Muscle Contraction Lab Report
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 …show more content…
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 to release larger amounts of calcium. Troponin is wrapped around actin and prevents myosin from binding to it. Calcium diffuses into the myofibrils where it binds to troponin causing a conformational shape change, revealing the myosin-binding site and facilitating myosin-actin interaction (Astrand & Rodahl, 2003).
The bound myosin head requires ATP in order to detach from actin. Once detached the myosin head hydrolyses ATP and the products adenosine diphosphate (ADP) and inorganic phosphate (Pi) remain in the myosin head. Hydrolysis of ATP initiates a change in the shape of the myosin head promoting myosin-actin interaction. Once rebound the myosin releases Pi, causing the head to swivel and drawing the actin in. At the end of its range the myosin head releases ADP and ATP is once again needed in order for myosin to detach from actin.
Released ADP can be used to create small amounts of adenosine mononphosphate (AMP), which is an important signal transducer(Astrand & Rodahl, 2003). The enzyme adenylate …show more content…
Adrenaline plays an important role in this through β-adrenergic stimulation resulting in increased cAMP (see below). Adrenaline is released via two mechanisms. Before exercise the anticipated exertion results in high sympathetic activity. When action potentials from the sympathetic pathway reach the adrenal medulla they cause it to release adrenaline into the blood (Connett & Sahlin, 1996). The second mechanism occurs in high intensity exercise such as a 100m sprint. Here the accumulation of potassium (k) and the low pH stimulates type 3 afferents which increase adrenaline secretion via the adrenal medulla (Astrand and Rodahl,
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 …show more content…
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 to release larger amounts of calcium. Troponin is wrapped around actin and prevents myosin from binding to it. Calcium diffuses into the myofibrils where it binds to troponin causing a conformational shape change, revealing the myosin-binding site and facilitating myosin-actin interaction (Astrand & Rodahl, 2003).
The bound myosin head requires ATP in order to detach from actin. Once detached the myosin head hydrolyses ATP and the products adenosine diphosphate (ADP) and inorganic phosphate (Pi) remain in the myosin head. Hydrolysis of ATP initiates a change in the shape of the myosin head promoting myosin-actin interaction. Once rebound the myosin releases Pi, causing the head to swivel and drawing the actin in. At the end of its range the myosin head releases ADP and ATP is once again needed in order for myosin to detach from actin.
Released ADP can be used to create small amounts of adenosine mononphosphate (AMP), which is an important signal transducer(Astrand & Rodahl, 2003). The enzyme adenylate …show more content…
Adrenaline plays an important role in this through β-adrenergic stimulation resulting in increased cAMP (see below). Adrenaline is released via two mechanisms. Before exercise the anticipated exertion results in high sympathetic activity. When action potentials from the sympathetic pathway reach the adrenal medulla they cause it to release adrenaline into the blood (Connett & Sahlin, 1996). The second mechanism occurs in high intensity exercise such as a 100m sprint. Here the accumulation of potassium (k) and the low pH stimulates type 3 afferents which increase adrenaline secretion via the adrenal medulla (Astrand and Rodahl,