<i>Lactic Acid Accumulation During Work. A Suggested Standardization of Work Classification</i>

Wells, Jennifer; Balke, Bruno; Fossan, Donald D. Van

doi:10.1152/jappl.1957.10.1.51

Cited by 45 publications

(15 citation statements)

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“…This was further evidenced by subject 4 achieving his highest V02 during AE (higher than FNS + AE). The lowest LA observed post-FNS exercise was 32 mg/ 100 ml (subject 2) and this was consistent with optimalstrenuous work done by normal sedentary subjects performing stress tests using a large muscle mass (20) . Only subject 3 was able to match his maximal AE power output during FNS + AE (Table 3) .…”

Section: Lactic Acid and Rersupporting

confidence: 78%

“…The subject with the highest RERs had the highest lactic acid reading (subject 4) and vice-versa (subject 2). Subject 4 had total blood LA accumulation of 115 mg/ 100 ml during FNS, which was consistent with maximal LA in sedentary normal subjects who performed maximal stress tests using a large muscle mass (20) . Mean MAP and maximal LA tolerance is usually much higher (2) when normal subjects use a large muscle mass (legs or arms and legs) compared to a small muscle mass (arms alone) .…”

Section: Lactic Acid and Rersupporting

confidence: 68%

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Metabolic responses to arm ergometry and functional neuromuscular stimulation

Edwards

Marsolais²

1990

JRRD

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The hips and lower extremities of four complete paraplegic male subjects (T-6, T-7, T-8, and T-11) were stimulated with functional neuromuscular stimulation (FNS) via transcutaneous intramuscular electrodes (20 mA, 0-150 pulse width, and 20 Hz) . Cardiopulmonary (CP) and/or cardiovascular (CV) responses were measured during maximal (seated) arm ergometry (AE), FNS, and FNS + AE . Subjects' lower extremities were stimulated with a 2 s walking cycle via a microprocessor computer. Data were collected with a SensorMedic MMC Horizon (VO 2 and VCO2 at STPD and VE at BPTS). The mean MET level (1 MET = 3.5 ml 0 2 /kg/min) during FNS was 4 .8. Mean METS during FNS + AE was 10 .3 and mean METS for AE was 7.2 . Mean lactic acid (LA) after FNS, AE, and FNS + AE was 73 mg percent, 77 mg percent and 115 mg percent respectively. Respiratory exchange ratio (RER) (VCO2 /VO2 ) was >1 .2 during the first 2 to 5 min of FNS but decreased to <1 .0 during the second 5 min of FNS . Steady state V02 and RER <1 .0 indicated a FNS transition from anaerobic to aerobic metabolism . Subject T-11 had CV limitations during FNS and FNS + AE due to excessive LA from FNS (115 mg percent) . Ventilatory (VE) responses during AE, FNS, and FNS + AE were consistent with V0 2 ; and mean maximal VE and V02 for subjects T-6, T-7, and T-8 during FNS + AE was greater than 90 percent of that observed in sedentary normals . The aerobic and anaerobic capacities of paraplegic subjects is primarily limited by available muscle mass rather than impaired CV or CP function.

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Section: Lactic Acid and Rersupporting

confidence: 78%

Section: Lactic Acid and Rersupporting

confidence: 68%

Metabolic responses to arm ergometry and functional neuromuscular stimulation

Edwards

Marsolais²

1990

JRRD

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“…The latter would indicate that the patients were performing at close to peak aerobic capacity. 15 The maximal A-V 02 reached by our patients was markedly lower than that reached by normal subjects, i.e., 9.6 vs 15.9 ml/100 ml. '6 The moderate anemia observed in our patients may partially explain this disparity.…”

Section: Discussioncontrasting

confidence: 46%

Acute substantial benefit of inotropic therapy with amrinone on exercise hemodynamics and metabolism in severe congestive heart failure.

Siskind¹,

Sonnenblick²,

Forman³

et al. 1981

Circulation

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SUMMARY The acute hemodynamic and metabolic effects of amrinone during exercise were studied in eight patients with severe congestive heart failure. The patients exercised to exhaustion on an upright bicycle ergometer at a fixed work load of 25 W. During the control period of exercise, exhaustion occurred at 3.16 + 1.39 minutes. Stroke volume increased from 29.5 ± 5.8 to 38.7 + 9.5 ml (p < 0.01), arteriovenous oxygen difference from 7.6 + 1.3 to 9.6 + 0.6 ml/100 ml (p < 0.001), oxygen consumption from 231 + 38 to 468 + 111 ml/min (p < 0.001) and arterial lactate concentration from 1.07 + 0.25 to 5.02 + 1.45 mmol/l (p < 0.01). During exercise after administration of amrinone, exhaustion occurred significantly later than during the control period: 6.28 ± 2.07 vs 3.16 ± 1.39 minutes (p < 0.05). At a time equal to the point of exhaustion during the control period, stroke volume was significantly greater after amrinone (46.7 + 9.8 vs 38.7 ± 9.5 ml, p < 0.05), arteriovenous oxygen difference and arterial lactate concentration were significantly lower (7.7 + 0.9 vs 9.6 ± 0.6 ml/100 ml [p < 0.05] and 2.96 t 1.01 vs 5.02 ± 1.45 mmol/l [p < 0.05], respectively) and oxygen consumption was similar.At the point of exhaustion during exercise after amrinone, there were further increases in stroke volume (to 54.0 ± 11.6 ml, p < 0.05), and oxygen consumption (to 674 ± 141 ml/min, p < 0.05), while arteriovenous oxygen difference and arterial lactate concentration reached values similar to those during control exercise. Thus, amrinone increased exercise capacity, improved exercise hemodynamics, and probably decreased anaerobic metabolism at a given duration of exercise.AMRINONE is a new synthetic cardiotonic agent that does not act through the mechanisms thought to mediate the action of digitalis glycosides or catecholamines.' Amrinone has been shown to improve left ventricular performance at rest in patients with severe congestive heart failure. This improvement occurs after either i.V.2' 8 or oral' administration of amrinone and is characterized by an increase in cardiac output (CO) and a reduction in left ventricular filling pressure without changes in mean arterial pressure (MAP) or heart rate (HR). Although preliminary data suggest that long-term therapy with amrinone can increase the exercise capacity of patients with severe chronic heart failure,517 the hemodynamic and metabolic responses to exercise after acute administration of the drug have not been evaluated.The major hemodynamic aims in the therapy of congestive heart failure are to control pulmonary and peripheral congestion and to improve exercise performance. Potent diuretics have helped to control the former problem, but do not acutely improve exercise performance. Short-term administration of vasodilators to patients with severe heart failure improves both resting and exercise hemodynamics, but does not increase exercise capacity.8 10 Accordingly, the effects of i.v. amrinone on the hemodynamic and metabolic response to upright exercise were evaluated in eight pat...

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“…The latter problem has been identified since the 1950s [34]. The transition to an exercise intensity that requires substantial supplementation by anaerobic metabolic pathways is commonly (although not without controversy) demarcated by the ventilatory or the lactate threshold (i.e., a nonlinear increase in expired carbon dioxide relative to the consumed oxygen or a rise in blood lactate concentration as a result of the rate of production exceeding the rate of clearance).…”

Section: Standardization Of Exercise Intensitymentioning

confidence: 99%