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