Norman L Jones

How should we measure function in patients with chronic heart and lung disease

To elucidate the characteristics of measures of function in patients with chronic heart failure and chronic lung disease we administered four functional status questionnaires, a 6-min walk test and a cycle ergometer exercise test, to 43 patients limited in their day to day activities as a result of their underlying heart or lung disease. Correlations between these measures were calculated using Spearmans rank order correlation coefficient. The walk test correlated well with the cycle ergometer (r = 0.579), and almost as well with the four functional status questionnaires (r = 0.473-0.590) as the questionnaires did with one another (0.423-0.729). On the other hand, correlations between cycle ergometer results and the questionnaires was in each case 0.295 or lower, and none of these correlations reached statistical significance. These results suggest that exercise capacity in the laboratory can be differentiated from functional exercise capacity (the ability to undertake physically demanding activities of daily living) and that the walk test provides a good measure of function in patients with heart and lung disease.

Effects on quality of life with comprehensive rehabilitation after acute myocardial infarction

Abstract This investigation was designed to determine the impact of a brief period of cardiac rehabilitation, initiated within 6 weeks of acute myocardial infarction (AMI), on both disease-specific and generic health-related quality of life, exercise tolerance and return to work after AMI. With a stratified, parallel group design, 201 low-risk patients with evidence of depression or anxiety, or both, after AMI, were randomized to either an 8-week program of exercise conditioning and behavioral counseling or to conventional care. Although the differences were small, significantly greater improvement was seen in rehabilitation group patients at 8 weeks in the emotions dimension of a new disease-specific, health-related Quality of Life Questionnaire, in their state of anxiety and in exercise tolerance. All measures of health-related quality of life in both groups improved significantly over the 12-month followup period. However, the 95% confidence intervals around differences between groups at the 12-month follow-up effectively excluded sustained, clinically important benefits of rehabilitation in disease-specific (limitations, −2.70, 1.40; emotions, −4.86, 1.10, where negative values favor conventional care and positive values favor rehabilitation) and generic health-related quality of life (time trade-off, −0.062, 0.052; quality of well-being, −0.042, 0.035) or in exercise tolerance (−38.5, 52.1 kpm/min); also, return to work was similar in the 2 groups (relative risk, 0.93; confidence interval, 0.71, 1.64). It is concluded that in patients with evidence of depression or anxiety, or both, exercise conditioning and behavioral counseling after AMI was associated with an accelerated recovery in some outcome measures at 8 weeks, but by 12 months similar improvements were seen in both diseasespecific and generic health-related quality of life and in other outcome measures when compared with conventional care in this community.

Economic evaluation of cardiac rehabilitation soon after acute myocardial infarction

Abstract Although there are extensive clinical evaluations of cardiac rehabilitation after acute myocardial infarction (AMI), no full economic evaluation is available. Patients with AMI and mild to moderate anxiety or depression, or both, while still in hospital were randomized to either an 8-week rehabilitation intervention (n = 99) or usual care (n = 102). Comprehensive costs and health-related quality of life, measured with the time trade-off preference score, were obtained in a 12-month trial, and together with survival data derived from published meta-analyses, cost-utility and cost-effectiveness of early cardiac rehabilitation were estimated. The best estimate of the incremental net direct 12-month costs for patients randomized to rehabilitation was

Regulation of skeletal muscle glycogen phosphorylase and PDH during maximal intermittent exercise.

480 (United States, 1991)/ patient. During 1-year follow-up, rehabilitation patients had fewer “other rehabilitation visits” (p

Usefulness of weightlifting training in improving strength and maximal power output in coronary artery disease

The time course for the activation of glycogen phosphorylase (Phos) and pyruvate dehydrogenase (PDH) and their allosteric regulators was determined in human skeletal muscle during repeated bouts of maximal exercise. Six subjects completed three 30-s bouts of maximal isokinetic cycling separated by 4-min recovery periods. Muscle biopsies were taken at rest and at 6, 15, and 30 s of exercise during bouts 1 and 3. Phos was rapidly activated within the first 6 s of bout 1 from 12% at rest to 47% at 6 s. The activation of PDH increased from 14% at rest to 48% at 6 s and 95% at 15 s of bout 1. Phos reverted back to basal values at the end of the first bout, whereas PDH remained fully activated. In contrast, in the third bout, PDH was 42% at rest and was activated more rapidly and was nearly completely activated by 6 s, whereas Phos remained at basal levels (range 14-20%). Lactate accumulation was marked in the first bout and increased progressively from 2.7 to 76.1 mmol/kg dry wt with no further increase in bout 3. Glycogen utilization was also marked in the first bout and was negligible in bout 3. The rapid activation of Phos and slower activation of PDH in bout 1was probably due to Ca2+ release from the sarcoplasmic reticulum. Lactate accumulation appeared to be due to an imbalance of the relative activities of Phos and PDH. The increase in H+ concentration may have served to reduce pyruvate production by inhibiting Phos transformation and may have simultaneously activated PDH in the third bout such that there was a better matching between pyruvate production and oxidation and minimal lactate accumulation. As each bout progressed and with successive bouts, there was a decreasing ability to stimulate substrate phosphorylation through phosphocreatine hydrolysis and glycolysis and a shift toward greater reliance on oxidative phosphorylation.

SPRINT TRAINING ENHANCES IONIC REGULATION DURING INTENSE EXERCISE IN MEN

The effects of 10 weeks (20 sessions) of combined weightlifting and aerobic training (n = 10) were compared with the effects of aerobic training alone (n = 8) on indexes of strength and aerobic exercise capacity in 18 men with coronary artery disease (CAD). Initial test performance was similar between groups. After aerobic training, the maximal load that could be lifted once only (1-repetition maximum) in single-arm curl, single-leg press and single-knee extension exercises increased by 13% (11.8 to 13.3 kg; p less than 0.01), 4% (97.0 to 101.0 kg; difference not significant) and 5% (28.2 to 29.7 kg; difference not significant), respectively; corresponding gains with combined weightlifting and aerobic training were 43% (12.2 to 17.4 kg; p less than 0.01), 21% (99.0 to 120.0 kg; p less than 0.01) and 24% (29.0 to 36.0 kg; p less than 0.01). After aerobic training, the initial 1-repetition maximum could be lifted an average of 4 times, compared with 14 times after combined training. Maximal progressive incremental cycle ergometer power output increased by 2% in the aerobic control group (1,088 to 1,113 kpm/min; difference not significant) and by 15% (1,030 to 1,180 kpm/min; p less than 0.05) in the experimental group. Cycling time at 80% of initial maximal power before attaining a Borg (0 to 10) rating of perceived exertion of 7 (very severe) increased by 11% (604 to 672 seconds; difference not significant) and by 109% (541 to 1,128 seconds; p less than 0.05) in the control and weight-trained patients, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Enhanced pulmonary and active skeletal muscle gas exchange during intense exercise after sprint training in men

1 This study investigated the effects of 7 weeks of sprint training on changes in electrolyte concentrations and acid‐base status in arterial and femoral venous blood, during and following maximal exercise for 30 s on an isokinetic cycle ergometer. 2 Six healthy males performed maximal exercise, before and after training. Blood samples were drawn simultaneously from brachial arterial and femoral venous catheters, at rest, during the final 10 s of exercise and during 10 min of recovery, and analysed for whole blood and plasma ions and acid‐base variables. 3 Maximal exercise performance was enhanced after training, with a 13% increase in total work output and a 14% less decline in power output during maximal cycling. 4 The acute changes in plasma volume, ions and acid‐base variables during maximal exercise were similar to previous observations. Sprint training did not influence the decline in plasma volume during or following maximal exercise. After training, maximal exercise was accompanied by lower arterial and femoral venous plasma [K+] and [Na+] across all measurement times (P < 0.05). Arterial plasma lactate concentration ([Lac−]) was greater (P < 0.05), but femoral venous plasma [Lac−] was unchanged by training. 5 Net release into, or uptake of ions from plasma passing through the exercising muscle was assessed by arteriovenous concentration differences, corrected for fluid movements. K+ release into plasma during exercise, and a small net K+ uptake from plasma 1 min post‐exercise (P < 0.05), were unchanged by training. A net Na+ loss from plasma during exercise (P < 0.05) tended to be reduced after training (P < 0.06). Release of Lac− into plasma during and after exercise (P < 0.05) was unchanged by training. 6 Arterial and venous plasma strong ion difference ([SID]; [SID] =[Na+]+[K+]–[Lac−]–[Cl−]) were lower after training (mean differences) by 2.7 and 1.8 mmol l−1, respectively (P < 0.05). Arterial and femoral venous C02 tensions and arterial plasma [HCO3−] were lower after training (mean differences) by 1.7mmHg, 4.5mmHg and 1.2mmol l−1, respectively (P < 0.05), with arterial plasma [H+] being greater after training by 2.2 nmol 1−1 (P < 0.05). 7 The acute changes in whole blood volume and ion concentrations during maximal exercise were similar to previous observations. Arterial and femoral whole blood [K+] and [Cl−] were increased, whilst [Na+] was lower, across all observation times after training (P < 0.05). 8 Net uptake or release of ions by exercising muscle was assessed by arteriovenous whole blood concentration differences, corrected for fluid movements. A net K+ uptake by muscle occurred at all times, including exercise, but this was not significantly different after training. An increased net Na+uptake by muscle occurred during exercise (P < 0.05) with greater Na+ uptake after training (P < 0.05). Net muscle Lac− release and Cl− uptake occurred at all times (P < 0.05) and were unchanged by training. 9 Sprint training improved muscle ion regulation, associated with increased intense exercise performance, at the expense of a greater systemic acidosis. Increased muscle Na+ and K+ uptake by muscle during the final seconds of exercise after training are consistent with a greater activation of the muscle Na+‐K+ pump, reduced cellular K+ loss and the observed lesser rate of fatigue. The greater plasma acidosis found after sprint training was caused by a lower arterial plasma [SID] due to lower plasma [K+] and [Na+], and higher plasma [Lac−].

A quantitative physicochemical approach to acid-base physiology

1 This study investigated the effects of 7 weeks of sprint training on gas exchange across the lungs and active skeletal muscle during and following maximal cycling exercise in eight healthy males. 2 Pulmonary oxygen uptake (V̇O2) and carbon dioxide output (V̇CO2) were measured before and after training during incremental exercise (n= 8) and during and in recovery from a maximal 30 s sprint exercise bout by breath‐by‐breath analysis (n= 6). To determine gas exchange by the exercising leg muscles, brachial arterial and femoral venous blood O2 and CO2 contents and lactate concentration were measured at rest, during the final 10 s of exercise and during 10 min of recovery. 3 Training increased (P < 0.05) the maximal incremental exercise values of ventilation (V̇E, by 15.7 ± 7.1%), V̇CO2 (by 9.3 ± 2.1%) and V̇O2 (by 15.0 ± 4.2%). Sprint exercise peak power (3.9 ± 1.0% increase) and cumulative 30 s work (11.7 ± 2.8% increase) were increased and fatigue index was reduced (by −9.2 ± 1.5%) after training (P < 0.05). The highest V̇E, V̇CO2 and V̇O2 values attained during sprint exercise were not significantly changed after training, but a significant (P < 0.05) training effect indicated increased V̇E(by 19.2 ± 7.9%), V̇CO2(by 9.3 ± 2.1%) and V̇O2(by 12.7 ± 6.5%), primarily reflecting elevated post‐exercise values after training. 4 Arterial O2 and CO2 contents were lower after training, by respective mean differences of 3.4 and 21.9 ml l−1 (P < 0.05), whereas the arteriovenous O2 and CO2 content differences and the respiratory exchange ratio across the leg were unchanged by training. 5 Arterial whole blood lactate concentration and the net lactate release by exercising muscle were unchanged by training. 6 The greater peak pulmonary V̇O2 and V̇CO2 with sprint exercise, the increased maximal incremental values, unchanged arterial blood lactate concentration and greater sprint performance all point strongly towards enhanced gas exchange across the lungs and in active muscles after sprint training. Enhanced aerobic metabolism after sprint training may contribute to reduced fatigability during maximal exercise, whilst greater pulmonary CO2 output may improve acid‐base control after training.

Measurement of mixed venous carbon dioxide pressure by rebreathing during exercise

An approach to acid-base physiology based on quantitative relationships between systems is presented. Key elements in the approach advocated by Stewart are, first, that changes in H+ or protons and bicarbonate are not considered primary, or initiating disturbances, but rather as changes that are dependent on the interactions between several systems. Secondly, the Henderson-Hasselbalch equation is not used as a control equation; [H%] is not controlled by changes in PCO2 and/or [HCO3]. Thirdly, the independent variables within the systems may be used to describe their interaction in aqueous solutions, using a series of equations easily solved by computer. In plasma, the systems and variables are strong ions (strong ion difference, SID); weak acids, or buffers (ion equivalence of total protein concentration, AtOt); and carbon dioxide (PCO2, as influenced by alveolar ventilation). This system provides a quantitative description of the interplay between systems, and it makes it much simpler to understand the effects of ion movements between cells and plasma, renal control of acid-base, the influence of metabolism, and management of acid-base disorders.

Effects of respiratory alkalosis on human skeletal muscle metabolism at the onset of submaximal exercise.

This study compared rebreathing methods currently used for the measurement of mixed venous PCO2 (PVCO2) during exercise. Four mathematical procedures were used to derive the asymptote of the exponential rise in end-tidal PCO2 during 15 sec rebreathing of low (2-6%) CO2 mixtures (exponential methods); the derived PVCO2 was compared to that obtained with an equilibrium method, in which high CO2 mixtures were rebreathed to obtain an equilibrium of CO2 between the lungs and rebreathing bag. Precision was established by analysing duplicate rebreathings at each power output. The most precise of the four exponential procedures (coefficient of determination 0.98) used iterative statistical analysis to obtain an equation for the best fit curve of end-tidal PCO2 with time (t), solved for t = 20 sec. The PVCO2 derived by this procedure was similar to that obtained by the equilibrium method (r = 0.96), and both yielded estimates of cardiac output that were within the previously published expected range. Variations in the initial rebreathing bag volume and CO2 concentration, and in the breathing frequency during rebreathing had little effect on the derived PVCO2.