*Equine Stress: Neuroendocrine Physiology and Pathophysiology DOI: http://dx.doi.org/10.5772/intechopen.105045*

for example, increased heart rate (i.e., presence of sinus tachycardia) and heart rate variability (i.e., presence of nonrespiratory sinus arrhythmia) [62, 182, 185, 186]. According to our recent investigations, sinus tachycardia and sinus arrhythmia are the most frequently diagnosed arrhythmia in equine clinic praxis [187]. Other clinical signs of acute stress are altered respiratory rate and increased body/eye temperatures [66, 182]. For studying the functional state of the brain, to test its bioelectric activity it is possible to use electroencephalographic (EEG) analysis in horses with or without stress conditions. We improved the methods for recording multichannel EEG in horses with specific six unipolar leads using overhead electrodes (Ippolitova/ Gauss method) (**Figure 2**) [188]. Comparative evaluation of electroencephalographic patterns in sporting horses with different types of higher nervous activity, as well as taking account for the age and training level was recently conducted for the first time. It allows the determination of an organism's potential capabilities, its resistance to stress, and thus the expected performance in competitions [188].

#### **5.2 Blood parameters during equine stress**

Various specific blood parameters can be used to assess the degree of stress activation. Commonly used were performance analyses of equine blood concentrations of E, NA, ACTH, cortisol, and β-EP [57, 111, 123, 125, 150]. However, E has a short half-life of only a few minutes, making this substance an impractical parameter for studies under field conditions [56]. Secretion of alpha-amylase from the salivary glands is controlled by autonomic nervous signals, and several studies have revealed that salivary alpha-amylase is correlated with SNS activity under stress conditions [189]. For ease of accessibility reasons equine cortisol is most often measured as a biomarker of the stress response, not only in blood but also in saliva, feces, and hair [123]. Interestingly cortisol concentration increases are noticed in saliva with a delay of approximately 20–30 min before the same observation in blood. However, it is becoming clear that relying on glucocorticoids to define stress is incomplete, and there is no current consensus that glucocorticoids should serve as the primary biomarker for defining the stress phenotype.

#### **5.3 Pathological changes during equine stress**

Stress-induced pathological changes also confirm the presence of chronic stress in the horse, for example, the occurrence of gastric ulcers. Parameters such as altered metabolism or suppressed immune function may have the potential to provide information on the long-term effects of stress, especially those which are related to blood chemistry (for example plasma or blood lactate levels, prolactin, iodothyronine, estradiol-17β, serum creatine kinase activity, IL-1, TNF). But these biochemical parameters are not specific for the measurement of stress in animals. Therefore, to date, there have been significant difficulties in measuring stress biomarkers in horses and their pathological effects, especially at the genetic, molecular, and cellular levels. In recent times in humans, different damage markers (e.g., lipid peroxidation, protein oxidation, stress-associated proteins, or oxidative stress mediators, as well length of telomeres) have been used to better reflect how people have coped with stress exposure [190].

Finally, it is necessary to take into account all these listed methods in the present day, not only in equine, but also in human medicine, and also to highlight that we have deficiencies in our abilities to analyze chronic stress before it becomes pathological. Thus far, there is a lack of understanding relating to the stress threshold, in analyses of the cumulative impact of multiple stressors over time, as well as the role of individual equine variation in reaction to stress and timing (e.g., time of day, season). Therefore, equine medicine requires improved contact sensing technology development that will allow for long-term, dynamic, noninvasive, multifactorial measurements of sets of stress mediators, as well as improvements in the diagnosis of stress damage at the cellular and genetic levels.
