Physiological responses of men and women during exercise in hot environments with equivalent WBGT.

Eight Japanese men and women participated in this study. They were randomly exposed to two environments: hot-dry; HD (Ta = 40 degrees C, rh 30%, wet bulb globe temperature (WBGT) = 32 degrees C) and hot-wet; HW (Ta = 31 degrees C, rh = 80%, WBGT = 32 degrees C) for 110 min. During the exposure, they rested on a bicycle ergometer for 20 min during rest and 30 min during recovery, then they pedaled it with an intensity of 40% VO2 max for 60 min. Tre, Tsk, and HR were recorded every minute. Total sweat loss and dripping were measured by independent bed balances which was connected to a computer processing with an accuracy of 1 g throughout the experiment. Sweat sodium concentration at forearm and back sites were collected by sweat capsule technique. These results showed that delta Tre, Tsk, evaporated sweat, dripping sweat, body heat storage of both sexes in HD were significantly higher than these in HW during exercise. HR of men in HD at the end of recovery was slightly higher than that of women. Whereas the sweat sodium concentration at forearm and back sites in both sexes remained unchanged either in HD or HW environment, it was found that HD was more stressful than HW environment under equivalent WBGT.

Physiological responses of women during exercise under dry-heat condition in winter and summer.

Fourteen young Japanese women were exposed to a dry-heat condition (Ta = 40 degrees C, rh = 30%) both in winter and summer. During an exposure for 110 min, they were rested on a bicycle ergometer for 20 min, exercised with an intensity of 40% Vo2 max for 60 min and recovery for 30 min. Their rectal and skin temperatures, and heart rate were determined every minute. Total sweat loss and dripping sweat were recorded throughout the experiment by independent bed balances which connected to a computer processor with an accuracy of 1 g. Sweat capsule with filter paper was used to measure sodium concentration on the forearm and back sites. Rectal temperature was not significantly different between winter and summer. Mean skin temperature was significantly higher in summer than in winter during exercise while heart rate was significantly lower in summer than in winter. Sweat evaporation and dripping in summer showed a tendency to increase much more than these in winter, but there were not significantly different. Sweat sodium concentration were significantly lower in summer than that in winter. It was found that sweating responses were not influenced by seasonal variation during exercise in dry-heat except the sweat sodium concentration.

Time course of changes in phospholipid in cardiac mitochondria from rats recovering from prolonged swimming.

The time course of the recovery of cardiac mitochondrial phospholipids was investigated in rats subjected to a 3 hour loaded swim. The 3 hour swim caused a 50% reduction in mitochondrial phospholipids compared with the level in sedentary controls. During the first 12 hours of the recovery period, phospholipids tended to increase but fell again before reaching control values by 120 hours after the swim ended. Phospholipid recovery in microsomes was completed in 12 hours. Total mRNA in cardiac tissue decreased by about 15% in rats subjected to a 3 hour loaded swim but recovered to control levels in the first 12 hours of the sedentary recovery period. Thus, fluctuations in cardiac mitochondrial phospholipids do not parallel the changes in total mRNA in cardiac tissue.

Studies on mitochondrial and microsomal phospholipids and phospholipase A2 in heart from rats subjected to prolonged exercise.

Alterations in phospholipids and phospholipase A2 activity produced in cardiac mitochondria and microsomes by prolonged exercise and the effect of quinacrine on these changes have been studied in two types of experiment done on rats subjected to prolonged swimming exercise. In Experiment I, rats swam for 0.5, 1.5 or 3 h carrying a weight representing 3% of body weight. At the end of exercise or after varying recovery periods, the hearts were removed, mitochondria and microsomes were isolated and phospholipid constituents, cholesterol and phospholipase A2 (PLA2) determined. The phosphatidylethanolamine (PE) and phosphatidylcholine (PC) levels in mitochondria were progressively reduced by exercise for 0.5, 1.5, and 3 h as compared with control rats (the rats which trained to swim with loading for 4 days and took rest for 1 night). After recovery periods of 6 and 12 h, levels were partially restored, but after 24 and 48 h they decreased slightly below the control values. By 120-240 h, PE and PC levels recovered to slightly higher values than control. In microsomes, PE and PC levels were also decreased at the end of exercise for 0.5, 1.5, or 3 h, but over recovery periods of 6 to 48 h, they gradually increased and stabilized. In Experiment II designed to study the cause of the exercise-induced decrease in PE and PC, intravenous quinacrine was used to inhibit PLA2. PE and PC in exercised rats injected with saline (ES group) were markedly decreased after prolonged exercise when compared with control rats injected with saline (CS group). In exercise rats injected with quinacrine (EQ group), PC was significantly decreased when compared with the CS group while PE was slightly decreased but was not significantly different. Total activity (TA) and specific activity (SA) of PLA2 in mitochondria did not differ significantly in the three groups. In microsomes, TA in the ES group was significantly increased compared with the CS group while that in EQ group was slightly increased but was not significantly different. SA was unchanged in three groups. These results suggest that quinacrine can partially prevent the decrease of phospholipid and partially inhibit the activity of PLA2 after prolonged exercise. RCR in ES group increased significantly after prolonged exercise while RCR in EQ group tended to increase. ADP/O ratio was not significantly different in all groups.

Suppressive effect of coenzyme Q10 on phospholipase A2 activation in cardiac cells after prolonged swimming.

Phospholipase A2 (PLA2) activity is elevated in cardiac microsomal fractions and phospholipids (PL) are much reduced in both the cardiac mitochondria and microsomal fractions from rats subjected to prolonged swimming. Preadministration of coenzyme Q10 (CoQ10 i.v. 30 mg/kg) significantly suppressed these changes. Two groups of 8-week-old male Wistar rats were trained to swim, receiving 30 min of training for 4 days. On the fifth day they were given an intravenous injection of either 30 mg/kg CoQ10 in saline or 1 ml saline. Thirty minutes later they began to swim for 3 hours carrying a weight representing 3% of body weight. On completion of the swim they were sacrified by instantaneous decapitation, and cardiac mitochondria were isolated. Mitochondria were also prepared from saline injected, unexercised control rats. Phosphatidylethanolamine (PE) and phosphatidylcholine (PC) concentrations were measured with HPLC and PLA2 activity was assayed fluorometrically. The mitochondrial concentrations (means +/- SEM, n = 6) of PE and PC were respectively 126 +/- 22 and 140 +/- 22 nmol/mg protein in the exercise-CoQ10 group against 66 +/- 4 and 50 +/- 10 nmol/mg protein in the exercise-saline group. The specific PLA2 activities (expressed as nmol degraded dipyrene phosphorylethanolamine substrate/hr/mg protein) in the microsomes was 0.20 +/- 0.02 in the exercise-CoQ10 group against 0.30 +/- 0.02 in the exercise-saline group. These results suggest CoQ10 has a protective effect against an excessive reduction in mitochondrial membrane phospholipids during prolonged exercise.

Changes in phospholipid constituents in mitochondrial membranes after long lasting exercise in rat heart.

Phosphatidylethanolamine, phosphatidylcholine and cholesterol were found to be significantly decreased to 44, 56 and 54% of the control values (p less than 0.001, 0.05 and 0.05, respectively), in cardiac mitochondria from rats which were made to swim bearing a weight representing 3% of body weight for 3 or more hours in water at 35 degrees C. The ratio of cholesterol to phospholipid did not change. Membrane viscosity tended to decrease very slightly. Steady-state anisotropy at infinite time, fluorescence life time and wobbling angle of phospholipids showed no significant change. Electron-microscopy showed no clear morphological damage, swelling or hypertrophy of cardiac mitochondria after long lasting exercise. The number of mitochondria was found to be increased by 19% in the long lasting exercise group compared with the control group. It was noteworthy that the dynamic microstructure and electron-microscopic structure of the cardiac mitochondria remained unaltered despite the remarkable changes in the phospholipid constituents.

Dynamic microstructure and hydration of peroxidized membrane of rat cardiac mitochondria and effects of adriamycin.

Nanosecond time-resolved fluorometry of diphenyl hexatriene, DPH, fluorescence was used to study the effects of lipid peroxidation caused by NADH or adriamycin treatment on the dynamic microstructure of mitochondrial membranes from rat myocardium. Isolated mitochondria were incubated with NADH, FeCl3, and ADP, or with adriamycin. Parameters for microdynamics were calculated from the fluorescence intensity and anisotropy decay curves for DPH fluorescence. Peroxidized lipids were measured as malondialdehyde (MDA) resulting from the thiobarbiturate reaction. As peroxidized lipids accumulated, the membrane viscosity increased and the wobbling angle of the phospholipids decreased. The structural changes induced in unsaturated phospholipids by peroxidation probably increased the friction of neighboring phospholipids and restricted the range of their wobbling motion. The fluorescence intensity and fluorescence lifetimes decreased significantly when MDA was higher than 10 nmol/mg protein. These alterations in the behavior of DPH fluorescence strongly suggest that the hydration of the phospholipid layer of the mitochondria is occurring as a consequence of lipid peroxidation, since the fluorophore, DPH, is hydrophobic and its fluorescence is known to be quenched by increasing the dielectric constant of the surrounding media. The present results provide experimental supports to the hypothesis of membrane hydration induced by lipid peroxidation.

Reaction time, impulse speed, overall synaptic delay and number of synapses in tactile reaction neuronal circuits of normal subjects and thinner sniffers.

In control subjects, warned auditory reaction time (RT) for a given effector organ was less than the warned visual RT for the same organ. The RT of the circuits between eye or ear or sites of tactile stimulation (SOS) and the index fingers were significantly shorter than that between eye or ear or the same SOS and the right or left big toes. The greater the distance between the SOS and the brain the longer the RT of the response by a given effector organ. The overall signal speed (OASS) from the neck to the index finger was less than that from the neck to the big toe. The OASS from the neck to a given effector was less than that from the toe to the same effector. Sensory nerve impulse speed was slightly faster than motor nerve impulse speed. The overall synaptic delay and estimated number of synapses (ENOS) of simple tactile reaction neuronal circuits of normal subjects did not significantly vary with site of tactile stimulation or effector organ. The mean number of synapses of various tactile reaction neuronal circuits of normal subjects was estimated to be between 69 and 77, which is far greater than the number of synapses in the touch-tactile and motor pathways combined. The overall synaptic delay in the tactile reaction neuronal circuits between SOS and the left and right big toes were significantly lower in sniffers than in control subjects. This may be due to a decrease in either the average synaptic delay, the number of synapses, or both in the tactile reaction neuronal circuits between sites of stimulation and big toes (but not index fingers) in sniffers.