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The respiratory compensation point (RCP) marks the onset of hyperventilation during incremental exercise. Its physiological meaning has not yet been definitely determined, but the most common explanation is a failure of the body’s buffering mechanisms which leads to metabolic (lactic) acidosis and an increase in dissolved CO2 causing an increase in VCO2 (Meyer, 2004). There has been extensive research to show that acidosis is part of the mechanism. In trained, young runners, it was seen that the degree of desaturation was inversely related to the degree of acidosis (Gledhill, 1980).

Gledhill concluded that with a reduced metabolic acidosis there is less of a compensatory hyperventilation which leads to a decrease in PAO2. This is consistent to other findings where another study showed that endurance training induces a reduced ventilatory response to submaximal exercise for a given workload. Concluding that due to the lactate threshold becoming present at a higher given work load in endurance trained individuals the ventilatory response is lower at a given work rate than in untrained individuals relaying the notion that acidosis is a trigger towards hyperventilation. It can be seen in some highly trained endurance athletes that because there lactate threshold is at such a high work rate when compared to non-trained individuals that a reduced ventilatory response can actually lead to an increase in PaCO2 during exercise.

This response was also observed in another study where higher levels of arterial partial pressure of CO2 (PaCO2) were reported in young and older highly trained athletes than in untrained individuals for the same maximal workload or a relative or absolute submaximal workload (Caillaud, 1993). This backing up the previous statement that endurance training can reduce the ventilatory response due to a decrease in lactacidaemia. Another adaptation to endurance training is a decrease in carbohydrate oxidation at moderate intensities (Brooks, 1994). The decreased reliance on carbohydrate oxidation has been linked more closely to a reduced ventilation rate than to the attenuated increase in blood lactate concentrations, leaving room for much debate over the mechanisms of the triggers causing exercise induced hyperventilation (MacRae, 1998)

Meyer et al tries to elucidate the physiological basis of RCP by directly, that is, intravenously, manipulating blood pH in human beings. Their findings showed that all subjects’ responses to the bicarbonate intervention was uniform. This gave rise to the fact that a decline in blood pH due to insufficient buffering of exercise induced lactic acidosis does indeed represent an important stimulus for hyperventilation during intense exercise. However, only a delayed hyperventilatory response was observed and not that one of complete absence even when blood pH remained constant.

This implies that additional factors must be involved in the stimulation of ventilation during high intensity exercise (Meyer, 2004). Other factors that could possibly be the cause of increased ventilation are local muscle mechanoreceptors or metaboreceptors (Smith, 1999), serum potassium, pain perception (Meyer, 2004) or other neuronal impulses (McCloskey, 1972). However, acidosis due to failure of lactate buffering seems to be a major determinant for exercise hyperventilation.

Effects of Different Exercise Modalities Many studies as we have seen before have studied the effects of an incremental exercise test on ventilatory responses. Though most have only looked at the effects when cycling or running. Only a few studies have actually examined the effect of using certain percentages of muscle mass on these ventilatory responses to exercise. One area of research was in haemoglobin saturation during incremental arm and leg exercise. In the research of this study PETCO2 and O2 were examined at different work rates for both arm and leg exercise. Powers et al found no significant differences between PETCO2 and O2 in either leg or arm exercises at any work rate when compared as a function of percent VO2 max (Powers, 1984).

However these findings are questionable due to other studies that have evidenced a significant difference between lactate levels between arm cranking and leg cycling (Jensen, 1993). Despite the smaller exercising muscle mass the release of lactate during exercise has been found to be nearly two fold higher during arm cranking than in leg cycling (Jensen, 1993). It was concluded by Jensen that the high arm vs. leg lactate release appeared to be associated with differences in the regional circulatory adaptation by the exercising limb.

However, these findings were all obtained by carrying out continuous arm and leg exercises which only increased by three intensities corresponding to 30%, 50%, and 80% of peak VO2. A more recent study investigated the physiological responses of arm and leg exercise during an incremental exercise test. They found that when the two modes of exercise were compared, total lactate accumulation was significantly lower for arm cranking than for leg cycling (Schneider, 2000).

Even though these two papers differ, their findings both seem to go against the findings from Powers, where no difference was seen in PETCO2 and O2 pressures during arm or leg cycling. However, if one of the modes of exercise produced more lactate, no matter which one, then surely a difference should have been seen in levels of PETCO2 due to the buffering of lactate from bicarbonate and with more lactate present more CO2 would be produced. In spite of this though a third study produced different findings to that of the two previously mentioned. In this study, the physiological responses to arm cranking and leg cycling were all similar at the same relative intensity.

This included blood lactate concentrations. The investigators concluded that substrate utilization (lactate response) is regulated by relative exercise intensity and not the exercising muscle mass (Hooker, 1990). This investigation fits in well with the findings from Powers. PETCO2, which found that no difference was exhibited between arm and leg exercise. This could be because exercise intensity and not the exercising muscle mass, as mentioned by Hooker, regulate lactate.

Even though there seems to be conflicting evidence the two studies by Hooker and Power are the only ones that do not conflict each other and at this moment seem to be the only binding evidence towards the actual accumulation of lactate between exercise modes. This evidence points towards the notion that lactate accumulation is reliant upon relative intensities and not just down to the exercising muscle mass. However, we should not dismiss other findings that show different exercising muscle masses accumulating more or less lactate than another. This just shows that there is more to be researched in this area and none of these findings should be taken as definite as there is a large amount of conflicting evidence.


In conclusion it has been seen that PETCO2 and PETO2 can vary significantly between people that exhibit different cardiovascular or respiratory diseases. During exercise testing when substituting PETCO2 and PETO2 for PaCO2 and PaO2 it is important to make sure that unless you are testing for responses to obesity or any other disease then testing healthy ‘normal’ subjects is required or you will get a lot of variability in the data.

This has never been more important than today with the ever increase in obesity and obesity related diseases. It can also be concluded that excess CO2 is produced as a product of the buffering process, during light to moderate intensity exercise, where bicarbonate buffers lactate ions (H+) as seen by a slight increase in PETCO2 also known as the ‘isocapnic buffering phase’. The start of is also to be said to coincide with the lactate threshold.

Excess CO2 triggers a response to increase the respiratory rate (respiratory compensation phase) and thus increases the VCO2. Metabolic acidosis is said to be the main trigger to this response but other variables also play a role in increasing the respiratory rate. During this phase PETCO2 falls due to a higher VCO2. No significant differences are seen between PETCO2 levels when exercising different muscle masses.

Concluding that PETCO2 may be governed by the relative intensities of arm cranking and leg cycling and not just down to the exercising muscle mass. Inconclusive evidence suggests that lactate could also be governed in the same way but due to variability between studies this cannot be taken as definite and thus more research is needed to be done to define the physiological responses to exercising different muscle masses. PETO2 however may behave differently when different sized muscle masses are exercise. Calbet (2005) examined O2 extraction during arm exercise and leg exercise.

They concluded that the upper extrimity muscles less O2 at a given intensity when compared to lower extremity exercise. In theory if more O2 is extracted from haemoglobin during leg exercise at the same relative intensity then the values for PETO2 will be lower due to there being less O2 being present in arterial blood when measurements are taken at the end of a tidal breath. These findings by Calbet (2005) allow the conclusion that PETO2 is governed by the size of the exercising muscle mass and not by the relative intensity at which they are exercising at.

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