3-nitrotyrosine And Soluble Vascular And Intracellular Adhesion Molecule Responses To High-intensity Interval And Steady-state Moderate-intensity Exercise: 626 Board #22 May 27, 2

TL;DR: Transient elevations in NT and sVCAM-1 after moderate-intensity SSE but not HIIE of similar average intensity and duration may indicate unique effects of interval exercise.

Abstract: Vascular endothelium may respond differently to high-intensity interval exercise (HIIE) when compared to moderate-intensity steady state exercise (SSE). We hypothesized that greater sympathetic stimulation of soluble vascular adhesion molecule-1 (sVCAM-1) and intracellular adhesion molecule-1 (sICAM-1) and greater oxidative and nitrative stress on the vascular endothelium may transiently result from HIIE. PURPOSE: Determine the influence of HIIE on sVCAM-1, sICAM-1 and 3-nitrotyrosine (NT), a marker of nitric oxide-dependent reactive nitrogen species and nitrative stress, relative to a comparable amount of moderate-intensity SSE and a dose that is half that of SSE. METHODS: Seventeen male participants (age 27.8 + 6.4 yr; weight 80.6 + 9.0 kg; BMI 25.1 + 2.4 kg/m2; %fat = 19 + 5; VO2max 52.1 + 7.5 ml/kg/min) underwent HIIE by treadmill running (90% and 40% of VO2reserve in 3:2 min ratio) to expend 500 kcals (H500); HIIE to expend 250 kcals (H250), and; SSE at 70% VO2reserve to expend 500 kcals (M500) in a randomized crossover design. Intensities of all exercise conditions averaged 70% VO2reserve. Blood measures of sVCAM-1 (ng/mL), sICAM-1 (ng/mL), NT (nM), epinephrine (EPI) and norepinephrine (NE) in pg/mL, were obtained just before, immediately after, 2 hr and 24 hr after exercise. Significant differences were determined using 3 by 4 repeated measures ANOVAs. Effect sizes were calculated to determine the magnitude of dependent variable responses to exercise. RESULTS: HIIE resulted in 2 to 2.5 fold greater EPI responses immediately after exercise versus SSE (p = 0.0059, H250 ES = 1.89; H500 ES = 3.04). NE increased an average of 5.4 times above pre-exercise values across all exercise conditions (p < 0.0001). NT decreased immediately after HIIE (H250 ES = 0.39; H500 ES = -0.97) and returned to baseline by 2 hr post-exercise; whereas, NT was elevated 111% 2 hr (ES = 2.46) and remained 24 hr after SSE (p = 0.0001). sVCAM-1 was unchanged with HIIE but increased 6% immediately following moderate-intensity SSE and remained elevated 24 hr post-exercise (p < 0.0005, ES = 1.01). SUMMARY: Our results are in direct opposition to our hypothesis. Transient elevations in NT and sVCAM-1 after moderate-intensity SSE but not HIIE of similar average intensity and duration may indicate unique effects of interval exercise. NT and sVCAM-1 were not elevated after HIIE in spite of a greater sympathetic response than what was observed after moderate-intensity SSE.

Summary

Summary

• Vascular endothelium may respond differently to high-intensity interval exercise (HIIE) when compared to moderate-intensity steady state exercise (SSE).
• The authors hypothesized that greater sympathetic stimulation of soluble vascular adhesion molecule-1 (sVCAM-1) and intracellular adhesion molecule-1 (sICAM-1) and greater oxidative and nitrative stress on the vascular endothelium may transiently result from HIIE.
• Determine the influence of HIIE on sVCAM-1, sICAM-1 and 3-nitrotyrosine (NT), a marker of nitric oxide-dependent reactive nitrogen species and nitrative stress, relative to a comparable amount of moderate-intensity SSE and a dose that is half that of SSE, also known as PURPOSE.
• Intensities of all exercise conditions averaged 70% VO2reserve.
• Blood measures of sVCAM-1 (ng/mL), sICAM-1 (ng/mL), NT (nM), epinephrine (EPI) and norepinephrine (NE) in pg/mL, were obtained just before, immediately after, 2 hr and 24 hr after exercise.
• Significant differences were determined using 3 by 4 repeated measures ANOVAs.
• Effect sizes were calculated to determine the magnitude of dependent variable responses to exercise.
• NE increased an average of 5.4 times above pre-exercise values across all exercise conditions (p < 0.0001).
• SVCAM-1 was unchanged with HIIE but increased 6% immediately following moderate-intensity SSE and remained elevated 24 hr post-exercise (p < 0.0005, ES = 1.01).
• The authors results are in direct opposition to their hypothesis, also known as SUMMARY.
• NT and sVCAM-1 were not elevated after HIIE in spite of a greater sympathetic response than what was observed after moderate-intensity SSE.

Full text

International Journal of Exercise Science www.tacsm.org
TACSM Abstract
3-Nitrotyrosine and Soluble Vascular and Intracellular Adhesion
Molecule Responses to High-Intensity Interval and Steady-State
Moderate-Intensity Exercise
Forsse JS
1
, Papadakis Z
1,
Bane AA
1
, Taylor JK
2
, Qian L
2
, Marroquín FEM
1
, Grandjean
PW
1
1
Department of Health, Human Performance, and Recreation; Baylor University; Waco,
TX
2
Clinical Laboratory Science; Auburn University-Montgomery; Montgomery, AL
Category: Doctoral
Advisor / Mentor: Grandjean, Peter (Peter_Grandjean@baylor.edu)
ABSTRACT
Vascular endothelium may respond differently to high-intensity interval exercise (HIIE) when compared
to moderate-intensity steady state exercise (SSE). We hypothesized that greater sympathetic stimulation of
soluble vascular adhesion molecule-1 (sVCAM-1) and intracellular adhesion molecule-1 (sICAM-1) and
greater oxidative and nitrative stress on the vascular endothelium may transiently result from HIIE.
PURPOSE: Determine the influence of HIIE on sVCAM-1, sICAM-1 and 3-nitrotyrosine (NT), a marker of
nitric oxide-dependent reactive nitrogen species and nitrative stress, relative to a comparable amount of
moderate-intensity SSE and a dose that is half that of SSE. METHODS: Seventeen male participants (age
27.8 + 6.4 yr; weight 80.6 + 9.0 kg; BMI 25.1 + 2.4 kg/m2; %fat = 19 + 5; VO2max 52.1 + 7.5 ml/kg/min)
underwent HIIE by treadmill running (90% and 40% of VO2reserve in 3:2 min ratio) to expend 500 kcals
(H500); HIIE to expend 250 kcals (H250), and; SSE at 70% VO2reserve to expend 500 kcals (M500) in a
randomized crossover design. Intensities of all exercise conditions averaged 70% VO2reserve. Blood
measures of sVCAM-1 (ng/mL), sICAM-1 (ng/mL), NT (nM), epinephrine (EPI) and norepinephrine (NE)
in pg/mL, were obtained just before, immediately after, 2 hr and 24 hr after exercise. Significant
differences were determined using 3 by 4 repeated measures ANOVAs. Effect sizes were calculated to
determine the magnitude of dependent variable responses to exercise. RESULTS: HIIE resulted in 2 to 2.5
fold greater EPI responses immediately after exercise versus SSE (p = 0.0059, H250 ES = 1.89; H500 ES =
3.04). NE increased an average of 5.4 times above pre-exercise values across all exercise conditions (p <
0.0001). NT decreased immediately after HIIE (H250 ES = - 0.39; H500 ES = -0.97) and returned to baseline
by 2 hr post-exercise; whereas, NT was elevated 111% 2 hr (ES = 2.46) and remained 24 hr after SSE (p =
0.0001). sVCAM-1 was unchanged with HIIE but increased 6% immediately following moderate-intensity
SSE and remained elevated 24 hr post-exercise (p < 0.0005, ES = 1.01). SUMMARY: Our results are in
direct opposition to our hypothesis. Transient elevations in NT and sVCAM-1 after moderate-intensity SSE
but not HIIE of similar average intensity and duration may indicate unique effects of interval exercise. NT
and sVCAM-1 were not elevated after HIIE in spite of a greater sympathetic response than what was
observed after moderate-intensity SSE.