Exercise and recovery ventilatory and VO2 responses of patients with McArdle's disease

1990 ◽  
Vol 68 (4) ◽  
pp. 1393-1398 ◽  
Author(s):  
J. M. Hagberg ◽  
D. S. King ◽  
M. A. Rogers ◽  
S. J. Montain ◽  
S. M. Jilka ◽  
...  
Keyword(s):  
Blood Lactate ◽  
High Intensity ◽  
Maximal Exercise ◽  
Matched Control ◽  
Slow Component ◽  
High Intensity Exercise ◽  
O2 Consumption ◽  
Control Subjects ◽  
Mcardle's Disease ◽  
Mcardle’S Disease

This study was designed to determine whether patients with McArdle's disease, who do not increase their blood lactate levels during and after maximal exercise, have a slow “lactacid” component to their recovery O2 consumption (VO2) response after high-intensity exercise. VO2 was measured breath by breath during 6 min of rest before exercise, a progressive maximal cycle ergometer test, and 15 min of recovery in five McArdle's patients, six age-matched control subjects, and six maximal O2 consumption- (VO2 max) matched control subjects. The McArdle's patients' ventilatory threshold occurred at the same relative exercise intensity [71 +/- 7% (SD) VO2max] as in the control groups (60 +/- 13 and 70 +/- 10% VO2max) despite no increase and a 20% decrease in the McArdle's patients' arterialized blood lactate and H+ levels, respectively. The recovery VO2 responses of all three groups were better fit by a two-, than a one-, component exponential model, and the parameters of the slow component of the recovery VO2 response were the same in the three groups. The presence of the same slow component of the recovery VO2 response in the McArdle's patients and the control subjects, despite the lack of an increase in blood lactate or H+ levels during maximal exercise and recovery in the patients, provides evidence that this portion of the recovery VO2 response is not the result of a lactacid mechanism. In addition, it appears that the hyperventilation that accompanies high-intensity exercise may be the result of some mechanism other than acidosis or lung CO2 flux.

Preexercise hypervolemia does not affect arterial hypoxemia in Thoroughbreds performing short-term high-intensity exercise

2003 ◽  
Vol 94 (6) ◽  
pp. 2135-2144 ◽  
Author(s):  
Murli Manohar ◽  
Thomas E. Goetz ◽  
Aslam S. Hassan
Keyword(s):  
Blood Lactate ◽  
Plasma Volume ◽  
High Intensity ◽  
Maximal Exercise ◽  
Lactate Concentration ◽  
High Intensity Exercise ◽  
Hydration Status ◽  
Mixed Venous Blood ◽  
Short Term ◽  
Arterial Hypoxemia

It is reported that preexercise hyperhydration caused arterial O2 tension of horses performing submaximal exercise to decrease further by 15 Torr (Sosa-Leon L, Hodgson DR, Evans DL, Ray SP, Carlson GP, and Rose RJ. Equine Vet J Suppl 34: 425–429, 2002). Because hydration status is important to optimal athletic performance and thermoregulation during exercise, the present study examined whether preexercise induction of hypervolemia would similarly accentuate the arterial hypoxemia in Thoroughbreds performing short-term high-intensity exercise. Two sets of experiments (namely, control and hypervolemia studies) were carried out on seven healthy, exercise-trained Thoroughbred horses in random order, 7 days apart. In resting horses, an 18.0 ± 1.8% increase in plasma volume was induced with NaCl (0.30–0.45 g/kg dissolved in 1,500 ml H2O) administered via a nasogastric tube, 285–290 min preexercise. Blood-gas and pH measurements as well as concentrations of plasma protein, hemoglobin, and blood lactate were determined at rest and during incremental exercise leading to maximal exertion (14 m/s on a 3.5% uphill grade) that induced pulmonary hemorrhage in all horses in both treatments. In both treatments, significant arterial hypoxemia, desaturation of hemoglobin, hypercapnia, acidosis, and hyperthermia developed during maximal exercise, but statistically significant differences between treatments were not found. Thus preexercise 18% expansion of plasma volume failed to significantly affect the development and/or severity of arterial hypoxemia in Thoroughbreds performing maximal exercise. Although blood lactate concentration and arterial pH were unaffected, hemodilution caused in this manner resulted in a significant ( P < 0.01) attenuation of the exercise-induced expansion of the arterial-to-mixed venous blood O2 content gradient.

Exercise hyperventilation in patients with McArdle's disease

1982 ◽  
Vol 52 (4) ◽  
pp. 991-994 ◽  
Author(s):  
J. M. Hagberg ◽  
E. F. Coyle ◽  
J. E. Carroll ◽  
J. M. Miller ◽  
W. H. Martin ◽  
...  
Keyword(s):  
Blood Lactate ◽  
Normal Subjects ◽  
O2 Consumption ◽  
Intense Exercise ◽  
Mcardle's Disease ◽  
Normal Individuals ◽  
Mcardle’S Disease ◽  
Muscle Phosphorylase ◽  
Lactate Levels ◽  
End Tidal

This study was undertaken to determine if patients who lack muscle phosphorylase (i.e., McArdle's disease), and therefore the ability to produce lactic acid during exercise, demonstrate a normal hyperventilatory response during progressive incremental exercise. As expected these patients did not increase their blood lactate above resting levels, whereas the blood lactate levels of normal subjects increased 8- to 10-fold during maximal exercise. The venous pH of the normal subjects decreased markedly during exercise that resulted in hyperventilation. The patients demonstrated a distinct increase in ventilation with respect to O2 consumption similar to that seen in normal individuals during submaximal exercise. However their hyperventilation resulted in an increase in pH because there was no underlying metabolic acidosis. End-tidal partial pressures of O2 and CO2 also reflected a distinct hyperventilation in both groups at approximately 70–85% maximal O2 consumption. These data show that hyperventilation occurs during intense exercise, even when there is no increase in plasma [H+]. Since arterial CO2 levels were decreasing and O2 levels were increasing during the hyperventilation, it is possible that nonhumoral stimuli originating in the active muscles or in the brain elicit the hyperventilation observed during intense exercise.

Influence of endurance training on muscle [PCr] kinetics during high-intensity exercise

2007 ◽  
Vol 293 (1) ◽  
pp. R392-R401 ◽  
Author(s):  
Andrew M. Jones ◽  
Daryl P. Wilkerson ◽  
Nicolas J. Berger ◽  
Jonathan Fulford
Keyword(s):  
Endurance Training ◽  
High Intensity ◽  
Slow Component ◽  
Knee Extension ◽  
High Intensity Exercise ◽  
Whole Body ◽  
Time To Exhaustion ◽  
Exercise Tests ◽  
Before And After ◽  
Knee Extension Exercise

We hypothesized that a period of endurance training would result in a speeding of muscle phosphocreatine concentration ([PCr]) kinetics over the fundamental phase of the response and a reduction in the amplitude of the [PCr] slow component during high-intensity exercise. Six male subjects (age 26 ± 5 yr) completed 5 wk of single-legged knee-extension exercise training with the alternate leg serving as a control. Before and after the intervention period, the subjects completed incremental and high-intensity step exercise tests of 6-min duration with both legs separately inside the bore of a whole-body magnetic resonance spectrometer. The time-to-exhaustion during incremental exercise was not changed in the control leg [preintervention group (PRE): 19.4 ± 2.3 min vs. postintervention group (POST): 19.4 ± 1.9 min] but was significantly increased in the trained leg (PRE: 19.6 ± 1.6 min vs. POST: 22.0 ± 2.2 min; P < 0.05). During step exercise, there were no significant changes in the control leg, but end-exercise pH and [PCr] were higher after vs. before training. The time constant for the [PCr] kinetics over the fundamental exponential region of the response was not significantly altered in either the control leg (PRE: 40 ± 13 s vs. POST: 43 ± 10 s) or the trained leg (PRE: 38 ± 8 s vs. POST: 40 ± 12 s). However, the amplitude of the [PCr] slow component was significantly reduced in the trained leg (PRE: 15 ± 7 vs. POST: 7 ± 7% change in [PCr]; P < 0.05) with there being no change in the control leg (PRE: 13 ± 8 vs. POST: 12 ± 10% change in [PCr]). The attenuation of the [PCr] slow component might be mechanistically linked with enhanced exercise tolerance following endurance training.

scholarly journals Exercise-Induced Lactate Release Mediates Mitochondrial Biogenesis in the Hippocampus of Mice via Monocarboxylate Transporters

2021 ◽  
Vol 12 ◽  
Author(s):  
Jonghyuk Park ◽  
Jimmy Kim ◽  
Toshio Mikami
Keyword(s):  
Blood Lactate ◽  
Mitochondrial Biogenesis ◽  
High Intensity ◽  
Lactate Concentration ◽  
High Intensity Exercise ◽  
Mtdna Copy Number ◽  
Single Bout ◽  
Extracellular Lactate ◽  
Exercise Induced ◽  
The Brain

Regular exercise training induces mitochondrial biogenesis in the brain via activation of peroxisome proliferator-activated receptor gamma-coactivator 1α (PGC-1α). However, it remains unclear whether a single bout of exercise would increase mitochondrial biogenesis in the brain. Therefore, we first investigated whether mitochondrial biogenesis in the hippocampus is affected by a single bout of exercise in mice. A single bout of high-intensity exercise, but not low- or moderate-intensity, increased hippocampal PGC-1α mRNA and mitochondrial DNA (mtDNA) copy number at 12 and 48h. These results depended on exercise intensity, and blood lactate levels observed immediately after exercise. As lactate induces mitochondrial biogenesis in the brain, we examined the effects of acute lactate administration on blood and hippocampal extracellular lactate concentration by in vivo microdialysis. Intraperitoneal (I.P.) lactate injection increased hippocampal extracellular lactate concentration to the same as blood lactate level, promoting PGC-1α mRNA expression in the hippocampus. However, this was suppressed by administering UK5099, a lactate transporter inhibitor, before lactate injection. I.P. UK5099 administration did not affect running performance and blood lactate concentration immediately after exercise but attenuated exercise-induced hippocampal PGC-1α mRNA and mtDNA copy number. In addition, hippocampal monocarboxylate transporters (MCT)1, MCT2, and brain-derived neurotrophic factor (BDNF) mRNA expression, except MCT4, also increased after high-intensity exercise, which was abolished by UK5099 administration. Further, injection of 1,4-dideoxy-1,4-imino-D-arabinitol (glycogen phosphorylase inhibitor) into the hippocampus before high-intensity exercise suppressed glycogen consumption during exercise, but hippocampal lactate, PGC-1α, MCT1, and MCT2 mRNA concentrations were not altered after exercise. These results indicate that the increased blood lactate released from skeletal muscle may induce hippocampal mitochondrial biogenesis and BDNF expression by inducing MCT expression in mice, especially during short-term high-intensity exercise. Thus, a single bout of exercise above the lactate threshold could provide an effective strategy for increasing mitochondrial biogenesis in the hippocampus.

Effects of glycogen depletion and work load on postexercise O2 consumption and blood lactate

1979 ◽  
Vol 47 (3) ◽  
pp. 514-521 ◽  
Author(s):  
S. S. Segal ◽  
G. A. Brooks
Keyword(s):  
Blood Lactate ◽  
Slow Component ◽  
Minute Ventilation ◽  
Co2 Flux ◽  
Work Load ◽  
Bicycle Ergometer ◽  
Co2 Production ◽  
O2 Consumption ◽  
Glycogen Depletion ◽  
Heavy Exercise

To study a possible relationship between blood lactate and O2 consumption (VO2) after exercise, 11 male subjects exercised on a bicycle ergometer at moderate and heavy work loads in both normal glycogen and glycogen-depleted states. At rest, glycogen depletion resulted in significantly lowered blood glucose and lactate concentrations, CO2 production (VCO2), respiratory exchange ratio (R), and minute ventilation (VE). With the exception of glucose, these variables changed more in response to heavy exercise (HE: 2 min at a mean of 1,750 kg.m/min) than to moderate exercise (ME: 2 min at a mean of 1,000 kg.m/min). At either work load, VCO2, R, and lactate showed consistently greater responses in the normal glycogen state. The slope of the initial component of the postexercise VO2 curve was unaffected by either work load or lactate. Although the slope of the slow component of the postexercise VO2 curve became significantly more negative after HE, it was unaffected by the level of lactate. These results are inconsistent with the hypothesis of a “lactacid O2 debt.” Exercise intensity was the predominant factor influencing the magnitude and kinetics of postexercise VO2. Glycogen depletion resulted in lower VCO2, R, and blood lactate, but higher VE during heavy exercise. The results suggest that factors, in addition to CO2 flux to the lungs, influence VE during exercise.

Pulmonary O2 uptake kinetics as a determinant of high-intensity exercise tolerance in humans

2011 ◽  
Vol 110 (6) ◽  
pp. 1598-1606 ◽  
Author(s):  
Scott R. Murgatroyd ◽  
Carrie Ferguson ◽  
Susan A. Ward ◽  
Brian J. Whipp ◽  
Harry B. Rossiter
Keyword(s):  
Steady State ◽  
High Intensity ◽  
Exercise Tolerance ◽  
Slow Component ◽  
Progressive Increase ◽  
High Intensity Exercise ◽  
Exercise Intolerance ◽  
Exercise Onset ◽  
O2 Uptake Kinetics ◽  
Two Parameters

Tolerance to high-intensity constant-power (P) exercise is well described by a hyperbola with two parameters: a curvature constant (W′) and power asymptote termed “critical power” (CP). Since the ability to sustain exercise is closely related to the ability to meet the ATP demand in a steady state, we reasoned that pulmonary O2 uptake (V̇o2) kinetics would relate to the P-tolerable duration (tlim) parameters. We hypothesized that 1) the fundamental time constant (τV̇o2) would relate inversely to CP; and 2) the slow-component magnitude (ΔV̇o2sc) would relate directly to W′. Fourteen healthy men performed cycle ergometry protocols to the limit of tolerance: 1) an incremental ramp test; 2) a series of constant-P tests to determine V̇o2max, CP, and W′; and 3) repeated constant-P tests (WR6) normalized to a 6 min tlim for τV̇o2 and ΔV̇o2sc estimation. The WR6 tlim averaged 365 ± 16 s, and V̇o2max (4.18 ± 0.49 l/min) was achieved in every case. CP (range: 171–294 W) was inversely correlated with τV̇o2 (18–38 s; R2 = 0.90), and W′ (12.8–29.9 kJ) was directly correlated with ΔV̇o2sc (0.42–0.96 l/min; R2 = 0.76). These findings support the notions that 1) rapid V̇o2 adaptation at exercise onset allows a steady state to be achieved at higher work rates compared with when V̇o2 kinetics are slower; and 2) exercise exceeding this limit initiates a “fatigue cascade” linking W′ to a progressive increase in the O2 cost of power production (V̇o2sc), which, if continued, results in attainment of V̇o2max and exercise intolerance. Collectively, these data implicate V̇o2 kinetics as a key determinant of high-intensity exercise tolerance in humans.

Blood lactate exchange and removal abilities after relative high-intensity exercise: effects of training in normoxia and hypoxia

2001 ◽  
Vol 84 (5) ◽  
pp. 403-412 ◽  
Author(s):  
Laurent Messonnier ◽  
Hubert Freund ◽  
Léonard Féasson ◽  
Fabrice Prieur ◽  
Josiane Castells ◽  
...  
Keyword(s):  
Blood Lactate ◽  
High Intensity ◽  
High Intensity Exercise ◽  
Lactate Exchange

Respiratory gas exchange and metabolic responses during exercise in McArdle's disease

1993 ◽  
Vol 75 (2) ◽  
pp. 745-754 ◽  
Author(s):  
M. Riley ◽  
D. P. Nicholls ◽  
A. M. Nugent ◽  
I. C. Steele ◽  
N. Bell ◽  
...  
Keyword(s):  
Gas Exchange ◽  
Anaerobic Threshold ◽  
Adenosine Monophosphate ◽  
Co2 Production ◽  
Control Subjects ◽  
Mcardle's Disease ◽  
Small Rise ◽  
Mcardle’S Disease ◽  
Purine Metabolite ◽  
Abrupt Rise

During normal progressive exercise, the gas exchange anaerobic threshold occurs when CO2 production (VCO2) and ventilation (VE) increase so as to depart from a linear relationship to O2 consumption (VO2). This is thought to represent a gas exchange response to metabolic acidosis due to lactate accumulation. Patients with McArdle's disease have previously been reported to exhibit a steepened ventilatory response relative to VCO2, despite an inability to produce lactate. However, the VCO2 response has not been studied. We therefore investigated the VCO2-VO2 and VE-VO2 relationships in seven McArdle's disease patients and seven control subjects during symptom-limited maximal treadmill exercise. Analysis of gas exchange showed that whereas all control subjects had an easily identifiable anaerobic threshold, four of the patients had none and the other three displayed an attenuated threshold. The occurrence of the threshold in one patient was associated with a small rise in lactate and in another patient with an abrupt rise in leg discomfort, suggesting a pain response. Ammonia and the purine metabolite hypoxanthine were elevated during exercise in all patients, suggesting that ammonia may be a product of adenosine monophosphate degradation. Free fatty acid levels were also elevated, and a shift toward utilization of lipid may contribute to abnormal gas exchange responses. It is concluded that lactic acidosis contributes to the gas exchange anaerobic threshold but that other factors, such as discomfort, may be involved in the excess Ve seen during heavy exercise.

Sign in / Sign up

Export Citation Format

Share Document