**1. Introduction**

In 1986, Reimer studied the contribution of ATP depletion in the genesis of myocardial damage in an experimental model that involved the production of a series of brief ischemic episodes, assuming that successive ischemia decreased ATP levels. Conversely, Reimer was found to initially decrease the ATP content during the first ischemic episode, but the remaining episodes did not imply significant variation in ATP levels and, in some animals, these periods of ischemia produced cardioprotection [1]. This finding, which challenged the concept of successive episodes of ischemia, produces infarction as a result of "cumulative damage" [2].

Murry postulated that the maintenance of ATP in Raimer's experiments, it could be because the myocyte needed less energy, as a consequence of the development of rapid adaptation to ischemia. To test this hypothesis, he performed a series of 4 periods of 5 minutes of ischemia and 5 minutes of reperfusion before the myocardium was submitted to a prolonged 40-minute ischemia. These brief periods of ischemia and reperfusion protect against ischemic damage and reduce 30% of the infarct size; He called this preconditioning or ischemic preconditioning (IPC) [3].

This finding contributed to the development of research lines to study the mechanisms involved in cardiac preconditioning, extending the concept of ischemic preconditioning in studies of: Arrhythmias [4], apoptosis [5] and endothelial dysfunction [6].

### *Cardiorespiratory Fitness*

In addition, other non-ischemic stimuli have been studied to protect the heart, such as hypoxia [7], cell stretching [8], accelerated cardiac pacemaking [8] and physical exercise.

Exercise has been used as therapy for the treatment of stable ischemic vascular syndrome, where it has been observed that it improves perfusion in ischemic tissues. Some mechanisms involved in improving the perfusion of ischemic tissues after exercise involve:

a. shear stress-associated improvement of endothelial function [9];

b.increase in phosphorylation and expression of endothelial nitric oxide synthase [9];

c.decrease in vascular oxidative stress; and

d.collateral formation of vascular tissue.

Something that has to be clear when we talk about ischemic preconditioning is its dependence on the intensity of the stimulus (ischemia) and its duration, under this principle we can establish adequate protocols for the treatment of cardiovascular and muscular diseases; as well as, to improve the physical performance of the athletes.

Physical exercise challenges the organism to maintain stable conditions of the internal environment (homeostasis), against hypoxic conditions, oxidative stress and tissue nutrient deficiency. It is a condition of physiological stress, to be carried out continuously and through appropriate physical training programs provides benefits in the body, ranging from better control of blood glucose levels to better long-term memory.

There are multiple studies of the benefit of exercise in health, in all the virtues of exercise are praised. The result is obvious, improves and maintains the physical fitness, health and wellness of the person who performs it.

It has direct effects on muscle strengthening and cardiovascular capacity, in addition to the systemic effects involved with the release of substances into the bloodstream or the tissue that contribute to the preconditioning of the heart and skeletal muscle can be attributed to exercise.

The biochemical and physiological advantages conferred by exercise-induced preconditioning can serve to improve exercise performance. Although not all studies achieve this result, it is important not to forget that the participation of mediators produced and released during physical exercise and that are responsible for the beneficial effects in the body.

This chapter focuses on discussing the physiological mechanisms that are produced following an exercise-induced preconditioning protocol, especially those that relate to the cardiovascular system, skeletal muscle and physical performance.
