Lactic acid, 'oxygen debt,' and strenuous exercise

1981 ◽  
Vol 141 (11) ◽  
pp. 1407
Author(s):  
Phil Gunby
1964 ◽  
Vol 19 (4) ◽  
pp. 623-628 ◽  
Author(s):  
R. Margaria ◽  
P. Cerretelli ◽  
F. Mangili

The speed of lactic acid formation in blood has been measured in man as a function of the intensity of exercise and was found to reach a maximum of about 36 mg lactic acid/liter blood per sec, corresponding to about 21.5 kcal (kg hr) or 0.034 hp/kg. The maximal energy release sustained by the alactacid mechanism is of the order of 45 kcal/(kg hr), or 0.07 hp/kg. The alactacid debt, as measured in man running on a treadmill, seems to be approximately proportional to the energy expenditure: it amounts at most to 0.1 kcal/kg or about 1.4 liters O2 for a man weighing 70 kg. The lactacid debt amounts at most to 0.22 kcal/kg or about 3 liters O2 for man, on the average. The alactacid oxygen debt contraction is a faster process and it requires 10–30 sec for completion, while the lactacid debt process is completed in about 40 sec in the most strenous exercise. Therefore, at the highest workloads, the only energy source available after 40 sec resides in oxidative processes. oxygen debt; lactic acid Submitted on July 5, 1963


1997 ◽  
Vol 273 (1) ◽  
pp. E92-E98 ◽  
Author(s):  
X. Wang ◽  
R. R. Fiscus

Previous data from our laboratory have shown that calcitonin gene-related peptide (CGRP) is released into the circulation during pathogenesis of endotoxic, hemorrhagic, and septic shock and appears to mediate in part the vascular problems of shock. Elevations in the levels of bradykinin (BK) and lactic acid and lowering of tissue pH also occur during shock and could be involved in CGRP release. In the present study, we have tested whether lactic acid, alone or in combination with BK or low pH, triggers release of CGRP-like immunoreactivity (CGRP-LI) from sensory nerves, using rat spinal cord slices as a tissue model. Lowering media pH from 7.4 to < or = 6.0 increased the release of CGRP-LI. Lactic acid (5 and 10 mM) by itself elevated CGRP-LI release from a control of 6.89 +/- 0.95 to 57.2 +/- 8.2 and 116 +/- 13 pg/mg protein, respectively. The combination of pH 6.0 and lactic acid (5 or 10 mM) caused more than additive stimulation of CGRP-LI release. BK (50 or 100 microM) elevated CGRP-LI release, which was greatly enhanced by lactic acid (2.5 or 5 mM). The data indicate that lactic acid potentiates BK- and low-pH-induced release of CGRP from sensory nerves in spinal cord. Similar mechanisms may occur at peripheral ends of sensory nerves, contributing to CGRP release during septic shock and other conditions with elevated lactic acid levels (e.g., strenuous exercise and tissue ischemia).


1981 ◽  
Vol 60 (5) ◽  
pp. 537-542 ◽  
Author(s):  
R. A. Iles ◽  
R. D. Cohen ◽  
P. G. Baron

1. Perfused rat livers were subjected to an acid perfusate and varying degrees of ischaemia in an attempt to simulate the conditions of strenuous exercise or shock. 2. Lactate uptake and glucose output from the liver decreased during moderate ischaemia alone and more so when, in addition, the perfusate was made acidic. 3. Hepatic ATP and ADP content increased in the presence of an acid perfusate. 4. It is concluded that both ischaemia and acidosis may contribute to the diminished hepatic uptake of lactic acid in strenuous exercise and shock.


1961 ◽  
Vol 39 (6) ◽  
pp. 767-776 ◽  
Author(s):  
P. W. Hochachka

Rainbow trout, Salmo gairdneri, conditioned to fast-flowing water, differ from untrained fish in several ways. The trained fish are able to acquire an oxygen debt three times as large as the untrained ones. Almost twice as much of the available glycogen in muscle can be used up during short bursts of swimming. The trained fish have higher levels of blood haemoglobin and relatively larger hearts. Following fatigue, the recovery of glycogen in muscle and liver is more rapid. The data suggest a modus operandi for short but severe bursts of swimming. The two critical factors are: (a) initial energy supplies and (b) tissue buffers. The former preclude the exhaustion of the muscle; the buffers allow a large utilization of the fuel, i.e., a large excess of lactic acid and, consequently, a large oxygen debt. Since even in trained trout only 70% of the muscle glycogen is used, fixed acid probably limits the stamina in both groups of fish.


2004 ◽  
Vol 54 (2) ◽  
pp. 119-130 ◽  
Author(s):  
Tinka Murk ◽  
Paul Balm ◽  
Ron Boot ◽  
Guido van den Thillart ◽  
Vincent van Ginneken

AbstractIn a Blazka swim tunnel swim trials with individual carp (Cyprinus carpio , N = 6, approximately 176 g) and rainbow trout (Oncorhynchus mykiss , N = 6 approximately 123 g) were performed until exhaustion at six body lengths per second (BL/s). Control carp (N = 6) and control trout (N = 6) were sampled after a moderate swim exercise at 1.5 BL/s. Significant differences were demonstrated in the exhausted carp group in comparison with the control group for plasma sodium (108.8%), lactic acid in red muscle (RM) (375.5%), lactic acid in white muscle (WM) (484.5%), triglycerids (133.9%), total protein (126.7%) and phospholipids (116.8%). In trout only, potassium was significantly elevated in the exhausted group (129.2%). T3- and T4-plasma values, as well as the T3/T4 ratio, were unaffected by the exercise protocol in both fish species. Despite the high lactic acid values in muscle tissue (RM: range 5-7 mM, WM: range 4-9 mM) in the exhausted groups of both fish species, the lactate in blood plasma in both fish species was not elevated (range 1.5-1.6 mM). This indicates that lactate is not released from the muscle compartment towards the blood and led to the concept of a 'non-release' lactic acid mechanism in cyprinid and a salmonid fish species after strenuous exercise.


2009 ◽  
Vol 41 ◽  
pp. 493
Author(s):  
Victoria Wiltshire ◽  
Veronica Poitras ◽  
Melissa Pak ◽  
Terence Hong ◽  
Jay Rayner ◽  
...  

1968 ◽  
Vol 25 (5) ◽  
pp. 837-851 ◽  
Author(s):  
F. W. H. Beamish

In Atlantic cod, muscle glycogen was reduced by about 50% at moderate swimming speeds and over 80% at higher speeds. Muscle glycogen for a given swimming speed was generally lower after 30 min exercise than after 15 min exercise. During the 8-hr period after strenuous exercise, muscle glycogen increased but remained well below the level for unexercised fish.At moderate swimming speeds, fish exhibited comparatively small amounts of muscle and blood lactic acid. At higher swimming speeds, fish accumulated significantly larger quantities of lactic acid in the muscle and blood. During the recovery period after strenuous exercise, muscle and blood lactic acid increased precipitously. Muscle lactic acid remained high for 1 hr after exercise and then decreased in 8 hr to levels similar to those of unexercised cod. Blood lactic acid followed a similar pattern except that it continued to increase for 1.5 hr after exercise.Serial samples of blood taken before and after 30 min strenuous exercise showed marked differences in lactic acid among individuals. Blood lactic acid usually continued to increase for 30–60 min after exercise, and decreased to the level for unexercised fish about 24 hr after exercise.No mortalities attributable to muscular fatigue occurred among cod.


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