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Origins of arterial and femoral venous acid–base responses during moderate-intensity bicycling exercise after glycogen depletion in men

Published online by Cambridge University Press:  01 November 2007

Michael I Lindinger ,
George JF Heigenhauser ,
Larry C Lands ,
Robert S McKelvie ,
Eric Hultman ,
Lawrence L Spriet ,
Charles T Putman  and
Norman L Jones
Michael I Lindinger*
Affiliation:
Department of Human Health and Nutritional Sciences, University of Guelph, Guelph, Ontario, CanadaN1G 2W1
George JF Heigenhauser
Affiliation:
Department of Medicine, McMaster University Medical Centre, Hamilton, Ontario, CanadaL8N 3Z5
Larry C Lands
Affiliation:
Department of Respiratory Medicine, McGill University Medical Centre, Montreal Children's Hospital, Montreal, Quebec, Canada
Robert S McKelvie
Affiliation:
Hamilton Health Sciences, McMaster University, Ontario, Canada
Eric Hultman
Affiliation:
Department of Medicine, McMaster University Medical Centre, Hamilton, Ontario, CanadaL8N 3Z5
Lawrence L Spriet
Affiliation:
Department of Human Health and Nutritional Sciences, University of Guelph, Guelph, Ontario, CanadaN1G 2W1
Charles T Putman
Affiliation:
Faculty of Physical Education and Recreation, Exercise Biochemistry Laboratory, and Faculty of Medicine and Dentistry, The Centre for Neuroscience, University of Alberta, Edmonton, Alberta, CanadaT6G 2H9
Norman L Jones
Affiliation:
Department of Medicine, McMaster University Medical Centre, Hamilton, Ontario, CanadaL8N 3Z5
*
*Corresponding author: [email protected]
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Abstract

The interactions between nutrition, energy status and acid–base balance during exercise are poorly understood. Exercise, under conditions of prior glycogen depletion (GD) and low-carbohydrate diet, results in a decreased rate of skeletal muscle glycogenolysis, greatly decreased muscle pyruvate and lactate contents with decreased plasma [lactate] (Putman et al., Am J Physiol, 265: E752, 1993). Therefore, it is hypothesized that exercise in GD, compared with normal (NG) or high-carbohydrate conditions, will result in a reduced magnitude of acidosis due to reduced production and accumulation of lactate. In two trials (GD, then NG) separated by 1–2 weeks, four men cycled at 75% of peak VO2 until the time of exhaustion in GD (57 ± 7 min). At 2 min of exercise, femoral vein (fv) plasma [H+] was increased by 21 ± 4 neq l− 1 (NG) and 14 ± 3 neq l− 1 (GD); increases in arterial [H+] were only c. 45% of those in fv plasma. The increase in fv PCO2 (NG, 25 ± 2 mm Hg and GD, 15 ± 2 mm Hg) was the primary variable responsible for the increased [H+]. During NG, the increase in fv [lactate− ] exceeded the decrease in strong ion difference [SID], with electrolyte charge balance mainly due to increased [Na+]. In the GD trial, arterial [SID] decreased and was the primary contributor to the increased [H+], as passage of blood through the lungs eliminated the CO2 contribution prevalent in fv plasma. Throughout GD, plasma [lactate− ] increased less than in NG and the decrease in [SID] in GD was also significantly less than in NG. In summary, in GD conditions, an attenuated production/release of lactate−  and CO2 from muscle resulted in reduced magnitude and duration of acidosis compared with NG conditions. In fv plasma, increased PCO2 was the primary variable responsible for the rapid and sustained elevation in [H+], whereas in arterial plasma decreased [SID], due to increased [lactate− ], was primarily responsible for increased [H+].

Keywords

plasma H+ concentrationacid–base regulationphysicochemical acid–base approachfemoral venousskeletal muscle
Type
Research Papers
Information
Equine and Comparative Exercise Physiology , Volume 4 , Issue 3-4 , November 2007 , pp. 123 - 133
Copyright
Copyright © Cambridge University Press 2008

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References

1Blomstrand, E. and Saltin, B. (1999). Effect of muscle glycogen on glucose, lactate and amino acid metabolism during exercise and recovery in human subjects. Journal of Physiology 514: 293–302.CrossRefGoogle ScholarPubMed
2Hargreaves, M, Hawley, JA. and Jeukendrup, A. (2004). Pre-exercise carbohydrate and fat ingestion: effects on metabolism and performance. Journal of Sports Science 22: 31–38.CrossRefGoogle ScholarPubMed
3Putman, CT, Spriet, LL, Hultman, E, Lindinger, MI, Lands, LC, McKelvie, RS, Cederblad, G, Jones, NL and Heigenhauser, GJF (1993). Pyruvate hydraogenase activity and acetyl-group accumulation during exercise after different diets. American Journal of Physiology: Endocrinology and Metabolic Physiology 265: E752–E760.Google ScholarPubMed
4Lacombe, V, Hinchcliff, KW, Geor, RJ and Baskin, CE (2001). Muscle glycogen depletion and subsequent replenishment affect anaerobic capacity of horses. Journal of Applied Physiology 91: 1782–1790.CrossRefGoogle ScholarPubMed
5Lindinger, MI (2004). acid–base physiology during exercise and in response to training. In: Hinchcliff, KW, Kaneps, AJ and Geor, RJ (eds) Equine Sports Medicine and Surgery: Basic and Clinical Sciences of the Athletic Horse. New York, NY: Elsevier, pp. 586–611.Google Scholar
6Stewart, PA (1981). How to Understand Acid–base. New York, NY: Elsevier.Google Scholar
7Stewart, PA (1983). Modern quantitative acid–base chemistry. Canadian Journal of Physiology and Pharmacology 61: 1444–1461.CrossRefGoogle ScholarPubMed
8Kowalchuk, JM, Heigenhauser, GJF, Lindinger, MI, Obminski, G, Sutton, JR and Jones, NL (1988). Role of lungs and inactive muscles in acid–base control after maximal exercise. Journal of Applied Physiology 65: 2090–2096.CrossRefGoogle ScholarPubMed
9Lindinger, MI, Heigenhauser, GJF, McKelvie, RS and Jones, NL (1992). Blood ion regulation during repeated maximal exercise and recovery in humans. American Journal Physiology: Regulatory, Integrative and Comparative Physiology 262: R126–R136.Google ScholarPubMed
10Lindinger, MI and Grudzien, SP (2003). Exercise-induced changes in plasma composition increases erythrocyte Na, K ATPase, but not NKCC, activity to stimulate net and unidirectional K+ transport. Journal of Physiology 553: 587–597.CrossRefGoogle Scholar
11McKelvie, RS, Lindinger, MI, Heigenhauser, GJF and Jones, NL (1991). Contribution of erythrocytes to the control of the electrolyte changes of exercise. Canadian Journal of Physiology and Pharmacology 69: 984–993.CrossRefGoogle Scholar
12Lindinger, MI, Heigenhauser, GJF, McKelvie, RS and Jones, NL (1990). Role of nonworking muscle on blood metabolites and electrolytes during and following intense intermittent exercise. American Journal Physiology: Regulatory, Integrative and Comparative Physiology 258: R1486–R1494.Google ScholarPubMed
13Hallen, J and Sejersted, OM (1993). Intravasal use of pliable K+ − selective electrodes in the femoral vein of humans during exercise. Journal of Applied Physiology 75: 2318–2325.CrossRefGoogle ScholarPubMed
14Bergmeyer, HU (1974). Methods in Enzymatic Analysis. New York, NY: Academic Press.Google Scholar
15Gillen, CM, Lee, R, Mack, GW, Tomaselli, CM, Nishiyasu, T and Nadel, ER (1991). Plasma volume expansion in humans after a single intense exercise protocol. Journal of Applied Physiology 71: 1914–1920.CrossRefGoogle ScholarPubMed
16Kowalchuk, JM and Scheuermann, BW (1994). Acid–base regulation: a comparison of quantitative methods. Canadian Journal of Physiology and Pharmacology 72: 818–826.CrossRefGoogle ScholarPubMed
17Wooten, EW (1999). Analytic calculation of physiological acid–base parameters in plasma. Journal of Applied Physiology 86: 326–334.CrossRefGoogle ScholarPubMed
18Miller, BF, Lindinger, MI, Fattor, JA, Jacobs, KA, LeBlanc, PJ, Duong, M-L, Heigenhauser, GJF and Brooks, GA (2005). Hematological and acid–base changes in men during prolonged exercise with and without sodium-lactate infusion. Journal of Applied Physiology 98: 856–865.CrossRefGoogle ScholarPubMed
19Putman, CT, Jones, NL and Heigenhauser, GJF (2003). Effects of short-term training on plasma acid–base balance during incremental exercise in man. Journal of Physiology 550: 585–603.CrossRefGoogle ScholarPubMed
20Spriet, LL, Soderlund, K, Bergstrom, M, Hultman, E et al. . (1987). Skeletal muscle glycogenolysis, glycolysis, and pH during electrical stimulation in men. Journal of Applied Physiology 62: 616–621.CrossRefGoogle ScholarPubMed
21Lindinger, MI (2003). Exercise: a paradigm for multi-system control of acid–base state. Journal of Physiology 550: 334.CrossRefGoogle ScholarPubMed
22Lindinger, MI, Spriet, LL, Hultman, E, Putman, CT, McKelvie, RS, Lands, LC, Jones, NL and Heigenhauser, GJF (1994). Plasma volume and ion regulation during exercise after low- and high-carbohydrate diets. American Journal Physiology: Regulatory, Integrative and Comparative Physiology 266: R1896–R1906.Google ScholarPubMed
23Clausen, T (2003). Na+–K+ pump regulation and skeletal muscle contractility. Physiological Reviews 83: 1269–1324.CrossRefGoogle ScholarPubMed
24Westen, EA and Prange, HD (2003). A reexamination of the mechanisms underlying the arteriovenous chloride shift. Physiological Biochemical Zoology 76: 603–614.CrossRefGoogle ScholarPubMed
25Hamasaki, N and Okubo, K (1996). Band 3 protein: physiology, function and structure. Cellular and Molecular Biology 42: 1025–1039.Google ScholarPubMed