Contemporary analysis of outcomes following lower extremity bypass in patients with end-stage renal disease.

This study was designed to compare outcomes following infrainguinal bypass between patients with end-stage renal disease (ESRD) and patients with normal renal function (NRF). Sixty-three patients with ESRD undergoing 78 infrainguinal bypasses from 1990 to 1999 were compared with a concurrent group of 132 age-, race-, and gender-matched patients with NRF undergoing 148 bypasses. Limb salvage and survival were calculated using Kaplan-Meier analysis. Markov decision analysis was used to calculate expected quality-adjusted life years (QALY) with intervention. Mean follow-up was 25 months (range 1-116). The results of our study show that infrainguinal bypass in patients with ESRD and tissue necrosis appears to provide a measurable, but marginal, degree of improvement in quality of life.

Protein kinase C activation before cardioplegic arrest: beneficial effects on myocyte contractility.

OBJECTIVE: A potential intracellular mechanism for the protective effects of myocardial preconditioning is the activation of protein kinase C. The present study tested the hypothesis that a brief period of protein kinase C activation before cardioplegic arrest would provide protective effects on myocyte contractility with subsequent reperfusion and rewarming. METHODS: Left ventricular porcine myocytes were assigned to the following treatments: (1) Protein kinase C/cardioplegia: Protein kinase C activation in myocytes (n = 39) for 3 minutes with a phorbol ester (10(-9) mol/L of phorbol 12-myristate 13-acetate) in oxygenated, normothermic (37 degrees C) cell media. Protein kinase C activation was followed by 2 hours of cardioplegic arrest (K+, 24 mEq/L; HCO3-, 30 mEq/L; 4 degrees C) and a 5-minute reperfusion period (37 degrees C media). (2) Cardioplegia: Myocytes (n = 31), 2 hours of cardioplegic arrest, and a 5-minute reperfusion and rewarming period. Myocyte contractility was measured by means of high-speed videomicroscopy. For comparison purposes, contractile function was examined in myocytes (n = 70) under normothermic control conditions. RESULTS: Myocyte shortening velocity was reduced after cardioplegic arrest when compared with normothermic values (22.3 +/- 1.6 vs 48.8 +/- 2.0 microm/sec, p < 0.0001). Protein kinase C activation before cardioplegic arrest normalized myocyte shortening velocity (48.8 +/- 2.5 microm/sec). Co-incubation with phorbol 12-myristate 13-acetate and chelerythrine (10(-6) mol/L), an inhibitor of protein kinase C, before cardioplegic arrest abolished the protective effects of phorbol 12-myristate 13-acetate pretreatment. CONCLUSION: These results suggest that an endogenous means of providing improved myocardial protection during prolonged cardioplegic arrest can be achieved through a brief period of protein kinase C activation.

Modulation of the renin-angiotensin pathway through enzyme inhibition and specific receptor blockade in pacing-induced heart failure: II. Effects on myocyte contractile processes.

BACKGROUND: The goal of this study was to determine the effects of ACE inhibition alone, AT1 angiotensin (Ang) II receptor blockade alone, and combined ACEI and AT1 Ang II receptor blockade in a model of congestive heart failure (CHF) on isolated LV myocyte function and fundamental components of the excitation-contraction coupling process. METHODS AND RESULTS: Pigs were randomly assigned to one of five groups: (1) rapid atrial pacing (240 bpm) for 3 weeks (n=9), (2) concomitant ACEI (benazeprilat, 0.187 mg x kg(-1) x d(-1)) and rapid pacing (n=9), (3) concomitant AT1 Ang II receptor blockade (valsartan, 3 mg/kg/d) and rapid pacing (n=9), (4) concomitant ACEI and AT1 Ang II receptor blockade (benazeprilat/valsartan, 0.05/3 mg x kg(-1) x d(-1)) and rapid pacing (n=9), and (5) sham controls (n=10). LV myocyte shortening velocity was reduced with chronic rapid pacing compared with control (27.2+/-0.6 versus 58.6+/-1.2 microm/s, P<.05) and remained reduced with AT1 Ang II receptor blockade and rapid pacing (28.0+/-0.5 microm/s, P<.05). Myocyte shortening velocity increased with ACEI or combination treatment compared with rapid pacing only (36.9+/-0.7 and 42.3+/-0.8 microm/s, respectively, P<.05). Myocyte beta-adrenergic response was reduced by >50% in both the rapid pacing group and the AT1 Ang II blockade group and improved by 25% with ACEI and increased by 54% with combined treatment. Both L-type Ca2+ channel density and the relative abundance of sarcoplasmic reticulum Ca2+ ATPase density were reduced with rapid pacing and returned to control levels in the combined ACEI and AT1 Ang II blockade group. CONCLUSIONS: The unique findings of this study were twofold. First, basic defects in specific components of the myocyte excitation-contraction coupling process that occur with CHF are reversible. Second, combined ACEI and AT1 Ang II blockade may provide unique benefits on myocyte contractile processes in the setting of CHF.

Left ventricular regional myocyte contractility in normal and heart failure states.

Fundamental determinants of left ventricular (LV) pump performance are preload, afterload and myocyte contractility. Regional variability in LV end systolic wall stress, an important index of LV afterload, has been well defined in both control and congestive heart failure (CHF) states. The goal of this study was to examine end systolic wall stress and myocyte contractile function in three circumferential regions of the LV in both control and CHF states. Accordingly, LV end systolic wall stress and myocyte velocity of shortening were measured from the basal, mid and apical regions in control pigs (n=5) and following the induction of pacing-induced CHF (3 weeks, 240 beats/min, n=5). LV mid wall, circumferential, end systolic wall stress decreased from base to apex in both control (35+/-7 v 16+/-4 g/cm2, P<0.05) and CHF (155+/-23 v 92+/-24 g/cm2, P<0.05) states. In the CHF group, LV end systolic wall stress was elevated by 300% compared to control values in all regions. LV myocyte velocity of shortening was equivalent in the basal and mid regions of control myocytes (52+/-2 v 57+/-2 m/s), and was higher in the apical region (63+/-3 microm/s, P<0.05). In the CHF group, LV myocyte velocity of shortening was reduced by 45% compared to controls with no regional variation. beta-adrenergic stimulation increased myocyte velocity in both the control and CHF groups, however, regional variation was observed only in the CHF group. These unique results demonstrated that minimal regional variations in myocyte contractile function exist in both control and congestive heart failure states, and does not necessarily parallel patterns of regional LV end systolic wall stress.

Myocardial electrophysiological properties in the presence of an AT1 angiotensin II receptor antagonist.

INTRODUCTION: Blockade of the AT1 angiotensin II (Ang II) receptor has been shown to provide anti-hypertensive effects. However, whether AT1 Ang II receptor antagonists influence myocardial electrophysiological properties remains unclear. METHODS AND RESULTS: Accordingly, atrial and ventricular myocardial electrophysiological properties were examined in adult rat (n = 13) and guinea pig (n = 9) myocardial preparations in the presence of the specific AT1 Ang II receptor antagonist, valsartan (CGP 48933; 0.5, 5, or 500 mumol/L). These concentrations reflect up to 100 fold higher drug concentrations than those observed in clinical trials. Transmembrane potential data were recorded using standard microelectrode techniques at baseline and following superfusion with valsartan. The lower concentrations of valsartan (0.5 and 5 mumol/L) had minimal effects on myocardial electrophysiology. In the presence of 500 mumol/L of valsartan, resting membrane potential increased from baseline in both rat (-82.3 +/- 4.1 vs -76.8 +/- 5.8 mV, p < 0.05) and guinea pig (-81.6 +/- 2.9 vs -76.9 +/- 2.0 mV, p < 0.05) atrial myocardium. Action potential duration at 90% repolarization was increased in guinea pig atrial (91.7 +/- 1.4 vs 80.0 +/- 5.6 ms, p < 0.05) and ventricular (131.1 +/- 8.1 vs 118.7 +/- 8.3 ms, p < 0.05) myocardium following exposure to 500 mumol/L of valsartan. In a separate series of experiments, Ang II (1.0 mumol/L) had no effect on atrial or ventricular action potential characteristics in either species. CONCLUSION: Thus, the effects of valsartan, which were observed only at concentrations 100 fold higher than those reported in clinical trials, may be due to non-specific drug interactions with the myocyte sarcolemma.

Protective effects of adenosine on myocyte contractility during cardioplegic arrest.

BACKGROUND: Adenosine delivery to the left ventricular myocardium has been demonstrated to provide protective effects in the setting of ischemia and reperfusion. However, whether adenosine has direct protective effects on isolated myocytes in the setting of cardioplegic arrest was unclear. METHODS: Isolated porcine left ventricular myocytes were assigned to one of the following treatment groups: (1) cardioplegia: 24 mEq/L K+, 4 degrees C for 2 hours followed by rewarming (cell media, 37 degrees C; n = 29); (2) cardioplegia augmented with adenosine (1 to 200 micromol/L) followed by rewarming (n = 98); and (3) normothermic control (cell media, 37 degrees C, 2 hours; n = 175). Myocyte contractility was measured by computer-aided videomicroscopy. RESULTS: Cardioplegic arrest and rewarming reduced myocyte shortening velocity compared with normothermic control (25.3 +/- 2.5 microm/s versus 50.9 +/- 1.4 microm/s, p < 0.05). Adenosine-augmented cardioplegic arrest improved myocyte contractility with rewarming in a concentration-dependent fashion. For example, cardioplegia augmented with 10 micromol/L adenosine improved myocyte shortening velocity by 33% (33.6 +/- 3.0 microm/s versus 25.3 +/- 2.5 microm/s, p < 0.05), whereas 200 micromol/L adenosine improved shortening velocity by 97% (49.9 +/- 3.4 microm/s vs 25.3 +/- 2.5 microm/s, p < 0.05) compared with conventional cardioplegia. CONCLUSIONS: This study demonstrated concentration-dependent protective effects of adenosine-augmented cardioplegia on myocyte contractile function with subsequent reperfusion and rewarming. These results suggest that stimulation of putative myocyte adenosine receptors may provide enhanced protective effects on myocyte contractile processes during cardioplegic arrest.

Differential effects of novel protamine variants on myocyte contractile function with left ventricular failure.

BACKGROUND: Protamine administration can cause left ventricular (LV) dysfunction, which may have clinical significance in the setting of congestive heart failure (CHF). Protamine variants have recently been constructed with heparin reversal capacity similar to protamine. The purpose of this study was to examine the potential differential effects of these protamine variants on isolated myocyte contractile function in normal myocytes and in myocytes after the development of CHF. METHODS: Contractile function was measured by means of computer-aided videomicroscopy in myocytes from five normal pigs and five pigs with CHF induced by rapid pacing (240 beats/min for 3 weeks). Myocyte contractility was examined in the presence of 40 micrograms/ml native protamine or one of three protamine variants: (1) reduced charge (+18) and lysine substituted for arginine; (2) lysine-substituted variant with glutamic acid substituted for the initial proline; or (3) arginine-rich peptide with a terminal arginine-glycine-aspartic acid (RGD) amino acid sequence. RESULTS: In the presence of native protamine, myocyte percent shortening fell from baseline in both the normal (2.86 +/- 0.15 versus 4.58 +/- 0.08, p < 0.05) and the CHF groups (1.01 +/- 0.06 versus 2.07 +/- 0.05, p < 0.05). With both of the lysine-substituted protamine variants, percent shortening fell from baseline in the normal group (3.42 +/- 0.20 for arginine and 3.74 +/- 0.20 for glutamic acid versus 4.58 +/- 0.08, p < 0.05), and was unchanged in the CHF group (1.94 +/- 0.13 versus 2.07 +/- 0.05, p = 0.34 for arginine; and 1.96 +/- 0.10 versus 2.07 +/- 0.05, p = 0.31, for glutamic acid). However, with the arginine/RGD variant, percent shortening fell from baseline in both the normal (2.86 +/- 0.23 versus 4.58 +/- 0.08, p < 0.05) and the CHF groups (1.32 +/- 0.10 versus 2.07 +/- 0.05, p < 0.05). CONCLUSIONS: Specific changes in the primary and secondary structures of protamine had different effects on myocyte contractile function. Furthermore, the negative effects of lysine-substituted protamine variants on myocyte contractility were less pronounced in both CHF and normal myocytes. Thus protamine variants may be of clinical use, particularly in the setting of preexisting LV dysfunction.

Exercise for coronary artery disease: a cornerstone of comprehensive treatment.

Exercise is effective in both preventing and treating coronary artery disease (CAD). Exercise improves cardiovascular efficiency and, in combination with other measures such as medication use, diet changes, and smoking cessation, may arrest or reverse atherosclerosis. Exercise prescriptions will vary according to disease level or risk, but the basic principle (physiologic evaluation followed by moderate exercise as tolerated) is the same for treatment or prevention. Most patients should work toward at least 20 to 30 minutes of moderate aerobic exercise three or more times a week.

Exercise for mild coronary artery disease.

Early warnings can be potent motivators. If your doctor has told you that you are at risk for the type of heart disease known as coronary artery disease (CAD) or that you have mild CAD, that's your call to action. Your doctor's exercise recommendation is something you can do that may help head off worsening symptoms or a heart attack.

Contributory mechanisms for the beneficial effects of myocyte preconditioning during cardioplegic arrest.

BACKGROUND: Preconditioning protects the myocardium from ischemia and may be a potent means of endogenous cardioprotection during cardioplegic arrest and rewarming. However, fundamental mechanisms that potentially contribute to the beneficial effects of preconditioning during cardioplegic arrest and rewarming remain unclear. Accordingly, the overall goal of the present study was to examine the potential mechanisms by which preconditioning protects myocyte contractile function during simulated cardioplegic arrest and rewarming. METHODS AND RESULTS: Left ventricular isolated porcine myocyte contractile function was examined with the use of videomicroscopy under three conditions: (1) normothermia, maintained in cell medium (37 degrees C) for 2 hours; (2) simulated cardioplegic arrest and rewarming, incubated in crystalloid cardioplegic solution (24 mEq/L K+, 4 degrees C) for 2 hours followed by normothermic reperfusion; and (3) preconditioning/cardioplegic arrest and rewarming, hypoxia (20 minutes) and reoxygenation (20 minutes) followed by simulated cardioplegic arrest and rewarming. Cardioplegic arrest and rewarming caused a decline in steady-state myocyte shortening velocity compared with normothermic controls (22.0 +/- 1.6 versus 57.2 +/- 2.6 microns/s, respectively, P < .05), which was significantly improved with preconditioning (36.1 1.7 microns/s, P < .05). In the next series of experiments, the influence of nonmyocyte cell populations with respect to preconditioning and cardioplegic arrest was examined. Endothelial or smooth muscle cell cultures were subjected to a period of hypoxia (20 minutes) and reoxygenation (20 minutes) and the eluent incubated with naive myocytes, which were then subjected to simulated cardioplegic arrest and rewarming. Pretreatment with the eluent from endothelial cultures followed by cardioplegic arrest and rewarming improved myocyte function compared with cardioplegia-alone values (31.7 +/- 2.2 versus 24.7 +/- 1.6 microns/s, respectively, P < .05), whereas smooth muscle culture eluent pretreatment resulted in no change (23.7 +/- 4.0 microns/s, P = .81). Molecular mechanisms for the protective effects of preconditioning on myocyte contractile processes with cardioplegic arrest and rewarming were examined in a final series of experiments. Adenosine-mediated pathways or ATP-sensitive potassium channels were activated by augmenting cardioplegic solutions with adenosine (200 mumol/L) or the potassium channel opener aprikalim (100 mumol/L), respectively. Both adenosine and aprikalim augmentation significantly improved myocyte function compared with cardioplegia-alone values (53.5 +/- 1.7, 57.6 +/- 2.0 versus 25.7 +/- 1.4 microns/s, respectively, P < .05). CONCLUSIONS: The unique findings from the present study demonstrated that preconditioning provides protective effects on myocyte contractile processes independent of nonmyocyte cell populations and that these effects are mediated in part through the activation of adenosine pathways or ATP-sensitive potassium channels. Thus, preconditioning adjuvant to cardioplegia may provide a novel means of protecting myocardial function after cardioplegic arrest and rewarming.

Direct and interactive effects of cardioplegic arrest and protamine on myocyte contractility.

BACKGROUND: Cardioplegic arrest with rewarming and protamine administration have been implicated in causing transient left ventricular dysfunction perioperatively. However, whether interactive effects between cardioplegic arrest and rewarming with protamine occur with respect to myocyte contractile processes remains unclear. Accordingly, using an isolated myocyte model, the present study tested the hypothesis that simulated cardioplegic arrest with rewarming and protamine would have direct and interactive effects on myocyte contractile function. METHODS: Left ventricular isolated myocyte contractile function was examined using computer-aided videomicroscopy under normothermic conditions (37 degrees C, cell medium; n = 183) and after simulated hypothermic, hyperkalemic cardioplegic arrest with rewarming (4 degrees C, 24 mEq/L K+, 2 hours; then 37 degrees C, cell medium, 5 minutes; n = 268). Myocyte function was then examined in the presence of protamine (10 to 40 micrograms/mL) under normothermic conditions (n = 102) and after cardioplegic arrest with rewarming (n = 175). RESULTS: Myocyte contractile function decreased by 43% from baseline after simulated cardioplegic arrest with rewarming. Under normothermic conditions, protamine (20 micrograms/mL) reduced myocyte contractile function by 43.9% +/- 4.3%, whereas myocyte contractile function decreased by only 31.1% +/- 2.7% with protamine (20 micrograms/mL) after cardioplegic arrest with rewarming. Thus, the negative effects of protamine on myocyte contractility were attenuated after cardioplegic arrest when compared with normothermic conditions. CONCLUSIONS: The present study demonstrated that simulated cardioplegic arrest with rewarming and protamine have direct and interactive effects on myocyte contractile function, which are not additive or synergistic.

Applied physiology of ice hockey.

Today's elite hockey players are physically bigger and have improved levels of physiological fitness when compared with their predecessors. Correspondingly, previous ice hockey studies that have become widely referenced may have little relevance to current players and the way the game is presently played. A great need exists to apply exercise science to the game of ice hockey. Although much has been written about the physiology of ice hockey, there is little information based on well controlled studies. Particularly, there is a paucity of knowledge concerning optimal training schedules, training specificity, recovery profiles and seasonal detraining. Moreover, the reports that do exist have attempted to make comparisons across all levels of skill and talent. Thus, fundamental questions remain as to actual physiological exercise response and specialised training programmes for ice hockey players, particularly at the elite level. There is a demand for new properly designed experiments to find answers pertaining to the appropriate training methods for today's ice hockey players. Future research directions should consider the relationships between performance and such variables as neuromuscular skills, strength, power, peripheral adaptations, travel, hydration, detraining and sport-specific training programmes. Incidence and severity of injury among ice hockey players in relation to fatigue and fitness must also be investigated. Much of the information currently used in ice hockey will remain speculative and anecdotal until these studies are conducted.

Application of impedance cardiography during exercise.

Impedance cardiography has been used over the last 30 years to measure stroke volume on a beat-by-beat basis. Cardiac output has been successfully measured with either upper or lower body exercise during light or moderate workloads. With strenuous exercise, movement artifacts severely limit the acquisition of a quality impedance cardiogram. Advances in computer technology and signal conditioning techniques have created the next generation of impedance cardiograph systems. The purpose of this study was to evaluate such a system, the noninvasive continuous cardiac output monitor (NCCOM3-R7), at rest and during submaximal upright cycle exercise. In addition, the relationships between thoracic impedance (Z(o)), first derivative of the change in thoracic impedance (dZ/dt) and posture were evaluated using the NCCOM3-R7 and the Minnesota impedance cardiograph 304B (MIC). Twenty-eight healthy men and women participated. The Z(o) progressively increased when moving from the supine to seated to standing position with both instruments. However, the NCCOM3-R7 yielded lower Z(o) values and higher dZ/dt values compared with the MIC for all postures. Z(o) and dZ/dt values appear to be dependent upon factors such as posture, gender, electrical current, and characteristics of the instrumentation. Exercise cardiac output values seemed reasonable for most subjects, although population subsets exist where the accuracy must be questioned. The general consensus supported by the impedance literature and reaffirmed by the present observations is that impedance cardiography provides a reasonable estimate of the directional changes in stroke volume and cardiac output during exercise and can be used to monitor changes in thoracic fluid balance. As this technology evolves and is further refined, it will undoubtedly play an increasing role in environmental medicine, exercise stress testing, cardiac rehabilitation, and sports medicine.

Prediction of maximal oxygen uptake from a modified Canadian aerobic fitness test.

The purpose of the present study was to increase the accuracy of prediction of VO2max from the Canadian Aerobic Fitness Test (CAFT) by modifying the protocol and developing a new equation. Males and females between the ages of 15 and 69 years (n = 129) were tested on four occasions. Each subject performed four submaximal step tests (modified CAFT protocol) and a maximal treadmill test. The modification of the protocol consisted of allowing each subject to complete the number of stages needed to reach a target heart rate of 85% of age-predicted maximum. This required adding a new Stage 8 for men and Stages 7 and 8 for women. The prediction equation resulting from regression analysis was, VO2max (ml.kg-1 x min-1) = 32.0 + 16.0 VO2 - 0.24 Age - 0.17 Wt (R2 - 0.77; delta 2 - 26.6), where VO2 = oxygen cost of stepping at the final level (L.min-1), Age = age (yrs), and Wt = body mass (kg).

Sources of variation in oxygen consumption during a stepping task.

Factors that determine oxygen uptake during stepping exercise (modified Canadian Aerobic Fitness Test, CAFT) were examined in 66 women and 55 men. Subjects ranged in age from 15 to 67 yr, VO2max from 22.5 to 76.9, leg length from 75.0 to 101.0 cm, and body mass from 48.4 to 107.7 kg. In accordance with the modified CAFT protocol, subjects stepped at cadences determined by their age and heart rate response. The oxygen demand of stepping at each cadence was measured on two occasions. A paired t-test revealed no significant (P > 0.05) difference in oxygen demand between the repeats and the intraclass correlation coefficient was 0.51. The coefficient of variation of oxygen uptake (ml O2.kg-1.min-1) at a given stepping cadence averaged 10.4%. Regression analysis indicated that little variation in oxygen demand could be explained by simple descriptors of the subjects. Age was weakly related to oxygen demand at a given level (males r = 0.26, females r = 0.58). Stepwise multiple regression of the oxygen uptake at selected stepping cadences on possible independent variables confirmed that little of the variation could be explained by age, aerobic fitness, leg length, or adiposity (maximum R2 = 0.34). We conclude that variation in the oxygen demand of a stepping task can account for a large portion of the error in predicting VO2max from a submaximal stepping test. Our ability to predict the oxygen demand of stepping from subject characteristics is limited.

Selection of a maximal test protocol to validate the Canadian Aerobic Fitness Test.

The purpose of this study was to select a maximal aerobic power test protocol with which to validate a submaximal step test prediction equation. Subjects (N = 129), males and females 15 to 69 years of age, performed one maximal step test and one maximal treadmill test. The maximal treadmill protocol yielded higher peak VO2, ventilation, heart rate, and RER values. An age-predicted maximum heart rate was achieved by 35% of subjects on the step test and 55% on the treadmill. An RER of 1.15 was attained by 22% of the subjects on the step test and 53% on the treadmill. Regression analysis indicated that the submaximal test was more predictive of VO2max when the maximum was attained using the treadmill rather than the maximal step protocol. Peak VO2 values obtained from subjects tested on the treadmill will be used to develop a new prediction equation for the Canadian Aerobic Fitness Test.

Reliability and validity of a fitness assessment for epidemiological studies.

A pilot study was conducted to investigate the applicability of the Canadian Aerobic Fitness Test (CAFT) for use in epidemiological studies. Thirty subjects ranging in age from 18 to 65 were evaluated for cardiorespiratory fitness on four separate visits. Protocols used included maximal treadmill testing, maximal step testing, and the CAFT. Results from these evaluations suggested that (a) habituation to the CAFT was negligible; (b) prediction of VO2max from the CAFT in fit subjects remains a problem and further equation development for this group may be necessary; (c) maximal step-test protocols do not result in unequivocal VO2max determinations and may lead to misclassification of fitness level; and (d) although the CAFT correlates highly to treadmill VO2max (r = 0.90), a relatively large standard error may result in as high as a 13% error in estimating VO2max and may lead to problems in classifying fitness in some populations (e.g., older unfit).

A study to validate the Canadian Aerobic Fitness Test.

Our purpose was to assess the validity of VO2 max values predicted from The Canadian Aerobic Fitness Test (CAFT) by comparing them with peak VO2 values measured during a maximal treadmill protocol. Male and female subjects, 15-69 yr (n = 129), performed two submaximal exercise tests (CAFT protocol), and one maximal treadmill test. There was no significant heart rate habituation between the first two CAFT protocols. Peak VO2 values measured during the treadmill test (TM) were significantly higher than those predicted from the CAFT whether the sample was analyzed overall or categorized by sex. When the sample was categorized by age group, all but groups 1 (15-19) and 6 (60-69) had treadmill peak VO2 values significantly higher than those predicted using Jetté's equation. Using treadmill measured peak VO2 scores as the gold standard, VO2 max predictions using the CAFT protocol and Jetté equation placed individuals of lower fitness levels more accurately than highly fit individuals, into one of five fitness categories.

Acute recovery profile of lung volumes and function after running 5 miles.

The purpose of this study was to characterize the acute changes and recovery profile of lung volumes and function subsequent to strenuous aerobic exercise. Eight experienced runners (X age = 25 yrs; wt = 73 kg; ht = 181 cm) completed three identical 5 mile runs. Determinations were made of forced vital capacity (FVC), residual volume (RV), closing capacity (CC), and pulmonary diffusion capacity (DLCO). Measurement of cardiac output (Q) and stroke volume (SV) occurred simultaneously with the 10 second DLCO breathhold maneuver. Measurements were obtained before and 5, 15 and 25 minutes after each run. FVC was reduced (-4.5%) 5 min post-run with a return to pre-run values by 15 min. CC (+16%) and RV (+18%) remained elevated for at least 30 min post-run. DLCO did not appear to be effected by the run. However, the single-breath DLCO breathhold maneuver consistently caused a fall in SV at rest and during recovery. The hypothesis has been forwarded that an increase in central blood volume post-run accounted for the acute reduction in FVC. The sustained elevation in RV resulted from early closure of the small airways possibly due to an increase in extra-vascular lung water.

Exercise training programs and cardiorespiratory adaptation.

Prudent, proper, and progressive aerobic exercise can improve the efficiency of the cardiorespiratory system. Several physiologic mechanisms interact to enhance the body's functional capabilities. Central cardiac adaptations such as improved pump efficiency and peripheral adjustments related to efficient energy transfer are the principle manifestations of proper exercise training. Related benefits of physical activity include reduction in risk from life style-related diseases, increased energy reserves for the activities of everyday living, and an improved quality of life. Functional exercise testing when administered properly can be used to establish safe exercise prescriptions, evaluate patients at risk, and determine program efficacy. The method of choice is a maximal exercise stress test with direct determination of oxygen uptake. Results from such evaluations help to accurately and safely determine the appropriate exercise prescriptions and establish a patient's physiologic profile. The exercise prescription should encompass an approach that denotes the proper application of frequency, intensity, duration, and mode of exercise. For the noncompetitive athlete, training programs should begin with a gentle progression of low-level intensity activities that encourages compliance and reduces risk. Short-term reachable goals documenting gradual increases in activity have been shown to be successful in terms of compliance and desired benefits. Although intense exercise training may be an ambitious goal for many persons, moderate levels of habitual physical activity are a more realistic goal. The clinician should realize that habitual physical activity is an integral part of a healthy life style. Lack of fitness has been strongly associated with all-cause morbidity and mortality. Obviously, the health potential of exercise cannot be realized if a society remains inactive. It is estimated that 40% of Americans are completely sedentary and another 40% are active at levels well below a threshold that would produce gains in cardiovascular fitness and health. This situation exists even though the US Public Health Service has prioritized the importance of physical fitness and habitual physical activity in maintaining preventive health measures and population health status.