Hideomi Takada

Three-month exercise and weight loss program improves heart rate recovery in obese persons along with cardiopulmonary function.

OBJECTIVE Heart rate recovery (HRR) after exercise is an independent risk factor for cardiovascular disease and mortality, and it is well known to be modifiable by weight loss. We investigated whether HRR was mainly improved by better cardiopulmonary function or by alteration of the metabolic profile. METHODS The weight loss program included 2h of group exercise per week and individual dietary instruction by a qualified dietician every week. Clinical assessment (including HRR) was done before and after the 3-month program. PATIENTS The subjects were 125 obese persons without a past history of stroke, cardiovascular events, or use of medications who participated in and completed our exercise plus weight loss program. RESULTS HRR (35.61+/-12.83 to 45.34+/-13.6 beats/min, p<0.0001) was significantly faster after the program. The change in HRR was significantly correlated (p<0.05) with the changes in body weight, body mass index, percent body fat, waist circumference, hip circumference, resting heart rate, peak exercise heart rate, exercise time, maximal work load, physical working capacity divided by body weight (PWC75%HRmax/weight), subcutaneous fat area, visceral fat area, low-density lipoprotein cholesterol, and leptin. Multivariate analysis showed that the change in HRR was significantly correlated (p<0.05) with the changes in resting heart rate, peak exercise heart rate, and PWC75%HRmax/weight. CONCLUSIONS Our data demonstrated that HRR can be improved in obese subjects by a 3-month exercise and weight loss program. Improvement in cardiopulmonary function by exercise seems to be the main contributor to the increment of HRR.

Range of ventricular ectopic complexes in healthy subjects studied with repeated ambulatory electrocardiographic recordings

The incidence and forms of ventricular premature complexes (VPCs) in apparently healthy subjects were studied to determine long-term reproducibility of day to day variation on Holter electrocardiogram. The study included 152 men and 68 women ranging in age from 20 to 78 years who were having routine check-ups that revealed no cardiovascular abnormalities. In addition to routine measurements, Holter electrocardiography was recorded during daily life, and the total number of VPCs occurring during 24 hours was visually calculated on replayed electrocardiographic tracings. Forms of VPCs and incidence of VPCs in 10-year age groups of the subjects were also recorded. No VPCs were observed in 56% of the subjects; 93% showed less than 50 VPCs and the other 7% of the 220 subjects had greater than or equal to 50 VPCs. Forty-one of the 220 subjects returned for routine follow-up 1 year later. Repeated Holter electrocardiograms at this time showed high reproducibility of less than 50 VPCs. A small number of multiform VPCs were reproducible but paired VPCs were not. Physiologic definition of VPCs in healthy subjects appears to be clinically significant.

Myocardial injury in a 100-km ultramarathon

Abstract Impaired cardiac function after strenuous exercise, such as an ultramarathon or triathlon, has been ascribed to “cardiac fatigue.” However, a reduction of cardiac function in strenuous sports in the absence of coronary artery disease might also be based on myocardial injury because of excess catecholamines. We studied the cardiac injury in runners of a 100-km ultramarathon by determination of levels of serum troponin T, which is highly specific for myocardial injury. Blood was collected from 13 healthy adult men before, immediately after, and the next morning after participation in a 100-km ultramarathon. Creatine kinase (CK), isozyme of CK with muscle and brain subunits (MB), and cardiac troponin T levels were determined. Creatine kinase levels were 207 ± 108 IU/L before the marathon, 10,313 ± 10,273 IU/L immediately after, and 10,799 ± 6593 IU/L on the next day. Creatine kinase MB levels at the same time points were 12 ± 14 IU/L, 197 ± 170 IU/L, and 166 ± 108 IU/L, respectively. Cardiac troponin T level was ⩽0.1 ng/mL in all subjects before the marathon and increased significantly to a mean of 0.68 ± 0.73 ng/mL immediately after, exceeding the normal limit in seven subjects. It then returned to normal (0.15 ± 0.07 ng/mL) on the next day, while CK, which referred to skeletal muscle damage, was still elevated at a high level. Because cardiac troponin T levels increased after the ultramarathon, myocardial injury was considered to have occurred.