Effects of physical training and detraining on intrinsic cardiac control mechanisms.
The effects of a moderate physical training program on the hearts of rats have been studied. The mechanical responses of these hearts are improved. Possible contributing factors in this improvement are increased coronary reserve and capacity to deliver oxygen to the myocardium, increased myocardial glycogen stores and increased turnover of fatty acids through the endogenous triglyceride pool. Myocardial oxidative compounds and high energy phosphate stores are not altered. Major changes are found in the energy utilization pathways. Actomyosin, myosin, and heavy meromyosin ATPase activity and binding activity of isolated sarcoplasmic reticulum are all enhanced. Sulfhydryl control of the active site of myosin ATPase is altered. The biochemical effects of conditioning are short lived when training is decreased or discontinued.
D000251:Adenosine Triphosphatases / Q000378:metabolism; D000818:Animals; D002118:Calcium / Q000378:metabolism; D004734:Energy Metabolism; D006321:Heart / Q000502:physiology*; D009206:Myocardium / Q000378:metabolism*; D015879:Myosin Subfragments / Q000378:metabolism; D009218:Myosins / Q000378:metabolism; D010101:Oxygen Consumption; D005082:Physical Exertion; D051381:Rats; D012519:Sarcoplasmic Reticulum / Q000378:metabolism; D013438:Sulfhydryl Compounds / Q000378:metabolism
D015879:Myosin Subfragments; D013438:Sulfhydryl Compounds; D000251:Adenosine Triphosphatases; D009218:Myosins; D002118:Calcium