Incremental Exercise Protocol Research Articles

Effect of body incline on cardiac performance.

Maximal cardiac performance is improved in man during upright compared to supine exercise. Whether cardiac performance in quadrupeds is dependent upon body position is unknown. Therefore, we undertook the present investigation to determine if peak cardiac output (Qpeak) would be influenced by body inclination in the Thoroughbred horse. To test the hypothesis, four Thoroughbred horses performed an incremental exercise protocol (speed increased by 1 m/s/min to fatigue) on both a level (L) and inclined (I: 6 degrees) treadmill. Specifically, we hypothesised that Qpeak would be increased on the incline, as this represents a progression towards upright exercise. Cardiac output was determined using the Fick relationship from continuous measurements of pulmonary VO2 and paired arterial (carotid artery or transverse facial) and mixed venous (pulmonary artery) samples. Qpeak was significantly increased on the incline (L: 279 +/- 20; I: 336 +/- 17 l/min; P<0.05), while CaO2 was not significantly different (L: 25.5 +/- 1.1; I: 25.4 +/- 1.9 ml/100 ml), and therefore, whole body O2 delivery (QO2) was significantly increased (L: 70.7 +/- 4.9; I: 84.4 +/- 3.1 l/min; P<0.05). In conclusion, within the scope of this investigation, these data suggest that cardiac performance, as judged by increased Qpeak and QO2, is enhanced in the inclined body position. Furthermore, these findings provide preliminary information that level and incline treadmill exercise tests may yield significantly different results in the Thoroughbred horse and consequently this factor should be considered when interpreting exercise testing and performance data.

Skin Blood Flow in Athletes After Heat Exposure and Exercise Training

Introduction: Exercise training has been shown to shift skin blood flow (SkBF) and sweating thresholds toward lower internal temperatures, and heat acclimation further lowered these thresholds (1). In athletes it is unclear as to whether SkBF to the active region after heat acclimation decreases, remains unchanged or increases during exhaustive competition in the heat. Using a laser-Doppler Blood Flowmeter (LDF) Hales (2) studied athletes with cycle exercise at moderate intensity in a high thermal condition and found relative upper limb SkBF drops near the end of exhaustive exercise. Traveling to international competitions is a way of life for today's top-level athletes. Often the athletes have to travel from a region of mild climate to a region of hot climate for competition, and have to deal with ambient heat and detraining problems. The concerns most coaches have are team traveling and the availability of a local training facility. It is of great interest to examine the extent of heat acclimation with vigorous exercise that could occur in a very short time period. The purpose of this study was to examine the effect of 5 daily sessions of vigorous cycle exercise in the heat on SkBF in athletes trained exclusively in an indoor facility. Methods: During off-season top-ranking male badminton (n = 7) and table-tennis (n = 7) players were recruited & randomly assigned into an experimental (EXP) or control (CON) group. The EXP trained on a cycle ergometer in a hot (37.9 °C) and the CON in a thermal neutral (24.2 °C) environment for 5 consecutive days. The duration of exercise was 25 min/day for day 1 and thereafter an increment of 5 min/day was added, and the intensity was increased from 10% below (day 1) to 5% above (day 5) their ventilatory threshold levels. The experimental protocol was approved by the Institutional Sports Science Research Committee, and informed consents were given by all participants. The following were measured before and after training using an incremental maximal cycle exercise (MXT) protocol: peak VO2, time to exhaustion (min), sweat volume (kg/m2/hr), O2-pulse, biceps (SkBFb) and quadriceps SkBF (SkBFq), mean skin temperature (Ts), and ear canal temperature (Te). SkBF were studied using a LDF (Vasamedics BPM2, MN), and a hardtip pencil probe placed on the surface of the skin, and were recorded at the same time as the skin and ear canal temperatures were taken. LDF values were recorded for 10 sec, and the peak and lowest values were averaged and reported as relative perfusion units. Two-way ANOVAs and Tukey post-hoc tests were used to analyze the data. All tests of statistical significance were set at p < .05 level. Results: The EXP subjects achieved heat acclimation (except sweat volume) in 5 days of repeated heat exposure and exercise. During the incremental MXT the EXP group exhibited: 1) increase in time to exhaustion, from 16.6 to 17.7 min in the hot (p < .05) and from 17.3 to 18.1 min in the thermoneutral conditions (p > .05), 2) lower heart rate in both conditions (p < .05), 3) increase in SkBFb during exercise in the thermoneutral condition (p < .05), 4) reduction in SkBFq during exercise in the hot (p < .05) and increase in SkBFq during exercise in the thermoneutral condition (p < .05), and 5) lower ear canal temperature during exercise in the hot condition (p < .05). These observations were not found in the CON group. Discussion: Two important adaptations were observed after heat acclimation: prolonged time to exhaustion and the ability to lower body temperature and heart rate during exhaustive exercise. After heat acclimation the %SkBFb during maximal cycle exercise in the hot condition was linearly related to workloads and was greater (p < .05) than before acclimation, suggesting that the increase in SkBF to the non-active limbs was needed to enhance the convective mechanism of heat exchange. Our results were inconsistent with Hales et al. (2), and agreed with those of Roberts et al. (1) who observed that after exercise training and heat acclimation during leg exercise forearm SkBF increases. They (1) also found that the threshold for skin vasodilation was shifted to lower internal temperatures relative to pre-acclimation levels. We conclude that reduction in SkBFq decreases blood perfusion to the working tissue, while increased SkBFb enhances convective heat exchange via the skin. The latter is beneficial to these athletes who compete indoors without the advantage of air-conditioning and convective cooling.

Effects of aerosolized albuterol on physiologic responses to exercise in standardbreds.

To examine the effects of an aerosolized beta2-adrenoreceptor agonist, albuterol, on performance during a standardized incremental exercise test in clinically normal horses. 8 Standardbred pacing mares. Clinically normal horses, as judged by use of physical examination, hematologic findings, serum biochemical analysis, and airway endoscopy, were randomly assigned to 2 groups and were given 900 microg of albuterol via a metered-dose inhaler 30 minutes before beginning a standardized incremental exercise test in a crossover design with a 7-day minimum washout. Further examination included measurement of baseline lung mechanics, response to histamine bronchoprovocation, and bronchoalveolar lavage. No significant differences (albuterol vs placebo) were seen for any incremental exercise test variables (ie, maximum oxygen consumption, maximum carbon dioxide consumption, respiratory quotient, treadmill speed at heart rate of 200 beats/min, or number of steps completed during an incremental exercise protocol). Mast cell percentage was significantly (r = -0.84) associated with the concentration of aerosolized histamine that evoked a 100% increase in total respiratory system resistance. No other direct correlations between bronchoalveolar lavage fluid cell types and any indices of exercise capacity or airway reactivity were found. Although no horse had exercise intolerance, 4 horses had airway hyperreactivity with bronchoalveolar lavage fluid mastocytosis; these horses may have been subclinically affected with inflammatory airway disease. In our study, albuterol did not enhance performance in 8 clinically normal racing-fit Standardbreds.

In-vivo intracellular pH at rest and during exercise in patients with essential hypertension

Several studies in isolated cells have reported that intracellular pH (pHi) in individuals with essential hypertension may be relatively alkaline compared to normotensive individuals. Such an abnormality of pHi in hypertension would be consistent with enhanced sodium-hydrogen exchanger activity and may provide potential mechanisms by which hypertension and its complications could develop. To determine in-vivo intracellular pH of skeletal muscle at rest and during recovery from exercise-induced acidosis in hypertensive and normotensive subjects. Using 31-phosphorus magnetic resonance spectroscopy, pHi of the dominant flexor digitorum superficialis was measured in 20 Caucasian subjects (14 male) with essential hypertension and 20 normotensive controls matched for gender, age, race and body mass index. Measurements were made at rest and during the exercise and recovery periods of a stepped incremental maximal exercise protocol. The rate of pHi recovery from exercise-induced acidosis was calculated by linear regression over the first 210 s of recovery from the pHi time plots of respective subjects. Mean resting pHi in the hypertensive (7.05 +/- 0.04) and normotensive groups (7.06 +/- 0.04) were not significantly different. There was a significant effect of gender on pHi: mean pHi was 7.07 +/- 0.03 in males and 7.02 +/- 0.03 in females, respectively (P < 0.0005). The mean intracellular pH achieved by exercise was 6.74 +/- 0.31 in hypertensive individuals and not significantly different in normotensive individuals (6.68 +/- 0.19; P = 0.4). The mean rate of pHi recovery in the hypertensives was 0.08 +/- 0.03 pH units/min and not significantly different in normotensives (0.08 +/- 0.02; P = 0.4). These results contrast with previously documented abnormalities in the control of pHi in hypertension and demonstrate the absence of major in-vivo disturbances of pHi in skeletal muscle, both at rest and during recovery from exercise-induced acidosis, in essential hypertension. Therefore, it is possible that previously documented abnormalities of pHi and activity of the exchanger may be either specific to cell type or not present under in-vivo conditions.

Nitric oxide synthase inhibition does not affect the exercise-induced arterial hypoxemia in Thoroughbred horses.

Because sensitivity of equine pulmonary vasculature to endogenous as well as exogenous nitric oxide (NO) has been demonstrated, we examined whether endogenous NO production plays a role in exercise-induced arterial hypoxemia. We hypothesized that inhibition of NO synthase may alter the distribution of ventilation-perfusion mismatching, which may affect the exercise-induced arterial hypoxemia. Arterial blood-gas variables were examined in seven healthy, sound Thoroughbred horses at rest and during incremental exercise protocol leading to galloping at maximal heart rate without (control; placebo = saline) and with N(omega)-nitro-L-arginine methyl ester (L-NAME) administration (20 mg/kg iv). The experiments were carried out in random order, 7 days apart. At rest, L-NAME administration caused systemic hypertension, pulmonary hypertension, and bradycardia. During 120 s of galloping at maximal heart rate, significant arterial hypoxemia, desaturation of hemoglobin, hypercapnia, hyperthermia, and acidosis occurred in the control as well as in NO synthase inhibition experiments. However, statistically significant differences between the treatments were not found. In both treatments, exercise caused a significant rise in hemoglobin concentration, but the increment was significantly attenuated in the NO synthase inhibition experiments, and, therefore, arterial O(2) content (Ca(O(2))) increased to significantly lower values. These data suggest that, whereas L-NAME administration does not affect pulmonary gas exchange in exercising horses, it may affect splenic contraction, which via an attenuation of the rise in hemoglobin concentration and Ca(O(2)) may limit performance at higher workloads.

Prolonged stage duration during incremental cycle exercise: effects on the lactate threshold and onset of blood lactate accumulation.

The aim of this study was to investigate whether increasing the duration of workloads from 3 min to 8 min during incremental exercise would influence workload (W), oxygen consumption (VO2) and heart rate (HR) at the lactate threshold (LT) and the onset of blood lactate accumulation (OBLA). Two groups of six male cyclists were assigned to a well-trained (WT) and recreational (REC) group on the basis of their performance in a maximal incremental ramp test. Each subject then performed two incremental lactate tests (EXT) consisting of six workloads of either 3 min (EXT3-min) or 8 min (EXT8-min) duration. At the completion of each workload whole capillary blood samples were obtained for the determination of blood lactate (BLa) concentration (mM). Power output (Watts, W), HR and VO2 were averaged in the final minute of each workload as well as in the third minute of the EXT8-min. The workload, HR and VO2 at the LT and OBLA were subsequently determined from the data of EXT3-min and EXT8-min. The results demonstrate that workload and VO2, but not HR, at the LT and OBLA were higher in the WT cyclists. At the same time, the workload at the LT obtained from the results of the EXT3-min was significantly (P < 0.05) higher then the value obtained in the EXT8-min in the WT subjects but not the REC subjects. However, the workload, VO2 and HR at the OBLA, together with the VO2 and HR at the LT were not significantly different when calculated from data obtained from EXT3-min or EXT8-min. The data obtained in this study suggest that incremental exercise protocols using workloads of duration longer than 3 min have the effect of increasing the workload at the LT in well-trained cyclists. However, the OBLA determined in exercise tests using stage increments of either 3 min or 8 min is similar in cyclists of different training status.

Examination of the validity and reliability of the accusport blood lactate analyser

Clough et al. (1997) reported that 95% of lactate values obtained using an Accusport analyser may be up to 2.6 mM below or 2.1 mM above YSI 2300 analyser values over the range 0-16 mM. This variability is substantial and unsuitable for research purposes, The objectives of this study were to re-examine the specific validity and reliability of an Accusport analyser and to develop a regression equation to improve the accuracy of Accusport measurements. Duplicate measurements of lactate concentration were made on both an Accusport (Boehringer Mannheim) and Analox LM3 Multi Channel analyser on 17 blood samples taken from two subjects performing a discontinuous incremental exercise protocol. Analysis of duplicate measurements revealed good test-retest reliability for Accusport (TEM 0.35 mM; SEM 0.24 mM; ICC r = 0.995) and Analox (TEM 0.07 mM; SEM 0.09 mM; ICC r = 0.999). The mean values for duplicate samples recorded on both the Accusport and Analox between the lactate range of 1-13 mM revealed an average difference between the two analysers of 1.7 mM (P< 0.01, range 1.0-2.9 mM) but values demonstrated a high level of association (ICC r = 0.853; P< 0.05). The level of agreement indicated that in 95% of cases the differences would lie between + 0.5 to + 3.0 mM with the Accusport values always higher than Analox. Linear regression analysis calculated the following equation to predict Analox values from Accusport values: Analox = -0.749 + 0.837Accusport (R2 = 0.990). The results showed the portable Accusport analyser to be reliable and it demonstrated good association with Analox LM3 lactate analyser measures. However, a need exists to develop specifically generated regressions from Accusport and Analox LM3 analyser measures to provide more accurate results when interpreting lactate values from Accusport measures taken in the field.

Inhibition of nitric oxide synthase with L-NAME does not increase lactate production at rest or during short-term high-intensity exercise in Thoroughbred horses.

The present study was carried out to determine whether inhibition of nitric oxide (NO) synthase promotes anaerobic metabolism in exercising horses, resulting in a significantly increased blood lactate concentration. N(omega)-nitro-L-arginine methyl ester (L-NAME) is a potent inhibitor of NO synthase that has been tested in horses and other species. Two sets of experiments, namely placebo (saline control) and L-NAME (20 mg/kg, i.v.) studies, were carried out on seven healthy, sound, exercise-trained, Thoroughbred horses in random order, 6 to 7 days apart. In both experiments, an incremental exercise protocol was used and data were obtained at rest, during submaximal exercise performed at 8 m/s on a 4.5% uphill grade, and during galloping at 14 m/s on a 4.5% uphill grade--a workload that not only elicited maximal heart rate and induced exercise-induced pulmonary haemorrhage, but also could not be sustained for more than 90 s. Measurements were also made in the recovery period. Mixed-venous blood samples, obtained at matched intervals in the two sets of experiments, were analysed in triplicate for determining the lactate concentration. Following administration of L-NAME, significant bradycardia occurred at rest (27 +/- 1 vs 37 +/- 2 beats/min in the placebo trials; p<0.0001) as well as during submaximal exercise (183 +/- 4 vs 200 +/- 4 beats/min in the placebo trials; p<0.001), but the heart rate increased during galloping at 14 m/s on a 4.5% uphill grade to reach values observed in the placebo trials (215 +/- 2 beats/min) and significant differences were not found. At rest, the mixed-venous blood lactate concentration was similar in the two experiments. With exercise, the mixed-venous blood lactate concentration increased progressively as work intensity increased in both trials, but significant differences were not found between the placebo and the L-NAME experiments during submaximal exercise, near-maximal exercise or recovery. These experiments demonstrated that inhibition of NO synthase in Thoroughbred horses does not promote enhanced anaerobic metabolism at rest or during short-term incremental exercise leading to galloping at maximal heart rate.

Dynamic exercise discloses different time-related responses in stress hormones.

Responses to stressful events are generally regarded as reactions of the organism to accommodate to or compensate for stress. This reaction is classically described as an activation of the sympathoadrenal system and the hypothalamic-pituitary-adrenocortical (HPA) axis. Activation of the release of growth hormone and prolactin in blood also occurs during various types of stress. Assuming that the stress response is a neuroendocrine mechanism that occurs in anticipation of physical exercise, we investigated whether an incremental exercise protocol can be used as a model stressor to disclose a distinct pattern of activation in these hormonal systems, which would support the notion that these systems have different roles in preparing the organism for physical activity and recovery. Moreover, such a model may help improve our understanding of the endocrine expressions of psychological stress. After an overnight fast, 8 healthy men (age, 19-26 years) cycled at 40, 60, 80, and 100% of the power output at VO2max in successive time blocks of 10 minutes each up to exhaustion. Venous blood was sampled immediately before exercise, at the end of each block, and during the recovery phase 5 and 30 minutes after exercise. Plasma adrenalin and noradrenalin were measured by high-performance liquid chromatography; plasma adrenocorticotropic hormone, beta-endorphin, cortisol, growth hormone, and prolactin were measured by specific immunoassays. Heart rate and levels of blood lactate and adrenalin were measured as markers of workload-related responses. Results showed that increases in heart rate, lactate, adrenalin, noradrenalin, and growth hormone reflected the relative workload, in contrast to increases in adrenocorticotropic hormone, beta endorphin, and prolactin, which were observed only after exercise reached an intensity of 80% VO2max. Increases in cortisol were found just after exhaustion. The delayed response of cortisol may be initiated by a drop in blood glucose levels but may also be considered preparatory to vigorous muscular effort and protective against tissue damage. Measurement of the cumulative response to exercise shows that activation of stress hormones occurs at different time points, supporting the notion that these hormones have different roles in preparing the organism for physical activity and recovery: ie, workload- and effort-related adaptation on one hand and protection against disturbed homeostasis on the other. The delayed response of the HPA axis during incremental exercise contrasts with the nondelayed HPA axis response observed during psychological stress and points to involvement of different neurobiological and cognitive emotional mechanisms.

Ventilation and locomotion coupling in varsity male rowers.

Ventilation and locomotion coupling (entrainment) has been observed and described in rowers during incremental exercise protocols but not during simulated race conditions. The purpose of this descriptive study was to examine ventilation and locomotion entrainment on a breath-by-breath and stroke-by-stroke basis in varsity male rowers during a maximal 2,000-m ergometer test. Eight of eleven rowers entrained ventilation at integral multiples of stroke rate (1:1, 2:1, or 3:1) for at least 120 consecutive seconds, with a 2:1 entrainment pattern being most common. In all 2:1-entrained subjects, inspiration occurred at catch and finish and expiration occurred during the latter portions of drive and recovery. In entrained and unentrained breaths from all rowers, peak flow rates and tidal volumes varied depending on when the breath was initiated during the stroke cycle. Entrained rowers made use of these differences and breathed in a pattern by which they avoided initiating breaths that resulted in reduced tidal volumes. The present data indicated that ventilation was impaired at stroke finish and not at catch, as hypothesized by some previous researchers. Ventilation also appeared to be subordinate to consistent locomotive patterns under race conditions.

Muscular and metabolic responses to moderate-intensity short-term training.

The objectives of this study were to determine the effects of 10 consecutive days of moderate-intensity training on 1) the muscular metabolic response to exercise at 100% of the pre-training maximum rate of oxygen consumption (VO2max); and 2) mitochondrial enzyme markers (citrate synthase, CS; succinate dehydrogenase, SDH; 3-hydroxy-acyl-CoA dehydrogenase, HAD) of oxidative capacity in middle gluteal muscle. Six mature, unfit Thoroughbred horses completed both incremental (for determination of VO2max) and high-intensity exercise protocols before (HI1) and after (HI2) training. Training consisted of 10 consecutive days of running at 55% VO2max for 60 min per day (13-14 km/day). For the HI, horses completed a 10 min warm-up, followed by exercise at 100% of pre-training VO2max (mean speed 9.8 m/s) until fatigue. Training resulted in an 8.9% increases in VO2max (Pre: 142 +/- 4 ml/kg bwt/min; Post: 155 +/- 4 ml/kg bwt/min) and a 24% increase in run time to fatigue during HI. Whereas VO2 during HI was not altered by training, peak values for VCO2 and R were significantly lower following training. Compared to HI1, there was a 45% reduction in the net rate of muscle glycogenolysis during HI2. Peak (end exercise) values for plasma and muscle lactate concentrations decreased by 22 and 23%, respectively, after training. Training also attenuated the exercise-associated increase in plasma norepinephrine, but there was no effect on plasma epinephrine concentrations. Maximal activities of CS, SDH, and HAD were unaltered by training. We conclude that 10 days of moderate-intensity exercise results in decreases in muscle glycogenolysis and anaerobic metabolism during high-intensity exercise at the same absolute workload. Furthermore, development of measurable increases in mitochondrial oxidative potential may not be required for expression of these metabolic adaptations in early training.

Skeletal muscle Na(+)-K(+)-ATPase and K+ homeostasis during exercise: effects of short-term training.

The objective of this study was to determine the effects of 10 consecutive days of moderate intensity training on 1) the concentration of middle gluteal muscle Na(+)-K(+)-ATPase as determined by vanadate-facilitated 3H[ouabain binding; and 2) plasma potassium regulation before, during and after exercise at 100% of the pre-training maximum rate of oxygen consumption (VO2max). Six mature, unfit Thoroughbred horses completed both incremental (for determination of VO2max) and high-intensity exercise protocols before (HI1) and after (HI2) training. There additional horses undertook no training or exercise tests and served as controls for determination of middle gluteal muscle Na(+)-K(+)-ATPase concentration. Training consisted of 10 consecutive days of running at 55% VO2max for 60 min per day (13-14 km/day). For each high intensity exercise protocol, horses completed a 10 min warm-up at 50% VO2max, followed by exercise at 100% of pre-training VO2max (6 degrees incline, mean speed 9.8 m/s) until fatigue. Training resulted in a 13.8% increase in resting plasma volume (pre: 20.9 +/- 0.8 l; post: 23.8 +/- 0.9 l; P = 0.03), and an 8.9% increase in VO2max (pre: 142 +/- 4 ml/kg/min; post: 155 +/- 4 ml/kg/min; P = 0.004) during HI. Peak values for plasma potassium concentration and content during exercise decreased by 13% (P = 0.02) and 7% (P = 0.0002), respectively, after training whereas training had no effect on increases in packed cell volume, plasma total solids, and erythrocyte K+ concentration and content during exercise. Following training, there was also a significant (23%) increase in Na(+)-K(+)-ATPase concentration in biopsies of middle gluteal muscle, as measured by vanadate-facilitated 3H[ouabain binding. We conclude that 10 days of moderate intensity exercise results in increases in skeletal muscle Na(+)-K(+)-ATPase and attenuation in the elevation in plasma K+ during high intensity exercise at the same absolute workload. The increase in middle gluteal muscle Na(+)-K(+)-ATPase concentration is consistent with decreases in K+ efflux from working muscle during exercise.

Pulmonary capillary pressure in horses undergoing alteration of pleural pressure by imposition of various upper airway resistive loads.

We hypothesized that changes in pleural pressure induced by resistive breathing would affect transmural pulmonary artery, pulmonary capillary, and pulmonary wedge pressures. Seven horses were assigned to exercise with each of 4 upper respiratory resistive loads in random order at intervals of at least 2 days: 1) control--no added resistive loads; 2) inspiratory resistive load (Iobst)--left laryngeal hemiplegia; 3) expiratory resistive load (Eobst)--one-way valve in the right nostril; and 4) combined inspiratory and expiratory resistive loads (CIEobst)--left nostril occlusion. On each occasion, the horses performed an incremental exercise protocol consisting of exercise episodes of 3 min duration at 75, 90, and 100% of maximal heart rate (HRmax). Pulmonary artery and oesophageal pressures were recorded continuously. Subsequent analysis was carried out on the pulmonary arterial pressure signal with the oesophageal pressure signal subtracted, hence the pulmonary vascular pressures in this paper approximate transmural pressures. Pulmonary vascular pressures, heart rate, and arterial blood gas tensions were measured at each level of exercise. Pulmonary capillary and pulmonary wedge pressures were determined from the pulmonary artery waveform after dynamic occlusion of a branch of the pulmonary artery. During exercise, peak expiratory oesophageal pressure was more positive in horses with Eobst and CIEobst (adjusted means = 43, and 39 mmHg, respectively) compared with control (adjusted mean = 23 mmHg) (P = 0.0001). Peak inspiratory oesophageal pressure was more negative in horses at exercise with Iobst and CIEobst (adjusted means = -42 and -39 mmHg, respectively) compared with control (adjusted mean = -26 mmHg) (P = 0.0012). Eobst was associated with an increase in mean oesophageal pressure while Iobst was associated with a decrease in mean oesophageal pressure. There were significant increases in mean pulmonary artery pressure in horses with CIEobst (adjusted means = 82 mmHg) and in pulmonary wedge pressure in horses with CIEobst and Iobst (adjusted means = 51, and 55 mmHg, respectively) when compared to control (73 and 42 mmHg, respectively) (P = 0.0001). Pulmonary capillary pressure was significantly increased in horses with CIEobst or Iobst (adjusted means = 61 mmHg, 63 mmHg, respectively) when compared to control (adjusted mean = 50 mmHg)(P = 0.0001). At maximal exercise intensity with inspiratory obstruction, the mean oesophageal (pleural) pressure was -17 mmHg while the mean pulmonary capillary pressure was 77 mmHg. The latter exceeds the reported 75 mmHg threshold for capillary failure in horses. We conclude that inspiratory resistive breathing can lead to a significant increase in transmural pulmonary capillary pressure which may contribute to loss of capillary integrity and rupture.

Nuclear magnetic resonance evidence of different muscular adaptations after resistance training

Objective: To evaluate muscle bioenergetics, muscle cross-sectional area (CSA), and soreness when the gastrocnemius was subjected to concentric and concentric/eccentric resistance training modes. Design: Prospective study, before and after training. The subjects served as their own controls. Setting: Rehabilitation center and nuclear magnetic resonance spectroscopy unit of a university hospital. Participants: Sixteen healthy young volunteers from the local physiotherapist school. Intervention: Two distinct resistive training programs were evaluated on the gastrocnemius: a protocol consisting of concentric contractions only and a mixed concentric/eccentric program. Main Outcome Measures: Maximal isometric resistance was measured after each training session. Before and after training, muscle CSA was appreciated using magnetic resonance imaging, whereas changes in muscle pH, phosphorus metabolite ratios, maximal oxidative power (P max), and oxidative phosphorylation were studied using 31P nuclear magnetic resonance spectroscopy at rest and during an incremental exercise protocol. Results: Magnetic resonance imaging revealed a significant increase (7.1%) in the gastrocnemius CSA in the concentriceccentric group only. The PCr/Pi (8.3 ± 0.9 vs 10.4 ± 1.7) and PCr/ATP (3.68 ± .36 vs 4.07 ± .27) resting ratios increased significantly (p = .008) after concentric-eccentric resistance training. P max was significantly improved in the concentriceccentric group (7.0 ± 2.1W vs 8.4 ± 1.8W: p < .02). This mixed protocol also reduced the incidence of muscular soreness. Conclusion: The data suggest that the improved oxidative mechanical power output could be due mainly to a greater muscle cross-section in the concentric-eccentric group, with circumstantial evidence suggesting a relatively higher type IIa fiber activity.

Physiological parameters during the initial stages of cardiopulmonary exercise testing in patients with chronic heart failure. Their value in the assessment of clinical severity and prognosis.

To analyse the relationship between initial exercise parameters and peak oxygen consumption and prognosis in 96 patients with congestive heart failure. Comparison of responses during the initial 6 min of cardiopulmonary exercise testing (Naughton modified protocol) in patients stratified to the Weber classification, and analysis of their predictive value with respect to peak oxygen uptake and prognosis. All patients had a left ventricular ejection fraction < 0.45 and a valid cardiopulmonary exercise test, during which they remained in sinus rhythm. Significant differences in several parameters were seen in the initial stages, including oxygen pulse (P < 0.04) and ventilation equivalent for oxygen (P < 0.004). These parameters remained as independent predictors of peak oxygen uptake in the algorithm derived from baseline and initial stage variables. In a multivariate Cox proportional hazards model, the predicted peak oxygen uptake (P < 0.003) was an independent predictor of mortality. In patients with congestive heart failure, the initial 6 min parameters of a cardiopulmonary exercise test have additional value in the assessment of clinical severity and prognosis. This may be of clinical relevance since a limited incremental exercise protocol may be more objective than more traditional 6 min walking tests and less demanding.

Cardiorespiratory Response to Exercise After Modified Fontan Operation: Determinants of Performance

Objectives. This study sought to measure the cardiorespiratory responses to exercise and to identify the perioperative determinants of exercise performance in children, adolescents and young adults who underwent the modified Fontan operation.Background. Several studies of the cardiorespiratory responses to exercise after the Fontan operation have demonstrated subnormal maximal oxygen uptake and exercise heart rate, but the perioperative variables that ultimately affect exercise responses have not been assessed systematically.Methods. The study included 59 of the 548 patients who underwent a modified Fontan operation between January 1, 1984 and December 31, 1993 at the Mayo Clinic. Spirometry was performed at rest in all patients before exercise testing. The patients then exercised using a previously calibrated cycle ergometer and a 3-min incremental cycle exercise protocol. Multiple linear regression analysis was used to determine a subset of variables associated with oxygen uptake at peak exercise (V̇o2max), blood oxygen saturation (O2sat) and heart rate at peak exercise (HRmax).Results. V̇o2max ranged from 29% to 95% of normal value; O2sat at peak exercise ranged from 77% to 96%; and HRmax ranged from 39.7% to 97.4% of normal value. Multivariate analysis showed that log V̇o2max/kg2/3was associated with age at exercise, male gender, body surface area, preoperative confluent pulmonary arteries and rest V̇o2max/kg2/3. Preoperative left pulmonary artery stenosis, the presence of a classic Glenn anastomosis at exercise and rest O2sat were associated with O2sat at peak exercise. Age, body surface area at exercise, heart rate at rest and diastolic blood pressure were associated with HRmax at exercise.Conclusions. Subnormal V̇o2max and HRmax values were demonstrated at peak exercise. Several perioperative variables were associated with V̇o2max and O2sat at peak exercise. The presence of a classic Glenn anastomosis was associated with decreased O2sat at peak exercise, suggesting intrapulmonary shunting with the classic Glenn anastomosis.(J Am Coll Cardiol 1997;29:785–90)

Oxygen uptake kinetics during low intensity exercise: relevance for rate adaptive pacemaker programming.

OBJECTIVE: To establish a normal database for oxygen uptake (VO2) kinetics during low intensity treadmill exercise (LITE) testing, to be used as a guideline for programming rate adaptive pacemakers, and...

Cellular bioenergetics after erythropoietin therapy in chronic renal failure.

After erythropoietin (rHuEPO) therapy, patients with chronic renal failure (CRF) do not improve peak O2 uptake (VO2 peak) as much as expected from the rise in hemoglobin concentration ([Hb]). In a companion study, we explain this phenomenon by the concurrent effects of fall in muscle blood flow after rHuEPO and abnormal capillary O2 conductance observed in CRF patients. The latter is likely associated with a poor muscle microcirculatory network and capillary-myofiber dissociation due to uremic myopathy. Herein, cellular bioenergetics and its relationships with muscle O2 transport, before and after rHuEPO therapy, were examined in eight CRF patients (27 +/- 7.3 [SD] yr) studied pre- and post-rHuEPO ([Hb] = 7.8 +/- 0.7 vs. 11.7 +/- 0.7 g x dl-1) during an incremental cycling exercise protocol. Eight healthy sedentary subjects (26 +/- 3.1 yr) served as controls. We hypothesize that uremic myopathy provokes a cytosolic dysfunction but mitochondrial oxidative capacity is not abnormal. 31P-nuclear magnetic resonance spectra (31P-MRS) from the vastus medialis were obtained throughout the exercise protocol consisting of periods of 2 min exercise (at 1.67 Hz) at increasing work-loads interspersed by resting periods of 2.5 min. On a different day, after an identical exercise protocol, arterial and femoral venous blood gas data were obtained together with simultaneous measurements of femoral venous blood flow (Qleg) to calculate O2 delivery (QO2leg) and O2 uptake (VO2leg). Baseline resting [phosphocreatine] to [inorganic phosphate] ratio ([PCr]/[Pi]) did not change after rHuEPO (8.9 +/- 1.2 vs. 8.8 +/- 1.2, respectively), but it was significantly lower than in controls (10.9 +/- 1.5) (P = 0.01 each). At a given submaximal or peak VO2leg, no effects of rHuEPO were seen on cellular bioenergetics ([PCr]/[Pi] ratio, %[PCr] consumption halftime of [PCr] recovery after exercise), nor in intracellular pH (pHi). The post-rHuEPO bioenergetic status and pHi, at a given VO2leg, were below those observed in the control group. However, at a given pHi, no differences in 31P-MRS data were detected between post-rHuEPO and controls. After rHuEPO, at peak VO2, Qleg fell 20% (P < 0.04), limiting the change in QO2leg to 17%, a value that did not reach statistical significance. The corresponding O2 extraction ratio decreased from 73 +/- 4% to 68 +/- 8.2% (P < 0.03). These changes indicate that maximal O2 flow from microcirculation to mitochondria did not increase despite the 50% increase in [Hb] and explain how peak VO2leg and cellular bioenergetics (31P-MRS) did not change after rHuEPO. Differences in pHi, possibly due to lactate differences, between post-rHeEPO and controls appear to be a key factor in the abnormal muscle cell bioenergetics during exercise observed in CRF patients.

Effects of erythropoietin on muscle O2 transport during exercise in patients with chronic renal failure.

Erythropoietin (rHuEPO) has proven to be effective in the treatment of anemia of chronic renal failure (CRF). Despite improving the quality of life, peak oxygen uptake after rHuEPO therapy is not improved as much as the increase in hemoglobin concentration ([Hb)] would predict. We hypothesized that this discrepancy is due to failure of O2 transport rates to rise in a manner proportional to [Hb]. To test this, eight patients with CRF undergoing regular hemodialysis were studied pre- and post-rHuEPO ([Hb] = 7.5 +/- 1.0 vs. 12.5 +/- 1.0 g x dl-1) using a standard incremental cycle exercise protocol. A group of 12 healthy sedentary subjects of similar age and anthropometric characteristics served as controls. Arterial and femoral venous blood gas data were obtained and coupled with simultaneous measurements of femoral venous blood flow (Qleg) by thermodilution to obtain O2 delivery and oxygen uptake (VO2). Despite a 68% increase in [Hb], peak VO2 increased by only 33%. This could be explained largely by reduced peak leg blood flow, limiting the gain in O2 delivery to 37%. At peak VO2, after rHuEPO, O2 supply limitation of maximal VO2 was found to occur, permitting the calculation of a value for muscle O2 conductance from capillary to mitochondria (DO2). While DO2 was slightly improved after rHuEPO, it was only 67% of that of sedentary control subjects. This kept maximal oxygen extraction at only 70%. Two important conclusions can be reached from this study. First, the increase in [Hb] produced by rHuEPO is accompanied by a significant reduction in peak blood flow to exercising muscle, which limits the gain in oxygen transport. Second, even after restoration of [Hb], O2 conductance from the muscle capillary to the mitochondria remains considerably below normal.

Factors which alter the relationship between ventilation and carbon dioxide production during exercise in normal subjects.

The slope of the linear relationship between ventilation (V(E)) and carbon dioxide production (VC0(2)) has been thought to indicate that VC0(2) is one of the major stimuli to V(E). A group of 15 normal subjects undertook different incremental treadmill exercise protocols to explore the relationship between V(E) and VCO(2). An incremental protocol using 1 instead of 3-min stages of exercise resulted in an increase in the V E to VCO(2) ratio [26.84 (SEM 1.23) vs 31.08 (SEM 1.36) (P <0.008) for the first stage, 25.24 (SEM 0.86) vs 27.83 (SEM 0.91) (P <0.005) for the second stage and 23.90 (SEM 0.86) vs 26.34 (SEM 0.81) (P = 0.001) for the third stage]. Voluntary hyperventilation to double the control level of V(E) during exercise resulted in an increase in the V(E) to VCO(2) slope [from 21.3 (SEM 0.71) for the control run to 35.1 (SEM 1.2) for the hyperventilation run (P <0.001)]. Prolonged hyperventilation (5 min) during exercise at stage 2 of the Bruce protocol resulted in a continued elevation of VCO(2) and the V(E)/VCO(2) slope. A steady state of V(E) and metabolic gas exchange can only be said to have been present after at least 3 min of exercise. Voluntary hyperventilation increased the slope of the relationship between V(E) and VCO(2). End-tidal carbon dioxide fell, but remained within the normal range. These results would suggest that a non-carbon dioxide factor may have been responsible for the increase we found in V(E) during exercise, and that factors other than increased dead space ventilation can cause an increased ventilation to VCO(2) slope, such as that seen in some pathophysiological conditions, such as chronic heart failure.