Protective effect of physical training on cardiovascular responses to hemorrhagic hypotension and shock.
The primary objective of this study was to determine if a measurable degree of protective cardiovascular adaptation to hypovolemic shock is developed in response to aerobic training. Twelve rats were trained (T) by running on a rodent treadmill 60 min/day, 5 days/wk at 30 m/min on a 5 degree incline for a period of 13-17 weeks. Elevated levels of SDH activity in the vastus intermedius muscles of the trained group (T) verified physiological training. Each T rat was weight matched with a sedentary untrained (UT) control, anesthetized with sodium pentobarbital, and subjected to a modified Wiggers hemorrhagic shock protocol. The parameters monitored were the maximum reduction in vascular capacitance (ie, maximum blood shed) when MAP was lowered to 30 mm Hg by hemorrhage; the time necessary to achieve maximum blood loss at 30 mm Hg (compensation time); and the time between maximum and 20% uptake of the shed volume from the reservoir (decompensation time). The data show that the initial MAPs for the UT group were significantly higher than the T group (133 +/- 3 mm Hg vs 121 +/- 4 mm Hg). The maximum blood loss normalized to body weight and pressure drop was .268 +/- .012 ml/kg/mm Hg for UT and .343 +/- .02 ml/kg/mm Hg for T (P less than .001), suggesting that T had a better ability to reduce total vascular capacitance. Also, both the compensation and decompensation times were greater in the T than UT groups. These data suggest that treadmill exercise-conditioned rats have a greater inherent cardiovascular compensatory ability than untrained rats.
D000818:Animals; D001794:Blood Pressure; D001810:Blood Volume; D008297:Male; D009132:Muscles / Q000201:enzymology; D010805:Physical Conditioning, Animal; D051381:Rats; D011919:Rats, Inbred Strains; D012771:Shock, Hemorrhagic / Q000201:enzymology / Q000503:physiopathology*; D013385:Succinate Dehydrogenase / Q000378:metabolism
D013385:Succinate Dehydrogenase