To evaluate the present status of physical fittness of Korean long distance runners, body fat, pulmonary functions, maximal oxygen intake and oxygen debt were measured in 5 elite marathoners (A group), 6 college student runners (B group) and 3 middle school student runners (C group). After laboratory tests, full course marathon running was performed in 2 elite marathoners during which their heart rates were monitored continuously. The results are summerized as follows: 1) Total body fat in all three groups are in the range of 13-15% of their body weight. 2) In all three groups, average values of various pulmonary functions were within the normal limits, but those of tidal volume were higher and respiratory rate were lower in comparison to normal values. These phenomena may represent respiratory adaptations against training. The average resting oxygen consumptions in A,B and C were $322{\pm}23$, $278{\pm}14$ and $287{\pm}16$m1/min, respectively. 3) In all three groups, resting blood pressures were in the normal range, but the resting heart rate was slightly lower in groups A $(56{\pm}3\;beats/min)$ and B $(64{\pm}2\;beats/min)$ and higher in group C $(82{\pm}9\;beats/min)$ in comparison to normal values. These changes in cardiovascular functions in marathoners may also represent adaptive phenomena. 4) During treadmill running the minute ventilation and oxygen consumption of the runners increased lineally with work load in all three groups. When the oxygen consumption was related to heart rate, it appeared to be a exponential function of the heart rate in all three groups. 5) The average maximal heart rates during maximal work were $196{\pm}3$, $191{\pm}3$ and $196{\pm}5\;beats/min$ for groups A,B and C, respectively. Maximal oxygen intakes were $84.2{\pm}3.3\;ml/min/kg$ in group A, $65.2{\pm}1.1\;ml/min/kg$ in group B and $58.7{\pm}0.4\;ml/min/kg$ in group C. 6) In all three groups, oxygen debts and the rates of recovery of heart rate after treadmill running were lower than those of long ditsance runners reported previously. 7) The 40 km running time in 2 elite marathoners was recorded to be $2^{\circ}42'25'$, and their mean speed was 243 m/min (ranged 218 to 274 m/min). The heart rate appeared to increase lineally with running speed, and the total energy expenditure during 40 km running was approximately 1360.2 Calories. From these it can be speculated that if their heart rates were maintained at 166 beats/min during the full course of marathon running, their records would be arround $2^{\circ}15'$. Based on these results, we may suspect that a successful long distance running is, in part, dependent on the economical utilization of one's aerobic capacity.

Studies have been conducted using isolated surviving skin of Rana temporalia in an attempt to evaluate the effect of N-ethylmaleimide (NEM) on the epithelial $Na^+$ transport. Active transport of $Na^+$ across the skin was estimated by measuring short circuit current (SCC). NEM administered to the outside surface of the skin in concentration of $0.5{\times}10^{-4}-2.5{\times}10^{-4}M$ induced $20{\sim}40%$ increase during the first 30 mintues, followed by a gradual reduction in SCC. With NEM above $4{\times}10^{-4}M$, SCC was inhibited from the beginning. Qualitatively similar results were obtained when NEM was added to the inside bathing medium. However, the concentration of NEM for a similar effect was much higher with the drug in the inside bathing medium than in the outside bathing medium. The oxygen consumption of the skin was inhibited by NEM of above $10^{-4}M$, the effect being of approximately the same magnitude as that on SCC. The activity of $Na^+-K^+$ ATPase of the skin was not inhibited by NEM below $10^{-3}M$, but it was dramatically reduced with $1.2{\times}M$ NEM. The effects of NEM $(10^{-4}M)$ on the SCC and oxygen consumption could be eliminated by adding cysteine $(10^{-4}-10^{-3}M)$ in the medium, indicating that the SH group is involved in the action of NEM in the frog skin. On the basis of these results, the mode of action of NEM on the $Na^+$ transport across the frog skin was discussed.

The following results were drawn from the experiment conducted to see the effect of ginseng alcohol extract on the mitochondrial oxidation of the rat liver. 1) Mitochondrial oxygen consumption increased in the low concentration and decreased in the high concentration of ginseng alcohol extract. 2) When the mitochondria was destroyed mechanically or was swollen by low concentration of $AgNO_3$, mitochondrial oxygen consumption was inhibited in all concentration of ginseng alcohol extract. 3) Oxygen consumption of intact mitochondria increased in the low concentration but decreased in the high concentration of sodium deoxycholate. 4) Ginseng alcohol extract inhibited cytochrome oxidase activities of liver mitochondria. These results suggest that low concentration of ginseng alcohol extract activates the oxygen consumption of liver mitochondria by increasing the permeability of the mitochondrial membrane and high concentration of the extract inhibit the oxygen consumption by inhibiting the enzyme activity related to respiration.

The present study was undertaken to investigate depressor action of tannic acid and the mechanism underlies it in the rabbit. The changes in arterial blood pressure were studied after intravenous administration of tannic acid in normal rabbits and the animals pretreated with atropine, propranolol, dibenamine, and hexamethonium. The results obtained were as follows; 1) Following administration of 1.5 mg/kg, 3.0 mg/kg, and 5.0 mg/kg of tannic acid into rabbits the maximum depressor responses observed were $12.0{\pm}0.9\;mmHg$, $23.4{\pm}1.0\;mmHg$, and $34.0{\pm}1.8\;mmHg$ respectively and generally depressor responses increased in proportion to dosage of tannic acid. 2) Since there were no changes in depressor responses to tannic acid in animals pretreated. separately with atropine, propranolol, dibenamine, and hexamethonium, the depressor responses appeared to be resulting from direct vasodilator action of tannic acid on the vascular smooth muscle. Comparing tannic acid and acorn extract in their mechanisms of depressor responses, it is strongly indicated that in acorn there might exist another depressor substance. 3) After administration of large doses of tannic acid, in addition to respiratory changes, the mean arterial blood pressure decreased markedly and was never recovered throughout the experiment. comma Therefore it is also suggested that the lethal action of tannic acid resides in a drastic decline of arterial blood pressure and in respiratory changes as well.

The present study was undertaken to investigate effect of water extracts of the mulberry leaves (MWE) on arterial blood pressure and respiration in cats. And also studied were depressor responses to intravenously administered MWE in the animals pretreated separately with atropine(2.5 mg/kg), propranolol(2 mg/kg), dibenamine (15 mg/kg), and hexamethonium (1.5 mg/kg) in order to find out the mechanism of depressor activity of MWE. The results obtained were as follows; 1) Following intravenous administration of 0.25 ml/kg and 0.5 ml/kg of MWE into the cat the maximum depressor responses observed were $60.2{\pm}2.3\;mmHg$ and $72.3{\pm}1.7\;mmHg$ respectively. 2) Since depressor responses to intravenously administered MWE were partially inhibited by hexamethonium and markedly by atropine, it is strongly suggested that depressor activity of MWE mainly results from its vagal effects. 3) After administration of MWE respiratory rate was invariably increased following a short period of apnea.

The activation mechanism of K-induced contracture was studied in renal vascular muscle which does not generate an action potential readily and in taenia coli which generates a spike potential spontaneously. Helical strips of arterial muscle from rabbit renal arteries and longitudinal strips of taenia coli from guinea-pig's colons, respectively, were prepared. All experiments were performed in Tris-buffered Tyrode solution which was aerated with 100% $O_2$ and kept $35^{\circ}C$. Renal arterial muscles developed the contracture rapidly, which was composed of a small phasic and a large tonic components, when exposed to a 40 mM K-Tyrode solution. In the absence of external $Ca^{++}$, however, no K-contracture appeared. The contracture induced by K-depolarization was abolished by the treatment with verapamil, which is known to be a selective $Ca^{++}-blocker$ through potential-sensitive $Ca^{++}-channel$. K-contracture of taenia coli showed the contracture composed of a large phasic and a small tonic components. In the $Ca^{++}-free$ Tyrode solution, only the tonic component was abolished and almost no change in the phasic component was observed. The amplitude of tonic component was dependent on the external $Ca^{++}$; The tonic component increased dose-dependently by a stepwise increase of the external $Ca^{++}$, and this component decreased in parallel with the increase of verapamil in the external medium. The results of this experiment suggest that K-contracture of rabbit renal artery is the direct result of the influx of the external $Ca^{++}$, while that of taenia coli is the result of both $Ca^{++}$ influx and the release of sequestered $Ca^{++}$.