Effects of exercise in normoxia and acute hypoxia on respiratory muscle metabolites

1986 ◽  
Vol 60 (4) ◽  
pp. 1274-1283 ◽  
Author(s):  
R. F. Fregosi ◽  
J. A. Dempsey
Keyword(s):  
Endurance Exercise ◽  
Muscle Glycogen ◽  
Respiratory Muscle ◽  
Acute Hypoxia ◽  
Lactate Concentration ◽  
Lactate Production ◽  
Exhaustive Exercise ◽  
Diaphragm Muscle ◽  
Arterial Blood ◽  
Glycogen Utilization

We determined changes in rat plantaris, diaphragm, and intercostal muscle metabolites following exercise of various intensities and durations, in normoxia and hypoxia (FIO2 = 0.12). Marked alveolar hyperventilation occurred during all exercise conditions, suggesting that respiratory muscle motor activity was high. [ATP] was maintained at rest levels in all muscles during all normoxic and hypoxic exercise bouts, but at the expense of creatine phosphate (CP) in plantaris muscle and diaphragm muscle following brief exercise at maximum O2 uptake (VO2max) in normoxia. In normoxic exercise plantaris [glycogen] fell as exercise exceeded 60% VO2max, and was reduced to less than 50% control during exhaustive endurance exercise (68% VO2max for 54 min and 84% for 38 min). Respiratory muscle [glycogen] was unchanged at VO2max as well as during either type of endurance exercise. Glucose 6-phosphate (G6P) rose consistently during heavy exercise in diaphragm but not in plantaris. With all types of exercise greater than 84% VO2max, lactate concentration ([LA]) in all three muscles rose to the same extent as arterial [LA], except at VO2max, where respiratory muscle [LA] rose to less than half that in arterial blood or plantaris. Exhaustive exercise in hypoxia caused marked hyperventilation and reduced arterial O2 content; glycogen fell in plantaris (20% of control) and in diaphragm (58%) and intercostals (44%). We conclude that respiratory muscle glycogen stores are spared during exhaustive exercise in the face of substantial glycogen utilization in plantaris, even under conditions of extreme hyperventilation and reduced O2 transport. This sparing effect is due primarily to G6P inhibition of glycogen phosphorylase in diaphragm muscle. The presence of elevated [LA] in the absence of glycogen utilization suggests that increased lactate uptake, rather than lactate production, occurred in the respiratory muscles during exhaustive exercise.

Exhaustive endurance exercise activates brain glycogen breakdown and lactate production more than insulin-induced hypoglycemia

2021 ◽  
Author(s):  
Takashi Matsui
Keyword(s):  
Endurance Exercise ◽  
Lactate Production ◽  
Severe Hypoglycemia ◽  
Exercise Group ◽  
Exhaustive Exercise ◽  
Endurance Capacity ◽  
Brain Glycogen ◽  
Insulin Group ◽  
Exercise Induced

Brain glycogen localized in astrocytes produces lactate via cAMP signaling, which regulates memory functions and endurance capacity. Exhaustive endurance exercise with hypoglycemia decreases brain glycogen, although the mechanism underlying this phenomenon remains unclear. Since insulin-induced hypoglycemia decreases brain glycogen, this study tested the hypothesis that hypoglycemia mediates exercise-induced brain glycogen decrease. To test the hypothesis, the effects of insulin- and exhaustive exercise-induced hypoglycemia on brain glycogen levels were compared using the microwave irradiation method in adult Wistar rats. The insulin challenge and exhaustive exercise induced similar levels of severe hypoglycemia. Glycogen in the hypothalamus and cerebellum decreased similarly with the insulin challenge and exhaustive exercise; however, glycogen in the cortex, hippocampus, and brainstem of the exercise group were lower compared to the insulin group. Blood glucose correlated positively with brain glycogen, but the slope of regression lines was greater in the exercise group compared to the insulin group in the cortex, hippocampus, and brainstem, but not the hypothalamus and cerebellum. Brain lactate and cAMP levels in the hypothalamus and cerebellum increased similarly with the insulin challenge and exhaustive exercise, but those in the cortex, hippocampus, and brainstem of the exercise group were higher compared to the insulin group. These findings support the hypothesis that hypoglycemia mediates the exercise-induced reduction in brain glycogen, at least in the hypothalamus and cerebellum. However, glycogen reduction during exhaustive endurance exercise in the cortex, hippocampus, and brainstem is not due to hypoglycemia alone, implicating the role of exercise-specific neuronal activity in brain glycogen decrease.

Adaptations of skeletal muscle to endurance exercise and their metabolic consequences

1984 ◽  
Vol 56 (4) ◽  
pp. 831-838 ◽  
Author(s):  
J. O. Holloszy ◽  
E. F. Coyle
Keyword(s):  
Skeletal Muscle ◽  
Blood Glucose ◽  
Exercise Training ◽  
Endurance Exercise ◽  
Muscle Glycogen ◽  
Lactate Production ◽  
Strenuous Exercise ◽  
Mitochondrial Content ◽  
Respiratory Capacity ◽  
Endurance Exercise Training

Regularly performed endurance exercise induces major adaptations in skeletal muscle. These include increases in the mitochondrial content and respiratory capacity of the muscle fibers. As a consequence of the increase in mitochondria, exercise of the same intensity results in a disturbance in homeostasis that is smaller in trained than in untrained muscles. The major metabolic consequences of the adaptations of muscle to endurance exercise are a slower utilization of muscle glycogen and blood glucose, a greater reliance on fat oxidation, and less lactate production during exercise of a given intensity. These adaptations play an important role in the large increase in the ability to perform prolonged strenuous exercise that occurs in response to endurance exercise training.

Menstrual cycle phase and sex influence muscle glycogen utilization and glucose turnover during moderate-intensity endurance exercise

2006 ◽  
Vol 291 (4) ◽  
pp. R1120-R1128 ◽  
Author(s):  
Michaela C. Devries ◽  
Mazen J. Hamadeh ◽  
Stuart M. Phillips ◽  
Mark A. Tarnopolsky
Keyword(s):  
Menstrual Cycle ◽  
Endurance Exercise ◽  
Muscle Glycogen ◽  
Constant Infusion ◽  
Moderate Intensity ◽  
Glucose Turnover ◽  
Cycle Phase ◽  
Metabolic Clearance ◽  
Menstrual Cycle Phase ◽  
Glycogen Utilization

Numerous studies from our and other laboratories have shown that women have a lower respiratory exchange ratio (RER) during exercise than equally trained men, indicating a greater reliance on fat oxidation. Differences in estrogen concentration between men and women likely play a role in this sex difference. Differing estrogen and progesterone concentrations during the follicular (FP) and luteal (LP) phases of the female menstrual cycle suggest that fuel use may also vary between phases. The purpose of the current study was to determine the effect of menstrual cycle phase and sex upon glucose turnover and muscle glycogen utilization during endurance exercise. Healthy, recreationally active young women ( n = 13) and men ( n = 11) underwent a primed constant infusion of [6,6-2H]glucose with muscle biopsies taken before and after a 90-min cycling bout at 65% peak O2 consumption. LP women had lower glucose rate of appearance (Ra, P = 0.03), rate of disappearance (Rd, P = 0.03), and metabolic clearance rate (MCR, P = 0.04) at 90 min of exercise and lower proglycogen ( P = 0.04), macroglycogen ( P = 0.04), and total glycogen ( P = 0.02) utilization during exercise compared with FP women. Men had a higher RER ( P = 0.02), glucose Ra ( P = 0.03), Rd ( P = 0.03), and MCR ( P = 0.01) during exercise compared with FP women, and men had a higher RER at 75 and 90 min of exercise ( P = 0.04), glucose Ra ( P = 0.01), Rd ( P = 0.01), and MCR ( P = 0.001) and a greater PG utilization ( P = 0.05) compared with LP women. We conclude that sex, and to a lesser extent menstrual cycle, influence glucose turnover and glycogen utilization during moderate-intensity endurance exercise.

scholarly journals Human skeletal muscle glycogen utilization in exhaustive exercise: role of subcellular localization and fibre type

2011 ◽  
Vol 589 (11) ◽  
pp. 2871-2885 ◽  
Author(s):  
Joachim Nielsen ◽  
Hans-Christer Holmberg ◽  
Henrik D. Schrøder ◽  
Bengt Saltin ◽  
Niels Ørtenblad
Keyword(s):  
Skeletal Muscle ◽  
Subcellular Localization ◽  
Muscle Glycogen ◽  
Fibre Type ◽  
Human Skeletal Muscle ◽  
Exhaustive Exercise ◽  
Skeletal Muscle Glycogen ◽  
Glycogen Utilization

Exercise-induced glycogen utilization by the respiratory muscles

1987 ◽  
Vol 62 (4) ◽  
pp. 1405-1409 ◽  
Author(s):  
C. D. Ianuzzo ◽  
M. J. Spalding ◽  
H. Williams
Keyword(s):  
Endurance Exercise ◽  
Treadmill Exercise ◽  
Periodic Acid ◽  
Respiratory Muscles ◽  
Diaphragm Muscle ◽  
Sprague Dawley ◽  
Periodic Acid Schiff ◽  
Sprague Dawley Rats ◽  
Glycogen Utilization ◽  
Exercise Induced

Some controversy exists in the literature as to whether or not diaphragmatic glycogen is utilized during exercise. In this study male Sprague-Dawley rats were used to determine whether prolonged treadmill exercise would result in a significant reduction of glycogen concentration in the respiratory muscles. Untrained rats were run to exhaustion at a speed of 24 m/min, up a 10% grade. Run time averaged 48:30 min. After exercise a significant reduction in glycogen was observed in the diaphragm (43% of control), intercostals (43%), heart (39%), and plantaris (76%). In the diaphragm a significant reduction was shown in both types I and II fibers using the periodic acid-Schiff (PAS) stain for glycogen. These findings show that muscles with vastly different aerobic capacities utilize endogenous glycogen during moderately intense submaximal endurance exercise and that the costal diaphragm muscle is not an exception as has recently been suggested.

Endurance exercise training reduces lactate production

1986 ◽  
Vol 61 (3) ◽  
pp. 885-889 ◽  
Author(s):  
R. J. Favier ◽  
S. H. Constable ◽  
M. Chen ◽  
J. O. Holloszy
Keyword(s):  
Exercise Training ◽  
Endurance Exercise ◽  
Contractile Activity ◽  
Lactate Concentration ◽  
Lactate Production ◽  
Endurance Exercise Training ◽  
Fast Twitch ◽  
Isotonic Contractions ◽  
Glycogen Sparing

In situ muscle stimulation in trained and untrained rats was used to reevaluate whether adaptations induced by endurance exercise training result in decreased lactate production by contracting muscles. The gastrocnemius-plantaris-soleus muscle group was stimulated to perform isotonic contractions. After 3 min of stimulation with 100-ms trains at 50 Hz at 60/min, the increases in lactate concentration in the plantaris, soleus, and fast-twitch red muscle (deep portion of lateral head of gastrocnemius) were only approximately 50% as great in trained as in sedentary rats. In the predominantly fast-twitch white superficial portion of the medial head of the gastrocnemius the increase in lactate concentration was 28% less in the trained than in the sedentary group. The decreases in muscle glycogen concentration seen after 3 min of stimulation at 60 trains/min were smaller in the trained than in the untrained group. The reduction in lactate accumulation that occurred in the different muscles in response to training was roughly proportional to the degree of glycogen sparing. These results show that endurance training induces adaptations that result in a slower production of lactate by muscle during contractile activity.

Sustained maximal ventilation after endurance exercise in athletes

1989 ◽  
Vol 67 (5) ◽  
pp. 1759-1763 ◽  
Author(s):  
J. D. Anholm ◽  
J. Stray-Gundersen ◽  
M. Ramanathan ◽  
R. L. Johnson
Keyword(s):  
Oxygen Consumption ◽  
Endurance Exercise ◽  
Muscle Function ◽  
Respiratory Muscle ◽  
Exhaustive Exercise ◽  
Muscle Performance ◽  
Maximum Oxygen Consumption ◽  
The Mean ◽  
Cross Country ◽  
Maximal Voluntary Ventilation

Although impaired respiratory muscle performance that persists up to 5 min after exercise is stopped has been demonstrated during exhaustive exercise in normal young men, it is not known whether impaired respiratory muscle function follows endurance exercise to exhaustion in highly trained athletes. To study the effects of exercise on sustained maximal voluntary ventilation immediately after exercise, eight elite cross-country skiers performed a 4-min maximal sustained ventilation (MSV) test before and immediately after exhaustive exercise. Subjects were encouraged to maintain maximal ventilation (VE) throughout the MSV test. To encourage greater effort, rapid visual feedback of VE was provided on a computer terminal along with a target VE based on their 12-s maximum voluntary ventilation (MVV). The subjects (7 males, 1 female) were 18.5 +/- 0.9 yr old (mean +/- SD) and exercised for 62.5 +/- 16.7 min at 77 +/- 5% of their maximum oxygen consumption during which average VE was 106.7 +/- 24.2 l/min BTPS. The mean MVV was 196.0 +/- 29.9 l/min or 107% of their age- and height-predicted MVV. Before exercise the MSV was 86% of the MVV or 176.7 +/- 30.5 l/min, whereas after exercise the MSV was 90% of the MVV or 180.3 +/- 28.9 l/min (P = NS). The total volume of gas expired during the 4-min MSV was 706.7 +/- 121.9 liters before and 721.2 +/- 115.5 liters after exercise (P = NS). In this group of athletes, exhaustive exercise produced no deleterious effects on the ability to perform a 4-min MSV test immediately after exercise.

α-Glycerophosphate metabolism in muscle under aerobic and hypoxic conditions

1964 ◽  
Vol 206 (3) ◽  
pp. 599-602 ◽  
Author(s):  
Ruth D. Peterson ◽  
David Gaudin ◽  
Rose Mary Bocek ◽  
Clarissa H. Beatty
Keyword(s):  
Skeletal Muscle ◽  
Lactate Concentration ◽  
Lactate Production ◽  
Fold Increase ◽  
Diaphragm Muscle ◽  
Dihydroxyacetone Phosphate ◽  
Hypoxic Conditions ◽  
Measurable Amount

A significant amount of α-glycerophosphate (α-GP) was present in voluntary skeletal muscle of rats when the hind limb was frozen in situ. Ischemia of this muscle in situ caused a 7-fold increase in α-GP concentration and a 12-fold increase in lactate concentration. In vitro experiments with diaphragm muscle from rats and adductor fiber groups from rats and monkeys also demonstrated that hypoxic conditions caused a 2.5- to 4-fold rise in α-GP levels. The α-GP concentration in hypoxic red muscle was higher than that in hypoxic white muscle from rats. Lactate diffused into the medium from all types of muscle preparations. However, under aerobic conditions no measurable amount of α-GP appeared in the medium surrounding the fibers and only a small amount diffused out of the diaphragm muscle. Even when incubation was carried out under hypoxic conditions little α-GP was present in fiber medium. Although the diaphragm released ten times as much α-GP as the fiber groups, this amount was small in relation to lactate production. These data indicate that under anaerobic and hypoxic conditions dihydroxyacetone phosphate can compete with pyruvate for the cytoplasmic NADH in diaphragm and voluntary skeletal muscle.

Elevated muscle acidity and energy production during exhaustive exercise in humans

1992 ◽  
Vol 263 (4) ◽  
pp. R891-R899 ◽  
Author(s):  
J. Bangsbo ◽  
T. Graham ◽  
L. Johansen ◽  
S. Strange ◽  
C. Christensen ◽  
...  
Keyword(s):  
Energy Production ◽  
Intermittent Exercise ◽  
Lactate Concentration ◽  
Lactate Production ◽  
Knee Extensor ◽  
Exhaustive Exercise ◽  
Time To Exhaustion ◽  
Intense Exercise ◽  
Muscle Lactate ◽  
Muscle Ph

This study examined the effect of previous intense exercise on energy production during exhaustive exercise. Subjects (n = 6) performed dynamic knee extensor exercise to exhaustion twice (Ex1 and Ex2) separated by 16 min of recovery consisting of 10 min of rest, 3.5 min of very high-intensity intermittent exercise, and a further 2.5 min of rest. This resulted in an elevated muscle lactate concentration of 13.1 mmol/kg wet wt before Ex2. Muscle lactate concentration was the same at end of Ex1 and Ex2, but the accumulation of lactate and net lactate release during Ex2 was reduced (P < 0.05) by 67 and 38%, respectively. The time to exhaustion was 3.73 and 2.98 min, respectively, and the mean rate of net lactate production for Ex2 was lower (P < 0.05) than for Ex1 (4.6 +/- 1.2 and 9.6 +/- 1.7 mmol.min-1.kg wet wt-1, respectively). Leg O2 uptake was the same for Ex1 and Ex2. Muscle pH (6.85) was lowered (P < 0.05) before Ex2, but at the end of Ex2 (6.77) it tended (P < 0.1) to be higher compared with that at the end of Ex1 (6.73). In summary, the net lactate production rate is reduced but the aerobic energy production is not significantly altered when intense exercise is repeated. Fatigue and the lowered glycolysis do not appear to be caused by the elevated acidity per se before exercise.

scholarly journals Astrocytic glycogen-derived lactate fuels the brain during exhaustive exercise to maintain endurance capacity

2017 ◽  
Vol 114 (24) ◽  
pp. 6358-6363 ◽  
Author(s):  
Takashi Matsui ◽  
Hideki Omuro ◽  
Yu-Fan Liu ◽  
Mariko Soya ◽  
Takeru Shima ◽  
...  
Keyword(s):  
Muscle Glycogen ◽  
Defense Mechanism ◽  
Lactate Production ◽  
Exhaustive Exercise ◽  
Endurance Capacity ◽  
Similar Response ◽  
Lactate Transport ◽  
Brain Glycogen ◽  
The Brain

Brain glycogen stored in astrocytes provides lactate as an energy source to neurons through monocarboxylate transporters (MCTs) to maintain neuronal functions such as hippocampus-regulated memory formation. Although prolonged exhaustive exercise decreases brain glycogen, the role of this decrease and lactate transport in the exercising brain remains less clear. Because muscle glycogen fuels exercising muscles, we hypothesized that astrocytic glycogen plays an energetic role in the prolonged-exercising brain to maintain endurance capacity through lactate transport. To test this hypothesis, we used a rat model of exhaustive exercise and capillary electrophoresis-mass spectrometry–based metabolomics to observe comprehensive energetics of the brain (cortex and hippocampus) and muscle (plantaris). At exhaustion, muscle glycogen was depleted but brain glycogen was only decreased. The levels of MCT2, which takes up lactate in neurons, increased in the brain, as did muscle MCTs. Metabolomics revealed that brain, but not muscle, ATP was maintained with lactate and other glycogenolytic/glycolytic sources. Intracerebroventricular injection of the glycogen phosphorylase inhibitor 1,4-dideoxy-1,4-imino-d-arabinitol did not affect peripheral glycemic conditions but suppressed brain lactate production and decreased hippocampal ATP levels at exhaustion. An MCT2 inhibitor, α-cyano-4-hydroxy-cinnamate, triggered a similar response that resulted in lower endurance capacity. These findings provide direct evidence for the energetic role of astrocytic glycogen-derived lactate in the exhaustive-exercising brain, implicating the significance of brain glycogen level in endurance capacity. Glycogen-maintained ATP in the brain is a possible defense mechanism for neurons in the exhausted brain.

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