Author(s): KUNIMASA, Y., AMANO, T.1, OKUSHIMA, D.2, KOGA, S.3, Institution: NIIGATA UNIVERSITY, Country: JAPAN, Abstract-ID: 1621

INTRODUCTION:
Near-infrared spectroscopy (NIRS) is a non-invasive technique to assess skeletal muscle oxygenation during exercise. Studies suggested that changes in skin blood flow (SkBF) would alter tissue oxygenations assessed by a conventional continuous-wave NIRS (CW-NIRS) which evaluates relative changes in muscle oxygenations (Buono et al. 2005; Koga et al. 2015). The time-resolved NIRS (TRS-NIRS), which can assess absolute changes in tissue oxygenations, has been suggested to be less influenced by the increases in SKBF, but not entirely insensitive (Koga et al. 2015). For both CW-NIRS and TRS-NIRS, eliminating potential changes in SkBF during the assessment of muscle oxygenations may improve physiological interpretation. We therefore investigated how a transdermal administration of adrenaline to induce sustained cutaneous vasoconstriction alters the assessment of muscle oxy- and deoxygenations during passive heating.
METHODS:
Eleven healthy males received 0.1% adrenaline into the medial gastrocnemius muscle using transdermal iontophoresis (0.5 mA, 20 min) to stimulate alpha adrenaline receptors inducing sustained cutaneous vasoconstrictions. After the normothermic baseline recording, participants were passively heated by wearing a water perfusion suit (47 °C) with concomitant elevations of ambient temperature to 35 °C for 60 minutes. SkBF, muscle oxy- and deoxygenation of hemoglogin+ myoglobin (Oxy [Hb+Mb] and deoxy [Hb+Mb]), total [Hb+Mb], and optical factors (path length: PL, scattering coefficient: SC, and absorption coefficient: AC ) were assessed at the site with and without (control) adrenaline treatments. Rectal and skin temperatures were assessed to evaluate the magnitude of heat stress.
RESULTS:
Heat stress elevated skin temperature by approximately 4 °C (P<0.001) while the elevation was small in rectal temperature (by 0.1 °C, P<0.01). Administration of adrenaline attenuates baseline SkBF by half (51%) of the control site. Cutaneous vasodilation was significantly suppressed at the adrenaline-treated site during heat stress as the changes were 4- and 2-fold from baseline at control and adrenaline treatment sites, respectively (both p<0.001). Heat stress increased CW-NIRS-derived oxy [Hb+Mb] and total [Hb+Mb] at both control and adrenaline-treated sites but this was only seen at the control for the assessment of TRS-NIRS (all P<0.05). TRS-NIRS-derived deoxy [Hb+Mb] at the control site was decreased by the heating (P<0.01), but not at the site with adrenaline treatments.
CONCLUSION:
The reduced SkBF by the adrenaline treatment abolished heat stress-mediated muscle oxygenations assessed by TRS-NIRS but it remains sensitive to the response assessed by CW-NIRS. These results suggest that cutaneous adrenaline treatment (or any other equivalent intervention to reduce SkBF) is important to interpret NIRS-derived muscle oxygenations when significant cutaneous vasodilation is expected. Notably, this treatment is more effective for assessing muscle oxygenations using TRS-NIRS.