Traditional models of fatigue and physical performance / Modelos tradicionais de fadiga e desempenho físico

ABSTRACT The origin of fatigue has been the focus of studies involved in sports performance, due to the necessity to clarify the mechanistic bases for the reduced capacity to perform considerable effort intensities. According to the traditional conception of fatigue, mechanisms may encompass peripheral and central sites of fatigue. Peripheral fatigue is understood as events related to an inefficient tissue oxygen delivery, metabolic accumulation, muscular acidosis and muscle substrate depletion. In contrast, the central fatigue is mostly related to events in the central nervous system (CNS) that may involve neurotransmitters changes, altered metabolic profile and elevated temperature. Therefore, the current review aimed to discuss the peripheral and central mechanisms of fatigue, thus driving interpretations of the phenomenon.

RESUMO A etiologia da fadiga tem sido objeto de estudo em pesquisas relacionadas ao desempenho esportivo em função da necessidade de esclarecer os mecanismos que reduzem a capacidade de manutenção do desempenho em intensidades elevadas de esforço. A concepção tradicional de fadiga assume que os mecanismos possam ser desencadeados em sítios de ação central ou periférica. A fadiga periférica é compreendida como uma oferta inadequada de oxigênio tecidual, acúmulo de metabólitos e depleção de substrato energético acelerando a acidose muscular. A fadiga central, por sua vez, oriunda do sistema nervoso central (SNC), apresenta alterações nos neurotransmissores, podendo alterar o perfil metabólico e temperatura do SNC. Desta forma, a presente revisão tem como intuito abordar os mecanismos de fadiga central e periférica, norteando futuras interpretações sobre o fenômeno.

Assessment of Abnormality in Skeletal Muscle Metabolism in Patients with Chronic Lung Desease by 31P Magnetic Resonance Spectroscopy / 결핵

The functional derangement of skeletal muscles which may be attributed to chronic hypoxia has been accepted as a possible mechanism of exercise impairment in patients with chronic obstructive pulmonary disease (COPD). The metabolc changes in skeletal muscle in patients with COPD are characterized by impaired oxidative phosphorylation early activation of anaerobic glycolysis and excessive lactate and hydrogen ion production with exercise. But the cause of exercise limitation in patients with chronic lung disease without hypoxia has not been known. In order to evaluate the change in the skeletal muscle metabolism as a possible cause of the exercise limitation in chronic lung disease patients without hypoxia, we compared the muscular metabolic data of seven male patients which had been derived from noninvasive 31P magnetic resonance spectroscopy(MRS) with those of five age-matched normal male control persons. 31P MRS was studied during the sustained isometric contraction of the dominant forearm flexor muscles up to the exhaustion state and the recovery period. Maximal voluntatry contraction(MVC) force of the muscle was measured before the isometric exercise, and the 30% of MVC force was constantly loaded to each patient during the isometric exercise. There were no differences of intracellular pH (pHi) and inorganic phosphate/phosphocreatine (Pi/PCr) at baseline, exhaustion state and recovery period between two groups. But pHi during the exercise was lower in patients group than the control group (p<0.05). Pi/PCr during the exercise did not show significant difference between two groups. These results suggest that the exercise limitation in chronic lung disease patients without hypoxia also could be attributed to the abnormalities in the skeletal muscle metabolism.