Maximal Dynamic Exercise Research Articles

Hyperkalemia During Progressive Dynamic Exercise

Serum potassium levels, catecholamines, and plasma renin activity are elevated during maximal dynamic exercise. Catecholamines and plasma renin activity have been shown to rise nonlinearly during exercise and to parallel changes in venous blood lactate. Since the hyperkalemia of exercise is modulated by catecholamines, we studied the changes in serum potassium in relation to attaining the exercise intensity associated with a rise in blood lactate (the lactate threshold). Eight healthy male subjects 25 to SO years of age underwent progressive cycle ergometry (PE) at increments of 25 W/4 min. During PE, absolute levels of peripheral venous potassium increased significantly only after the lactate threshold was exceeded (T < .01). In a control study (TC), subjects exercised to their lactate threshold and remained at that work rate for a time equal to that of PE. During TC, there were no significant increases in potassium until the final four minutes of exercise (T < .05). Plasma aldosterone levels rose comparably during PE and TC. These results demonstrate that significant potassium elevation during dynamic exercise begins at the lactate threshold. This threshold response of potassium may have clinical implications for exercise prescription in patients with impaired potassium homeostasis.

Blood pressure during exercise in healthy children.

During maximal dynamic exercise the blood pressure (BP) was measured in 497 healthy 9- to 18-year-old children. Systolic BP increased more in the postpubertal groups than in the prepubertal ones. It was also higher in the boys than in the girls of the same age. This was due to a higher work load in boys than girls. Twenty-two subjects had a systolic BP of 200 mmHg or more during the exercise. Only 2 had a resting systolic BP exceeding the mean by 2 standard deviations or more. Three postpubertal boys reached a systolic BP of 240 mmHg at heart rate 170. None had an elevated resting BP. It may be concluded that it cannot be predicted on the basis of the resting BP whether or not an individual is going to have an excessive increase in systolic BP during exercise. The increase in systolic BP to dangerous levels, e.g. 240 mmHg or more, during exercise can only be excluded by means of an individual exercise test.

Cardiovascular, ventilatory and catecholamine responses to maximal dynamic exercise in partially curarized man.

1. In ten young men the ventilatory, cardiovascular, catecholamine and metabolic responses to maximal dynamic leg exercise on a stationary bicycle were followed during partial neuromuscular blockade with tubocurarine. Maximal exercise was performed when the drug effect was at its maximum as well as during the subsequent reduction in the effect allowing a gradually increasing work intensity. The results were compared with those obtained during submaximal and maximal exercise performed without tubocurarine. Partial neuromuscular blockade decreased hand-grip strength to 41 +/- 1.1% (S.E. of mean) and the maximal work load to 27 +/- 2.4% of control values. Voluntary effort was maximal and the rate of perceived exertion was high at all levels of exercise with tubocurarine indicating a maintained intense central nervous motor command. 2. During maximal action of the drug oxygen uptake was 1.67 +/- 0.11 l/min while only 0.91 +/- 0.13 l/min (P less than 0.01) at the same work intensity without neuromuscular blockade. This difference may reflect a dominant reliance on fast-twitch muscle fibres when work was performed under the influence of tubocurarine. 3. Compared at a given oxygen uptake ventilation was higher during work with tubocurarine than during control exercise (e.g. 55 +/- 4.2 and 40 +/- 2.2 l/min, respectively (P less than 0.01), at a mean oxygen uptake of 1.9 l/min), while heart rate did not differ significantly (146 +/- 4.4 and 139 +/- 3.0 beats/min). With decreasing drug effect both variables increased towards the maximum values of 138 +/- 4.5 l/min and 183 +/- 3.9 beats/min, respectively, achieved in control experiments at an oxygen uptake of 3.8 +/- 0.2 l/min. Like heart rate the mean arterial blood pressure increased with increasing work load and was similar at a given oxygen uptake with and without tubocurarine. 4. During maximal exercise at peak tubocurarine effect plasma adrenaline and noradrenaline concentrations were smaller than during control maximum, 1.6 +/- 0.27 versus 3.4 +/- 0.55 nmol/l (P less than 0.01) and 7.5 +/- 1.3 versus 12.6 +/- 1.8 nmol/l (P less than 0.05), respectively. However, comparisons at identical oxygen uptake rates revealed that catecholamine responses were markedly enhanced during tubocurarine treatment. Also, blood lactate concentrations were smaller at peak tubocurarine action than during control maximum, 1.9 +/- 0.42 mmol/l and 6.1 +/- 0.49 mmol/l (P less than 0.01).(ABSTRACT TRUNCATED AT 400 WORDS)

Stress induced right ventricular dysfunction: an indication of reversible right ventricular ischaemia.

Stress induced changes in left ventricular ejection fraction are widely used in the detection and assessment of coronary artery disease. This study demonstrates that right ventricular dysfunction may also occur, and assesses its significance in terms of coronary artery anatomy. This study involved 14 normal subjects and 26 with coronary artery disease investigated by equilibrium radionuclide ventriculography, at rest and during maximal dynamic exercise. Mean normal resting right ventricular ejection fraction (RVEF) was 0.40 (SD 0.118), and all normal subjects increased RVEF with stress (mean delta RVEF + 0.13 SD 0.099). Mean delta RVEF in the subjects with coronary artery disease was significantly lower at 0.00 (SD 0.080), but there was overlap between the two groups. The largest falls in RVEF were seen if the right coronary artery was occluded without retrograde filling. In this subgroup with the most severely compromised right ventricular perfusion (nine subjects), RVEF always fell with stress, and mean delta RVEF was -0.08 (SD 0.050). There was no significant correlation between delta LVEF and delta RVEF, implying that the right ventricular dysfunction was due to right ventricular ischaemia, rather than secondary to left ventricular dysfunction. Stress induced right ventricular ischaemia can therefore be detected readily by radionuclide ventriculography.

An evaluation of the effect of fasting on the exercise-induced changes in pH and Pi/PCr from skeletal muscle.

The changes in the response of skeletal muscle to maximal dynamic exercise were investigated in going from a fasted state to a refed state by means of 31P NMR spectroscopy. It was found that in the fasted state, exercise-induced changes in Pi/PCr and in pH were both inhibited, in comparison with those in the refed state.

Leg glucose uptake during maximal dynamic exercise in humans.

Leg glucose uptake (LGU) during submaximal (50% maximal O2 uptake) and maximal dynamic exercise (97%) has been quantified from the product of the leg blood flow and the arterial minus femoral venous glucose concentration. Muscle biopsies were also obtained. During 15 min of submaximal exercise the mean LGU values ranged from 1.07 to 1.25 mmol/min, which demonstrates that LGU was stable under this condition. In contrast, during maximal exercise LGU increased continuously, reaching 2.38 +/- 0.22, 2.95 +/- 0.32, and 3.82 +/- 0.34 mmol/min after 2, 4, and 5.2 min (fatigue), respectively. The mean LGU was negatively related to the mean muscle phosphocreatine content (r = -1.00;P less than 0.01). Intracellular glucose-6-phosphate (G-6-P) and glucose were very low at rest and did not change significantly during submaximal exercise (P greater than 0.05). However, at fatigue G-6-P and glucose increased substantially and were both 8.5 mmol/kg dry muscle (P less than 0.001). These findings demonstrate that during heavy exercise glucose accumulates in the cell probably due to hexokinase inhibition by G-6-P, and thus the rate of glucose utilization appears to be lower than the rate of glucose uptake. It is suggested that 1) LGU during short-term exercise is dependent on the energy state of the muscle and 2) LGU is equal to leg glucose utilization during submaximal exercise but is in excess of utilization during heavy exercise.

Human muscle metabolism during sprint running.

Biopsy samples were obtained from vastus lateralis of eight female subjects before and after a maximal 30-s sprint on a nonmotorized treadmill and were analyzed for glycogen, phosphagens, and glycolytic intermediates. Peak power output averaged 534.4 +/- 85.0 W and was decreased by 50 +/- 10% at the end of the sprint. Glycogen, phosphocreatine, and ATP were decreased by 25, 64, and 37%, respectively. The glycolytic intermediates above phosphofructokinase increased approximately 13-fold, whereas fructose 1,6-diphosphate and triose phosphates only increased 4- and 2-fold. Muscle pyruvate and lactate were increased 19 and 29 times. After 3 min recovery, blood pH was decreased by 0.24 units and plasma epinephrine and norepinephrine increased from 0.3 +/- 0.2 nmol/l and 2.7 +/- 0.8 nmol/l at rest to 1.3 +/- 0.8 nmol/l and 11.7 +/- 6.6 nmol/l. A significant correlation was found between the changes in plasma catecholamines and estimated ATP production from glycolysis (norepinephrine, glycolysis r = 0.78, P less than 0.05; epinephrine, glycolysis r = 0.75, P less than 0.05) and between postexercise capillary lactate and muscle lactate concentrations (r = 0.82, P less than 0.05). The study demonstrated that a significant reduction in ATP occurs during maximal dynamic exercise in humans. The marked metabolic changes caused by the treadmill sprint and its close simulation of free running makes it a valuable test for examining the factors that limit performance and the etiology of fatigue during brief maximal exercise.

Quantitative analysis of segmental wall motion during maximal upright dynamic exercise: variability in normal adults.

Twenty-five healthy adults underwent subcostal-view, four-chamber two-dimensional echocardiographic examination while upright at rest and at the peak of maximal bicycle exercise. The purpose of the study was to determine whether the variability in regional left ventricular endocardial motion, previously demonstrated to be present at rest, persisted at peak exercise. The rest and exercise end-diastolic and end-systolic endocardial contours were visually identified, digitized, and divided into 32 radial segments after realignment by the computer. At rest there was similar percent segmental area reduction for the septum (segments 1 to 12) (54 +/- 4%, mean +/- 1 SD), apex (segments 13 to 20) (67 +/- 3%), and lateral wall (segments 21 to 32) (67 +/- 8%). At peak exercise the percent area reduction increased significantly: septum 84 +/- 5%, apex 88 +/- 2%, lateral wall 83 +/- 6% (p less than .001 compared with rest for all areas). However, there was considerable variability in percent area reduction between different radial segments in the same individual. At rest the difference between minimal and maximal percent area reduction within the same individual was 49 +/- 17 percentage units (range 21 to 83) and that at peak exercise was 32 +/- 17 percentage units (range 0 to 66). It is concluded that, because the range of standard deviation of normal endocardial motion and the degree of variability between radial segments in the same healthy individual are significant, qualitatively determined "hypokinesis," as commonly assessed clinically, may be a normal event. However, segmental akinesis or dyskinesis, which occurred rarely at rest and never at peak exercise, must be considered abnormal events.

Muscle performance and metabolism in maximal isokinetic cycling at slow and fast speeds.

To provide a description of the metabolic changes in muscle during maximal dynamic exercise, muscle biopsies were obtained in five healthy subjects before and after 30 s of isokinetic exercise at two pedaling frequencies (60 and 140 rpm) associated with contrasting fatigue characteristics. Higher peak power was attained at 140 rpm (1,473 + 185 W) (mean +/- SE) than at 60 rpm (1,122 +/- 70 W), but the decline in power during 30 s (fatigue index) was greater at 140 rpm (61.6 +/- 3.2 vs. 21.5 +/- 2.4%), total work in 30 s being similar (18.1 +/- 1.10 vs. 20.1 +/- 1.10 kJ). Changes in the concentration of muscle metabolites were similar; creatine phosphate concentration fell to approximately 50% of resting values, and the glycolytic intermediates glucose 6-phosphate, fructose 6-phosphate, and fructose 1,6-biphosphate increased up to 30-fold. Muscle lactate concentration ([La-]) was 29.0 +/- 3.98 and 31.0 +/- 4.31 mmol/kg wet wt immediately postexercise at 140 and 60 rpm, respectively. Even after only 10 s exercise (n = 2), large increases were measured in glycolytic intermediates and [La-]. In the two subjects, muscle [La-] increased to 17.2 and 15.1 mmol/kg at 140 rpm and to 14.3 and 14.2 mmol/kg at 60 rpm. In this type of exercise, glycogenolysis is activated very rapidly at both pedal speeds; the changes in glycolytic intermediates were consistent with rate-limiting steps at the phosphofructokinase and pyruvate dehydrogenase reactions. The greater fatigue at the higher speed is not accompanied by different biochemical changes than at 60 rpm.

Autonomic mechanisms regulating myocardial contractility in conscious animals

In this review some of the issues and controversies involved in the neural control of the myocardial inotropic response to stress have been discussed. For example, it is surprising that either direct or reflex activation of the sympathetic nerves induces a relatively small increase (20–40%) in the left ventricular inotropic state when compared with the three-five-fold increase associated with maximal dynamic exercise. Studies contrasting the levels of circulating catecholamines with the left ventricular inotropic responses induced by hemorrhage, exercise and exogenously administered catecholamines, suggest that the catecholamine concentration at the synaptic cleft is the primary determinant of the left ventricular inotropic response. Although parasympathetic neural activation alone appears to have little direct influence on the left ventricular inotropic state and central nervous system integration of the autonomic nervous system usually insures there is a reciprocal relationship between sympathetic and parasympathetic neural activity, the potential for parasympathetic inhibition of the response to sympathetic or sympathomimetic augmentation of the inotropic response exists. The importance of sympathetic-parasympathetic nervous system interaction in physiologic and pathologic conditions has yet to be defined. It is this type of knowledge of the interactions of reflex pathways which will be critical to the full understanding of autonomic reflex control of myocardial performance under physiologic and pathologic conditions.

Radionuclide imaging correlatives of heart rate impairment during maximal exercise testing

A lower than normal heart rate response to maximal dynamic exercise, known as chronotropic incompetence or heart rate impairment, has been demonstrated to have a poor prognosis. In order to better describe patients with this finding, 156 men with coronary heart disease were evaluated. All patients were studied with maximal exercise testing, including measurements of oxygen consumption, exercise electrocardiograms, thallium scintigraphy and radionuclide ventriculography. Chronotropic incompetence was defined as a maximal heart rate 1 standard error of the estimate below the regression line of age versus maximal heart rate on two separate exercise tests. In patients so defined, mean maximal oxygen consumption was significantly lowered and angina was the major reason for stopping exercise on the treadmill. Patients with chronotropic incompetence not limited by angina had more evidence of myocardial scar and dysfunction and had a greater prevalence of three vessel coronary disease than did patients with a normal heart rate response. Radionuclide testing results suggest that among patients with chronotropic incompetence, those with angina have a better prognosis than those who do not have angina but who may have myocardial dysfunction.

Effect of beta-adrenergic blockade on circulating catecholamines and dopamine-beta-hydroxylase activity during exercise in normal subjects

We investigated the effects of beta-adrenergic blockade with propranolol (P) on circulating catecholamines at rest and during isometric and dynamic exercise. By means of a radioenzymatic assay, we measured plasma norepinephrine (NE) and epinephrine (E) concentrations in nine normal, sedentary men, aged 22 to 34 years. Measurements were made during resting conditions, at 3 minutes of 30% maximal isometric handgrip exercise (IHE), and during submaximal and maximal dynamic treadmill exercise. Measurements were repeated one week later after the subjects received P in doses ranging from 40 to 80 mg four times a day (plasma P levels at the time of exercise ranged from 96 to 303 ng/ml with a mean of 178 ng/ml). We also measured serum dopamine-beta-hydroxylase (DBH) activity to detect changes in chronic sympathetic tone. Changes in NE from rest to exercise were significant ( p < 0.01) at all exercise loads with or without P. Changes in E from rest to exercise were significant ( p < 0.01) at all exercise loads with or without P except for submaximal dynamic exercise during the control study ( p > 0.05). For NE, there were no significant differences between the control and P values either at rest or during any form of exercise. For E, there were no significant changes between the control and p values at rest or at maximal dynamic exercise, although there were mild increases ( p < 0.05) with IHE and submaximal dynamic exercise. DBH activity increased significantly ( p < 0.01) from rest to exercise for all exercise points with and without P, but there were no significant differences between the control and p values either at rest or during any form of exercise. In conclusion, we have demonstrated that competitive blockade of beta-adrenergic receptors at the tissue level does not alter neural release of NE or DBH and has little effect on adrenal release of E.

Predictability of blood pressure response to isometric stress

Isometric exercise causes transient systemic hypertension, but with individual differences. An attempt was made to delineate predictors of those differences by analyzing the blood pressure (BP) response in terms of variables readily measured in clinical practice. For each of 270 office patients, we determined blood pressure, heart rate (HR), electrocardiographic findings, and symptoms in response to maximal isometric and maximal dynamic exercise. For systolic BP response as the predicted measure, 4 predictor variables in combination, including age, sex, resting systolic BP, and maximal treadmill systolic BP, yielded 70% predictability. For diastolic BP, 5 predictors in combination, including handgrip strength, resting diastolic BP, treadmill HR, systolic BP, and diastolic BP, allowed 66% prediction. Not predictive of either were resting HR, abnormality of treadmill test, presence of heart disease, and certain other medical diagnoses.

Muscle fatigue and its relation to lactate accumulation and LDH activity in man.

The lactate concentration in different muscle fibre types was determined in biopsy specimens from human vastus lateralis muscle after 30 and 60 s of maximal dynamic leg exercise. In addition, muscle fibre type distribution, total lactate dehydrogenase (LDH) activity, and isozymes of LDH were determined. In accordance with previous studies (Thorstensson and Karlsson 1976, Nilsson et al. 1977) it was found that an increasing proportion of slow twitch (ST) fibres corresponded to better sustained muscle force. Lactate was found preferentially in fast twitch (FT) fibres after 30 s, but after 60 s this difference was abolished. Differences between the two main muscle fibre types in muscle lactate, total LDH activity, and M-LDH activity were correlated to muscle fatigue. It was concluded that lactate or associated pH changes primarily in FT fibres could be one factor responsible for the impaired muscle function.

Comparative response to isometric (static) and dynamic exercise tests in coronary disease

Forty-six patients with arteriosclerotic heart disease manifested significant electrocardiographic changes (accompanied by angina in 35) during maximal exercise testing. These patients subsequently performed isometric exercise at levels representing various percentages of maximal voluntary contraction. Twenty-two patients also performed combined isometric and submaximal dynamic exercise. The prevalence rate of S-T segment changes during isolated isometric exercise depended on the percent of maximal voluntary contraction applied but was far lower than the rate observed during maximal dynamic exercise. Angina seldom occurred. Manifestations of coronary insufficiency appeared more often during combined submaximal dynamic and isometric exercise than during isolated isometric testing. Aortic pressure was measured in eight cases. Tension-time index and pressure-heart rate product were lower when maximal dynamic exercise was stopped owing to coronary insufficiency than at the end of isolated isometric exercise or combined submaximal dynamic and isometric exercise. However, the latter two tests produced fewer ischemic manifestations. The reasons for these discrepancies are discussed. We conclude that isometric exercise tests are unsuitable for diagnosing coronary insufficiency.