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 VO
2
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 PCO
2
(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 CO
2
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 CO
2
from muscle resulted in reduced magnitude and duration of acidosis compared with NG conditions. In fv plasma, increased PCO
2
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
+
].