Thesis (M.S.)--Virginia Polytechnic Institute and State University, 1992. / Vita. Abstract. Includes bibliographical references (leaves 97-98). Also available via the Internet.

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The ability to exercise for more than a short period requires energy to be supplied by using oxygen (aerobic energy supply). How quickly we can supply energy depends on how much oxygen we can deliver to muscles. Similarly, delivery of oxygen (O2 del) to the brain is important as brief, transient disruptions can cause nausea or fainting. Therefore, regulation of O2 del so that the O2 supply matches the metabolic requirement (O2 del matching metabolic demand) is essential to exercise tolerance and brain function. O2 del to the brain is often researched in response to orthostatic stress, however little is known about vascular responses protecting O2 del. In muscle, use of a forearm exercise model is common as measuring O2 del is difficult in other exercise modalities. Unfortunately, it is also difficult to measure/test metabolism in the forearm. Hence, measuring O2 del response to exercise at a known metabolic intensity is difficult. Purpose: To investigate O2 del matching metabolic demand in the following manner: 1) develop a repeatable and reliable critical power (CP, highest sustainable rate of aerobic metabolism) test for the forearm exercise model 2) discover if individual differences in O2 del account for differences in forearm CP (fCP) 3) determine if fCP is sensitive to changes in O2 del 4) characterize cerebral vascular response to an orthostatic challenge Methods: Echo and Doppler ultrasound measured blood flow through the brachial artery. Venous blood samples were used to measure hemoglobin and O2 content for calculations of O2 del and consumption. Middle cerebral blood velocity measured via transcranial Doppler ultrasound. Blood pressure was measured using finger photoplethysmography. Results: 1) fCP can be accurately estimated from a maximal effort handgripping test 2) Inter-individual differences in O2 del account for most of the variance in fCP 3) fCP is sensitive to changes in O2 del 4) cerebral vascular responses blunt cerebral hypoperfusion in response to initial orthostatic hypotension. Conclusions: CP is an exercise characteristic of aerobic metabolism which is dependent on and sensitive to O2 del. Therefore, fCP can be used in the forearm exercise model to research O2 del-metabolism matching. / Thesis (Ph.D, Kinesiology & Health Studies) -- Queen's University, 2013-01-04 15:04:44.391

Thesis (M.S.)--University of British Columbia, 2004. / Includes bibliographical references (leaves 113-121). Also available online (PDF file) by a subscription to the set or by purchasing the individual file.

Thesis (M.S.)--University of British Columbia, 2004. / Includes bibliographical references (leaves 113-121).

Effects of a Short Work/Shorter Rest Intermittent Exercise on Muscle Metabolic Status, VO2, Hemoglobin Saturation and Performance, PhD, 2010, Glen Robert Belfry, Exercise Science, University of Toronto. Abstract Many sports require short duration work periods and short duration rest periods (INT). This dissertation examines the engagement of aerobic and anaerobic energy systems in acute exercise with brief (10 seconds) work and recovery (5 seconds) and the effect of chronic exposure on those systems. The differences between INT and continuous exercise (CONT) of deoxygenated hemoglobin saturation (ΔHHb), the pattern of breath-by-oxygen uptake (VO2) and muscle metabolic status, including, [Pi], [Pi]/[PCr], and [H+] were studied in young healthy adults. The physiological and performance responses to a four week, 12 session cycle ergometer training regime of the CONT and INT protocols were observed. Fluctuations in VO2, ∆HHb, [PCr], and [H+] were observed within the work : recovery duty cycle of INT. Fluctuations of VO2, ΔHHb, and [PCr] may be a function of the priming effects of previous high intensity exercise, inhibition at the locus of metabolic control, and elevated blood flow over the recovery-work transitions. Fluctuations in oxidative phosphorylation were associated with concurrent fluctuations in [PCr]. [Pi] and [PCr] were greater in INT vs CONT, whereas no differences were observed for [H+] between conditions. Reduced [PCr] may be the most appropriate indicator of metabolic stress, not increased [Pi] or [H+]. Similar improvements in aerobic power were observed for CONT and INT training, whereas anaerobic performance was enhanced post-INT training. Collectively the findings indicate that a unique INT exercise protocol facilitates increased muscle blood flow versus continuous exercise, the temporal association of muscle metabolic status, ΔHHb, and pulmonary VO2 with work rate, the apt use of [PCr] as a proxy for metabolic stress, and when this unique INT bout is utilized as a training protocol, adaptations in both aerobic and anaerobic metabolism will occur.

Effects of a Short Work/Shorter Rest Intermittent Exercise on Muscle Metabolic Status, VO2, Hemoglobin Saturation and Performance, PhD, 2010, Glen Robert Belfry, Exercise Science, University of Toronto. Abstract Many sports require short duration work periods and short duration rest periods (INT). This dissertation examines the engagement of aerobic and anaerobic energy systems in acute exercise with brief (10 seconds) work and recovery (5 seconds) and the effect of chronic exposure on those systems. The differences between INT and continuous exercise (CONT) of deoxygenated hemoglobin saturation (ΔHHb), the pattern of breath-by-oxygen uptake (VO2) and muscle metabolic status, including, [Pi], [Pi]/[PCr], and [H+] were studied in young healthy adults. The physiological and performance responses to a four week, 12 session cycle ergometer training regime of the CONT and INT protocols were observed. Fluctuations in VO2, ∆HHb, [PCr], and [H+] were observed within the work : recovery duty cycle of INT. Fluctuations of VO2, ΔHHb, and [PCr] may be a function of the priming effects of previous high intensity exercise, inhibition at the locus of metabolic control, and elevated blood flow over the recovery-work transitions. Fluctuations in oxidative phosphorylation were associated with concurrent fluctuations in [PCr]. [Pi] and [PCr] were greater in INT vs CONT, whereas no differences were observed for [H+] between conditions. Reduced [PCr] may be the most appropriate indicator of metabolic stress, not increased [Pi] or [H+]. Similar improvements in aerobic power were observed for CONT and INT training, whereas anaerobic performance was enhanced post-INT training. Collectively the findings indicate that a unique INT exercise protocol facilitates increased muscle blood flow versus continuous exercise, the temporal association of muscle metabolic status, ΔHHb, and pulmonary VO2 with work rate, the apt use of [PCr] as a proxy for metabolic stress, and when this unique INT bout is utilized as a training protocol, adaptations in both aerobic and anaerobic metabolism will occur.

We sought to determine if compensatory vasodilator and/or pressor responses protect exercising muscle O2 delivery (O2D) under conditions of reduced arterial perfusion pressure, if this is exercise intensity-dependent, and if distinct cardiovascular response phenotypes exist. Ten healthy male subjects (19.5±0.4 years) completed two trials of a ramp protocol forearm isometric handgrip exercise test to exhaustion (2.5 kg increments every 3.5 minutes) in each of forearm above and below heart level (forearm arterial perfusion pressure (FAPP) difference of 29.5±0.97 mmHg). Forearm blood flow ((FBF (ml/min; brachial artery Doppler and echo ultrasound), mean arterial blood pressure (MAP; finger photoplethysmography), and exercising forearm venous effluent (ante-cubital vein catheter) measurements at the end of each work rate (WR) revealed the following. Group level (n=10) Δ FBF was compromised beyond 5 kg WR in above vs. below (P<0.05). There was no evidence of compensatory vasodilator (P=0.21) or pressor (P=0.63) responses. Peak O2D, WR and VO2 were significantly compromised by reduced FAPP (115.6±16.8 vs. 152.0±13.4 mlO2/min, 25.5±1.22 vs. 28.94±1.50 kg and 75.9±5.3 vs. 100.2±8.6 ml/min; P<0.05). In contrast, examination of individual responses revealed distinct cardiovascular response groups with (n=6) vs. without (n=4) compensatory vasodilation with the former having less compromise to submaximal O2D and peak WR (-94.12±23.42 vs. -223.40±36.01 mlO2/min), P<0.05 and -2.5±0.32 vs. -5.32±0.79 kg, P<0.05). In conclusion, exercising forearm muscle hypoperfusion due to reduced FAPP is not compensated for by pressor responses. However, there appear to be distinct phenotypes in which vasodilatory compensation does vs. does not occur, which in the former partially protects O2D and exercise performance. / Thesis (Master, Kinesiology & Health Studies) -- Queen's University, 2012-09-13 16:42:41.751

Doctor of Philosophy / Department of Kinesiology / David C. Poole / The onset of skeletal muscle contractions induces rapid and robust increases in metabolic rate (V̇O₂) and blood flow (Q̇) in order to supply the energetic demands of the muscle. In young healthy populations, these variables increase proportionally to maintain oxygen flux into the myocyte for both sexes. However, while the resultant changes in V̇O₂ and Q̇ conflate to establish adequate driving pressures of oxygen (PO₂), it appears that the underlying control processes express distinct sexual dimorphism. Estrogen is crucial for cardiovascular control for young women through its relationship with nitric oxide (NO) and results in lower blood pressure and risk of cardiovascular disease for women. However, in post-menopausal women and some disease states, such as heart failure (HF), these protections are lost due to reductions in estrogen and NO bioavailability which causes women to catch and surpass men in rates of hypertension and cardiovascular disease. The purpose of this dissertation is to explore the mechanisms responsible for establishing the oxygen delivery-to-utilization matching (Q̇O₂/V̇O₂) necessary for skeletal muscle contractions in health and disease. In the first investigation (Chapter 1), we explored the effect of altered NO bioavailability on spinotrapezius muscle interstitial space PO₂ (PO₂is; determined by Q̇O₂/V̇O₂) of healthy male and female rats. We show that both sexes regulate PO₂is to similar levels at rest and during skeletal muscle contractions. However, modulating NO bioavailability exposes sex differences in this regulation with females having greater reliance on basal NO bioavailability and males having greater responsiveness to exogenous NO. In the second investigation (Chapter 2), we sought to determine whether measures of central and peripheral function in HF rats predicted exercise tolerance (as critical speed (CS)). We showed for the first time, that CS can be resolved in HF animals and that decrements in central cardiac (echocardiography) and peripheral skeletal muscle function (PO₂is) predicted CS. Building upon these findings, the third investigation (Chapter 3) aimed to determine if the sex differences in the control of PO₂is seen in healthy rats translated to greater deficits in HF for females. Furthermore, this investigation sought to determine if five days of dietary nitrate supplementation (an exogenous NO source) would raise PO₂is in HF rats, with a greater effect seen in females. We revealed that HF reduces PO₂is at rest and during skeletal muscle contractions and this negative effect is exacerbated for females. However, elevating NO bioavailability with dietary nitrate increases resting PO₂is and alters the dynamic response during contractions with females potentially being more responsive than males. The results herein reveal the importance of NO in the control of Q̇O₂/V̇O₂ in health. The onset of HF results in deleterious declines in exercise tolerance, which are mediated through reductions in central and peripheral function, due, in part, to attenuated NO bioavailability. This creates intensified Q̇O₂/V̇O₂ dysfunction in females with HF; however, this can potentially be countered with dietary supplementation of inorganic nitrate. Altogether, the present dissertation suggests that targeting NO bioavailability, particularly in female HF patients, could be a beneficial non-pharmaceutical therapeutic strategy.

Master of Science / Kinesiology / Timothy I. Musch / Exercise intolerance characteristic of diseases such as chronic heart failure (CHF) and diabetes is associated with reduced nitric oxide (NO) bioavailability from nitric oxide synthase (NOS), resulting in an impaired microvascular O₂ driving pressure (PO₂mv: O₂ delivery – O₂ utilization) and metabolic control. Infusions of the potent NO donor sodium nitroprusside augment NO bioavailability yet decrease mean arterial pressure (MAP) thereby reducing its potential efficacy for patient populations. To eliminate or reduce hypotensive sequellae NO₂⁻ was superfused onto the spinotrapezius muscle. It was hypothesized that local NO₂⁻ administration would elevate resting PO₂mv and slow PO₂mv kinetics (increased τ: time constant, MRT: mean response time) following the onset of muscle contractions. In 12 anesthetized male Sprague-Dawley rats, PO₂mv of the circulation-intact spinotrapezius muscle was measured by phosphorescence quenching during 180 s of electrically-induced twitch contractions (1 Hz) before and after superfusion of NaNO₂ (30 mM). NO₂⁻ superfusion elevated resting PO₂mv (CON: 28.4 ± 1.1 vs NO₂⁻: 31.6 ± 1.2 mmHg, P ≤ 0.05), τ (CON: 12.3 ± 1.2 vs NO₂⁻: 19.7 ± 2.2 s, P ≤ 0.05) and MRT (CON: 19.3 ± 1.9 vs NO₂⁻: 25.6 ± 3.3 s, P ≤ 0.05). Importantly, these effects occurred in the absence of any reduction in MAP (103 ± 4 vs 105 ± 4 mmHg, pre- and post-superfusion respectively; P ˃ 0.05). These results indicate that NO₂⁻ supplementation delivered to the muscle directly through NO₂⁻ superfusion enhances the blood-myocyte driving pressure of oxygen without compromising MAP at rest and following the onset of muscle contraction. This strategy has substantial clinical utility for a range of ischemic conditions.