The heart is one of the muscular organs that pump blood through the blood vessels by repeated, rhythmic contractions. The heart is composed of cardiac muscle, an involuntary muscle tissue which is found exclusively within this organ where the term cardiac from the Greek καρδία or kardia meaning “heart”. It is said that the average human heartbeat is at 72 BPM and that it will beat approximately 2.5 billion times during a lifetime of 66 years (OBGyn.net, 2008).
The Structure of the Heart
The heart is situated in the middle of the thorax with the largest part of the heart slightly offset to the left but for dextrocardia, it is on the right. It is located underneath the breastbone. It is usually felt on the left side because the left heart or left ventricle pumps stronger as it directs to all body parts. The sac pericardium encloses the heart and is surrounded by the lungs. The pericardium is made of two parts: the fibrous pericardium, a dense fibrous connective tissue; and the serous pericardium which is a double membrane structure containing a serous fluid to reduce friction during heart contractions. The mediastinum is the name of the heart cavity and is a subdivision of the thoracic cavity (DuBose, 2008).
The heart has a natural pacemaker that regulates the pace or rate of the heart. It sits in the upper portion of the right atrium (RA) and is a collection of specializes electrical cells known as the SINUS or SINO-ATRIAL (SA) node (Heart Site, 2008).
The heart is like the spark plug of an automobile generating a number of ‘sparks’ per minute. It was described that each ‘spark’ travels across a specialized electrical pathway and stimulates the muscle wall of the four chambers of the heart to contract and empty in a certain sequence or pattern. First stimulated are the upper chambers or atria followed by a slight delay to allow the two atria to empty. Then, the two ventricles are finally electrically stimulated (Heart Site, 2008).
In the heart, like the automobile, adrenaline acts as a gas pedal and causes the sinus node to increase the number of sparks per minute that increases the heart rate. The nervous system controls the release of adrenaline. Normal beats are at around 72 times per minute and the sinus node speeds up during exertion, emotional stress, fever, or when the body needs an extra boost of blood supply. It and slows down during rest or under the influence of certain medications. It was found that well-trained athletes also tend to have a slower heartbeat (Heart Site, 2008).
The sequence of electrical activity within the heart
Heart Site (2008) further described that as the SA node fires, each electrical impulse travels through the right and left atrium causing the two upper chambers of the heart to contract. The electrical activity is recorded from the surface of the body as a “P wave” on the patient’s EKG or ECG (electrocardiogram). The electrical impulse moves to an area known as the AV (atrioventricular) node and is held up for a brief period to allows the right and left atrium to continue emptying its blood contents into the two ventricles. The delay is known as a “PR interval” where the AV node acts as a “relay station” (Heart Site, 2008).
After the delay, the electrical impulse travels through both ventricles through the right and left bundle branches with the electrically stimulated ventricles contract. Blood is pumped into the pulmonary artery and aorta and is recorded from the surface of the body as a “QRS complex”. The ventricles then generate an “ST segment” and T wave on the EKG (Heart Site, 2008).
Hemodynamic effects of breath-holding
Finoff et al (2003) found that voluntary breath-holding significantly affected the heart rate response during exercise (P=.03). In their study, “breath-holding during all 3 exercises resulted in a mean heart rate increase of 18.5±7.3bpm, compared with a mean increase of 20.0±6.7bpm when subjects breathed freely.” There is significant interaction between exercise type and breath-holding (P=.01), the effect of exercise on heart rate was analyzed separately for each level of the breath-holding. In addition, the heart rate increase during OPSU with breath-holding was greater than that for the SPSU with breath-holding (21.0±8.1bpm vs 16.3±7.3bpm; P=.04).
The report indicated that voluntary breath-holding significantly increased the SBP, DBP, and mean blood pressure for all 3 exercises compared with the free-breathing condition (table 2). Likewise, ANOVA revealed no interactions between exercise type and blood pressure responses as a function of breath-holding. Breath-holding significantly increased the RPP elevations during all 3 exercises (mean, 38.2±19.3bpm•mmHg with breath-hold vs 31.5±12.4bpm•mmHg without breath-hold; P=.02), without any interaction between exercise type and breath-holding response.
Breath-holding was confirmed by a nasal cannula that monitored airflow, or lack thereof, while the subject performed the exercise with the mouth closed. The report suggested that even if these differences are not likely clinically meaningful, the slightly blunted heart rate increase with breath-holding may be a result of a Valsalva-like effect induced by breath-holding. The initial phase of a Valsalva response is characterized by a brief duration, mild reflex tachycardia, followed by more prolonged bradycardia caused by an increase in vagal tone.
Enoff et all (2003) added that the quantitative SBP, DPB, and mean blood pressure increases during the 3 abdominal exercises performed with breath-holding were approximately twice those seen when the same exercises were performed without breath-holding. There are only minor, insignificant differences between exercises. It only meant that breath-holding would increase blood pressure parameters.
The effect of breath-holding on blood pressure parameters and the RPP, regardless of the etiology, is of potential clinical significance as breath-holding doubles the average blood pressure increase, with some of our normal subjects exhibiting SBP and DBP elevations of over 60mmHg.
The study concluded that when performing the OPSU, SPSU, or the AbSculptor exercises as used in this investigation, normal individuals may experience peak heart rate and mean blood pressure increases that may exceed 30bpm and 50mmHg, respectively. Likewise, Enoff et all suggested that voluntary breath-holding significantly increased the peak blood pressure elevations and RPP for all 3 exercises, but particularly for the OPSU.
Based on their findings, they suggest that:
- the acute hemodynamic changes of abdominal exercise are potentially clinically relevant,
- clinicians should consider avoiding the OPSU exercise as used in this study in patients with vascular risk factors, and
- patients should be instructed to avoid breath holding during abdominal exercise training to avoid potentially detrimental increases in blood pressure and cardiac stress (Enoff et al, 2003).
The Cardiac Cycle
The cardiac cycle is the sequence of events that occur when the heart beats with the two phases:
- Diastole – Ventricles are relaxed.
- Systole – Ventricles contract (Wikipedia, 2008).
In the diastole phase, the atria and ventricles are relaxed and the atrioventricular valves are open. In this process, de-oxygenated blood from the superior and inferior vena cava flows into the right atrium and the open atrioventricular valves allow blood to pass through to the ventricles (Wikipedia, 2008).
As described in the Wikipedia (2008), the systole phase has the right ventricle receives impulses from the Purkinje fibers and contracts while the atrioventricular valves close and the semilunar valves open. De-oxygenated blood is then pumped into the pulmonary artery where the pulmonary valve prevents the blood from flowing back into the right ventricle.
“The pulmonary artery carries the blood to the lungs. There the blood picks up oxygen and is returned to the left atrium of the heart by the pulmonary veins. In the next diastole period, the semilunar valves close and the atrioventricular valves open. Blood from the pulmonary veins fills the left atrium. (Blood from the vena cava is also filling the right atrium.) The SA node contracts again triggering the atria to contract. The left atrium empties its contents into the left ventricle. The mitral valve prevents the oxygenated blood from flowing back into the left atrium,” (Wikipedia, 2008).
Frank-Starling law of the heart
The Frank-Starling law of the heart or the Frank-Starling mechanism states that the more the ventricle is filled with blood during diastole (end-diastolic volume), the greater the volume of ejected blood will be during the resulting systolic contraction (stroke volume) (Wikiedia, 2008).
The force of contractions will increase as the heart is filled with more blood and is a direct consequence of the effect of an increasing load on a single muscle fiber. The increased load consequently stretches the myocardium and enhances the affinity of troponin C for Calcium, hence increasing the contractile force (Wikipedia, 2008).
This is usually the case of premature ventricular contraction where it causes early emptying of the left ventricle (LV) into the aorta (Wikipedia, 2008).
Reference
OBGyn.net. (2007) “Embryonic Heart Rates.” Web.
Terry J. DuBose. Web.
Finnoff, Jonathan T., Jay Smith, Phillip A. Low, Diane L. Dahm, & Shawn P. Harrington MDa (2003). “Acute hemodynamic effects of abdominal exercise with and without breath holding.” Sports Medicine Center, Mayo Clinic, Rochester, MN, USA, Department of Neurology, Mayo Clinic, Rochester, MN, USA.
Heart Site.com (2008). “Heart Electrical Activity.” Web.
Wikipedia (2008) “Frank-Starling law of the Heart.” Web.