The physiological cardiac remodeling caused by aerobic exercise training involves a set of microRNAs, as discussed in the study by Fernandes et al. (2015). The increase in venous return during exercise is facilitated by the auxiliary pumping action of contracting skeletal muscles. This, in turn, leads to increases in heart rate and myocardial contractility through activation of cardiac sympathetic nerves. These changes enable the heart to pump blood to the pulmonary and systemic circulations, resulting in an increase in cardiac output. However, stroke volume only increases slightly. Additionally, aerobic exercise leads to increased oxygen consumption, blood oxygen extraction, systolic pressure, and mean blood pressure. As body temperature rises during exercise, the blood vessels in the skin dilate. However, during severe exercise when the heart rate reaches its maximum, the skin vessels constrict. This effectively increases blood volume but also causes greater increases in body temperature and a feeling of exhaustion. The limiting factor in exercise performance is the delivery of blood to the active muscles. 

Acute blood loss triggers various compensatory mechanisms, including tachycardia, hypotension, generalized arteriolar constriction, and generalized venoconstriction. These mechanisms help to restore blood volume and pressure. Negative feedback mechanisms such as baroreceptor and chemoreceptor reflexes, responses to cerebral ischemia, reabsorption of tissue fluids, release of vasoconstrictors, and renal conservation of water and electrolytes are activated. However, there are also positive feedback mechanisms that can lead to decompensation, such as cardiac failure, acidosis, central nervous system depression, aberrations in blood coagulation, and depression of the mononuclear phagocytic system. The outcome of acute blood loss depends on the interactions between these positive and negative feedback mechanisms.

The control of blood flow to cardiac and skeletal muscles during exercise is discussed by Laughlin et al. (1996). The respiratory system plays a crucial role in exercise and cardiovascular health, as highlighted in the review by Lavie et al. (2015). Modeling acute traumatic injury and understanding its impact is explored by Valparaiso et al. (2015). 

In Section 5, the respiratory system is examined by Cloutier and Thrall. The chapter covers topics such as the anatomical structure/function relationships of the upper and lower components of the respiratory system, the differences between the pulmonary and bronchial circulatory systems, the roles of innervation and muscles in respiration control, the functions of conducting airways and components of the respiratory unit, the effects of parasympathetic and sympathetic nervous system stimulation on respiratory responses, and lung development and alveolar repair after injury.
Fernandes T, Baraúna VG, Negrão CE, et al. Aerobic exercise training promotes physiological cardiac remodeling involving a set of microRNAs. Am J Physiol. 2015;309:H543.
Gruen RL, Brohi K, Schreiber M, et al. Haemorrhage control in severely injured patients. Lancet. 2012;380:1099.
which, along with the auxiliary pumping action of the contracting skeletal muscles, greatly increases venous return. The increases in heart rate and myocardial contractility, both induced by the activation of cardiac sympathetic nerves, enables the heart to transfer blood to the pulmonary and systemic circulations, thereby increasing cardiac output. Stroke volume increases only slightly. O2 consumption and blood O2 extraction increase, and systolic pressure and mean blood pressure increase slightly. As body temperature rises during exercise, the skin blood vessels dilate. However, when the heart rate becomes maximal during severe exercise, the skin vessels constrict. This increases the effective blood volume but causes greater increases in body temperature and a feeling of exhaustion. The limiting factor in exercise performance is delivery of blood to the active muscles.
6. Acute blood loss induces tachycardia, hypotension, generalized arteriolar constriction, and generalized venoconstriction. Acute blood loss invokes a number of negative feedback (compensatory) mechanisms, such as baroreceptor and chemoreceptor reflexes, responses to moderate cerebral ischemia, reabsorption of tissue fluids, release of endogenous vasoconstrictors, and renal conservation of water and electrolytes. Acute blood loss also invokes a number of positive feedback (decompensatory) mechanisms, such as cardiac failure, acidosis, central nervous system depression, aberrations in blood coagulation, and depression of the mononuclear phagocytic system. The outcome of acute blood loss depends on the sum of gains of the positive and negative feedback mechanisms and on the interactions between these mechanisms.
Laughlin MH, Korthuis RJ, Duncker DJ, et al. Control of blood flow to cardiac and skeletal muscles during exercise. In: Rowell LB, Shepherd JT, eds. Handbook of Physiology, Section 12: Exercise: Regulation and Integration of Multiple Systems. Bethesda, MD: Oxford University Press; 1996.
Lavie CJ, Arena R, Swift DL, et al. Exercise and the cardiovascular system: clinical science and cardiovascular outcomes. Circ Res. 2015;117:207.
Valparaiso AP, Vicente DA, Bograd BA, et al. Modeling acute traumatic injury. J Surg Res. 2015;194:220.
SECTION 5The Respiratory System MICHELLE M. CLOUTIER AND ROGER S. THRALL
Upon completion of this chapter, the student should be able to answer the following questions: 1.
Explain the anatomical structure/function relationships of the upper and lower components of the respiratory system.
2.
Compare and contrast the pulmonary and bronchial circulatory systems.
3.
Explain the relationships between innervation and muscles in the control of respiration.
4.
Compare and contrast the roles of the conducting airways and components of the respiratory unit.
5.
Compare and contrast the effects of stimulation of the parasympathetic and sympathetic nervous systems on respiratory responses.
6 Describe lung development and alveolar repair after injury to regeneration of normal architecture.