Energetics of karate kumite

It is speculated that anaerobic metabolism is the predominant source of energy in karate kumite. However, no experimental proof is currently available. The metabolic cost and fractions of aerobic and anaerobic energy of karate kumite fighting were investigated. Ten male nationally or internationally ranked karateka [means (SD) age 26.9 (3.8) years, height 1.80 (0.08) m, mass 77.2 (12.8) kg] performed two to four fights scheduled and judged like a championship. Oxygen uptake was measured continuously with a portable spirometric device. Blood lactate was determined immediately before, and minute by minute after, each fight. Aerobic, anaerobic alactic and anaerobic lactic energy were calculated from oxygen uptake during the fight (VO₂), the fast component of the post-fight oxygen uptake (VO_2PCr) above resting values and changes in blood lactate concentration (Net-BLC), respectively. Altogether, 36 fights lasting 267 (61) s were analysed. The referees decisions caused an activity-to-break ratio of approximately 2:1. VO₂, VO_2PCr, and Net-BLC per fight were 165.3 (52.4) ml^.kg^–1, 32.2 (7.2) ml^.kg^–1and 4.2 (1.9) mmol^.l^–1; the overall energy cost above rest was 334.3 (86.3) kJ per fight. Fractions of aerobic, anaerobic alactic, and lactic energy sources were 77.8 (5.8)%, 16.0 (4.6)%, and 6.2 (2.4)%, respectively. The results indicate a high metabolic rate in karate kumite. However, the acyclic activity profile implies that aerobic metabolism is the predominant source of energy and there is anaerobic supplementation, mainly by high-energy phosphates.     

金属硫蛋白对培养神经细胞迟发性损伤的作用和一氧化氮的表达

本文以新生大鼠原代培养皮质神经元为实验材料，造成迟发性神经元损伤模型．在不同时程内，测试培养液中的细胞乳酸脱氢酶漏出量和用还原型尼克酰胺腺嘌呤二核着苷酸脱氢酶染色反应，观察培养细胞中一氧化氮合酶的表达水平．结果表明，缺血组在缺血与再灌流中，细胞乳酸脱氢酶漏出量明显高于对照组，差异显著（Ｐ＜０．００１）．一氧化氮合酶阳性神经元数量在缺血组的缺血时即明显高于对照组（Ｐ＜０．０１），再灌流后一氧化氮合酶表达仍然强烈，与对照组相比有显著差异（Ｐ＜０．０１）．当损伤细胞再灌流时，同时加入金属硫蛋白后，显示一氧化氮合酶表达减弱，和缺血组相比有显著差异（Ｐ＜０．０５～０．００１），细胞乳酸脱氢酶漏出量在再灌流后的早期近似于对照组．结合文献和本实验结果提示：在迟发性神经元损伤形成过程中一氧化氮起着重要作用；金属硫蛋白对脑缺血后迟发性神经元损伤有一定保护作用，是一种细胞保护剂，可望用于临床，控制缺血再灌流损伤。     

Negative accumulated oxygen deficit during heavy and very heavy intensity cycle ergometry in humans

The concept of the accumulated O₂ deficit (AOD) assumes that the O₂ deficit increases monotonically with increasing work rate (WR), to plateau at the maximum AOD, and is based on linear extrapolation of the relationship between measured steady-state oxygen uptake (O₂) and WR for moderate exercise. However, for high WRs, the measured O₂ increases above that expected from such linear extrapolation, reflecting the superimposition of a "slow component" on the fundamental O₂ mono-exponential kinetics. We were therefore interested in determining the effect of the O₂ slow component on the computed AOD. Ten subjects [31 (12) years] performed square-wave cycle ergometry of moderate (40%, 60%, 80% and 90% ), heavy (40%), very heavy (80%) and severe (110% O_{2 peak}) intensities for 10–15 min, where is the estimated lactate threshold and is the WR difference between and O_{2 peak}. O₂ was determined breath-by-breath. Projected "steady-state" O₂ values were determined from sub- tests. The measured O₂ exceeded the projected value after ~3 min for both heavy and very heavy intensity exercise. This led to the AOD actually becoming negative. Thus, for heavy exercise, while the AOD was positive [0.63 (0.41) l] at 5 min, it was negative by 10 min [–0.61 (1.05) l], and more so by 15 min [–1.70 (1.64) l]. For the very heavy WRs, the AOD was [0.42 (0.67) l] by 5 min and reached –2.68 (2.09) l at exhaustion. For severe exercise, however, the AOD at exhaustion was positive in each case: +1.69 (0.39) l. We therefore conclude that the assumptions underlying the computation of the AOD are invalid for heavy and very heavy cycle ergometry (at least). Physiological inferences, such as the "anaerobic work capacity", are therefore prone to misinterpretation.     

Growth resistance-sized arteries in response to bladder hypertrophy in the rat: time-course,DNA-synthesis and LDH-isoform pattern

Bladder growth was induced by partial urethral obstruction. Bladder hypertrophy was evident at 53 h after obstruction and continued over a 6 weeks period. Small bladder arteries were taken from fixed anatomical locations of the bladder circulation, mounted in a small vessel myograph and the optimal diameter for maximal isometric force development was determined (L_max, K⁺=125 mm stimulation). Bladder hypertrophy was associated with an enlarged L_max from 53 h onward (compared with sham-operated controls) and L_max continued to increase until 10 days after urethral obstruction. Between 10 days and 6 weeks no further increase of the diameter was observed. Increased diameters in vitro were accompanied by a transiently increased [³H]Thymidine uptake in the small arteries which peaked at 53 h after obstruction but was still above background at 10 days. At this time point, small arterial growth was associated with a significant relative increase in the M isoform of LDH as determined with agarose electrophoresis on tissue homogenates. Thus organ growth induced small vessel growth in the rat is characterized by a rapid onset, increased but transient DNA-turnover and LDH-isoform changes. The latter mimic changes seen in other types of smooth muscle growth.     

Changes in glutamate-related enzyme activities in the striatum of the rat following lesion of corticostriatal fibres

Summary The behaviour of enzymes putatively involved in glutamate/aspartate transmitter metabolism (glutamate dehydrogenase, aspartate aminotransferase, alanine aminotransferase,-glutamyltranspeptidase) was studied in the striatum 3, 7, 14 days and 7 weeks after mechanical destruction of corticostriatal fibres. For a period of up to seven days after unilateral lesion, enzyme activities were significantly diminished (by up to 13% based on protein) in the ipsilateral striatum as compared to the striatum of the intact side. Later, the enzyme activities in the ipsilateral striatum recovered. After seven weeks, an increase was observed for glutamate dehydrogenase activity, whereas the activity of alanine aminotransferase showed a transient rise at the end of the second week. The decrease in enzyme levels is interpreted as being attributable to the destruction of nerve endings which are considered to be glutamatergic, interfering with various compensating processes (e.g. glial cell proliferation) which occur with advancing times after lesion.     

Calretinin- and parvalbumin-immunoreactive neurons in the rat main olfactory bulb do not express NADPH-diaphorase activity

The presence of nitric oxide synthase (NOS) in neuronal elements expressing the calcium-binding proteins calretinin (CR) and parvalbumin (PV) was studied in the rat main olfactory bulb. CR and PV were detected by using immunocytochemistry and the nitric oxide (NO) -synthesizing cells were identified by means of the reduced nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-diaphorase) direct histochemical method. The possible coexistence of NADPH-diaphorase and each calcium-binding protein marker was determined by sequential histochemical-immunohistochemical double-labeling of the same sections. Specific neuronal populations were positive for these three markers. A subpopulation of olfactory fibers and olfactory glomeruli were positive for either NADPH-diaphorase or CR. In the most superficial layers, groups of juxtaglomerular cells, superficial short-axon cells and Van Gehuchten cells demonstrated staining for all three markers. In the deep regions, abundant granule cells were NADPH-diaphorase- and CR-positive and a few were PV-immunoreactive. Scarce deep short-axon cells demonstrated either CR-, PV-, or NADPH-diaphorase staining. Among all these labeled elements, no neuron expressing CR or PV colocalized NADPH-diaphorase staining. The present data contribute to a more detailed classification of the chemically- and morphologically-defined neuronal types in the rodent olfactory bulb. The neurochemical differences support the existence of physiologically distinct groups within morphologically homogeneous populations. Each of these groups would be involved in different modulatory mechanisms of the olfactory information. In addition, the absence of CR and PV in neuronal groups displaying NADPH-diaphorase, which moreover are calmodulin-negative, indicate that the regulation of NOS activity in calmodulin-negative neurons of the rat olfactory bulb is not mediated by CR or PV.     

Alteration of regulatory enzyme activities in fast-twitch and slow-twitch muscles and muscle fibres in low-intensity endurance-trained rats

The effect of progressive, low-intensity endurance training on regulatory enzyme activities in slow-twitch (ST) and fast-twitch (FT) muscle fibres was studied in 32 rats. Of those rats 16 were trained on a treadmill at a running speed of 10m · min^–1 5 days a week over an 8-week period. Running time was progressively increased from 15 min to 2 h · day^–1. Of the rats 4 trained and 4 sedentary rats were also subjected to acute exhausting exercise. Enzyme activities of phosphofructokinase 1 (PFKI) from glycolysis, -ketoglutarate dehydrogenase (-KGDH) from the Krebs cycle and carnitine palmitoyltransferase (CPT I and II) from fatty acid metabolism in soleus, tibialis anterior and gastrocnemius muscles were measured in trained and sedentary rats. Enzyme activities of individual ST and FT fibres were measured from the freeze-dried gastrocnemius muscle of 8 trained and 8 sedentary rats. In the sedentary rats the activity of PFK1 in tibialis anterior and soleus muscles was 141% and 41% of the activity in gastrocnemius muscle, respectively. The activity of -KGDH in tibialis anterior and soleus muscles was 164% and 278% of the activity in gastrocnemius muscle, respectively. The activity of CPT I in tibialis anterior and gastrocnemius muscles were at the same level, but in soleus muscle the activity was 127% of that in mixed muscle. Endurance training increased enzyme activities of -KGDH and CPT I significantly (P < 0.05) in gastrocnemius muscle but not in soleus or tibialis anterior muscle. After training both -KGDH and CPT II activities were elevated significantly (P < 0.05) in the ST fibres of gastrocnemius muscle, whereas in FT fibres only -KGDH was increased. For PFK1 activity no significant change was observed in ST or FT fibres. After acute exercise, activities of mitochondrial enzymes -KGDH and CPT I tended to be elevated in all muscles. Thus, low-intensity endurance training induced significant peripheral changes in regulatory enzyme activities in oxidative and fatty acid metabolism in individual ST or FT muscle fibres.     

Irreversible shock of rats after acute renal vein thrombosis

Summary After occlusion of the renal veins rats die quickly in progressive shock (within 4.5 h), but after ligating the renal hilum of both Kidneys they survive 27 h. To learn why renal vein occlusion is so rapidly lethal, and what substances are given off and by what method from the hemorrhagically infarcted kidneys, we studied eight groups of rats, each containing at least seven animals. The groups differed in the combination of hilar structures (renal veins, ureters, lymphatics) ligated. We compared: survival times, changes in blood pressure, blood volume, levels of plasma kinins, adenosine, and lactate, changes of blood pH, responses to Indomethacin, Trasylol^®, and plasma expanders, tubular and capillary flow rates, histopathological changes in organs and cerebral blood flow and changes in the blood coagulation system. Our results suggest that the venous stasis, anoxia, and hemorrhagic necrosis caused by bilateral venous occlusion release into renal lymphatics toxic substances which reach the systemic circulation and induce irreversible shock. We have excluded prostaglandins and adenosine as the toxic substances inducing shock but could not rule out an action of the kallikrein-kinin-system. We postulate that the striking degenerative changes occurring in the arterioles of the brain after bilateral venous occlusion may mean these vessels are especially susceptible to high levels of lactic acid and that this may explain why these animals die so quickly. Our conclusions should help not only in understanding why high levels of lactate in shock portend a poor prognosis but also help in formulating appropriate therapy for circulatory failure of renal origin and for protracted hypotension after extensive tissue injury.The studies were supported by the German Research Foundation within the SFB 90 Cardiovasculäres SystemPresented in part: Jäckh and Steinhausen, 1976; Dallenbach et al., 1978; Zimmerhackl et al., 1979We dedicate this paper to Wilhelm Doerr, Dr. med., Professor of Pathology, University of Heidelberg on the occasion of his 65th birthday (August 25th, 1979)     

Lactate kinetics during passive and partially active recovery in endurance and sprint athletes

We investigated the effects of passive and partially active recovery on lactate removal after exhausting cycle ergometer exercise in endurance and sprint athletes. A group of 14 men, 7 endurance-trained (ET) and 7 sprint-trained (ST), performed two maximal incremental exercise tests followed by either passive recovery (20 min seated on cycle ergometer followed by 40 min more of seated rest) or partially active recovery [20 min of pedalling at 40% maximal oxygen uptake ( O_2max) followed by 40 min of seated rest]. Venous blood samples were drawn at 5 min and 1 min prior to exercise, at the end of exercise, and during recovery at 1, 2, 3, 4, 5, 6, 8, 10, 15, 20, 30, 40, 50, 60 min post-exercise. The time course of changes in lactate concentration during the recovery phases were fitted by a bi-exponential time function to assess the velocity constant of the slowly decreasing component (₂) expressing the rate of blood lactate removal. The results showed that at the end of maximal exercise and during the 1st min of recovery, ET showed higher blood lactate concentrations than ST. Furthermore, ET reached significantly higher maximal exercise intensities [5.1 (SEM 0.5) W · kg^–1 vs 4.0 (SEM 0.3) W · kg^–1,P < 0.05] and O_2max [68.4 (SEM 1.1) ml · kg^–1 · min^–1 vs 55.5 (SEM 5.1) ml · kg^–1 · min^–1,P < 0.01]. There was no significant difference between the two groups during passive recovery for ₂ During partially active recovery, ₂ was higher than during passive recovery for both groups (P < 0.001), but ET recovered faster and sooner than ST (P < 0.05). Compared to passive recovery, the ₂ measured during partially active recovery was increased threefold in ET and only 1.5-fold in ST. We concluded that partially active recovery potentiates the enhanced ability to remove blood lactate induced by endurance training.     

Caffeine increases maximal anaerobic power and blood lactate concentration

Summary The aim of this study was to specify the effects of caffeine on maximal anaerobic power (W _max). A group of 14 subjects ingested caffeine (250 mg) or placebo in random double-blind order. TheW _max was determined using a force-velocity exercise test. In addition, we measured blood lactate concentration for each load at the end of pedalling and after 5 min of recovery. We observed that caffeine increasedW _max [964 (SEM 65.77) W with caffeine vs 903.7 (SEM 52.62) W with placebo;P<0.02] and blood lactate concentration both at the end of pedalling [8.36 (SEM 0.95) mmol · l^–1 with caffeine vs 7.17 (SEM 0.53) mmol · l^–1 with placebo;P<0.011 and after 5 min of recovery [10.23 (SEM 0.97) mmol · l^–1 with caffeine vs 8.35 (SEM 0.66) mmol · l^–1 with placebo;P<0.04]. The quotient lactate concentration/power (mmol · l^–1 · W^–1) also increased with caffeine at the end of pedalling [7.6 · 10^–3 (SEM 3.82 · 10^–5) vs 6.85 · 10^–3 (SEM 3.01 · 10^–5);P<0.01] and after 5 min of recovery [9.82·10^–3 (SEM 4.28 · 10^–5) vs 8.84 · 10^–3 (SEM 3.58 · 10^–5);P<0.02]. We concluded that caffeine increased bothW _max and blood lactate concentration.