Muscle Fatigue

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Muscle adaptations to the increase in energy demands at the start of exercise

Introduction

The transition from rest to exercise is associated with a huge upsurge in energy expenditure, due primarily to skeletal muscle contractions (Connett & Sahlin, 1996). Contractions require energy in the form of adenosine tri-phosphate (ATP). ATP stores in muscle are around 8mmol/l and are exhausted within 2s of exercise (Connett & Sahlin, 1996). To continue exercise and maintain ATP homeostasis, ATP production must increase rapidly. The adaptations that occur are tailored to suit the energy requirements of the exercise, therefore the adaptations during marathon running are different to those seen during sprinting. Breakdown of phosphocreatine (PC) is the first adaptation to increased energy demand and has been called the alactic energy system because it does not result in lactate formation. As this fails the process of glycolysis is turned on and glucose utilization begins. Anaerobic respiration at the onset of exercise was traditionally attributed to insufficient oxygen supply to muscle. However the finding that fully oxygenated muscles still utilize glycolysis at the onset of exercise put this theory out of contention (Conley et al, 1998). Today the mechanisms by which glycolysis are activated are better understood and a review of current understandings will ensue. Fat oxidation is also increased during exercise and adaptations leading to this also need attention. Muscle Contraction

Muscle contraction is the result of a complex chain of command stemming from the motor cortex in the brain (Connett & Sahlin, 1996). In the muscle fibre the immediate steps leading to contraction involve action potentials and calcium. T tubules conduct action potentials into the interior of the fibre. Dihydropyridine (DHP) receptors on the T tubule membrane release calcium when an action potential arrives. This stimulates the Ryanodine receptors (RyR) on the sacroplasmic reticulum...
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