W Darlene Reid1, A William Sheel, Babak Shadgan, S Jayne Garland, Jeremy D Road. 1. Department of Physical Therapy, University of Toronto, Toronto, Ontario, Canada (Dr Reid); and School of Kinesiology (Dr Sheel), Center for International Collaboration on Repair Discoveries (Dr Shadgan), and Respiratory Division (Dr Road), University of British Columbia, Vancouver, British Columbia, Canada; Faculty of Health Sciences, University of Western Ontario, London, Ontario, Canada (Dr Garland).
Abstract
PURPOSE: To evaluate changes in oxygenated (O2Hb), deoxygenated (HHb), and total hemoglobin (tHb) of the sternocleidomastoid (SCM), parasternal (PS), biceps (BC), and tibialis anterior (TA) using near-infrared spectroscopy during incremental loading of the inspiratory muscles and the elbow flexors in people with stable chronic obstructive pulmonary disease. METHODS:Fifteen participants with obstructive pulmonary disease were recruited in a repeated-measures crossover design. Near-infrared spectroscopy optodes were applied over the SCM, PS, BC, and TA to measure O2Hb, HHb, and tHb. Participants were randomly assigned to perform incremental inspiratory threshold loading or elbow flexor loading that imposed higher loads every 2 minutes until task failure. At least 1 week later, participants performed the other test. Arterial oxygen saturation (SpO2) was monitored continuously. RESULTS: O2Hb of the main agonist muscles, SCM and BC, decreased compared with the other muscles during inspiratory threshold loading and elbow flexor loading, respectively. SCM O2Hb and BC O2Hb decreased at higher loads compared with baseline. SCM tHb and HHb increased, whereas TA tHb decreased during inspiratory threshold loading. tHb did not change among any muscles during elbow flexor loading. SpO2 did not change from baseline to task failure. CONCLUSIONS: Our data suggest that the SCM was recruited progressively during incremental inspiratory threshold loading; however, O2Hb was not maintained in this muscle. Similarly, O2Hb was not maintained in the biceps during elbow flexor loading. This regional deoxygenation in SCM and BC during incremental loading protocols was not reflected by a decrease in SpO2.
RCT Entities:
PURPOSE: To evaluate changes in oxygenated (O2Hb), deoxygenated (HHb), and total hemoglobin (tHb) of the sternocleidomastoid (SCM), parasternal (PS), biceps (BC), and tibialis anterior (TA) using near-infrared spectroscopy during incremental loading of the inspiratory muscles and the elbow flexors in people with stable chronic obstructive pulmonary disease. METHODS: Fifteen participants with obstructive pulmonary disease were recruited in a repeated-measures crossover design. Near-infrared spectroscopy optodes were applied over the SCM, PS, BC, and TA to measure O2Hb, HHb, and tHb. Participants were randomly assigned to perform incremental inspiratory threshold loading or elbow flexor loading that imposed higher loads every 2 minutes until task failure. At least 1 week later, participants performed the other test. Arterial oxygen saturation (SpO2) was monitored continuously. RESULTS: O2Hb of the main agonist muscles, SCM and BC, decreased compared with the other muscles during inspiratory threshold loading and elbow flexor loading, respectively. SCM O2Hb and BC O2Hb decreased at higher loads compared with baseline. SCM tHb and HHb increased, whereas TA tHb decreased during inspiratory threshold loading. tHb did not change among any muscles during elbow flexor loading. SpO2 did not change from baseline to task failure. CONCLUSIONS: Our data suggest that the SCM was recruited progressively during incremental inspiratory threshold loading; however, O2Hb was not maintained in this muscle. Similarly, O2Hb was not maintained in the biceps during elbow flexor loading. This regional deoxygenation in SCM and BC during incremental loading protocols was not reflected by a decrease in SpO2.