Predicting the oxygen cost of air-braked ergometry.
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The results of a randomized double-blind study with two comparable treatment groups are reported. In the course of treatment the frequency of angina pectoris during exercise as measured by a 4-point rating scale of symptom intensity decreased significantly for both groups. In comparison to the base line data the mean total workload increased significantly in both treatment groups (Molsidomin from 379 to 526 watt min; ISDN from 382 to 524 watt min-1). The product of systolic blood pressure and heart rate (BP X HR) under maximal workload increased significantly in both groups (Molsidomin from 17.5 to 20.9 mmHg min-1 1000(-1); ISDN from 17.7 to 20.2 mmHg min-1 1000(-1). The decrease in the ischaemic ST-segment depression on the level of maximal workload of the base line test was significant for both groups for all measures (Molsidomin from 0.27 to 0.08 mV; ISDN from 0.28 to 0.07 mV). The decrease of the ST-segment depression on the individual maximal workload level was significant for all measures in the Molsidomin group, but only on the first day of treatment in the ISDN group.
Exercise prescription has traditionally been based on the heart rate/work rate relationship. Many post-myocardial (MI) patients are now taking medications such as beta-blockers that alter this relationship, necessitating an alternative method for exercise prescription. The directly measured maximal oxygen intake (VO2max) is not substantially affected by such medications, but direct determinations of VO2max are time consuming, costly, and vulnerable to both local muscle weakness and poor motivation. We have therefore re-examined the relationship between work rate and maximal oxygen intake in order to derive a simple formula which will give an indirect estimate of the latter. Our results, obtained on 28 patients receiving beta-blockers, 13 receiving calcium channel blockers, 10 receiving combined therapy, and 49 who received neither treatment, indicate that the peak oxygen intake can be estimated accurately, using the expression VO2max.ml.min-1 = 2W, where W is the peak power output, measured in kp.m.min-1, or 12.3 W, where W is the peak power output in Watts.
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The purpose of this study was to investigate the effects of arm cranking speed on heart rate (HR), systolic blood pressure (SBP), and rate-pressure product (RPP) using an isokinetic upper extremity ergometer. Fifteen healthy men exercised for one minute at a work load of 300 kg X m/min and for five minutes at a work load of 600 kg X m/min on three different occasions at speeds of 30, 60, and 90 rpm. An analysis of variance and a Duncan's multiple range test were performed on all immediate postexercise (IPE) values. Significant differences were found in IPE HR and RPP across the exercise speeds. No significant differences were found in IPE SBP. The 60-rpm speed elicited significantly lower HR and RPP responses than the 30- or 90-rpm speeds. The 90-rpm speed elicited significantly lower HR responses than the 30-rpm speed. These results indicated that the 60-rpm speed caused the least cardiovascular stress at a submaximal work load of 600 kg X m/min.
To evaluate the accuracy of continuous non-invasive blood pressure measurements in the finger during exercise, Finapres blood pressures of six normotensive healthy males were measured during increasing levels of bicycle exercise, using simultaneously registered ipsilateral intrabrachial artery pressures as a reference. At rest, finger systolic blood pressure was higher and finger diastolic and mean arterial pressures were lower than the corresponding intrabrachial pressures in five of the six subjects. During exercise, average finger diastolic and mean arterial pressures did not differ further from these intrabrachial pressures, but finger systolic pressure increased considerably more than the direct systolic pressure, exceeding it by 26 +/- 20 mmHg (mean +/- s.d.) at maximal exercise. This latter finding potentially limits the use of finger blood pressure measurements during exercise.
PURPOSE: The relationship between oxygen consumption and power is not linear. The purpose of this investigation was to examine the nature of the relationship and the cause of the nonlinearity. METHODS: Eight male cyclists (60.5 +/- 3.8 mL O2.min-1.kg(-1) VO2 peak) completed an incremental exercise test (1 W.5 s(-1)) to exhaustion. VO2 was measured every breath, and rmsEMG was recorded continuously over the belly of vastus lateralis, biceps femoris, and lateral gastrocnemius. RESULTS: VO2 is a linear function of power in moderate exercise; the slope of the linear portion was approximately 9.7 mL O2.min(-1).W(-1), which is consistent with the steady state gain for moderate exercise. Beyond this initial break from linearity, the VO2.W(-1) plot demonstrates a second break that is not different from the point of respiratory compensation (break in VE.VCO2(-1)). These breaks were coincident with increased neuromuscular activity (1st break: 194 +/- 27 W for VO2, 191 +/- 25 W for vastus lateralis; 2nd break: 262 +/- 34 W for VO2, 258 +/- 27 W for vastus lateralis) and corresponded to approximately 58% VO2 peak for the first and 75% VO2 peak for the second break. CONCLUSIONS: VO2 is not a linear function of power. During an incremental test, neuromuscular activity and VO2 increase more rapidly in heavy exercise. Both VO2 and neuromuscular activity exhibit a second break at very high power output, which may mark an upper limit for sustainable exercise.
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OBJECTIVES: Patients with peripheral arterial disease (PAD) and aorto-iliac atherosclerotic lesions suffer from a broad range of complaints, such as pain at the hip, the thigh, and calf claudication. The purpose of this study was to investigate the high-energy metabolism in the calf muscle of patients with PAD with isolated aorto-iliac stenoses during incremental plantar flexion exercise. MATERIALS AND METHODS: Using a 1.5 T whole-body magnetic resonance (MR) scanner, 12 patients with PAD with uni- or bilateral aorto-iliac atherosclerotic lesions and 10 healthy male controls underwent serial phosphor-31 MR spectroscopy during incremental exercise at 2, 3, 4, and 5 W. The phosphocreatine (PCr) time constants were calculated for each increment and recovery using a monoexponential model. In the patient group, the run-off resistance was determined on MR angiograms. In both the patients and the controls, the ankle brachial pressure index was measured. RESULTS: The diseased legs exhibited significantly increased PCr time constants during the second and the third workload increment at 3 and 4 W, but not during the first increment at 2 W and recovery compared with normal controls. Only 3 diseased legs succeeded the last increment at 5 W. We detected significant correlations between the ankle brachial pressure index scores and the PCr time constants when including both the diseased and the control legs. The diseased legs showed a significant correlation with the run-off resistance only during the first increment. CONCLUSIONS: Our study shows that the impairment of muscle metabolism, expressed by prolonged PCr time constants, occurs with greater work intensities in patients with aorto-iliac disease compared with patients with multisegmental PAD, as recently published, whereas our patients collective exhibited normal PCr recovery time constants. Our findings may help to understand variability of clinical symptoms in aorto-iliac PAD.
A sample of 66 healthy, unrelated males with normal blood pressure were studied for a possible association between an insertion/deletion polymorphism in the gene coding for the angiotensin converting enzyme and blood pressure response to physical exercise. No association was found between the polymorphism and systolic blood pressure at rest and during stress. Statistically significant associations between the polymorphism and diastolic blood pressure were observed during exercise and post-stress. At maximal workload, among homozygotes for the deletion, the mean diastolic blood pressure was 93 (+/- 10) mmHg, among homozygotes for the insertion it was 82 (+/- 8) mmHg, among heterozygotes it was 85 (+/- 10) mmHg. The difference was still statistically significant 3 minutes post-stress. The angiotensin converting enzyme polymorphism may be a marker for genetically determined differences in the response of the cardiovascular system to physical stress.
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The purpose of this investigation was to determine if a new proposed arm ergometer protocol was advantageous in eliciting higher peak oxygen uptake (peak VO2) when compared with two protocols currently referred to in the literature. Ten male subjects were tested on three different exercise protocols; a discontinuous test (DT), a continuous test (CT) and a new proposed jump-max test (JMT). The CT began at a work rate of 33 watts (W) (40 rpm) with the power output (PO) being increased 16 W every 3 minutes. The DT began without resistance on the ergometer flywheel (50 rpm) and the work rate was increased by 25 W every 3 minutes with a 1-minute rest between stages. The JMT began with a 3-minute pretest to determine a PO which elicited a HR of 120 +/- 5 beat min-1. After a 2-minute rest, subjects began exercise at the predetermined work rate (80 rpm) with the PO being increased 20 W each minute of the test. Oxygen uptake was measured minute by minute via open circuit spirometry. Peak VO2 was higher (p less than 0.05) in the JMT (mean +/- SEM = 2.36 +/- 0.06 l.min-1) when compared with either (means +/- SEM = 2.16 +/- 0.07 l.min-1) or the CT (means +/- SEM = 2.04 +/- 0.10 l.min-1). No difference (p greater than 0.05) existed in peak VO2 between the CT and the DT. These data suggest that the proposed JMT may result in a higher measured peak VO2 in subjects when compared with either DT or CT of moderate to long duration.
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The purpose of this study was to investigate excess post-exercise oxygen consumption (EPOC) following a continuous 30 min bout of upper-body exercise (UBE) compared with 3 consecutive 10 min bouts of UBE. Ten male subjects (age (mean +/- standard deviation), 25.7 +/- 5.83 years; arm VO(2) (peak), 2.2 +/- 0.25 L x min(-1), on separate days (48 h between trials) and in counterbalanced order, performed a continuous 30 min bout of arm exercise at 60% of arm VO2 peak and 3 separate 10 min bouts of arm exercise at 60% of arm VO(2) (peak). Subjects reported to the laboratory rested and after a 12 h fast. Each test was preceded by a 30 min baseline test to determine resting metabolic rate. Post-exercise VO2 was continuously monitored until baseline was re-established. Results showed that the combined magnitude of the EPOCs from the intermittent exercise sessions was significantly (p > .05) greater (4.47 +/- 1.58 L O2) than that elicited from the continuous exercise session (1.54 +/- 1.25 L O2). These data indicate that separating a continuous 30 min arm exercise into 3 equal 10 min arm exercises will elicit a small but significantly higher EPOC, and thus result in greater post-exercise energy expenditure. This could be beneficial for those unable to perform lower-body exercise (LBE), or for those with limited exercise capacities.