Muscle Deoxygenation Kinetics Research Articles

VO2 and Muscle Blood Flow and Deoxygenation Kinetics In Different Regions of Moderate-In tensity Exercise

VO2 and Muscle Blood Flow and Deoxygenation Kinetics In Different Regions of Moderate-In tensity Exercise

Effects of prior heavy-intensity exercise on pulmonary O2 uptake and muscle deoxygenation kinetics in young and older adult humans

Pulmonary O2 uptake (VO2p) and muscle deoxygenation kinetics were examined during moderate-intensity cycling (80% lactate threshold) without warm-up and after heavy-intensity warm-up exercise in young (n = 6; 25 +/- 3 yr) and older (n = 5; 68 +/- 3 yr) adults. We hypothesized that heavy warm-up would speed VO2p kinetics in older adults consequent to an improved intramuscular oxygenation. Subjects performed step transitions (n = 4; 6 min) from 20 W to moderate-intensity exercise preceded by either no warm-up or heavy-intensity warm-up (6 min). VO2p was measured breath by breath. Oxy-, deoxy-(HHb), and total hemoglobin and myoglobin (Hb(tot)) of the vastus lateralis muscle were measured continuously by near-infrared spectroscopy (NIRS). VO2p (phase 2; tau) and HHb data were fit with a monoexponential model. After heavy-intensity warm-up, oxyhemoglobin (older subjects: 13 +/- 9 microM; young subjects: 9 +/- 8 microM) and Hb(tot) (older subjects: 12 +/- 8 microM; young subjects: 14 +/- 10 microM) were elevated (P < 0.05) relative to the no warm-up pretransition baseline. In older adults, tauVO2p adapted at a faster rate (P < 0.05) after heavy warm-up (30 +/- 7 s) than no warm-up (38 +/- 5 s), whereas in young subjects, tauVO2p was similar in no warm-up (26 +/- 7 s) and heavy warm-up (25 +/- 5 s). HHb adapted at a similar rate in older and young adults after no warm-up; however, in older adults after heavy warm-up, the adaptation of HHb was slower (P < 0.01) compared with young and no warm-up. These data suggest that, in older adults, VO2p kinetics may be limited by a slow adaptation of muscle blood flow and O2 delivery.

Muscle deoxygenation as related to work rate.

The kinetics of the decrease in venous O(2) content in response to constant work rate exercise below the lactic acidosis threshold (LAT) is very rapid, reaching a constant value by approximately 1 min. However, for work rates above the LAT, a slow further decrease in venous O(2) content takes place that is attributable to the Bohr effect rather than further decrease in end capillary PO. We hypothesized that similar differences, with respect to the LAT, will be observed in muscle deoxygenation kinetics when studied with near-infrared spectroscopy (NIRS). Twelve normal subjects performed three constant work rate tests from unloaded cycling at 60% of LAT, 80% LAT, each with four repetitions, and above LAT (LAT + 35% between LAT and VO(2max) three times, on a cycle ergometer for 6 min. We measured tissue deoxygenation with NIRS, with the probe over the vastus lateralis muscle, time-averaging the repetitions. Gas exchange and heart rate (HR) were measured breath-by-breath and beat-by-beat. Tissue deoxygenation kinetics were significantly faster than VO(2) and HR at 60%- and 80%-LAT work rates. By 1 min of exercise, deoxygenation was constant for the work rate below the LAT. At 30 s, tissue deoxygenation was 70-95% complete, whereas VO(2) and HR were only 30-60% complete. For the work rate above the LAT, a steady state for muscle deoxygenation was not reached during the 6 min of exercise. After 1 min of above-LAT exercise, either one of two patterns of slow change in tissue oxygenation developed, deoxygenation or reoxygenation. It is postulated that these different responses might be due to effects of the exercise lactic acidosis. H accompanying lactate increase might cause further deoxygenation due to the Bohr effect, and acidosis-induced vasodilatation might cause reoxygenation after the initial deoxygenation. 1) The kinetics of tissue deoxygenation are significantly more rapid than VO(2) and HR kinetics at all work rates studied, and 2) steady-state in tissue deoxygenation is seen by 1 min of constant work rate exercise below the LAT, but this is much delayed for work rates above the LAT.

THE RELATIONSHIP BETWEEN PULMONARY O2 UPTAKE KINETICS AND MUSCLE DEOXYGENATION.

The temporal relationship between the kinetics of phase 2 pulmonary O2 uptake (VO2 p) and deoxygenation of the vastus lateralis muscle was examined during constant-load leg cycling exercise. Young adults (6 male, 6 female; 23 ± 3 yr; mean ± S.D.) performed repeated transitions on 3 separate days from 20 W to exercise intensities corresponding to moderate (80% ventilatory threshold; MOD) and heavy (δ50%; HVY) exercise. Breath-by-breath VO2 p was measured by mass spectrometer and volume turbine. Oxy-(HbO2), deoxy-(HHb) and total hemoglobin/myoglobin (Hbtot) were determined by near-infrared spectroscopy (NIRS; Hamamatsu NIRO-300). VO2 p data were filtered, interpolated to 1 s, and averaged to 5 s bins. HHb-NIRS data were filtered and averaged to 5 s bins. VO2 p and HHb data were fit with a single-component exponential model; NIRS data were further analyzed by determining the time delay from exercise onset to the start of an increase in HHb. The delay prior to an increase in HHb was 13 ± 2 s (MOD) and 7 ± 1 s (HVY). This delay may reflect either a delay in activation of muscle O2 consumption and/or an early close matching of muscle O2 consumption and local muscle blood flow. The phase 2 time constants (τ) for VO2 p, 30τ 8 s (MOD) and 35 ± 5 s (HVY) were slower (p < 0.01) than the ± HHb, 10 ± 3 s (MOD) and 12 ± 5 s (HVY) and in several subjects, the initial rise in HHb during MOD showed an early overshoot relative to the exponential fit. These data demonstrate that the kinetics of local muscle deoxygenation assessed by NIRS are faster than those of phase 2 VO2 p during both MOD and HVY intensity exercise and suggest that a mismatch exists between O2 delivery and utilization during the exercise on-transient. Supported in part by NSERC, Canada

Mechanisms of action of hypocapnic alkalosis on limb blood vessels in man and dog

ARTICLESMechanisms of action of hypocapnic alkalosis on limb blood vessels in man and dogHA Kontos, DW Richardson, AJ Raper, Zubair-ul-Hassan, and Patterson JL JrHA Kontos, DW Richardson, AJ Raper, Zubair-ul-Hassan, and Patterson JL JrPublished Online:01 Dec 1972https://doi.org/10.1152/ajplegacy.1972.223.6.1296MoreSectionsPDF (3 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformationCited ByEffects of Pre-Exercise Voluntary Hyperventilation on Metabolic and Cardiovascular Responses During and After Intense Exercise28 September 2022 | Research Quarterly for Exercise and Sport, Vol. 164Hemodynamic characteristics of postural hyperventilation: POTS with hyperventilation versus panic versus voluntary hyperventilationJulian M. Stewart, Paul Pianosi, Mohamed A. Shaban, Courtney Terilli, Maria Svistunova, Paul Visintainer, and Marvin S. Medow1 November 2018 | Journal of Applied Physiology, Vol. 125, No. 5ButeykoRepeated Pre-Syncope from Increased Inspired CO 2 in a Background of Severe HypoxiaHigh Altitude Medicine & Biology, Vol. 15, No. 1Biochemical aspects of breathingChanges in arterial blood pressure elicited by severe passive heating at rest is associated with hyperthermia-induced hyperventilation in humans9 May 2012 | European Journal of Applied Physiology, Vol. 113, No. 1Effect of voluntary hypocapnic hyperventilation on cutaneous circulation in resting heated humansNaoto Fujii, Yasushi Honda, Stephane Delliaux, Bun Tsuji, Kazuhito Watanabe, Akira Sugihara, Narihiko Kondo, and Takeshi Nishiyasu1 November 2012 | American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, Vol. 303, No. 9Pulmonary O2 uptake and leg blood flow kinetics during moderate exercise are slowed by hyperventilation-induced hypocapnic alkalosisLisa M. K. Chin, George J. F. Heigenhauser, Donald H. Paterson, and John M. Kowalchuk1 June 2010 | Journal of Applied Physiology, Vol. 108, No. 6Effect of hyperventilation and prior heavy exercise on O2 uptake and muscle deoxygenation kinetics during transitions to moderate exercise28 November 2009 | European Journal of Applied Physiology, Vol. 108, No. 5Cardiovascular and cerebrovascular responses to acute isocapnic and poikilocapnic hypoxia in humansCraig D. Steinback, and Marc J. Poulin1 February 2008 | Journal of Applied Physiology, Vol. 104, No. 2Hyperventilation-induced hypocapnic alkalosis slows the adaptation of pulmonary O 2 uptake during the transition to moderate-intensity exercise7 August 2007 | The Journal of Physiology, Vol. 583, No. 1Effects of hyperventilation on phosphocreatine kinetics and muscle deoxygenation during moderate-intensity plantar flexion exerciseS. C. Forbes, J. M. Kowalchuk, R. T. Thompson, and G. D. Marsh1 April 2007 | Journal of Applied Physiology, Vol. 102, No. 4Ventilatory responses to isocapnic and poikilocapnic hypoxia in humansRespiratory Physiology & Neurobiology, Vol. 155, No. 2Differential sensitivities of cerebral and brachial blood flow to hypercapnia in humansJimmy S. Vantanajal, Jon C. Ashmead, Todd J. Anderson, Russell T. Hepple, and Marc J. Poulin1 January 2007 | Journal of Applied Physiology, Vol. 102, No. 1Biochemical Aspects of BreathingOpioid peptide modulation of circulatory response to hyperventilation in humansPeptides, Vol. 21, No. 8Hyperventilation — a rose by any other nameComplementary Therapies in Medicine, Vol. 4, No. 3The Pathophysiology of Hyperventilation DisordersChest, Vol. 109, No. 2Adverse Events during IV TherapyJournal of Vascular Access Devices, Vol. 1, No. 2Hyperventilation SyndromesHyperventilation-induced changes of blood cell counts depend on hypocapniaEuropean Journal of Applied Physiology and Occupational Physiology, Vol. 69, No. 5Differential contractile effects of changes in carbon dioxide tension on rat mesenteric resistance arteries precontracted with noradrenalinePfl�gers Archiv European Journal of Physiology, Vol. 419, No. 1Hyperventilation Syndrome-Hiding Behind Pseudonyms?Chest, Vol. 97, No. 6Gas Exchange in Acid‐Base Disturbances1 January 2011Hyperventilation Syndromes in Medicine and Psychiatry: A Review7 March 2018 | Journal of the Royal Society of Medicine, Vol. 80, No. 4Optimum ventilation levels for maintenance of normal arterial blood pO2, pC02, and pH in the pithed rat preparationJournal of Pharmacological Methods, Vol. 10, No. 3Differences in the regulation of vascular resistance in guinea pigs with right and left heart failure.Circulation Research, Vol. 41, No. 1Impairment of myocardial O2 supply due to hyperventilation.Circulation, Vol. 52, No. 5 More from this issue > Volume 223Issue 6December 1972Pages 1296-1307 Copyright & PermissionsCopyright © 1972 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1972.223.6.1296PubMed4123706History Published online 1 December 1972 Published in print 1 December 1972 Metrics

Systemic circulatory responses to hypocapnia in man.

Systemic circulatory responses to hypocapnia in man.

Hemodynamic response to work with different muscle groups, sitting and supine.

Hemodynamic response to work with different muscle groups, sitting and supine.