Ioannis Vogiatzis1, Zafeiris Louvaris2, Peter D Wagner3. 1. Department of Sport, Exercise and Rehabilitation, Northumbria University Newcastle, Newcastle upon Tyne, UK. 2. Department of Rehabilitation Sciences, Faculty of Kinesiology and Rehabilitation Sciences, Rehabilitation for Internal Disorders Research Group, KU Leuven, Leuven, Belgium. 3. Division of Pulmonary, Critical Care, and Sleep Medicine, Department of Medicine, University of California San Diego, San Diego, CA, USA.
Abstract
NEW FINDINGS: What is the topic of this review? The work presented here focuses mostly on testing the theory of blood flow redistribution from the locomotor to the respiratory muscles during heavy exercise in healthy participants and in patients with COPD. What advances does it highlight? Studies presented and the direct experimental approach to measure muscle blood flow by indocyanine green dye detected by near infrared spectroscopy, show that exercise interferes with respiratory muscle blood flow especially in COPD, but even in healthy. ABSTRACT: We have developed an indicator-dilution method to measure muscle blood flow at rest and during exercise using the light absorbing tracer indocyanine green dye (ICG) injected as an intravenous bolus, with surface optodes placed over muscles of interest to record the ICG signal by near-infrared spectroscopy. Here we review findings for both quadriceps and intercostal muscle blood flow (measured simultaneously) in trained cyclists and in patients with chronic obstructive pulmonary disease (COPD). During resting hyperpnoea in both athletes and patients, intercostal muscle blood flow increased with ventilation, correlating closely and linearly with the work of breathing, with no change in quadriceps flow. During graded exercise in athletes, intercostal flow at first increased, but then began to fall approaching peak effort. Unexpectedly, in COPD, intercostal muscle blood flow during exercise fell progressively from resting values, contrasting sharply with the response to resting hyperpnoea. During exercise at peak intensity, we found no quadriceps blood flow reduction in favour of the respiratory muscles in either athletes or patients. In COPD at peak exercise, when patients breathed 21% oxygen in helium or 100% oxygen, there was no redistribution of blood flow observed between legs and respiratory muscles in either direction. Evidence of decrease in leg blood flow and increase in respiratory muscle flow was found only when imposing expiratory flow limitation (EFL) during exercise in healthy individuals. However, because EFL caused substantial physiological derangement, lowering arterial oxygen saturation and raising end-tidal P C O 2 and heart rate, these results cannot be projected onto normal exercise.
NEW FINDINGS: What is the topic of this review? The work presented here focuses mostly on testing the theory of blood flow redistribution from the locomotor to the respiratory muscles during heavy exercise in healthy participants and in patients with COPD. What advances does it highlight? Studies presented and the direct experimental approach to measure muscle blood flow by indocyanine green dye detected by near infrared spectroscopy, show that exercise interferes with respiratory muscle blood flow especially in COPD, but even in healthy. ABSTRACT: We have developed an indicator-dilution method to measure muscle blood flow at rest and during exercise using the light absorbing tracer indocyanine green dye (ICG) injected as an intravenous bolus, with surface optodes placed over muscles of interest to record the ICG signal by near-infrared spectroscopy. Here we review findings for both quadriceps and intercostal muscle blood flow (measured simultaneously) in trained cyclists and in patients with chronic obstructive pulmonary disease (COPD). During resting hyperpnoea in both athletes and patients, intercostal muscle blood flow increased with ventilation, correlating closely and linearly with the work of breathing, with no change in quadriceps flow. During graded exercise in athletes, intercostal flow at first increased, but then began to fall approaching peak effort. Unexpectedly, in COPD, intercostal muscle blood flow during exercise fell progressively from resting values, contrasting sharply with the response to resting hyperpnoea. During exercise at peak intensity, we found no quadriceps blood flow reduction in favour of the respiratory muscles in either athletes or patients. In COPD at peak exercise, when patients breathed 21% oxygen in helium or 100% oxygen, there was no redistribution of blood flow observed between legs and respiratory muscles in either direction. Evidence of decrease in leg blood flow and increase in respiratory muscle flow was found only when imposing expiratory flow limitation (EFL) during exercise in healthy individuals. However, because EFL caused substantial physiological derangement, lowering arterial oxygen saturation and raising end-tidal P C O 2 and heart rate, these results cannot be projected onto normal exercise.