Skeletal Muscle Contraction

Skeletal muscle is a voluntary and striated muscle that attaches to the skeleton to allow control over posture and movement. Each skeletal muscle consists of bundles of muscles fibers called fascicles. These fascicles are composed of many individual muscle fibers or muscle cells that can be up to several millimeters long. These muscle fibers are composed of myofibrils, which are organized into thick filaments, myosin, and thin filaments, actin. These filaments are organized into repeating structures called sarcomeres, which are the subunits of skeletal muscle. In order to generate force, these filaments must slide past one another (Widmaier 2011). Muscle fibers are innervated by motor neurons. A motor unit is a single motor neuron and all muscle fibers it innervates. Contraction occurs through a mechanism called excitation-contraction coupling when an action potential propagates down a motor neuron axon to initiate contraction. As the action potential then travels down these transverse tubules it opens ion channels, which releases calcium into the sarcoplasm. When this calcium is released, binding sites on the thin filaments become available that allow the thick filaments to bind and pull the thin filaments toward the center of the sarcomere, generating
contraction. ATP allows the myosin heads to release and reattach therefore, calcium and ATP must continue be present in order for this process to repeat (Widmaier 2011). When a muscle declines in its ability to generate force this is called fatigue. Although the major cause of fatigue is unknown, it can be due to a buildup of ions causing a shift in the ion gradient. It can also be due to a lack of availability of ATP, which happens when a cell uses energy (Widmaier 2011). Fatigue can be measured by combining an EMG with dynamometry. Dynamometry is a measure of power or output of power by a muscle. By measuring the decrease in power over time, fatigue of a muscle can be measured (Pflanzer 2006). Fatigue can additionally be affected by temperature. A lower body temperature of the muscle can cause the muscle to fatigue faster than normal (Roots 2008) Reaction time is a measure of how quickly a subject can respond to a given stimulus. It is controlled by both the skeletal and nervous system. Both work physiologically to respond to changes in the surrounding environment, also known as stimuli. The body can respond either voluntarily or involuntarily to these stimuli to maintain its stable internal environment. The body can respond to these stimuli with a reflex, an automatic or involuntary reaction to a stimulus in the surrounding environment (Widmaier 2011). A reflex begins when a stimulus is received by a receptor at a sensory or afferent neuron.
This sensory neuron then relays this information to the central nervous system where afferent neurons synapse with interneurons which in turn synapse with efferent or motor neurons. This motor neuron then relays the information out of the brain to an effector. In this case, the effector is a skeletal muscle that causes the reflex response to occur. Reaction time is a measure of the time between when the stimulus is delivered and the response occurs. This speed can vary person-to-person depending on the speed of transmission of the signal from neuron to neuron, as well as the number of neurons involved (Widmaier
2011). Caffeine is a central nervous stimulant that has a number of physiological effects on the body. It increases the effects of the sympathetic nervous system or the flight or fight mechanism of the body, it increases the firing of skeletal muscle motor units, and finally increases the efficiency of neurotransmissions in the cerebral cortex therefore causing the increase in alertness people look for with caffeine. Due to this increased alertness and arousal, caffeine could also correlate with a decrease in reaction time to a stimulus (Chawla 2015). Additionally, caffeine has been linked to a greater increase in plasma epinephrine levels, leading to a greater endurance level for individuals (Graham 1998).