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The purpose of the project was to test the widely endorsed assumption that pedometers produce or encourage more physical activity participation in the form of walking. The investigators hypothesized that pedometers would not increase the amount of walking cardiac patients participated in after their cardiac rehabilitation program compared to patients without pedometers.
As evidenced by the media attention given to pedometers and recent physical activity promotional efforts focused on pedometers, people seem to think that owning a pedometer will influence activity levels.
However, an examination of a few social cognitive theories produces no theoretical rationale that would support any sustained positive influence of pedometers in the absence of some other conditional factor, such as a behavioural goal or a social support system. We believe that once people determine how many steps their usual routes and daily activity typically amounts to, that the pedometer will no longer be used. We based our contentions on two theories: self efficacy theory (Bandura, 1986;1997) and self-determination theory (Deci & Ryan, 2000).
Allocation: Randomized, Control: Active Control, Endpoint Classification: Efficacy Study, Intervention Model: Parallel Assignment, Masking: Open Label, Primary Purpose: Treatment
Glenrose Rehabilitation Hospital
University of Alberta, Physical Education
Published on BioPortfolio: 2014-07-23T21:46:26-0400
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To evaluate the impact of pedometer use on the physical activity (PA) and functional walking capacity (FWC) of adolescents with juvenile idiopathic arthritis (JIA) and lower extremity (LE) involvement...
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Coronary artery disease accounts for the majority of sudden cardiac deaths (SCD) in the older population whereas cardiomyopathies and arrhythmogenic abnormalities predominate in younger SCD victims (
A group of cardiac arrhythmias in which the cardiac contractions are not initiated at the SINOATRIAL NODE. They include both atrial and ventricular premature beats, and are also known as extra or ectopic heartbeats. Their frequency is increased in heart diseases.
Blocking of a blood vessel in the SKULL by an EMBOLUS which can be a blood clot (THROMBUS) or other undissolved material in the blood stream. Most emboli are of cardiac origin and are associated with HEART DISEASES. Other non-cardiac sources of emboli are usually associated with VASCULAR DISEASES.
A state of subnormal or depressed cardiac output at rest or during stress. It is a characteristic of CARDIOVASCULAR DISEASES, including congenital, valvular, rheumatic, hypertensive, coronary, and cardiomyopathic. The serious form of low cardiac output is characterized by marked reduction in STROKE VOLUME, and systemic vasoconstriction resulting in cold, pale, and sometimes cyanotic extremities.
Inflammatory processes of the muscular walls of the heart (MYOCARDIUM) which result in injury to the cardiac muscle cells (MYOCYTES, CARDIAC). Manifestations range from subclinical to sudden death (DEATH, SUDDEN). Myocarditis in association with cardiac dysfunction is classified as inflammatory CARDIOMYOPATHY usually caused by INFECTION, autoimmune diseases, or responses to toxic substances. Myocarditis is also a common cause of DILATED CARDIOMYOPATHY and other cardiomyopathies.
Unexpected rapid natural death due to cardiovascular collapse within one hour of initial symptoms. It is usually caused by the worsening of existing heart diseases. The sudden onset of symptoms, such as CHEST PAIN and CARDIAC ARRHYTHMIAS, particularly VENTRICULAR TACHYCARDIA, can lead to the loss of consciousness and cardiac arrest followed by biological death. (from Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine, 7th ed., 2005)