load, intracellular calcium, hypoxia, and redox state. Because of our biased interest in exercise, it was our goal to review these relatively well-studied systems so that we might provide insight into potential mechanisms that govern exercise-induced transcriptional changes. What becomes obvious, when reaching the end of this review, is that there are many common themes among the different physiological responses described. Some examples include the activation of IEGs, such as c-jun and c-fos, the phosphorylation of the transcription factor CREB, and the importance of the serum response element and the serum response factor. These commonalities across the different physiological systems suggest a certain redundancy or shared mechanism(s) for regulating transcription in response to physiological stimuli. While very little is known at this time about how exercise regulates transcription, it is an exciting time in this field of research. The recent growth in the molecular biological research literature of more physiologically-based studies provides exciting new molecular and cellular tools for those researchers willing to take on the challenge of understanding the complex mechanisms of exercise-induced adaptations.

39 citations



Journal ArticleDOI
TL;DR: Evidence shows that the respiratory muscles demand a significant portion of the cardiac output during maximal exercise, and it appears that respiratory muscle work during strenuous exercise affects exercise performance.
Abstract: In summary, evidence shows that the respiratory muscles demand a significant portion of the cardiac output during maximal exercise. Estimates of both animal and human blood flow and VO2 to the respiratory muscles during maximal exercise approximate 14-16% of the total cardiac output and VO2. During heavy exercise, this metabolic demand of the respiratory muscles affects the distribution of cardiac output between the respiratory muscles and the legs such that leg vascular conductance and blood flow increases with respiratory muscle unloading and decreases with respiratory loading. The reflex effects underlying this blood flow redistribution remain unknown; however, these data do clearly support the existence of a significant sympathetic effect output to working skeletal muscle in heavy exercise. These data also invite the exciting (although speculative) prospect of important chemo- or mechano-induced reflexes emanating from respiratory muscle under load.Finally, while not yet completely understood or investigated, it appears that respiratory muscle work during strenuous exercise affects exercise performance.

Journal ArticleDOI
TL;DR: Based on the structural and functional homology between myosin and other molecular motors, these findings have implications not only for understanding muscle contraction, but for understanding numerous aspects of motility in all cellular systems as well.
Abstract: Recent experimental advances in structural biology, biophysics, and molecular biology have dramatically increased our understanding of the molecular mechanism of muscle contraction, as well as the assembly of myosin filaments. Future studies are required to detail, for example, the molecular cause of the conformational change during the power stroke and ATP hydrolysis, as well as the nature of the communication between nucleotide and actin binding sites. Based on the structural and functional homology between myosin and other molecular motors, these findings have implications not only for understanding muscle contraction, but for understanding numerous aspects of motility in all cellular systems as well.