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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*
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: mlinding@uoguelph.ca
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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+].

Type
Research Papers
Copyright
Copyright © Cambridge University Press 2008

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References

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