Intermittent claudication: prevalence and risk factors.

Risk factors for intermittent claudication (IC) were studied in 54 patients--that is, all patients with IC on the lists of two general practices--and 108 controls. Smoking was the factor most strongly associated with the development of IC, but systolic and diastolic blood pressures and concentrations of triglyceride, urate, and fibrinogen were all significantly higher among the patients with IC than the controls. The presence of more than one factor appeared to be associated with a multiplicative increase in risk. Cholesterol, an important risk factor for ischaemic heart disease, was not associated with an increased risk of IC. IC was present in about 2% of the men and 1% of the women, who were aged 45-69 years. These findings suggest that IC, a common and disabling manifestation of atheroslcerosis, may be largely preventable.     

The effect of training and detraining on lactate dehydrogenase isoenzymes in the horse

In the horse, total LDH activity increased with training and the H and M subunit activity parallelled this increase. It is suggested that these increases are in response to a stimulus from the type of training program utilised. The first half of a detraining program decreased the activity of the H and M subunits as might be expected. A sharp rise in the total LDH and the M subunit activity occurred during the latter half of the detraining program. This unexpected increase may be due to relatively more hypoxic conditions prevailing in the muscle during the detraining period.     

The effect of lactate concentration on the handgrip strength during judo bouts

Judo is a combat sport in which the athletes attempt to hold and control their adversary through gripping techniques (kumi-kata) to apply opportune throwing techniques (nage-waza). Twelve male judo athletes, representing national teams, were recruited to investigate the changes in the maximal isometric strength in both hands before (pre) and after (post) 4 judo bouts and its relationship with the maximal blood lactic acid concentration. The subjects performed a maximal isometric contraction with each hand immediately before and after each bout. A blood sample was taken at 1, 3, and 14 minutes after each bout, and the lactic acid concentration was determined. An overall effect of the successive bouts on the maximal isometric handgrip strength of prebouts was observed for both hands (p < 0.05) but not in that of postbouts (p > 0.05). The dominant hand showed an overall decrease in the maximal isometric strength because of the bout, with the decrease being significant for the first, third, and fourth bouts (p < 0.05). The nondominant hand only showed a significant decrease in the first prebout and postbout (p < 0.05). We observed an inverse relationship between the maximal isometric handgrip strength of postbouts and maximum lactic acid concentration (Lacmax), and between the maximal isometric handgrip strength of postbouts and the lactic acid concentration at minute 14 of the recovery period (Lac14) (p < 0.05). These results show that successive judo bouts significantly reduce the maximal isometric strength of both hands and may suggest that fatigue of each hand depends on different factors. An enhanced understanding of the behavior of the isometric handgrip strength, and the factors that affect grip fatigue during judo bouts in the dominant and nondominant hands, can aid coaches in developing optimal training and exercise interventions that are aimed at mitigating decreases in the capacity of judo athletes to perform a grip.     

The effect of mepyramine on the development of morphine tolerance and physical dependence in mice.

Latency relaxation (LR) as well as resting tension and twitch tension of frog toe muscles are studied in an isotonic solution (= 1 T) and in solutions made hypotonic by leaving out the appropriate amounts of NaCl and KCl (0.54 T and 0.76 T). In hypotonic solutions there is an increase in peak twitch tension as well as a decrease in the depth of the LR: the resting tension is increased at sarcomere lengths which are greater than 2.8 μm and is decreased at sarcomere lengths which are less than this value. The behaviour of twitch tension is discussed with respect to the influence of the sarcoplasmic ionic strength on the interaction between the contractile filaments. Concerning the decrease in both the LR and the resting tension, it is assumed that these effects are induced osmotically, the tension of the membranes of the longitudinal sarcoplasmic reticulum being the particular parameter which is influenced.     

The effect of high temperatures on tissue lactate,pyruvate and venous blood properties in the rat

Brain, muscle and liver pyruvate and L(+) lactate were determined in rats (1) control, T_re=37.2°C; (2) thermal stress T_re=40.8°C; (3) terminal thermal stress T_re=43.8°C, and (4) hypoxic death at reduced oxygen tension. A second experiment was conducted to examine venous blood acid-base parameters in heated rats at imminent death. Group 2 failed to show a significant change in brain lactate concentration, but muscle lactate decreased and liver lactate increased significantly (27 and 48%, respectively). Group 3 showed significant increases of 65 and 125% in the lactate content of brain and liver, respectively, but in this instance no significance was attributed to the 12% decrease in muscle lactate. Hypoxia in Group 4 resulted in the greatest increases in tissue lactate in brain, muscle and liver (130, 50 and 171%, respectively). The pyruvate concentrations of brain and liver in Group 2 exhibited no change, but muscle pyruvate decreased significantly (59%). Group 3 brain and muscle pyruvate decreased significantly by 57 and 74%, while liver pyruvate remained unchanged. Hypoxia (4) produced no significant differences in pyruvate levels from those observed in Group 3. The changes in venous blood properties of rats heated until respiratory movement ceased suggested acute and severe metabolic acidosis while animals exhibiting heat induced spasms and loss of coordination showed only slight decreases in blood pH and bicarbonate levels. Brain water content did not change, but muscle was dehydrated and liver tissue water content increased in rats exposed to lethal temperatures. The results indicate that hypoxia probably occurs in rat tissues at high temperatures, but not to a degree that would result in death.

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Zusammenfassung Gehirn, Muskel und Leberpyruvat and 1-Laktat wurden bestimmt in Ratten (1) Kontrollen, T_re=37,2°C; (2) Hitze T_re=40,8°C; (3) tödliche Belastung T_re=43,8°C und (4) Tod durch Hypoxie bei reduziertem PO₂. In einem zweiten Experiment wurde der Säure Basengehalt des venösen Blutes in erhitzten Tieren vor Eintritt des Todes bestimmt. Gruppe 2 zeigte keine signifikante Änderung in der Gehirnlaktatkonzentration, dagegen fiel das Muskellaktat (–27%) und das Leberlaktat stieg significant(+48%). Gruppe 3 zeigte einen signifikanten Anstieg des Gehirn- (+65%) und Leberlaktats (+125%), während das Muskellaktat fiel (–11%). Hypoxie in Gruppe 4 bewirkte den grössten Anstieg des Laktats im Gehirn (+130%), Muskel (+50%) und Leber (+171%). Die Pyruvatkonzentration in Gruppe 2 zeigte nur im Muskel einen Anstieg auf +59%. In Gruppe 3 fielen das Gehirn- (–57%) und Muskelpyruvat (–74%) signifikant, ohne Änderung in der Leber. Ähnliche Resultate ergaben sich bei Hypoxie in Gruppe 4. Vor dem Eintritt des Hitzetodes war im Blut hochgradige Acidose nachweisbar, während Tiere mit Hitzespasmus und Koordinationsstörungen nur gering niedrigere pH- und Bikarbonatwerte aufwiesen. Der Gehirnwassergehalt blieb unverändert, der Muskel war dehydriert und die Leber zeigte einen höheren Wassergehalt bei letal hohen Temperaturen. Die Ergebnisse zeigen, dass Hypoxia bei Hyperthermie auftritt, doch nicht in dem Ausmasse, um zum Tod zu führen.

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Resume On a déterminé les pyruvates et lactates du cerveau, des muscles et du foie de rats présentant 4 particularités différentes: (1) T_re (température rectale) = 37,2°C (contrôle); (2) T_re = 40,8°C (contrainte de chaleur); (3) T_re = 43,8°C (contraite de chaleur limite) et (4) morts par hypoxie par suite de la réduction de la pression partielle de l'oxygène. Dans un second essai, on a déterminé le rapport acides/bases dans le sang veineux de rats sous contrainte de chaleur, juste avant leur trépas. Dans le groupe 2, on n'a pas trouvé de modification significative de la concentration des lactates du cerveau. Par contre, celle des muscles a diminué (–27%) et celle du foie a augmenté (+48%) et cela de façon significative. Dans le groupe 3, on constate une hausse du taux de lactates dans le cerveau (+65%) et dans le foie (+125%), alors que celui des muscles diminue (–11%). L'hypoxie du groupe 4 a provoqué une forte augmentation des lactates aussi bien dans le cerveau (+130%), les muscles (+50%) que le foie (+171%). La concentration des pyruvates ne fut sensiblement modifiée dans le groupe 2 que pour les muscles (+59%). Dans le groupe 3, on en note une diminution significative dans le cerveau (–57%) et dans les muscles (–74%) alors que le taux du foie reste inchangé. On a obtenu des résultats analogues par l'hypoxie dans le groupe 4. On a pu constater une acidose aigue du sang juste avant la mort de chaleur, alors que les animaux atteints de spasmes et de perturbations dans la coordination ne présentaient que peu de variations du pH et du taux de bicarbonate. Dans un état létal par hautes températures, la teneur en eau du cerveau est restée inchangée. Les muscles étaient par contre déshydratés et le foie contenait davantage d'eau. Ces résultats ont montré que, lorsque la température augmente, les animaux souffrent d'hypoxie, mais pas au point d'en mourir.

     

The effect of diabetes and insulin on adipose lactate dehydrogenase isozymes.

Adipose lactate dehydrogenase (LDH) (EC 1.1.1.27) isozyme distribution was altered in streptozotocin-diabetic and fasting rats resulting from a relative reduction of subunit A. Treatment with insulin for 2 days partially restored the relative content of isozyme 5 to control values in the diabetic rats, and the effect of insulin was not inhibited by simultaneous injection of actinomycin D or puromycin. When the epididymal adipose tissues isolated from control animals were incubated in vitro with dibutyryl adenosine 3',5'-cyclic monophosphate or epinephrine, a relative decrease in subunit A was observed; whereas, either compound caused an increase in subunit A in diabetic tissues. The findings suggest that the redistribution of LDH isozyme under these conditions is to prevent excessive accumulation of lactate in the tissue.     

Intermittent versus continuous stimulation: effect of time interval on the development of sensitization or tolerance

Studies from several disciplines support the concept that the temporal characteristics of repeated drug, electrophysiological, or psychological stimuli can affect the direction of cellular and behavioral adaptation. While chronic, continuous stimulation is often associated with the development of tolerance, intermittant stimulation, under some circumstances, may have the opposite effect and be associated with sensitization or reverse tolerance. While many other variables can affect the development of sensitization or tolerance, it is suggested that the interval between electrical, drug, or psychological stimuli is important in determining subsequent responsivity. Temporal characteristics should be carefully considered both in relation to experimental design and theoretical implications; they may shed light on similarities and differences in mechanisms underlying tolerance and sensitization.     

Effects of 2-chloropropionate on venous plasma lactate concentration and anaerobic power during periods of incremental intensive exercise in humans

We investigated the effects of a stimulation of pyruvate dehydrogenase (PDH) activity induced by 2-chloropropionate (2-CP) on venous plasma lactate concentration and peak anaerobic power (W _{an, peak}) during periods (6 s) of incremental intense exercise, i.e. a force-velocity (F-) test known to induce a marked accumulation of lactate in the blood. TheF- test was performed twice by six subjects according to a double-blind randomized crossover protocol: once with placebo and once with 2-CP (43 mg · kg^–1 body mass). Blood samples were taken at ingestion of the drug, at 10, 20, and 40 Min into the pretest period, at the end of each period of intense exercise, at the end of each 5-min recovery period, and after completion of theF- test at 5, 10, 15, and 30 min. During theF- test, venous plasma lactate concentrations with both placebo and 2-CP increased significantly when measured at the end of each period of intense exercise (F = 33.5,P < 0.001), and each 5-min recovery period (F = 24.6,P < 0.001). Venous plasma lactate concentrations were significantly lower with 2-CP at the end of each recovery period (P < 0.01), especially for high braking forces, i.e. 8 kg (P < 0.05), 9 kg (P < 0.02), and maximal braking force (P < 0.05). After completion of theF- test, venous plasma lactate concentrations were also significantly lower with 2-CP (P < 0.001). The percentage of lactate decrease between 5- and 30-min recovery was significantly higher with 2-CP than with the placebo [59 (SEM 4)% vs 44.6 (SEM 5.5)%,P < 0.05]. Furthermore,W _{an, peak} was significantly higher with 2-CP than with the placebo [1016 (SEM 60) W vs 957 (SEM 55) W,P < 0.05]. In conclusion, PDH activation by 2-CP attenuated the increase in venous plasma lactate concentration during theF- test. Ingestion of 2-CP led to an increasedW _{an, peak}.