Academic literature on the topic 'Oxygen Consumption, VO2 kinetics, Exercise Physiology'

Abstract Oxygen uptake (VO2) and heart rate (HR) kinetics after exercise are important indicators of fitness and cardiovascular health. However, these variables have been little investigated in resistance exercise (RE). The current study compared post-exercise kinetics of VO2 and the HR among different types of REs. The study included 14 males (age: 26.5±5.4 years, body mass: 80.1±11.4 kg, body height: 1.77±0.07 m, fat content: 11.3±4.6%) with RE experience. Dynamic muscle strength was measured using one repetition maximum (1RM) with regard to the half-squat, bench press, pull-down, and triceps pushdown exercises. The participants performed a maximum number of repetitions at 80% of 1RM for each exercise, separated by a recovery period of 60 minutes. VO2 was measured using ergospirometry. VO2 and HR kinetics were assessed using the time constant of the recovery curves, and excess oxygen consumption (EPOC) was calculated afterward. Significant differences were not observed across the exercises with regard to VO2 kinetics. However, the half-squat exercise elicited a greater EPOC than the bench press and triceps pushdown exercises (p<.05). HR kinetics was slower for the half-squat exercise than for the other exercises (p<.05). These findings confirm that the type of RE influences both the cardiac autonomic response post-exercise and EPOC, but not VO2 kinetics

The purpose of this study is to directly compare the dynamic responses of phosphocreatine (PCr) and P(i) to those oxygen uptake (VO2) measured at the lung during transitions to and from moderate-intensity exercise. Changes in PCr and P(i) were measured by 31P-nuclear magnetic resonance spectroscopy, and changes in VO2 were measured breath by breath by mass spectroscopy during transitions to and from moderate-intensity square-wave ankle plantar flexion exercise in 11 subjects (7 men and 4 women; mean age 27 yr). Three repeated transitions were averaged for improvement in signal-to-noise ratio of phosphate data, and 12 transitions were averaged for VO2 measurements. Averaged transitions were fit with a monoexponential curve for determination of the time constant (tau) of the responses. Mean tau values for on transients of PCr, P(i), and phrase 2 VO2 were 47.0, 57.7, and 44.5 s, respectively, whereas means tau values for off transients were 44.8, 42.1, and 33.4 s, respectively. There were no significant differences between tau values for phosphate- and VO2-measured transients or on and off transients. The similarity of on and off kinetics supports linear first-order respiratory control models. Measurement of phase 2 pulmonary VO2 kinetics to and from moderate-intensity small-muscle-mass exercise reflect muscle phosphate kinetics (and muscle oxygen consumption).

Abstract Abstract 2109 The clinical burden of sickle cell anemia (SCA) has a tremendous impact on physical functioning, including cardiopulmonary fitness, among affected individuals. However, the physiologic basis of exercise limitation remains poorly understood in this population. The objective of our study was to characterize the cardiopulmonary response to maximal exercise and to delineate the physiologic mechanisms responsible for decreased fitness among children and young adults with SCA. Methods: We prospectively performed maximal cardiopulmonary exercise testing (CPET) on 60 subjects with SCA (hemoglobin SS or S/β0 thalassemia) and 20 controls without SCA or sickle cell trait matched for race and gender. CPET was completed using a graded, symptom-limited cycle ergometry protocol with breath-by-breath, gas exchange analysis and pre/post spirometry. The primary outcome of fitness was defined by weight-adjusted, peak oxygen consumption (peak VO2). Slopes for determining oxygen uptake kinetics and ventilatory efficiency were calculated using 10-second averages of data points. We used the V-slope method to determine ventilatory threshold. Bivariate comparisons of continuous data were performed using Student's t-test for independent samples (IBM, SPSS V20). We used multivariate analysis to derive a model for determining independent contributors to peak VO2 in subjects. Results: There was no difference in gender distribution among subjects and controls, but subjects were older (15.1 ± 3.44 vs. 13.2 ±2.9 years, p = 0.03) and had lower hemoglobin (8.8 ±1.3 vs. 12.8 ±1.5 g/dL, p < 0.0001). All subjects met criteria for a maximal test as defined by a respiratory exchange ratio (RER) ≥ 1.1, and in all, testing was terminated due to excessive fatigue. No major adverse events occurred during CPET in any subject. Only 1/60 (1.7%) subjects developed vaso-occlusive pain requiring hospitalization in the 2-week follow-up period after testing. Nearly all of the major indicators of CPET performance and gas exchange were adversely affected in our subjects. Compared to controls, subjects demonstrated significantly lower mean peak VO2 (26.9 ±6.9 vs. 40.6 ±8.2 mL/kg/min, p < 0.0001), even after adjustment for age and hemoglobin. Average total test time (5.6 ±1.3 vs. 7.8 ±2.2 min, p = 0.012) and peak work rate (108 ±37 vs. 151 ±57 watts, p = 0.011) were similarly reduced as was ventilatory threshold (1.01 ±0.29 vs. 1.34 ±0.34 L/min, p < 0.0001), indicating earlier transition to anaerobic metabolism during exercise. Heart rate reserve, the difference between achieved maximal and baseline heart rates, was significantly lower (99 ±14 vs. 111 ±15, p = 0.002) in subjects. Slopes calculated using minute ventilation (VE), expired CO2 (VCO2), VO2 and work rate also indicated significantly reduced ventilatory efficiency (ΔVE/ΔVCO2), oxygen delivery (ΔVO2/ΔWR) and oxygen uptake (ΔVO2/ΔVE) kinetics in subjects versus controls. To examine the physiologic contributors to peak VO2 in subjects with SCA alone, we developed a multivariate model that included age, baseline hemoglobin, heart rate reserve, maximal VE, pre-exercise forced expiratory volume in 1 second, and ventilatory threshold. This model explained 67% of the variability observed in peak VO2 in subjects, with age, maximal VE and ventilatory threshold retaining independent contributions to peak VO2 and ventilatory threshold making the largest contribution with an non-standardized β coefficient of 11.9 (SE ±3.2), p < 0.0001. Conclusions: Maximal CPET is safe in children and young adults with SCA, suggesting that acute exercise challenge is well tolerated in this population even at high levels of exercise intensity and physical exertion. When compared to their peers, children and young adults with SCA demonstrate significantly reduced fitness levels. Exercise limitation in SCA may be attributed to complex derangements in the cardiopulmonary and metabolic responses to exercise that are independent of anemia. Our findings highlight the need to develop targeted exercise training strategies aimed at improving fitness in this population and to assess its impact on overall disease severity. Disclosures: No relevant conflicts of interest to declare.

Previous work with pregnant ewes has shown that acute bouts of exercise may cause changes in plasma hormone concentrations, blood flow distribution, and maternal and fetal temperatures. However, most of these studies do not quantify the chosen exercise intensity through measurement of oxygen consumption (VO2). Therefore the purpose of this study was to statistically model the VO2 response of pregnant sheep to treadmill (TM) exercise to determine the exercise intensities (% maximal VO2) of previous studies. Ewes with either single (n = 9) or twin (n = 5) fetuses were studied from 100 to 130 days of gestation. After 1–2 wk of TM habituation, maximal VO2 (VO2max) was determined by measurements of VO2 (open flow-through method) and blood lactate concentration. VO2 was measured as a function of TM incline (0, 3, 5, and 7 degree) and speed (0.8–3.4 m/s). VO2max averaged 57 +/- 7 (SD) ml.min-1.kg-1, and peak lactate concentration during exercise averaged 22 +/- 2 mmol/l. The relationship between VO2 (ml.min-1.kg-1) and incline (INC) and speed (SP) [VO2 = 0.70(INC) + 13.95(SP) + 1.07(INC x SP) - 1.18] was linear (r2 = 0.94). Our findings suggest that most previous research used exercise intensities less than 60% VO2max and indicate the need for further research that examines the effect of exercise during pregnancy at levels greater than 60% VO2max.

Our purpose was to examine the gas exchange response to exercise in heart transplant (HT) patients and to characterize the O2 uptake kinetics (tau VO2) during successive square-wave on-transients from loadless cycling to moderate exercise. We hypothesized that with a slow heart rate response (and O2 transport limitation) O2 kinetics would be slowed but that with a repeated exercise initiated while the heart rate remained elevated the tau VO2 would be faster. Six male HT patients performed two ramp-function tests to determine peak O2 uptake (1.32 +/- 0.23 l/min) and ventilation threshold (1.02 +/- 0.16 l/min). Patients subsequently completed two repeats of a square-wave forcing function and repeated this on 2 days. Alveolar gas exchange was measured breath by breath. A monoexponential fit of signal-averaged data of the first exercise on-transient (between days) yielded a significantly slower tau VO2 in HT subjects than in healthy men (mean age 47 yr; n = 8) (77 +/- 26 vs. 45 +/- 4 s). With successive exercise (2nd transition) initiated while HR remained elevated the tau VO2 of HT patients was 46 +/- 17 s. The faster O2 kinetics of the second transition suggests that O2 delivery was enhanced and therefore that the tau VO2 may reflect bioenergetic processes controlling the rate of oxidative metabolism.

The work of breathing (WB), and thus the energy requirement of the respiratory muscles, is increased any time minute ventilation (VE) is elevated, by either exercise or voluntary hyperventilation. Respiratory muscle O2 consumption (VRMO2) in humans has generally been estimated by having subjects breathe at a level comparable to that during exercise while the change in O2 consumption (VO2) is measured. The difference between VO2 at rest and during hyperventilation is attributed to the respiratory muscles and is assumed to be similar to VRMO2 during exercise at the same VE. However, it has been suggested that WB differs between exercise and hyperventilation and that WB during exercise is lower than during hyperventilation at the same VE. In this study we measured WB during exercise and hyperventilation and from these measurements estimated VRMO2. WB, VE, and VO2 were measured in five male subjects during rest and during exercise or hyperventilation at levels of VE ranging from 30 to 130 l/min. VE/WB relationship was determined for both hyperventilation and exercise. Multiple regression analysis showed that the shape of the two curves was different (P < 0.0001), with WB at high levels of VE being < or = 25% higher in hyperventilation than in exercise. In a second study in which frequency, tidal volume, and duty cycle were controlled as well as VE, there was no difference in WB between exercise and hyperventilation. VO2 was significantly correlated with WB, and the estimated VRMO2 did not increase as a fraction of total VO2 as exercise intensity rose.(ABSTRACT TRUNCATED AT 250 WORDS)

The present study tested whether, during moderate exercise, 1) the dynamic responses of ADP and changes in free energy of ATP hydrolysis (delta GATP) were similar to those of phosphocreatine [PCr; as would be expected for a simple controller of muscle respiration (QO2)] and 2) the rise in pulmonary O2 uptake (VO2) during cycle exercise would reflect the rise in muscle QO2 indicated by the calf PCr kinetics. The responses of PCr, Pi, ADP, and delta GATP were measured from the calf in five subjects during supine treadle exercise using 31P-magnetic resonance spectroscopy and compared with those for VO2, measured breath by breath during upright cycle exercise. The time constants for delta GATP [24.2 +/- 14.2 (SE) s] were not significantly different from those for PCr (26.3 +/- 17.3 s) and Pi (30.7 +/- 22.5 s) (P > 0.05). The time constants for phase 2 VO2 (29.9 +/- 16.8 s) were also similar to those of PCr. In contrast, the dynamics of ADP were distorted from those of PCr due to dynamic changes in pH. These results are consistent with mechanisms of respiratory control that feature substrate control by PCr or thermodynamic control through changes in delta GATP. However, these results are not consistent with substrate control by ADP in a simple fashion. Furthermore, the similarity of time constants for phase 2 VO2 and muscle PCr suggests that phase 2 VO2 kinetics reflect those of muscle QO2 in healthy subjects during moderate exercise.

Requirements for cellular homeostasis appear to be unchanged between childhood and maturity. We hypothesized, therefore, that the kinetics of O2 uptake (VO2) in the transition from rest to exercise would be the same in young children as in teenagers. To test this, VO2 and heart rate kinetics from rest to constant work rate (75% of the subject's anaerobic threshold) in 10 children (5 boys and 5 girls) aged 7–10 yr were compared with values found in 10 teenagers (5 boys and 5 girls) aged 15–18 yr. Gas exchange was measured breath to breath, and phases I and II of the transition and phase III (steady-state exercise) were evaluated from multiple transitions in each child. Phase I (the VO2 at 20 s of exercise expressed as percent rest-to-steady-state exercise VO2) was not significantly correlated with age or weight [mean value 42.5 +/- 8.9% (SD)] nor was the phase II time constant for VO2 [mean 27.3 +/- 4.7 (SD) s]. The older girls had significantly slower kinetics than the other children but were also found to be less fit. When the teenagers exercised at work rates well below 75% of their anaerobic threshold, phase I VO2 represented a higher proportion of the overall response, but the phase II kinetics were unchanged. The temporal coupling between the cellular production of mechanical work at the onset of exercise and the uptake of environmental O2 appears to be controlled throughout growth in children.

We assessed the linearity of oxygen uptake (VO2) kinetics for several work intensities in four trained cyclists. VO2 was measured breath by breath during transitions from 33 W (baseline) to work rates requiring 38, 54, 85, and 100% of maximal aerobic capacity (VO2max). Each subject repeated each work rate four times over 8 test days. In every case, three phases (phases 1, 2, and 3) of the VO2 response could be identified. VO2 during phase 2 was fit by one of two models: model 1, a double exponential where both terms begin together close to the start of phase 2, and model 2, a double exponential where each of the exponential terms begins independently with separate time delays. VO2 rose linearly for the two lower work rates (slope 11 ml.min-1 W-1) but increased to a greater asymptote for the two heavier work rates. In all four subjects, for the two lighter work rates the double-exponential regression reduced to a single value for the time constant (average across subjects 16.1 +/- 7.7 s), indicating a truly monoexponential response. In addition, one of the responses to the heaviest work rate was monoexponential. For the remaining seven biexponential responses to the two heaviest work rates, model 2 produced a significantly better fit to the responses (P less than 0.05), with a mean time delay for the slow component of 105 +/- 46 s.(ABSTRACT TRUNCATED AT 250 WORDS)

To test the hypothesis that O2 uptake (VO2) dynamics are different in adults and children, we examined the response to and recovery from short bursts of exercise in 10 children (7–11 yr) and 13 adults (26–42 yr). Each subject performed 1 min of cycle ergometer exercise at 50% of the anaerobic threshold (AT), 80% AT, and 50% of the difference between the AT and the maximal O2 uptake (VO2max) and 100 and 125% VO2max. Gas exchange was measured breath by breath. The cumulative O2 cost [the integral of VO2 (over baseline) through exercise and 10 min of recovery (ml O2/J)] was independent of work intensity in both children and adults. In above-AT exercise, O2 cost was significantly higher in children [0.25 +/- 0.05 (SD) ml/J] than in adults (0.18 +/- 0.02 ml/J, P less than 0.01). Recovery dynamics of VO2 in above-AT exercise [measured as the time constant (tau VO2) of the best-fit single exponential] were independent of work intensity in children and adults. Recovery tau VO2 was the same in both groups except at 125% VO2max, where tau VO2 was significantly smaller in children (35.5 +/- 5.9 s) than in adults (46.3 +/- 4 s, P less than 0.001). VO2 responses (i.e., time course, kinetics) to short bursts of exercise are, surprisingly, largely independent of work rate (power output) in both adults and children. In children, certain features of the VO2 response to high-intensity exercise are, to a small but significant degree, different from those in adults, indicating an underlying process of physiological maturation.

The collective purpose of these two studies was to determine a link between the V02 slow component and the muscle activation patterns that occur during cycling. Six, male subjects performed an incremental cycle ergometer exercise test to determine asub-TvENT (i.e. 80% of TvENT) and supra-TvENT (TvENT + 0.75*(V02 max - TvENT) work load. These two constant work loads were subsequently performed on either three or four occasions for 8 mins each, with V02 captured on a breath-by-breath basis for every test, and EMO of eight major leg muscles collected on one occasion. EMG was collected for the first 10 s of every 30 s period, except for the very first 10 s period. The V02 data was interpolated, time aligned, averaged and smoothed for both intensities. Three models were then fitted to the V02 data to determine the kinetics responses. One of these models was mono-exponential, while the other two were biexponential. A second time delay parameter was the only difference between the two bi-exponential models. An F-test was used to determine significance between the biexponential models using the residual sum of squares term for each model. EMO was integrated to obtain one value for each 10 s period, per muscle. The EMG data was analysed by a two-way repeated measures ANOV A. A correlation was also used to determine significance between V02 and IEMG. The V02 data during the sub-TvENT intensity was best described by a mono-exponential response. In contrast, during supra-TvENT exercise the two bi-exponential models best described the V02 data. The resultant F-test revealed no significant difference between the two models and therefore demonstrated that the slow component was not delayed relative to the onset of the primary component. Furthermore, only two parameters were deemed to be significantly different based upon the two models. This is in contrast to other findings. The EMG data, for most muscles, appeared to follow the same pattern as V02 during both intensities of exercise. On most occasions, the correlation coefficient demonstrated significance. Although some muscles demonstrated the same relative increase in IEMO based upon increases in intensity and duration, it cannot be assumed that these muscles increase their contribution to V02 in a similar fashion. Larger muscles with a higher percentage of type II muscle fibres would have a larger increase in V02 over the same increase in intensity.

Peripheral arterial disease results in varying degrees of functional disability. Although principally a disease of the vascular tree, evidence demonstrates a significant contribution from metabolic alterations within ischaemically affected skeletal muscle. This thesis was concerned with better characterising the nature of these metabolic alterations, and their contribution to the functional disability in PAD patients. It also examined the efficacy of dietary carbohydrate supplementation as a therapeutic intervention in PAD. The activity of the pyruvate dehydrogenase complex (PDH) is an important determinant of carbohydrate metabolism, experiment I examined the possibility that the active fraction of PDH (PDHa) is lower than normal in skeletal muscle of patients with intermittent claudication (IC) or patients with chronic limb ischaemia and rest pain (RP). A resting muscle biopsy was taken from the medial gastrocnemius of 11 patients with IC, seven patients with RP and eight healthy control subjects (CON). Biopsies were analysed for PDHa, acetylcarnitine, glycogen and phosphocreatine. In the RP group resting PDHa was 60 percent lower than CON (0.19 ± 0.21 versus 0.53 ± 0.27 mmol.min·1.kg·1 wet wt), but not significantly different (p = 0.09) from IC (0.42 ± 0. i 7 mmol.min·1.kg·1 wet wt); PDHa was not different between IC and CON (p = 0.54). There was no difference in muscle acetylcarnitine and glycogen between the groups, nor were there any associations between PDHa and resting acetylcamitine. Further work is warranted in determining the significance of the reduction in PDHa in the RP group, its relationship to symptoms and amenability to treatment. Study two examined the extent to which resting metabolic changes within ischaemic muscle account for the exercise intolerance in PAD patients with intermittent claudication. Specifically, study two tested the hypothesis that walking intolerance in intermittent claudication (IC) is related to both slowed whole body V02 kinetics and depressed activity of the active fraction of pyruvate dehydrogenase (PDHa) in skeletal muscle. Ten patients displaying IC and eight healthy controls performed two familiarisation and then three maximal incremental walking tests. From these tests averaged estimates of walking time, peak V02 and the time constant of V02 ('t) during submaximal walking were obtained. A muscle sample was taken from the medial gastrocnemius muscle at rest and analysed for PDHa and several other biochemical variables. Walking time and peak V02 were -50 percent lower in IC than controls, and 't was 2-fold higher (p < 0.05). 't was significantly correlated with walking time (r = - 0.72) and peak V02 (r = -0.66) in IC; but not in controls. Resting muscle PDHa tended to be correlated with 't (r = -0.56; p = 0.09) in IC; but not in controls (r = -0.14). A similar correlation was observed between resting ABI and 't (r = -0.63, p = 0.05) in IC. This data demonstrates that impaired V02 kinetics contribute to the reduced walking capacity in IC, and that slowed V02 kinetics may result from both haemodynamic and metabolic factors in claudicants. The final experiment examined the effects of a three-day dietary carbohydrate supplementation regime on walking capacity in claudications and in healthy control subjects. Previous work has demonstrated an ergogenic effect of CHO loading in claudicants, but failed to accurately quantify the magnitude of the improvement in walking capacity, or potential mechanisms involved in the effect. Continuing from study II, eleven PAD patients with intermittent claudication and eight control subjects performed a further two maximal treadmill tests, each preceded by a three day supplemental period. In a randomised blinded fashion, all subjects consumed a total of 700g of glucose polymer dissolved into 6 L of water (CHO), or an equal volume of artificially sweetened water (PLAC) (2Uday with meals). From baseline, walking time was significantly improved in the IC group (660 ± 331 s to 697 ± 313 s) and significantly reduced in the CON group (1335 ± 264 s to 1290 ± 250 s) following CHO. In the IC group the improvement in walking capacity was inversely associated with the initial walking capacity of the patient (r = -0.73, p < 0.05) such that for patients with an initial walking capacity of less than 400 s (n=4) there was a 23% improvement following CHO. Resting, steady state, peak V02 and the kinetics of the transitional response ('t) were unaffected by CHO, however there was an association between the change in walking time and change in 't in the IC group only (r = -0.70, p < 0.05). Resting, steady-state and maximal RER was significantly elevated following CHO in both groups. In the CON group the reduction in walking time was strongly associated with increases in body weight (r = 0.87, p < 0.05). There was no association between the change in walking performance and any muscle measure in the CON group, but in IC the improvement in walking time was inversely associated with resting PDHa (r = -0.65, p < 0.05). This data demonstrates the benefits of CHO supplementation are mainly confined to those patients with greater functional impairments and may be mediated via improvements in V02 uptake kinetics resulting from metabolic alterations within the exercising musculature.

Introdução: A reabilitação cardiopulmonar e metabólica (RCPM) é uma importante estratégia no tratamento da insuficiência cardíaca isquêmica. Entretanto, os seus principais mecanismos de melhora e as correlações com aumento na capacidade de exercício e menos sintomas ainda não estão totalmente esclarecidos. Objetivos: Investigar os efeitos de um programa multidisciplinar de RCPM sobre o tempo de tolerância ao esforço (TLim) e a resposta da fase rápida (fase II) da cinética do consumo de oxigênio (variável relacionada ao desempenho oxidativo muscular) em cardiopatas isquêmicos. Adicionalmente, avaliar as variáveis cardiovasculares, ventilatórias e metabólicas nos TCPE máximo (TRIM) e de endurance (TSCC), além da composição corporal pela bioimpedância elétrica, fração de ejeção (FE) e qualidade de vida. Métodos: Cento e seis pacientes com cardiopatia isquêmica encaminhados ao PRCPM foram submetidos ao TRIM em esteira rolante e, após intervalo de 1 a 7 dias, ao TSCC, com 80% da carga atingida no TRIM. Trinta e sete (37) pacientes foram excluídos, 31 por adesão < 50% às sessões de treinamento, 3 com IMC> 35kg.m-2 e 3 com FE<35%. Após 12 semanas de RCPM, 69 pacientes foram ressubmetidos aos mesmos testes e analisados os efeitos sobre o TLim, fase II da cinética do V\'O2 e a qualidade de vida. Resultados: Os pacientes tiveram evidente redução da sua limitação funcional e 95,6% tornaram-se classe I (pré-RCPM era 62,3%), 4,3% classe II (31,8% antes intervenção) e nenhum mais na classe III da NYHA (5,8% anteriormente), após a intervenção da RCPM. Apresentaram melhora significativa no desempenho ao esforço em ambos protocolos TRIM e TSCC, no entanto, o aumento no tempo de tolerância ao esforço foi quase 3 vezes superior no TSCC. Dentre os diversos sistemas avaliados pelo TCPE, o componente periférico foi o que apresentou melhora mais significativa, principalmente pelo incremento na fase II da cinética do V\'O2, com redução da constante de tempo (tau) ? (p<0,001) e de modo paralelo o mean response time (p <0,001), que engloba também a fase III. Houve redução dos índices isquêmicos ao esforço, bem como da densidade arritmogênica significativa em 37%. Houve melhora significativa em todos os domínios do questionário de vida (p<0,001) e modesta, mas com significância estatística na composição corporal pela BIE com incremento da massa magra e redução da massa gorda após treinamento e, também, da FE. A qualidade de vida se correlacionou com a fase II da cinética do V\'O2 (tau), tanto no sumário físico quanto mental. Na análise de regressão múltipla, o sumário físico pós-RCPM teve como variáveis preditoras a fase II da cinética do V\'O2 e a FE. Conclusões: A RCPM resultou em importantes benefícios fisiológicos e de qualidade de vida aos pacientes com cardiopatia isquêmica com CF predominante I e II. A qualidade de vida esteve associada à obtenção da resposta mais rápida da cinética do V\'O2, que reflete a melhora no metabolismo oxidativo muscular. O treinamento físico regular promoveu retardamento do limiar de isquemia miocárdica e redução da densidade arritmogênica. O TSCC, em relação ao TRIM, detectou ganhos de maior magnitude após o programa de RCPM, como o TLim, e proporcionou a mensuração de novos índices na avaliação das respostas à intervenção do treinamento físico como a cinética do V\'O2
Introduction: Cardiopulmonary and Metabolic Rehabilitation (CPMR) is an important strategy in the treatment of ischemic heart failure. However, their main mechanisms of improvement and correlations with increased exercise capacity and fewer symptoms are still not fully understood. Objectives: To investigate the effects of a multidisciplinary CPMR program on exercise tolerance time (TLim) and the response of the fast phase (phase II) of the kinetics of oxygen consumption (variable related to muscle oxidative performance) in ischemic cardiomyopathy. Additionally, to evaluate cardiovascular, ventilatory and metabolic variables in maximal (Max) and endurance (End) cardiopulmonary tests, and body composition by bioelectrical impedance analysis, ejection fraction (EF) and quality of life. Methods: One hundred and six patients with ischemic cardiomyopathy referred to CPMR underwent Max on a treadmill and, after an interval of 1 to 7 days, the End with 80% load achieved in Max. Thirty-seven (37) patients were excluded, 31 with participation of <50% in the training sessions, 3 with BMI> 35kg.m-2 and 3 with EF <35%. After 12 weeks of CPMR, 69 patients underwent the same tests and analyzed the effects on TLim. Results: The patients had an evident reduction in functional limitation and 95.6% became Class I (pre-CPMR was 62.3%), 4.3% class II (31.8% before intervention) and no longer in class III (5.8% previously), after the intervention of the CPMR. They had significant improvement in performance when effort on both Max and End protocols, however, the increase in exercise tolerance time was nearly 3 times higher in End. Among the various systems assessed by CPET, peripheral component showed the most significant improvement, especially the increase in the phase II kinetics V\'O2, reducing the time constant (tau) ? (p <0.001) and so parallel the mean response time (p <0.001), which also includes the phase III. There was a reduction of ischemic effort indices as well as the significant arrhythmogenic density by 37%. There was significant improvement in all domains of quality of life (p <0.001) and modest, but with statistical significance, in body composition by bioelectrical impedance with increasing lean mass and decreasing fat mass after training and also the EF. The quality of life was correlated with the phase II kinetics V\'O2 (tau), both physical and mental domains. In multiple regression analysis, the physical summary post CPMR had as predictors phase II kinetics V\'O2 and EF. Conclusions: The CPMR has resulted in important physiological benefits and quality of life for patients with ischemic heart disease with predominant NYHA I and II. The quality of life was associated with obtaining more rapid response kinetics V\'O2, reflecting the improvement in muscle oxidative metabolism. Regular physical training promoted retardation in the threshold of myocardial ischemia and reduced arrhythmogenic density. The End, when compared to Max, detected gains of greater magnitude after CPMR as Tlim, and provided the measurement of new indices in the evaluation of responses to the intervention of physical training as the kinetics of V\'O2

The purpose of this dissertation series was to examine oxygen uptake kinetics in skeletal muscle by evaluating responses of local muscle deoxygenation during incremental exercise in healthy individuals using near-infrared spectroscopy (NIRS). Metabolic activity in skeletal muscle, as part of the integrative responses of the cardiovascular, respiratory and neuromuscular systems, are major determinants of an individual’s physical capacity and function. The workings of these systems, called whole-body metabolism, affect the capability of an individual to engage in activities of daily living, to exercise, and participate in athletic performance. Thus, they have a strong impact on health as engagement in physical activity is well known to be effective in improving cardiorespiratory fitness and reducing the risks of chronic disease. At this time, the in vivo relationships between whole-body metabolism and local muscle metabolic activity are not well understood, but with the availability of NIRS technology this is possible. NIRS is a noninvasive optical technique used to continuously measure changes in muscle tissue oxygen saturation locally, allowing interrogation of the functional integration between muscle metabolism and the cardiovascular system in intact human beings, which is what the series of studies in this dissertation evaluate. Healthy adults and adolescents were enrolled as healthy control participants into an observational study evaluating changes in local muscle oxygen uptake in neuromuscular disease during exercise. Participants performed a maximal cardiopulmonary exercise test (CPET) on a recumbent cycle ergometer. Changes in muscle deoxygenation (HHb), reflecting local oxygen uptake, were measured using NIRS and whole-body metabolism was assessed synchronously via expired gas analysis. After an initial increase in HHb at exercise onset, a consistent pattern of plateau in HHb was observed in the healthy participants near the end of peak exercise. Despite increasing workload and oxygen uptake (VO2) in the final minutes of the test, it was unclear what mechanisms were contributing to this HHb response. It was hypothesized that the HHb-Workload relationship evaluated at the time of VO2peak would be non-linear, such that a greater maximum workload achieved at VO2peak would not be linearly matched by greater ΔHHb (i.e., greater total change from rest to VO2peak). First, a critical evaluation of the literature was conducted to explore this hypothesis. Chapter 2 provides the results of a scoping review that was performed in order to better understand the scientific evidence using NIRS that describes the relationships between indices of muscle oxygen saturation and workload during incremental exercise. This formed the basis to pursue the hypothesis-driven research presented in the subsequent chapters, interrogating the overarching question of this dissertation related to the HHb-Workload relationship. The review revealed there are three methodological approaches to examining changes in muscle oxygen saturation and workload, the least common of which was examination of HHb and workload at the VO2peak time point. Changes in muscle oxygen saturation and work have also been studied as the change in muscle oxygenation over the duration of exercise and at a certain time point or intensity during incremental exercise. Based on the literature, it was clear that there was a dearth of research examining the HHb plateau response in relation to work at VO2peak. Accordingly, chapter 3 provides the results of a pilot study that evaluated the relationship between change in HHb (ΔHHb) and the maximum workload (MW) achieved at VO2peak, where it was hypothesized that the relationship at this time point would be non-linear. A polynomial regression model was used to describe the relationship. The results of this study showed that at lower maximum workloads there were initial increases in ΔHHb with increasing maximum workload but at the highest maximum workloads, ΔHHb attenuated. A polynomial model including ΔHHb and MW, with VO2peak (an indicator of cardiorespiratory fitness) as a covariate, best characterized the relationship. Age was not significantly related to ΔHHb or MW, and VO2peak appeared to play a partial role as its inclusion as a covariate helped explain approximately a quarter of the variance, suggesting other factors may be contributing to the attenuated HHb response. From this pilot work it was hypothesized that the attenuation in ΔHHb at higher maximum workloads, and the HHb plateau observed during CPET, could be explained by muscle efficiency. If so, a longer duration and lesser slope of the HHb plateau in the minutes leading up to VO2peak occurs in muscles with higher metabolic efficiency. As muscle efficiency is defined as a ratio of external work accomplished to internal energy expended, the hypothesis, if true, would support a better matching of the internal work (VO2) to the external work (workload on the ergometer). Chapter 4 provides the results of a secondary analysis that sought to determine whether the observed plateau in HHb reflected muscular efficiency by comparing the slope of the HHb plateau (HHb[s]) to a commonly used method of assessing muscle efficiency, delta efficiency (DE). It was hypothesized that HHb[s] and DE would be inversely and significantly correlated, providing a potential mechanism for the attenuated HHb response and a noninvasive method for assessing muscle efficiency. In contrast to the hypothesis, HHb[s] and DE were not associated, suggesting that a mechanism other than muscle efficiency is contributing to the HHb plateau. Collectively, this series of studies demonstrate that there is a need to better understand the relationship between HHb and workload in healthy individuals, because of a paucity of evidence exploring the HHb-MW relationship at VO2peak, the finding that ΔHHb attenuates at higher maximum workloads, and that results suggest the HHb plateau phenomenon cannot be explained by muscle efficiency. Future work should seek to elucidate the mechanism that allows healthy individuals to achieve higher workloads (i.e., continue exercising at high intensity) without further increasing muscle oxygen uptake, in a larger more heterogeneous sample.

This chapter uses an analytic approach to the factors limiting maximal aerobic exercise. A person’s maximal aerobic work is determined by their maximal oxygen consumption (VO2max). Cardiac output is the dominant determinant of VO2 and thus the primary determinant of population differences in VO2max. Furthermore, cardiac output is the product of heart rate and stroke volume and maximum heart rate is determined solely by a person’s age. Thus, maximum stroke volume is the major factor for physiological differences in aerobic performance. Stroke output must be matched by stroke volume return, which is determined by the mechanical properties of the systemic circulation. These are primarily the compliances of each vascular region and the resistances between them. I first discuss the physiological principles controlling cardiac output and venous return. Emphasis is placed on the importance of the distribution of blood flow between the parallel compliances of muscle and splanchnic beds as described by August Krogh in 1912. I then present observations from a computational modeling study on the mechanical factors that must change to reach known maximum cardiac outputs during aerobic exercise. A key element that comes out of the analysis is the role of the muscle pump in achieving high cardiac outputs.