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Status:Closed    Asked:May 28, 2013 - 09:35 AM

what exactly does it mean when you say ventilation is non-linear at VT1?

I am a little confused about VT1 and VT2 - just want to clarify the ventilatory relationship. Specifically it being non-linear at VT1

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In general, heart rate (HR) increases incrementally as exercise intensity increases [i.e., the heart’s beats per minute (bpm) increase as exercise intensity increases]. This is necessary so that oxygen and nutrients can be delivered at an appropriate rate to the exercising muscles. The breathing rate (or ventilatory rate), which is measured in respirations per minute, does not follow the same increase as is seen with the HR as exercise intensity is increased. There is a lag in time between when the ventilatory rate starts to show a marked increase and when exercise has begun. The reason for this lag time (which can also be thought of as a “nonlinear increase in ventilation”) is due to lactate build up in the blood during exercise. In a practical sense, this means that the ventilatory rate up until the lactate build-up reached a critical point is a certain level, and then once the critical point of blood lactate is reached, the ventilatory response shows an exaggerated increase (i.e., nonlinear).

Lactate is produced at a higher rate as exercise intensity increases. At approximately 50% of an individual’s power output during incremental exercise, the ability to remove lactate from the circulation starts to become limited, and a net accumulation of lactate in the blood begins. This break in the pattern of blood lactate accumulation with increasing exercise intensity is called the first ventilation threshold (VT1). From a scientific standpoint, this is defined as the blood lactate threshold, but it really means the same thing as VT1. Blood lactate threshold and VT1 are the same because of the need to prevent the accumulation of lactate from causing disturbances in the blood pH (i.e., acid–base) balance of the body, the acid associated with lactate is buffered by the bicarbonate buffering system in the blood. This produces extra carbon dioxide (CO2), which causes a subsequent increase in the amount of breathing (VT1) and the subsequent challenge to talking continuously. Thus, this increase in blood lactate and VT1 occur at about the same exercise intensity.

At higher intensities, when the buffering mechanism cannot keep up with the extra acid production, and the pH of the blood begins to fall (due to accumulating lactate), the respiratory center is strongly stimulated, and there is yet another increase in breathing called the second ventilatory threshold (VT2). This is the point at which the intensity is so high that the body can no longer sustain an activity [also called “onset of blood lactate accumulation” (OBLA)], given the accumulation of lactate, and begins to shut down. In most healthy people, this marker is associated with a flattening of the HR response to increasing intensity, referred to as the HR turnpoint.


May 28, 2013 - 09:35 AM

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