The fight or flight response is a physiological response to stressful situations, developed as a protective measure against perceived danger. ‘Fight’ refers to fighting or reacting to the situation; ‘flight’ refers to fleeing or retreating from the situation. Both responses to danger require the muscles and body to be ready for, as described by Olin Health Center at Michigan State University, “vigorous” activity. The response is involuntary and the signals in fight or flight are mediated by the sympathetic portion of the autonomic nervous system, resulting in the release of stress hormones by the endocrine system.
One such part of the stress response involves the beta-adrenergic receptors. These receptors are the targets of treatment for various cardiovascular and breathing related disorders, such as asthma and hypertension, and are bound by norepinephrine and adrenaline (also known as epinephrine), which is probably the most famous hormone released in the fight or flight response – referred to as an adrenaline rush. The beta-adrenergic receptors play a role in increasing muscle contractility during the fight or flight response via calcium channels.
The beta-adrenergic receptors, like other cell surface receptors, activate a signaling cascade when they are bound by their ligand. The signaling cascade is known to activate a cAMP-dependent protein kinase pathway, which William Catterall’s group at the University of Washington showed in September 2010 (published in PNAS) to result in the phosphorylation of Cav1.1 channels in skeletal muscle. Cav1 is a family of calcium channels that are upregulated in skeletal and heart muscle as a result of the sympathetic nervous system response. The same research group also showed that Cav1.2 channels, which conduct L-type calcium ion currents, are phosphorylated as part of an adenylyl cyclase/protein kinase A pathway in cardiac muscle (published in Science Signaling).
Calcium channels play a role in muscle contraction because the flow of the ions into the muscle fiber from the external environment or across the sarcoplasmic reticulum of the muscle turns them “on”. This occurs in both skeletal and vascular smooth muscle. Activation of the calcium channels, such as via phosphorylation, allows the flow of calcium ions across the membrane. Calcium works with a protein called calmodulin to activate an enzyme that regulates myosin, specifically myosin light chain kinase. Myosin works with actin to contract the muscle fiber. Phosphorylation-activated calcium channels, such as Cav1, act faster than voltage-dependent calcium channels (see comparison diagram), but the recent research described above suggests that the beta-adrenergic activation is coupled in the fight or flight response, which would allow for the faster muscle reaction.
See a diagram of the autonomic nervous system and the organs affected at Encylcopedia Britannica.
The University of Utah Genetic Science Learning Center provides an overview of the physiological response of each organ and tissue to the fight or flight response.
For an overview of the hormone response involving adrenaline, see Discovery Health.