Alrocket, below is some info from UpToDate, a medical info source for physicians, that might be helpful to you (the numbers in square brackets are references--you can ignore them):
"Sinus bradycardia is a rhythm in which fewer than the normal number of impulses arise from the sinoatrial (SA) node. The normal heart rate has been considered historically to range from 60 to 100 beats/min, with sinus bradycardia being defined as a sinus rhythm with a rate below 55 to 60 beats/min. However, a study in 500 normal subjects using an electrocardiographically recorded heart rate found the mean afternoon heart rate for men and women to be about 70 beats/min with two standard deviation limits of 46 and 93 beats/min in men and 51 and 95 beats/min for women; there was no significant age-related effect...
"Sinus bradycardia occurs in normal children  and adults [4,5], particularly during sleep when rates of 30 beats/min and pauses of up to 2 seconds are not uncommon [4,6]. It may also be seen in the absence of heart disease in the following settings:
At rest, in 25 to 35 percent of asymptomatic individuals under 25 years of age .
In well-conditioned athletes [8,9].
In some elderly patients .
There is no prognostic significance to sinus bradycardia in otherwise healthy subjects. In subjects over the age of 40, for example, there is no adverse effect on longevity.
PATHOPHYSIOLOGIC SINUS BRADYCARDIA — Sinus bradycardia can be seen in a variety of pathophysiologic settings (show table 1):
Exaggerated vagal activity — Vasovagal responses may be associated with a profound bradycardia due to heightened parasympathetic activity and sympathetic withdrawal on the SA node. The combination of the slow heart rate and an associated decline in peripheral vascular resistance is often sufficient to produce presyncope or syncope. (See "Neurocardiogenic (vasovagal) syncope and carotid sinus hypersensitivity").
There are a variety of stimuli for vagal activation:
Pressure on the carotid sinus, as may occur with a tight collar or with the impact of the stream of water in a shower
Vomiting or coughing
Valsalva maneuver when straining at stool
Sudden exposure of the face to cold water
Prolonged standing via a Bezold-Jarisch reflex
Hypervagotonia can also result in chronic (ie, nonepisodic) resting sinus bradycardia. This is the primary mechanism of resting bradycardia in well-trained athletes (see "Athletes" below). Junctional bradycardia and Mobitz type I AV block can also be seen in this setting.
Increased intracranial pressure — Increased intracranial pressure should be excluded when sinus bradycardia occurs in a patient with neurologic dysfunction. (See "Evaluation and management of elevated intracranial pressure in adults", section on Clinical manifestations).
Sinus node dysfunction — Sinus bradycardia may be the first manifestation of SA node dysfunction and the sick sinus syndrome [12,13]. This problem can be induced by virtually any disorder affecting the SA node. (See "Manifestations and causes of the sick sinus syndrome").
Acute myocardial infarction — Sinus bradycardia occurs in 15 to 25 percent of patients with acute myocardial infarction, particularly those affecting the inferior wall since the right coronary artery supplies the SA node in approximately 60 percent of people. Increased vagal activity is primarily responsible, and the bradycardia is typically transient. If treatment is necessary because of hemodynamic compromise or ischemia, sinus bradycardia usually responds well to intravenous atropine (0.6 to 1.0 mg in the majority of cases) (show table 2A-2B). (See "Supraventricular arrhythmias after myocardial infarction", section on Sinus bradycardia).
Athletes — The majority of well-trained endurance athletes have a sinus bradycardia at rest [8,9]. This has traditionally been attributed to increased vagal tone induced by exercise conditioning. However, studies in which atropine and propranolol are given to block the parasympathetic and sympathetic pathways suggest that the intrinsic physiology of the sinoatrial node may be altered . (See "Arrhythmia in athletes").
Obstructive sleep apnea — Individuals with obstructive sleep apnea frequently have sinus bradycardia that may be severe (<30 beats per minute) during apneic episodes [15-17]. Therapies to improve the apnea frequently alleviate the bradycardia . On the other hand, pacing for sinus node dysfunction may improve indices of apnea . (See "Cardiovascular and cerebrovascular effects of sleep apnea").
Drugs — A number of drugs can depress the SA node and slow the heart rate. These include parasympathomimetic agents, sympatholytic drugs (beta blockers, reserpine, guanethidine, methyldopa, clonidine), cimetidine, digitalis, calcium channel blockers, amiodarone and other antiarrhythmic drugs, and lithium.
Other — Other causes of sinus bradycardia include hypothyroidism, hypothermia, hypoxia, and some infections.
TREATMENT — Treatment is not indicated in asymptomatic patients with sinus bradycardia...."