| Research Abstract |
The purpose of the present project was to develop a exercise training program which can be applied to over several thousands elderly people by developing a novel handy calorie meter and an IT network, and moreover, to establish animal models to investigate individually different responses to the program from genetic background. Summary of the project is as follows,
1)The development of a calorie meter :
We successfully developed a novel handy calorie meter to measure energy expenditure precisely during exercise above the intensity of walking. Moreover, we are able to estimate muscle strength of the thigh by measuring acceleration in the 3 dimensions : fore back, right-left, and up-down, during walking at the maxial speed.
2)The development of exercise training program suitable for individuals by IT network :
We confirmed in 200 elderly voluanteers that estimated maximal aerobic power (VO_<2,max>) increased by 10-20% after the training regimen ; walking at the high speed of 60-70% VO_<2,max
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>, 3Omin/ day, 3 day/week, for 6 months. The individual enegy expenditure during the training period was recorded by the calorie meter. The data were transferred to a host computer through terminal computers at a given interval, and inversely, the effects by the training on blood chemicals, blood pressure, and physical fitness were sent to the teriminal computer for the individuals in a feed back manner. By this system, several thousands of elderly people will be able to participate the program even though there are riot satisfactory number of facilities for physical training or trainers.
3)The development of animal models to discover the genes well responding to physical training :
We developed animal models to discover the gene well responding to physical training. For example, we investigated the role of calponin in arterial pressure regulation. Calponin is known to be a mediator in the vascular smooth muscle associating with α-adrenergic vasoconstriction. We found that arterial pressure regulation was impaired in the calponin knockout mice, genetically deficient of calponin, and that. they were not able to run at the high intensity as control mice. Moreover, we found that arterial pressure regulation was impaired in CRY, a key gene to generate circadian rhythm of activity, double knockout mice since α-adrenergic receptors were not expressed. in the vascular smooth muscles. These are promising findings to fill the gap between molecular bilogy and system physiology. We will be able to extend these to human studies by introducing the system stated above. Less
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