OBJECTIVE:To determine the mechanisms underlying the obesity-induced increase in myocardial lipid peroxidation in the faafa rat. We hypothesized that elevated heart work (ie rate-pressure product), an increased rate of superoxide (O 2 À ) production, total myocardial lipid content, andaor insuf®cient antioxidant defenses are potential contributors to myocardial lipid peroxidation in obesity. DESIGN: Comparative, experimental study of myocardial tissue in 16-week-old lean control (Faa?, normal diet), obese high-fat fed (Faa?, 45% dietary fat), and obese fatty (faafa, normal diet) Zucker rats. MEASUREMENTS: Myocardial work (heart rate  systolic blood pressure), myocardial lipid content, oxidative and antioxidant enzyme activities (citrate synthase (CS), catalase (CAT), glutathione peroxidase (GPX), superoxide dismutase (SOD)), the rate of papillary muscle superoxide radical production in vitro, thiol content, basal and post-oxidative challenge myocardial lipid peroxidation levels using thiobarbituric reactive acid substances (TBARS) and lipid hydroperoxides (PEROX) as indices of lipid peroxidation. RESULTS: Compared to lean controls, the high-fat fed and fatty animals had similar elevations (P`0.05) in myocardial TBARS and PEROX (23%, 25% and 29% 45%, respectively; P`0.05), and elevated susceptibilities to oxidative stress in vitro following exposure to oxidizing agents (P`0.05). Resting heart work was slightly higher (P`0.05) in both the high-fat fed and fatty animals compared to controls. Myocardial lipid content, SOD activities and non-protein thiol (glutathione) levels were elevated (P`0.05) in high-fat fed and fatty animals compared to controls. The rate of superoxide formation by isolated papillary muscles in vitro did not differ among groups (P`0.05). Regression analysis revealed that the myocardial lipid content contributed most to myocardial lipid peroxidation (R 2 0.76, P`0.05). CONCLUSIONS: Myocardial oxidative injury is closely associated with myocardial lipid content, but is not closely correlated with heart work, insuf®cient antioxidant defenses or a greater rate of superoxide production.

The accuracy of two pulse oximeters (Ohmeda 3700 and Biox IIa) was evaluated during cycle ergometer incremental exercise in 10 healthy subjects. The exercise protocol began at 30 W with the power output being increased 15 W.min-1 until volitional fatigue. Ear and finger probe pulse oximetry measurements of available hemoglobin (%Spo2) were compared with arterial oxyhemoglobin fraction of total hemoglobin (%HbO2) measured directly from arterial blood samples using a CO-oximeter. To provide a wide range of %HbO2 values, four subjects exercised under hypoxic conditions [inspired partial pressure of O2 (PIo2) = 107 Torr], while the remaining six subjects exercised under normoxic conditions (PIo2 = 150 Torr). Because carboxyhemoglobin (HbCO) or methemoglobin (MetHb) is not measured by pulse oximeters, %HbO2 was corrected for HbCO and MetHb and expressed as percent arterial O2 saturation of available Hb (%Sao2). Small and insignificant differences (P greater than 0.05) existed between SpO2 (all 3 instruments) and %SaO2 at the lowest work rate and the highest power output achieved. Regression analyses of %SpO2 vs. %SaO2 produced correlation coefficients of r = 0.82 [standard error of the estimate [(SEE) = 1.79], r = 0.89 (SEE = 1.48), and r = 0.93 (SEE = 1.14) for the Biox IIa, Ohmeda 3700 (ear), and the Ohmeda 3700 (finger) pulse oximeters, respectively. We conclude that pulse oximetry, within the above limits of accuracy, is useful in estimating %SaO2 during exercise in healthy subjects.

This investigation was designed to describe alterations in O2 uptake (VO2) and tension development in a contracting in situ gastrocnemious-plantaris muscle preparation during three conditions of reduced O2 delivery [arterial O2 concentration X blood flow (Q)]. The three conditions, hypoxemia (H), ischemia (I), and anemia (A), were matched for O2 delivery. A normoxic normal flow condition was also utilized for comparison. H was produced by respiring the animals with 9% O2 in N2; I was produced by lowering Q, and A was produced by hemodilution with 6% dextran. The stimulation pattern for the isometric tetanic contractions used was 1 train/s, and each train was 200 ms, 70 Hz, and 6 V. The muscle was maximally contracted during each of the experimental conditions, and the conditions were administered in random order. In each bout the contractions continued for 5 min with 30 min of rest between bouts. Samples of arterial and muscle venous blood were obtained during the last 30 s of each bout. VO2 during I (125 ml.kg-1.min-1) was less than during N (145 ml.kg-1.min-1; P < 0.05) and greater than during H or A (104 and 101 ml.kg-1.min-1, respectively; P < 0.05). Venous PO2 (PVO2) was significantly lower during H (17.1 Torr) compared with the other conditions; no differences existed between N, I, and A (26.8, 26.0, and 28.1 Torr, respectively). Tension development was reduced by the reduction of O2 delivery during I, H, and A compared with N. Tension developed among the reduced O2 delivery groups was not significantly different.(ABSTRACT TRUNCATED AT 250 WORDS)

Seven human spinal cord-lesioned subjects (SPL) underwent electrically induced muscle contractions (EMC) of the quadriceps and hamstring muscles for 10 min: 5 min control, 2 min with venous return from the legs occluded, and 3 min postocclusion. Group mean changes in CO2 output compared with rest were +107 +/- 30.6, +21 +/- 25.7, and +192 +/- 37.0 (SE) ml/min during preocclusion, occlusion, and postocclusion EMC, respectively. Mean arterial CO2 partial pressure (PaCO2) obtained from catheterized radial arteries at 15- to 30-s intervals showed a significant (P less than 0.05) hypocapnia (36.2 Torr) during occlusion and a significant (P less than 0.05) hypercapnia (38.1 Torr) postocclusion relative to a group mean preocclusion EMC PaCO2 of 37.5 Torr. Relative to preocclusion EMC, expired ventilation (VE) decreased during occlusion and increased after release of occlusion. However, changes in VE always occurred after changes in end-tidal PCO2 (mean 41 s after occlusion and 10 s after release of occlusion). In the two subjects investigated during hyperoxia, the VE and PaCO2 responses to occlusion and release did not differ from normoxia. We conclude that the data do not support mediation of the EMC hyperpnea in SPL by humoral mechanisms that others have proposed for mediation of the exercise hyperpnea in spinal cord-intact humans.

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