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Regulation of Mitochondrial Oxygen Consumption at Exercise Onset: O 2 delivery or O 2 utilization?. F.W. Kolkhorst Kasch Exercise Physiology Lab San Diego State University, San Diego, CA. Why study VO 2 kinetics?. Grassi et al., JAP , 1996.

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Regulation of Mitochondrial Oxygen Consumption at Exercise Onset: O 2 delivery or O 2 utilization?

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Regulation of mitochondrial oxygen consumption at exercise onset o 2 delivery or o 2 utilization l.jpg

Regulation of Mitochondrial Oxygen Consumption at Exercise Onset:O2 delivery or O2 utilization?

F.W. Kolkhorst

Kasch Exercise Physiology Lab

San Diego State University, San Diego, CA


Why study vo 2 kinetics l.jpg

Why study VO2 kinetics?

Grassi et al., JAP, 1996


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VO2 response to heavy exercise in a representative subject

Kolkhorst et al., MSSE, 2004


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What is primary regulator of mitochondrial respiration at exercise onset?

  • Oxygen utilization? (Grassi et al.)

    • infers metabolic inertia

  • Oxygen delivery? (Hughson & Morrisey, JAP, 1982)

    • infers that PmitO2 is not saturating in all active muscle fibers at all time points


Regulation of mitochondrial respiration o 2 utilization metabolic inertia l.jpg

Regulation of mitochondrial respiration:O2 utilization (metabolic inertia)?

Peripheral O2 diffusion (capillary-to-mitochondria) as a limiting factor?

  • hyperoxic air had no effect on VO2 kinetics (MacDonald et al., JAP 1997)

  •  PO2 in isolated canine muscle had no effect on VO2 kinetics (Grassi et al., JAP 1998)


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VO2 response to electrical stimulation in isolated canine muscleThere were no differences in the time constant between the three conditions. (RSR13 is a drug that shifts O2-Hb dissociation curve to the right) (Grassi et al., JAP 1998)


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O2 deficit during electrical stimulation in isolated canine muscleBlood flow enhanced with administration of adenosine was compared to control. O2D was ~25% less during enhanced blood flow at high-intensity stimulation (Grassi et al., 1998, 2000).


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Effect of Cr supplementation on VO2 kinetics

  • no effect on VO2 response after supplementation (Balsom et al., 1993; Stroud et al. 1994)

  •  rapid component amplitude during exercise >VT after supplementation (Jones et al., 2002)

  • faster kinetics after supplementation (Rico-Sands & Mendez-Marco, 2000)


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Effect of Cr supplementation on VO2 kinetics during heavy exercise

Shedden et al., unpublished observations


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Effect of Cr supplementation on repeated bouts of supramaximal cycling

O2D in the later bouts was 15% greater after Cr supplementation (P = 0.040)

*

Kolkhorst et al., unpublished observations


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Regulation of mitochondrial respiration:O2 utilization (metabolic inertia)?

Potential mechanisms

  • Pyruvate dehydrogenase complex (PDH)

    • pharmacological intervention spared PCr during exercise transition (Timmons et al., AJP, 1998)

  • PCr/Cr

    • Cr will  and PCr will  mitochondrial respiration in vitro(Walsh et al., 2002)

      • when PCr:Cr was decreased from 2.0 (resting) to 0.5 (low-intensity), small  in respiration

      • when PCr:Cr was further decreased to 0.1 (high-intensity), large  in respiration


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Regulation of mitochondrial respiration:O2 delivery?

Can O2 supply during entire adaptation phase precisely anticipate/exceed O2 demand? (Hughson et al., ESSR, 2001)

  • feed forward control from motor cortex/skeletal muscle and CV control center

  • matching steady-state O2 delivery requires feedback control mechanisms


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Effects of prior exercise on VO2 kinetics

Light warmup exercise

  • no affect on VO2 kinetics of subsequent bout

    Heavy warmup exercise (Bohnert et al., Exp Physiol, 1998; Gerbino et al., JAP, 1996)

  • speeded VO2 kinetics

  • metabolic acidosis thought to enhance O2 delivery


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Bout 2

Bout 1

Top: VO2 responses to repeated bouts of supra-LT exercise.

Bottom: VO2 responses to repeated bouts of sub-LT exercise.

Gerbino et al., JAP, 1996


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Effects of prior exercise on VO2 kinetics

  • later studies suggested that warmup bouts affected only slow component amplitude, not the kinetics (Burnley et al., 2000, 2001)

    • used more sophisticated analyses of VO2 kinetics

    • no effect on rapid component time constant

  • breathing hypoxic air slows VO2 kinetics

  • breathing hyperoxic air speeds VO2 kinetics at exercise >VT(MacDonald et al., 1997)

    • faster MRT,  O2D,  Phase III amplitude


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Hypotheses

Bicarbonate ingestion would:

slow rapid component

decrease magnitude of slow component

Purpose

To investigate effects of bicarbonate ingestion on VO2 kinetics


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Methods

  • 10 active subjects (28  9 yr; 82.4  11.2 kg)

  • On separate days, performed two 6-min bouts at 25 W greater than VT

    • ingested 0.3 gkg-1 body weight of sodium bicarbonate with 1 L of water or water only

  • Measured pre-exercise blood pH and [bicarbonate]

  • VO2 measured breath-by-breath

    • used 5-s averages in analysis


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Three-component model of VO2 kinetics

Phase I

Phase II

Phase III

3

A'3

2

VO2

A'2

1

A'1

VO2base

TD2

TD3

Time

Initiation of exercise

VO2(t) = VO2base + A1 • (1-e-(t-TD1)/1)

+ A2• (1-e-(t-TD2/2)

+ A3• (1-e-(t-TD3)/3)


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Pre-exercise blood measurements (mean  SE)

* P < 0.001


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VO2 kinetics from heavy exercise (mean  SE)

* P < 0.05


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VO2 response to heavy exercise in a representative subject

Kolkhorst et al., MSSE, 2004


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Discussion

  • Bicarbonate altered manner in which VO2 increased

    • slower rapid component

    • smaller slow component

  • Why did bicarbonate affect slow component?

    • bicarbonate attenuates decreases in muscle pH (Nielsen et al., 2002; Stephens et al., 2002)

    • Does pH cause fatigue?

      • Westerblad et al. (2002) suggested Pi accumulation primary cause

      • bicarbonate ingestion  performance


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Why did bicarbonate affect rapid component?

alkalosis decreased vasodilation and caused leftward shift of O2-Hb dissociation curve

effects of prior heavy exercise on rapid component are equivocal

 2 and MRT (MacDonald et al., 1997; Rossiter et al., 2001; Tordi et al., 2003)

n/c in 2, but A'2 and  A'3(Burnley et al., 2001; Fukuba et al., 2002)

Why did bicarbonate affect slow component?

bicarbonate attenuates decreases in muscle pH (Nielsen et al., 2002; Stephens et al., 2002)

Does pH cause fatigue?

Westerblad et al. (2002) suggested Pi accumulation primary cause

bicarbonate ingestion  performance


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Potential effects of bicarbonate ingestion on slow component

  • Slow component may reflect increased motor unit recruitment

    • fatigue may be due to metabolic acidosis

  • Nonsignificant tendencies of smaller ΔVO2(6-3) after bicarbonate ingestion (Santalla et al., 2003; Zoladz et al., 1998)


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Pulmonary VO2 kinetics are known to be:

  • faster in trained than untrained

  • faster during exercise with predominantly ST fibers than FT fibers

  • slower after deconditioning

  • slower in aged population

  • slower in patients with respiratory/CV diseases as well as in heart and heart/lung transplant recipients

VO2 kinetics appears to be more sensitive than VO2max or LT to perturbations such as exercise training


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What is primary regulator of mitochondrial respiration at exercise onset?

  • Oxygen utilization?

  • Oxygen delivery?


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