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  • American Physiological Society  (4)
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  • American Physiological Society  (4)
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  • 1
    Online Resource
    Online Resource
    American Physiological Society ; 2006
    In:  American Journal of Physiology-Regulatory, Integrative and Comparative Physiology Vol. 291, No. 1 ( 2006-07), p. R235-R237
    In: American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, American Physiological Society, Vol. 291, No. 1 ( 2006-07), p. R235-R237
    Abstract: The development of acidosis during intense exercise has traditionally been explained by the increased production of lactic acid, causing the release of a proton and the formation of the acid salt sodium lactate. On the basis of this explanation, if the rate of lactate production is high enough, the cellular proton buffering capacity can be exceeded, resulting in a decrease in cellular pH. These biochemical events have been termed lactic acidosis. The lactic acidosis of exercise has been a classic explanation of the biochemistry of acidosis for more than 80 years. This belief has led to the interpretation that lactate production causes acidosis and, in turn, that increased lactate production is one of the several causes of muscle fatigue during intense exercise. This review presents clear evidence that there is no biochemical support for lactate production causing acidosis. Lactate production retards, not causes, acidosis. Similarly, there is a wealth of research evidence to show that acidosis is caused by reactions other than lactate production. Every time ATP is broken down to ADP and P i , a proton is released. When the ATP demand of muscle contraction is met by mitochondrial respiration, there is no proton accumulation in the cell, as protons are used by the mitochondria for oxidative phosphorylation and to maintain the proton gradient in the intermembranous space. It is only when the exercise intensity increases beyond steady state that there is a need for greater reliance on ATP regeneration from glycolysis and the phosphagen system. The ATP that is supplied from these nonmitochondrial sources and is eventually used to fuel muscle contraction increases proton release and causes the acidosis of intense exercise. Lactate production increases under these cellular conditions to prevent pyruvate accumulation and supply the NAD + needed for phase 2 of glycolysis. Thus increased lactate production coincides with cellular acidosis and remains a good indirect marker for cell metabolic conditions that induce metabolic acidosis. If muscle did not produce lactate, acidosis and muscle fatigue would occur more quickly and exercise performance would be severely impaired.
    Type of Medium: Online Resource
    ISSN: 0363-6119 , 1522-1490
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2006
    detail.hit.zdb_id: 1477297-8
    SSG: 12
    Library Location Call Number Volume/Issue/Year Availability
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  • 2
    Online Resource
    Online Resource
    American Physiological Society ; 2007
    In:  Journal of Applied Physiology Vol. 102, No. 2 ( 2007-02), p. 582-586
    In: Journal of Applied Physiology, American Physiological Society, Vol. 102, No. 2 ( 2007-02), p. 582-586
    Abstract: Whether structural changes of the erythrocyte membrane increase the susceptibility to hemolysis particularly of the relatively older cell population during the early phase of a 216-km ultrarace was tested in six male runners (age 53.6 ± 10.4 yr, height 175.8 ± 11.1 cm, body mass 75.9 ± 8.4 kg). Erythrocyte membrane spectrins were lowest ( P 〈 0.001) after 42 km (75.59 ± 5.25% of prerace) and increased ( P 〈 0.001) toward 216 km (88.27 ± 3.37%). Susceptibility to osmotic hemolysis was highest ( P 〈 0.01) after 42 km (107.34 ± 3.02 mOsm sodium phosphate buffer) with almost identical ( P 〉 0.05) values prerace (97.98 ± 3.41 mOsm) and postrace (98.61 ± 3.26 mOsm). Haptoglobin indicated intravascular hemolysis of 9.27 × 10 9 cells/l ( P 〈 0.05) during the initial 84 km. Changes in hematocrit and plasma proteins indicated an estimated total net erythrocyte loss of 3.47 × 10 11 cells/l ( P 〈 0.05) after 21 km. This was compensated by a gain in erythrocytes ( P 〈 0.05) of 3.31 × 10 11 cells/l during the final 132 km. A main effect ( P 〈 0.05) on erythropoietin suggests increased erythropoiesis throughout the race. Exercise-induced hemolysis reflects alterations in erythrocyte membrane spectrins and occurs particularly in the early phase of an ultraendurance race because of a relative older cell population.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    RVK:
    RVK:
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2007
    detail.hit.zdb_id: 1404365-8
    SSG: 12
    SSG: 31
    Library Location Call Number Volume/Issue/Year Availability
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  • 3
    Online Resource
    Online Resource
    American Physiological Society ; 2005
    In:  American Journal of Physiology-Regulatory, Integrative and Comparative Physiology Vol. 289, No. 3 ( 2005-09), p. R902-R903
    In: American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, American Physiological Society, Vol. 289, No. 3 ( 2005-09), p. R902-R903
    Type of Medium: Online Resource
    ISSN: 0363-6119 , 1522-1490
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2005
    detail.hit.zdb_id: 1477297-8
    SSG: 12
    Library Location Call Number Volume/Issue/Year Availability
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  • 4
    Online Resource
    Online Resource
    American Physiological Society ; 2005
    In:  Journal of Applied Physiology Vol. 99, No. 2 ( 2005-08), p. 499-504
    In: Journal of Applied Physiology, American Physiological Society, Vol. 99, No. 2 ( 2005-08), p. 499-504
    Abstract: Whether age-related differences in blood lactate concentrations (BLC) reflect specific BLC kinetics was analyzed in 15 prepubescent boys (age 12.0 ± 0.6 yr, height 1.54 ± 0.06 m, body mass 40.0 ± 5.2 kg), 12 adolescents (16.3 ± 0.7 yr, 1.83 ± 0.07 m, 68.2 ± 7.5 kg), and 12 adults (27.2 ± 4.5 yr, 1.83 ± 0.06 m, 81.6 ± 6.9 kg) by use of a biexponential four-parameter kinetics model under Wingate Anaerobic Test conditions. The model predicts the lactate generated in the extravasal compartment (A), invasion ( k 1 ), and evasion ( k 2 ) of lactate into and out of the blood compartment, the BLC maximum (BLC max ), and corresponding time (TBLC max ). BLC max and TBLC max were lower ( P 〈 0.05) in boys (BLC max 10.2 ± 1.3 mmol/l, TBLC max 4.1 ± 0.4 min) than in adolescents (12.7 ± 1.0 mmol/l, 5.5 ± 0.7 min) and adults (13.7 ± 1.4 mmol/l, 5.7 ± 1.1 min). No differences were found in A related to the muscle mass (A MM ) and k 1 between boys (A MM : 22.8 ± 2.7 mmol/l, k 1 : 0.865 ± 0.115 min −1 ), adolescents (22.7 ± 1.3 mmol/l, 0.692 ± 0.221 min −1 ), and adults (24.7 ± 2.8 mmol/l, 0.687 ± 0.287 min −1 ). The k 2 was higher ( P 〈 0.01) in boys (2.87 10 −2 ± 0.75 10 −2 min −1 ) than in adolescents (2.03 × 10 −2 ± 0.89 × 10 −2 min −1 ) and adults (1.99 × 10 −2 ± 0.93 × 10 −2 min −1 ). Age-related differences in the BLC kinetics are unlikely to reflect differences in muscular lactate or lactate invasion but partly faster elimination out of the blood compartment.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    RVK:
    RVK:
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2005
    detail.hit.zdb_id: 1404365-8
    SSG: 12
    SSG: 31
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
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