Glycogen depletion-induced lactate reductions attenuate reflex responses in exercising humans

1992 ◽  
Vol 263 (5) ◽  
pp. H1499-H1505 ◽  
Author(s):  
L. I. Sinoway ◽  
K. J. Wroblewski ◽  
S. A. Prophet ◽  
S. M. Ettinger ◽  
K. S. Gray ◽  
...  

Post leg exercise circulatory arrest (PLE-CA) raises blood pressure (BP) and reduces peak forearm vascular conductance (C). This reflex is evoked by activation of muscle afferents that are often sensitive to lactic acid. We tested the hypothesis that lactic acid reductions induced by muscle glycogen depletion would attenuate the lower-limb metaboreceptor-mediated pressor and forearm vasoconstrictor responses. Eleven subjects had C measured (plethysmography) during post leg exercise circulatory arrest (PLE-CA) (supine bicycle exercise for 9 min, 10 s at 75% VO2max before and after undergoing a glycogen-depletion paradigm (24-h fast followed by 10 min of supine leg exercise at 75% VO2max). In six subjects with lower lactate values, C during PLE-CA was higher after glycogen depletion (0.39 +/- 0.05 vs. 0.21 +/- 0.01 ml.min-1.100 ml-1 x mmHg-1; P < 0.01) and BP was lower (113 +/- 6 vs. 128 +/- 6 mmHg, P < 0.01). In five subjects without attenuated lactate responses, C and BP during PLE-CA were not different. Muscle biopsies (n = 5) demonstrated that the paradigm lowered muscle glycogen concentrations. Thus glycogen depletion-induced reductions in muscle lactate are associated with reduced muscle metaboreceptor-mediated responses.

1996 ◽  
Vol 270 (2) ◽  
pp. E328-E335 ◽  
Author(s):  
A. Chesley ◽  
G. J. Heigenhauser ◽  
L. L. Spriet

The purpose of this study was to examine the regulation (hormonal, substrate, and allosteric) of muscle glycogen phosphorylase (Phos) activity and glycogenolysis after short-term endurance training. Eight untrained males completed 6 days of cycle exercise (2 h/day) at 65% of maximal O2 uptake (Vo2max). Before and after training subjects cycled for 15 min at 80% of Vo2max, and muscle biopsies and blood samples were obtained at 0 and 30 s, 7.5 and 15 min, and 0, 5, 10, and 15 min of exercise. Vo2max was unchanged with training but citrate synthase (CS) activity increased by 20%. Muscle glycogenolysis was reduced by 42% during the 15-min exercise challenge following training (198.8 +/- 36.9 vs. 115.4 +/- 25.1 mmol/kg dry muscle), and plasma epinephrine was blunted at 15 min of exercise. The Phos a mole fraction was unaffected by training. Muscle phosphocreatine utilization and free Pi and AMP accumulations were reduced with training at 7.5 and 15 min of exercise. It is concluded that posttransformational control of Phos, exerted by reductions in substrate (free Pi) and allosteric modulator (free AMP) contents, is responsible for a blunted muscle glycogenolysis after 6 days of endurance training. The increase in CS activity suggests that the reduction of muscle glycogenolysis was due in part to an enhanced mitochondrial potential.


2000 ◽  
Vol 10 (3) ◽  
pp. 326-339 ◽  
Author(s):  
G. Gregory Haff ◽  
Alexander J. Koch ◽  
Jeffrey A. Potteiger ◽  
Karen E. Kuphal ◽  
Lawrence M. Magee ◽  
...  

The effects of carbohydrate (CHO) supplementation on muscle glycogen and resistance exercise performance were examined with eight highly resistance trained males (mean ± SEM, age: 24.3 ± 1.1 years, height: 171.9±2.0 cm, body mass: 85.7 ± 3.5 kg; experience 9.9 ± 2.0 years). Subjects participated in a randomized, double blind protocol with testing sessions separated by 7 days. Testing consisted of an initial isokinetic leg exercise before and after an isotonic resistance exercise (IRT) session consisting of 3 leg exercises lasting ~39 min. Subjects consumed a CHO (1.0 g CHO ·kg body mass−1) or placebo treatment (PLC), prior to and every 10-min (0.5 g CHO ·kg body mass−1) during the IRT. Muscle tissue was obtained from the m vastus lateralis after a supine rest (REST) immediately after the initial isokinetic test (POST-ISO) and immediately after the IRT (POST-IRT). The CHO treatment elicited significantly less muscle glycogen degradation from the POST-ISO to POST-IRT (126.9 ± 6.5 to 109.7 ± 7.1 mmol·kg wet weight−1) compared to PLC (121.4±8.1 to 88.3±6.0 mmol·kg wet weight−1). There were no differences in isokinetic performance between the treatments. The results of this investigation indicate that the consumption of a CHO beverage can attenuate the decrease in muscle glycogen associated with isotonic resistance exercise but does not enhance the performance of isokinetic leg exercise.


2001 ◽  
Vol 52 (7) ◽  
pp. 723 ◽  
Author(s):  
G. E. Gardner ◽  
R. H. Jacob ◽  
D. W. Pethick

This study was a series of experiments designed to test the influence of supplemental magnesium oxide (MgO) on muscle glycogen concentration in sheep exposed to stress (exercise) and the commercial slaughter process, and to test the effectiveness of this supplement in the commercial scenario. In Expt 1, Merino wethers maintained on a mixed ration (metabolisable energy 11 MJ/kg and crude protein 16.3% in DM) were supplemented with MgO at the rate of 0%, 0.5%, or 1% of their ration for 10 days prior to a single bout of exercise and for 10 days prior to slaughter at a commercial abattoir. The exercise regimen consisted of 4 intervals of 15 min, with muscle biopsies taken by biopsy drill from the m. semimembranosis (SM) and m. semitendinosis (ST) pre-exercise and immediately post-exercise, and at 36 and 72 h post-exercise. Muscle biopsies were also taken 1 week prior to slaughter from the SM and ST, with further samples taken approximately 30 min post-slaughter. Ultimate pH (pHu) of the SM, ST, and m. longissimus dorsi (LD) was measured 48 h after slaughter. Sheep supplemented with MgO lost less muscle glycogen in the ST during exercise, and repleted more muscle glycogen in the SM during the post-exercise repletion phase, than unsupplemented sheep. The supplemented animals also had higher muscle glycogen concentrations in the ST at slaughter. In Expt 2, MgO was administered to Merino wether lambs for 4 days prior to slaughter in the form of a water-borne slurry at a rate equivalent to 1% of their ration. This treatment resulted in significantly reduced muscle glycogen concentrations in both the SM and ST at slaughter. In Expts 3–5, MgO was used as an ‘in-feed’ supplement in the commercial scenario. In each case, slaughter-weight Merino lambs were supplemented with MgO at the rate of 1% of their ration for 4 days prior to commercial slaughter. Positive responses were seen in 2 of the 3 experiments, with increased glycogen concentrations and a reduced pHu. The animals that demonstrated no response to MgO had the lowest pHu after slaughter, suggesting a minimal stress load, thus providing very little scope for an effect of the MgO supplement. We conclude that MgO can reduce the effects of exercise, leading to a subsequent reduction in glycogen loss, and an increase in the rate of glycogen repletion in skeletal muscle following exercise. The results support MgO supplementation as a viable option for reducing the stress associated with commercial slaughter.


1986 ◽  
Vol 60 (5) ◽  
pp. 1466-1470 ◽  
Author(s):  
E. Jansson ◽  
P. Hjemdahl ◽  
L. Kaijser

Epinephrine increases glycogenolysis in resting skeletal muscle, but less is known about the effects of epinephrine on exercising muscle. To study this, epinephrine was given intraarterially to one leg during two-legged cycle exercise in nine healthy males. The epinephrine-stimulated (EPI) and non-stimulated (C) legs were compared with regard to glycogen, glucose, glucose 6-phosphate (G6P), alpha-glycerophosphate (alpha-GP), and lactate contents in muscle biopsies taken before and after the 45-min submaximal exercise, as well as brachial arterial-femoral venous (a-fv) differences for epinephrine, norepinephrine, lactate, glucose, and O2 during exercise. During exercise the arterial plasma epinephrine concentration was 4.8 +/- 0.8 nmol/l and the femoral venous epinephrine concentrations were 10.3 +/- 2.1 and 3.9 +/- 0.6 nmol/l, respectively, in the EPI and C leg. During exercise the a-fv difference for lactate was greater (-0.41 +/- 0.14 vs. -0.21 +/- 0.14 mmol/l; P less than 0.001), and the a-fv difference for glucose was smaller (0.07 +/- 0.12 vs. 0.24 +/- 0.12 mmol/l; P less than 0.01) in the EPI than in the C leg, but the a-fv differences for O2 were similar. Muscle glycogen depletion (137 +/- 63 vs. 99 +/- 43 mmol/kg dry muscle; P less than 0.1) and the muscle concentrations of glucose (P less than 0.05), alpha-GP (P less than 0.1), G6P (P greater than 0.1), and lactate (P greater than 0.1) tended to be higher in the EPI than the C leg after exercise. These findings suggest that physiological concentrations of epinephrine may enhance muscle glycogenolysis during submaximal exercise in male subjects.


1985 ◽  
Vol 59 (6) ◽  
pp. 1929-1935 ◽  
Author(s):  
A. J. Young ◽  
M. N. Sawka ◽  
L. Levine ◽  
B. S. Cadarette ◽  
K. B. Pandolf

The influence of heat acclimation on skeletal muscle metabolism during submaximal exercise was studied in 13 healthy men. The subjects performed 30 min of cycle exercise (70% of individual maximal O2 uptake) in a cool [21 degrees C, 30% relative humidity (rh)] and a hot (49 degrees C, 20% rh) environment before and again after they were heat acclimated. Aerobic metabolic rate was lower (0.1 l X min-1; P less than 0.01) during exercise in the heat compared with the cool both before and after heat acclimation. Muscle and plasma lactate accumulation with exercise was greater (P less than 0.01) in the hot relative to the cool environment both before and after acclimation. Acclimation lowered (P less than 0.01) aerobic metabolic rate as well as muscle and plasma lactate accumulation in both environments. The amount of muscle glycogen utilized during exercise in the hot environment did not differ from that in the cool either before or after acclimation. These findings indicate that accumulation of muscle lactate is increased and aerobic metabolic rate is decreased during exercise in the heat before and after heat acclimation; increased muscle glycogen utilization does not account for the increased muscle lactate accumulation during exercise under extreme heat stress; and heat acclimation lowers the aerobic metabolic rate and muscle and blood lactate accumulation during exercise in a cool as well as a hot environment.


1968 ◽  
Vol 25 (5) ◽  
pp. 837-851 ◽  
Author(s):  
F. W. H. Beamish

In Atlantic cod, muscle glycogen was reduced by about 50% at moderate swimming speeds and over 80% at higher speeds. Muscle glycogen for a given swimming speed was generally lower after 30 min exercise than after 15 min exercise. During the 8-hr period after strenuous exercise, muscle glycogen increased but remained well below the level for unexercised fish.At moderate swimming speeds, fish exhibited comparatively small amounts of muscle and blood lactic acid. At higher swimming speeds, fish accumulated significantly larger quantities of lactic acid in the muscle and blood. During the recovery period after strenuous exercise, muscle and blood lactic acid increased precipitously. Muscle lactic acid remained high for 1 hr after exercise and then decreased in 8 hr to levels similar to those of unexercised cod. Blood lactic acid followed a similar pattern except that it continued to increase for 1.5 hr after exercise.Serial samples of blood taken before and after 30 min strenuous exercise showed marked differences in lactic acid among individuals. Blood lactic acid usually continued to increase for 30–60 min after exercise, and decreased to the level for unexercised fish about 24 hr after exercise.No mortalities attributable to muscular fatigue occurred among cod.


2019 ◽  
Vol 317 (1) ◽  
pp. R59-R67 ◽  
Author(s):  
Ida E. Clark ◽  
Anni Vanhatalo ◽  
Christopher Thompson ◽  
Lee J. Wylie ◽  
Stephen J. Bailey ◽  
...  

It is not clear how the parameters of the power-duration relationship [critical power (CP) and W′] are influenced by the performance of prolonged endurance exercise. We used severe-intensity prediction trials (conventional protocol) and the 3-min all-out test (3MT) to measure CP and W′ following 2 h of heavy-intensity cycling exercise and took muscle biopsies to investigate possible relationships to changes in muscle glycogen concentration ([glycogen]). Fourteen participants completed a rested 3MT to establish end-test power (Control-EP) and work done above EP (Control-WEP). Subsequently, on separate days, immediately following 2 h of heavy-intensity exercise, participants completed a 3MT to establish Fatigued-EP and Fatigued-WEP and three severe-intensity prediction trials to the limit of tolerance (Tlim) to establish Fatigued-CP and Fatigued-W′. A muscle biopsy was collected immediately before and after one of the 2-h exercise bouts. Fatigued-CP (256 ± 41 W) and Fatigued-EP (256 ± 52 W), and Fatigued-Wʹ (15.3 ± 5.0 kJ) and Fatigued-WEP (14.6 ± 5.3 kJ), were not different ( P > 0.05) but were ~11% and ~20% lower than Control-EP (287 ± 46 W) and Control-WEP (18.7 ± 4.7 kJ), respectively ( P < 0.05). The change in muscle [glycogen] was not significantly correlated with the changes in either EP ( r = 0.19) or WEP ( r = 0.07). The power-duration relationship is adversely impacted by prolonged endurance exercise. The 3MT provides valid estimates of CP and W′ following 2 h of heavy-intensity exercise, but the changes in these parameters are not primarily determined by changes in muscle [glycogen].


1996 ◽  
Vol 81 (4) ◽  
pp. 1658-1663 ◽  
Author(s):  
M. Jackman ◽  
P. Wendling ◽  
D. Friars ◽  
T. E. Graham

Jackman, M., P. Wendling, D. Friars, and T. E. Graham.Metabolic, catecholamine, and endurance responses to caffeine during intense exercise. J. Appl. Physiol. 81(4): 1658–1663, 1996.—This study examined the possible effects of caffeine ingestion on muscle metabolism and endurance during brief intense exercise. We tested 14 subjects after they ingested placebo or caffeine (6 mg/kg) with an exercise protocol in which they cycled for 2 min, rested 6 min, cycled 2 min, rested 6 min, and then cycled to voluntary exhaustion. In each exercise the intensity required the subject’s maximal O2 consumption. Eight subjects had muscle and venous blood samples taken before and after each exercise period. The caffeine ingestion resulted in a significant increase in endurance (4.12 ± 0.36 and 4.93 ± 0.60 min for placebo and caffeine, respectively) and resulted in a significant increase in plasma epinephrine concentration throughout the protocol but not in norepinephrine concentration. During the first two exercise bouts, the power and work output were not different; blood lactate concentrations were not affected significantly by caffeine ingestion, but during the exercise bouts muscle lactate concentration was significantly increased by caffeine. The net decrease in muscle glycogen was not different between treatments at any point in the protocol, and even at the time of fatigue there was at least 50% of the original glycogen concentration remaining. The data demonstrated that caffeine ingestion can be an effective ergogenic aid for exercise that is as brief as 4–6 min. However, the mechanism is not associated with muscle glycogen sparing. It is possible that caffeine is exerting actions directly on the active muscle and/or the neural processes that are involved in the activity.


1998 ◽  
Vol 275 (2) ◽  
pp. R418-R425 ◽  
Author(s):  
Richard A. Howlett ◽  
Michelle L. Parolin ◽  
David J. Dyck ◽  
Eric Hultman ◽  
Norman L. Jones ◽  
...  

This study investigated the transformational and posttransformational control of skeletal muscle glycogen phosphorylase and pyruvate dehydrogenase (PDH) at three exercise power outputs [35, 65, and 90% of maximal oxygen uptake (V˙o 2 max)]. Seven untrained subjects cycled at one power output for 10 min on three separate occasions, with muscle biopsies at rest and 1 and 10 min of exercise. Glycogen phosphorylase in the more active ( a) form was not significantly different at any time across power outputs (21.4–29.6%), with the exception of 90%, where it fell significantly to 15.3% at 10 min. PDH transformation increased significantly from rest (average 0.53 mmol ⋅ kg wet muscle−1 ⋅ min−1) to 1 min of exercise as a function of power output (1.60 ± 0.26, 2.77 ± 0.29, and 3.33 ± 0.31 mmol ⋅ kg wet muscle−1 ⋅ min−1at 35, 65, and 90%, respectively) with a further significant increase at 10 min (4.45 ± 0.35) at 90%V˙o 2 max. Muscle lactate, acetyl-CoA, acetylcarnitine, and free ADP, AMP, and Pi were unchanged from rest at 35% V˙o 2 max but rose significantly at 65 and 90%, with accumulations at 90% being significantly higher than 65%. The results of this study indicate that glycogen phosphorylase transformation is independent of increasing power outputs, despite increasing glycogenolytic flux, suggesting that flux through glycogen phosphorylase is matched to the demand for energy by posttransformational factors, such as free Pi and AMP. Conversely, PDH transformation is directly related to the increasing power output and the calculated flux through the enzyme. The rise in PDH transformation is likely due to increased Ca2+concentration and/or increased pyruvate. These results demonstrate that metabolic signals related to contraction and the energy state of the cell are sensitive to the exercise intensity and coordinate the increase in carbohydrate use with increasing power output.


1962 ◽  
Vol 19 (1) ◽  
pp. 127-136 ◽  
Author(s):  
P. W. Hochachka ◽  
A. C. Sinclair

Changes in the glycogen reserves of epaxial and heart muscle of trout were followed after stream planting. Muscle glycogen recovered quickly in large fish; more slowly in smaller ones, and was related to earlier reported changes in liver glycogen and blood lactic acid. Heart glycogen increased initially, but fell again shortly after feeding became stabilized. Muscle glycogen reserves of wild trout were lower in the presence of hatchery fish than in their absence. A depletion of some metabolite, such as glycogen, in conjunction with an increased body demand due to raised basal metabolism was suggested as a factor in delayed mortality.


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