Heavy and moderate interval exercise training alters low-flow-mediated constriction but does not increase circulating progenitor cells in healthy humans

Mark Rakobowchuk, Emma Harris, Annabelle Taylor, Vivek Baliga, Richard M. Cubbon, Harry B. Rossiter, Karen M. Birch

Research output: Contribution to journalArticle

39 Citations (Scopus)

Abstract

Moderate-intensity endurance exercise training improves vascular endothelial vasomotor function; however, the impact of high-intensity exercise training has been equivocal. Thus, the effect of the physiological stress of the exercise remains poorly understood. Furthermore, enhanced vascular repair mediated by circulating progenitor cells may also be improved. To address whether the physiological stress of exercise training is an important factor contributing to these adaptations, 20 healthy participants trained for 6 weeks. Training involved either moderate (MSIT; n= 9) or heavy metabolic stress (HSIT; n= 11) interval exercise training programmes matched for total work and duration of exercise. Before and after training, flow-mediated dilatation, low-flow-mediated constriction and total vessel reactivity were measured at the brachial artery using Doppler ultrasound. Circulating progenitor cells (CD34 +, CD133 + and CD309/KDR +) were measured by flow cytometry (means ± SD). Relative (MSIT pre- 5.5 ± 3.4 versus post-training 6.6 ± 2.5%; HSIT pre- 6.6 ± 4.1 versus post-training 7.0 ± 3.4%, P= 0.33) and normalized (P= 0.16) flow-mediated dilatation did not increase with either training programme. However, low-flow-mediated constriction was greater after training in both groups (MSIT pre- -0.5 ± 3.2 versus post-training -1.9 ± 3.1%; HSIT pre- -1.0 ± 1.7 versus post-training -2.9 ± 3.0%, P= 0.04) and contributed to greater total vessel reactivity (MSIT pre- 7.4 ± 3.3 versus post-training 10.1 ± 3.7%; HSIT pre- 10.9 ± 5.9 versus post-training 12.7 ± 6.2%, P= 0.01). Peak reactive hyperaemia and the area under the shear rate curve were not different between groups, either before or after training. Although circulating progenitor cell numbers increased following heavy-intensity interval exercise training, variability was great amongst participants [MSIT pre- 16 ± 18 versus post-training 14 ± 12 cells (ml whole blood) -1; HSIT pre- 8 ± 6 versus post-training 19 ± 23 cells (ml whole blood) -1, P= 0.50]. Overall, vasoconstrictor function may be augmented by moderate- and heavy-intensity interval exercise training in young adults. However, circulating progenitor cell numbers were not increased, suggesting that these cells are not likely to be upregulated as a result of training.

LanguageEnglish
Pages375-385
Number of pages11
JournalExperimental Physiology
Volume97
Issue number3
Early online date16 Dec 2011
DOIs
Publication statusPublished - Mar 2012
Externally publishedYes

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Constriction
Stem Cells
Exercise
Physiological Stress
Blood Vessels
Dilatation
Cell Count
Education
Doppler Ultrasonography
Brachial Artery
Hyperemia
Vasoconstrictor Agents
Young Adult
Healthy Volunteers
Flow Cytometry

Cite this

Rakobowchuk, Mark ; Harris, Emma ; Taylor, Annabelle ; Baliga, Vivek ; Cubbon, Richard M. ; Rossiter, Harry B. ; Birch, Karen M. / Heavy and moderate interval exercise training alters low-flow-mediated constriction but does not increase circulating progenitor cells in healthy humans. In: Experimental Physiology. 2012 ; Vol. 97, No. 3. pp. 375-385.
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title = "Heavy and moderate interval exercise training alters low-flow-mediated constriction but does not increase circulating progenitor cells in healthy humans",
abstract = "Moderate-intensity endurance exercise training improves vascular endothelial vasomotor function; however, the impact of high-intensity exercise training has been equivocal. Thus, the effect of the physiological stress of the exercise remains poorly understood. Furthermore, enhanced vascular repair mediated by circulating progenitor cells may also be improved. To address whether the physiological stress of exercise training is an important factor contributing to these adaptations, 20 healthy participants trained for 6 weeks. Training involved either moderate (MSIT; n= 9) or heavy metabolic stress (HSIT; n= 11) interval exercise training programmes matched for total work and duration of exercise. Before and after training, flow-mediated dilatation, low-flow-mediated constriction and total vessel reactivity were measured at the brachial artery using Doppler ultrasound. Circulating progenitor cells (CD34 +, CD133 + and CD309/KDR +) were measured by flow cytometry (means ± SD). Relative (MSIT pre- 5.5 ± 3.4 versus post-training 6.6 ± 2.5{\%}; HSIT pre- 6.6 ± 4.1 versus post-training 7.0 ± 3.4{\%}, P= 0.33) and normalized (P= 0.16) flow-mediated dilatation did not increase with either training programme. However, low-flow-mediated constriction was greater after training in both groups (MSIT pre- -0.5 ± 3.2 versus post-training -1.9 ± 3.1{\%}; HSIT pre- -1.0 ± 1.7 versus post-training -2.9 ± 3.0{\%}, P= 0.04) and contributed to greater total vessel reactivity (MSIT pre- 7.4 ± 3.3 versus post-training 10.1 ± 3.7{\%}; HSIT pre- 10.9 ± 5.9 versus post-training 12.7 ± 6.2{\%}, P= 0.01). Peak reactive hyperaemia and the area under the shear rate curve were not different between groups, either before or after training. Although circulating progenitor cell numbers increased following heavy-intensity interval exercise training, variability was great amongst participants [MSIT pre- 16 ± 18 versus post-training 14 ± 12 cells (ml whole blood) -1; HSIT pre- 8 ± 6 versus post-training 19 ± 23 cells (ml whole blood) -1, P= 0.50]. Overall, vasoconstrictor function may be augmented by moderate- and heavy-intensity interval exercise training in young adults. However, circulating progenitor cell numbers were not increased, suggesting that these cells are not likely to be upregulated as a result of training.",
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Heavy and moderate interval exercise training alters low-flow-mediated constriction but does not increase circulating progenitor cells in healthy humans. / Rakobowchuk, Mark; Harris, Emma; Taylor, Annabelle; Baliga, Vivek; Cubbon, Richard M.; Rossiter, Harry B.; Birch, Karen M.

In: Experimental Physiology, Vol. 97, No. 3, 03.2012, p. 375-385.

Research output: Contribution to journalArticle

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T1 - Heavy and moderate interval exercise training alters low-flow-mediated constriction but does not increase circulating progenitor cells in healthy humans

AU - Rakobowchuk, Mark

AU - Harris, Emma

AU - Taylor, Annabelle

AU - Baliga, Vivek

AU - Cubbon, Richard M.

AU - Rossiter, Harry B.

AU - Birch, Karen M.

PY - 2012/3

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N2 - Moderate-intensity endurance exercise training improves vascular endothelial vasomotor function; however, the impact of high-intensity exercise training has been equivocal. Thus, the effect of the physiological stress of the exercise remains poorly understood. Furthermore, enhanced vascular repair mediated by circulating progenitor cells may also be improved. To address whether the physiological stress of exercise training is an important factor contributing to these adaptations, 20 healthy participants trained for 6 weeks. Training involved either moderate (MSIT; n= 9) or heavy metabolic stress (HSIT; n= 11) interval exercise training programmes matched for total work and duration of exercise. Before and after training, flow-mediated dilatation, low-flow-mediated constriction and total vessel reactivity were measured at the brachial artery using Doppler ultrasound. Circulating progenitor cells (CD34 +, CD133 + and CD309/KDR +) were measured by flow cytometry (means ± SD). Relative (MSIT pre- 5.5 ± 3.4 versus post-training 6.6 ± 2.5%; HSIT pre- 6.6 ± 4.1 versus post-training 7.0 ± 3.4%, P= 0.33) and normalized (P= 0.16) flow-mediated dilatation did not increase with either training programme. However, low-flow-mediated constriction was greater after training in both groups (MSIT pre- -0.5 ± 3.2 versus post-training -1.9 ± 3.1%; HSIT pre- -1.0 ± 1.7 versus post-training -2.9 ± 3.0%, P= 0.04) and contributed to greater total vessel reactivity (MSIT pre- 7.4 ± 3.3 versus post-training 10.1 ± 3.7%; HSIT pre- 10.9 ± 5.9 versus post-training 12.7 ± 6.2%, P= 0.01). Peak reactive hyperaemia and the area under the shear rate curve were not different between groups, either before or after training. Although circulating progenitor cell numbers increased following heavy-intensity interval exercise training, variability was great amongst participants [MSIT pre- 16 ± 18 versus post-training 14 ± 12 cells (ml whole blood) -1; HSIT pre- 8 ± 6 versus post-training 19 ± 23 cells (ml whole blood) -1, P= 0.50]. Overall, vasoconstrictor function may be augmented by moderate- and heavy-intensity interval exercise training in young adults. However, circulating progenitor cell numbers were not increased, suggesting that these cells are not likely to be upregulated as a result of training.

AB - Moderate-intensity endurance exercise training improves vascular endothelial vasomotor function; however, the impact of high-intensity exercise training has been equivocal. Thus, the effect of the physiological stress of the exercise remains poorly understood. Furthermore, enhanced vascular repair mediated by circulating progenitor cells may also be improved. To address whether the physiological stress of exercise training is an important factor contributing to these adaptations, 20 healthy participants trained for 6 weeks. Training involved either moderate (MSIT; n= 9) or heavy metabolic stress (HSIT; n= 11) interval exercise training programmes matched for total work and duration of exercise. Before and after training, flow-mediated dilatation, low-flow-mediated constriction and total vessel reactivity were measured at the brachial artery using Doppler ultrasound. Circulating progenitor cells (CD34 +, CD133 + and CD309/KDR +) were measured by flow cytometry (means ± SD). Relative (MSIT pre- 5.5 ± 3.4 versus post-training 6.6 ± 2.5%; HSIT pre- 6.6 ± 4.1 versus post-training 7.0 ± 3.4%, P= 0.33) and normalized (P= 0.16) flow-mediated dilatation did not increase with either training programme. However, low-flow-mediated constriction was greater after training in both groups (MSIT pre- -0.5 ± 3.2 versus post-training -1.9 ± 3.1%; HSIT pre- -1.0 ± 1.7 versus post-training -2.9 ± 3.0%, P= 0.04) and contributed to greater total vessel reactivity (MSIT pre- 7.4 ± 3.3 versus post-training 10.1 ± 3.7%; HSIT pre- 10.9 ± 5.9 versus post-training 12.7 ± 6.2%, P= 0.01). Peak reactive hyperaemia and the area under the shear rate curve were not different between groups, either before or after training. Although circulating progenitor cell numbers increased following heavy-intensity interval exercise training, variability was great amongst participants [MSIT pre- 16 ± 18 versus post-training 14 ± 12 cells (ml whole blood) -1; HSIT pre- 8 ± 6 versus post-training 19 ± 23 cells (ml whole blood) -1, P= 0.50]. Overall, vasoconstrictor function may be augmented by moderate- and heavy-intensity interval exercise training in young adults. However, circulating progenitor cell numbers were not increased, suggesting that these cells are not likely to be upregulated as a result of training.

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