Model for the behaviour of compartmental CO2 stores during incremental exercise

Abstract

The respiratory exchange ratio (RER) is a valid method for determining fat and carbohydrate oxidation during exercise when the exchange of respiratory gas is in a state of steady flux between the tissue and fluid compartments and the alveoli. However, under incremental intensity or heavy exercise conditions, the movement of electrolytes, fluids, and CO(2) between body-fluid compartments is accentuated, leading to increased hydrogen-ion concentration ([H(+)]), decreased bicarbonate-ion concentration ([HCO(3) (-)]) and CO(2) stores, and the excretion of additional CO(2) at the alveoli (i.e. H(+)+HCO(3) (-) --> CO(2)+H(2)O) elevating the CO(2) minute volume. This non-respiratory CO(2) excretion can invalidate use of the RER for determination of fat and carbohydrate oxidation. Direct measurement of the labile CO(2) store and non-respiratory CO(2) excretion during exercise is difficult. Therefore, physicochemical models were derived to illustrate the likely behaviour of compartmental CO(2) stores during 8 W.min(-1) incremental cycling exercise to formulate correction factors to the RER for the non-respiratory CO(2) component. From these models, a polynomial regression equation was derived to describe the change in the total labile CO(2) store volume during incremental exercise from the relationship with blood HCO(3) (-) content: CO(2) volume (ml) = -17x(2)+464x+650, where x is the arterialised blood standard HCO(3) (-) concentration (mmol.l(-1)), relative to resting conditions. Non-respiratory CO(2) excretion (ml.min(-1)) was then determined from the rate of change in CO(2) volume. The modelling method could allow for straightforward calculation of the non-respiratory CO(2) excretion rate for future validation work.

Effect of breakfast glycemic index on metabolic responses during rest and exercise in overweight and non-overweight adolescent girls

“…Although we did not measure blood lactate, higher postprandial lactate concentrations have been reported following LGI compared with HGI breakfasts (Stevenson et al, 2006). In addition, blood lactate can affect the validity of indirect calorimetry for fat oxidation estimations (Rowlands, 2005). However, it is unlikely that this was a factor in this study because the girls exercised at a moderate intensity (50% VO 2peak ) and additional steps were taken to increase the validity of indirect calorimetry (for example, removing individual VO 2 and VCO 2 values X3 s.d.s from the mean and verifying a steady state in VO 2 and VCO 2 ).…”

Effect of energy expenditure on postprandial triacylglycerol in adolescent boys

“…It was not possible to identify a clear determinant of this inter-individual variation within our study; differences in exercise substrate metabolism and energy expenditure between the individual boys did not appear to be significant contributory factors. A limitation of the indirect calorimetry estimations is that we assumed that the urinary nitrogen excretion rate was negligible and did not account for non-respiratory carbon dioxide excretion that may have resulted in an underestimation of fat oxidation in some individuals (Rowlands 2005). However, a study with adults, where a lipolysis inhibitor (acipimox) was used to reduce exercise lipid metabolism, showed that reductions in postprandial lipaemia were independent of specific substrate metabolism during exercise (Malkova et al 1999)-we are not aware of a similar study with adolescents.…”

Group- and individual-level coincidence of the ‘Fatmax’ and lactate accumulation in adolescents

“…The fat oxidation estimations from respiratory measurements were restricted to low-moderate exercise intensities. However, we assumed that the urinary nitrogen excretion rate was negligible and did not account for an increase in nonrespiratory carbon dioxide excretion that could have led to an underestimation of fat oxidation at some of the higher exercise intensities (Rowlands 2005).…”