Metabolic response of equine muscle to intermittent maximal exercise

Four thoroughbred horses performed 4 gallops (G1-G4) with intervals of 5 min. With one exception, gallops were sustained at maximal speed over 620 m. Muscle biopsy samples of the middle gluteal and brachiocephalicus were taken before, during, and after exercise and assayed for ATP and intermediary metabolites. The results showed a major involvement of the brachiocephalicus, in addition to the middle gluteal, during galloping. In three horses, who were clearly fatigued, muscle ATP decreased by up to 50% by the end of G4. This was matched by an equal rise in inosine 5'-monophosphate. Pronounced accumulations of glycerol 3-phosphate, glycerol, and lactate (up to 204 mmol X kg dry muscle-1) occurred with exercise. In the fourth horse, which was less fatigued, a decrease in ATP and increases in intermediary metabolites were much less. Postexercise there was little or no recovery in muscle ATP or lactate during 30 min. The decreases in ATP are consistent with a high activity of adenosine 5'-monophosphate deaminase in horse muscle and indicative also of the high level of anaerobic stress of the exercise program. There was evidence to suggest that the increase in muscle glycerol resulted from hydrolysis of glycerol 3-phosphate and not from the utilization of triglyceride.     

Adenine nucleotide degradation in the thoroughbred horse with increasing exercise duration

Adenine nucleotide (AN) degradation has been shown to occur during intense exercise in the horse and in man, at or close to the point of fatigue. The aim of the study was to compare the concentrations of muscle inosine 5'-monophosphate (IMP) and plasma ammonia (NH3) during intense exercise with the concentrations of muscle and blood lactate. Seven trained thoroughbred horses were used in the study. Each exercised on a treadmill for periods of between 30 s and 150 s, at 11 and/or 12 m.s-1. Blood and muscle samples were taken and analysed for lactate and NH3 and adenosine 5'-triphosphate (ATP), phosphorylcreatine (PCr), IMP, creatine, lactate and glycerol-3-phosphate respectively. Horses showed varying degrees of AN degradation as indicated by plasma [NH3] and muscle [ATP] and [IMP]. Comparisons of [IMP] with muscle [lactate], and plasma [NH3] with that of blood [lactate] indicated a threshold to the start of AN degradation. This threshold corresponded to a lactate content of around 80 mmol.kg-1 dry muscle and 15 mmol.l-1 in blood. We discuss the mechanisms which have been proposed to account for AN degradation and suggest that IMP formation occurs as a result of a sudden rise in the concentration of adenosine 5'-diphosphate (ADP) and consequently the concentration of adenosine 5'-monophosphate. The data suggest a critical pH below which there may be a substantial reduction in the kinetics of ADP rephosphorylation provided by PCr resulting in an increase in [ADP], which is the stimulus to AN degradation during intense exercise.     

Cerebral hemodynamic response to maximal exercise

The response of central and cerebral hemodynamics to a stepwise increase in dynamic exercise until failure was studied in healthy young men. Each subject was examined using Doppler ultrasound assessment of blood flow in the middle cerebral artery (MCA), Doppler echocardiography, and spiroergometry. Hemodynamic parameters were recorded before the study and during the last several seconds of each step of the dynamic exercise. The central hemodynamic and energy exchange parameters exhibited typical changes with increasing exercise intensity. The peak systolic blood flow velocity in the MCA increased only in response to exercise of a moderate intensity (1 W/kg body weight, 45% of the maximal oxygen uptake); the further increase in exercise intensity did not affect the blood flow velocity. The cerebral vascular resistance index at the last step of the exercise was 24% higher than at rest. The increase in the MCA resistance index during the exercise was moderately correlated with the increase in the pulse pressure and systolic blood pressure, whereas the increase in blood pressure was not related to the increase in the peak systolic blood flow velocity in the MCA in response to an exercise intensity at which the oxygen uptake was higher than 45% of its maximal value. The differences between the responses of central and cerebral hemodynamics to the stepwise increase in exercise intensity reflect the phenomenon of cerebral hemodynamic autoregulation.     

Plasma adrenomedullin response to maximal exercise in healthy subjects.

The aim of the study was to find out whether maximal exercise performed by healthy young men influences plasma adrenomedullin concentration (ADM) and is the peptide level related to the cardiovascular, metabolic and hormonal changes induced by exercise. Ten subjects (age 24+/-1.0 yr) participated in the study. They performed graded bicycle ergometer exercise until exhaustion. Heart rate (HR) and blood pressure (BP) were measured throughout the test. Before and at the end of exercise venous blood samples were taken for [ADM], noradrenaline [NA], adrenaline [A], growth hormone [hGH], cortisol and lactate [LA] determination. Plasma [ADM] decreased during exercise from 1.71+/-0.09 to 1.53+/-0.10 pmol x l(-1) (p<0.01). This was accompanied by increases in plasma catecholamines and [hGH], while plasma cortisol level did not change. Positive correlation was found between the exercise-induced decreases in plasma ADM and diastolic BP. Blood [LA], systolic and mean BP at the end of exercise correlated negatively with plasma [ADM]. No significant interrelationships were found between plasma ADM, catecholamines or the other hormones measured. The present data suggests, that maximal exercise inhibits ADM secretion in young healthy men. Metabolic acidosis and a decrease in peripheral resistance might be involved in this effect.     

Ventilatory dynamics and control of blood gases after maximal exercise in the Thoroughbred horse.

Despite enormous rates of minute ventilation (Ve) in the galloping Thoroughbred (TB) horse, the energetic demands of exercise conspire to raise arterial Pco(2) (i.e., induce hypercapnia). If locomotory-respiratory coupling (LRC) is an obligatory facilitator of high Ve in the horse such as those found during galloping (Bramble and Carrier. Science 219: 251-256, 1983), Ve should drop precipitously when LRC ceases at the galloptrot transition, thus exacerbating the hypercapnia. TB horses (n = 5) were run to volitional fatigue on a motor-driven treadmill (1 m/s increments; 14-15 m/s) to study the dynamic control of breath-by-breath Ve, O(2) uptake, and CO(2) output at the transition from maximal exercise to active recovery (i.e., trotting at 3 m/s for 800 m). At the transition from the gallop to the trot, Ve did not drop instantaneously. Rather, Ve remained at the peak exercising levels (1,391 +/- 88 l/min) for approximately 13 s via the combination of an increased tidal volume (12.6 +/- 1.2 liters at gallop; 13.9 +/- 1.6 liters over 13 s of trotting recovery; P < 0.05) and a reduced breathing frequency [113.8 +/- 5.2 breaths/min (at gallop); 97.7 +/- 5.9 breaths/min over 13 s of trotting recovery (P < 0.05)]. Subsequently, Ve declined in a biphasic fashion with a slower mean response time (85.4 +/- 9.0 s) than that of the monoexponential decline of CO(2) output (39.9 +/- 4.7 s; P < 0.05), which rapidly reversed the postexercise arterial hypercapnia (arterial Pco(2) at gallop: 52.8 +/- 3.2 Torr; at 2 min of recovery: 25.0 +/- 1.4 Torr; P < 0.05). We conclude that LRC is not a prerequisite for achievement of Ve commensurate with maximal exercise or the pronounced hyperventilation during recovery.     

Metabolic response to carbohydrate ingestion during exercise in males and females

The present study investigated potential sex-related differences in the metabolic response to carbohydrate (CHO) ingestion during exercise. Moderately endurance-trained men and women (n = 8 for each sex) performed 2 h of cycling at approximately 67% Vo(2 max) with water (WAT) or CHO ingestion (1.5 g of glucose/min). Substrate oxidation and kinetics were quantified during exercise using indirect calorimetry and stable isotope techniques ([(13)C]glucose ingestion, [6,6-(2)H(2)]glucose, and [(2)H(5)]glycerol infusion). In both sexes, CHO ingestion significantly increased the rates of appearance (R(a)) and disappearance (R(d)) of glucose during exercise compared with WAT ingestion [males: WAT, approximately 28-29 micromol x kg lean body mass (LBM)(-1) x min(-1); CHO, approximately 53 micromol x kg LBM(-1) x min(-1); females: WAT, approximately 28-29 micromol x kg LBM(-1) x min(-1); CHO, approximately 61 micromol x kg LBM(-1) x min(-1); main effect of trial, P < 0.05]. The contribution of plasma glucose oxidation to the energy yield was significantly increased with CHO ingestion in both sexes (from approximately 10% to approximately 20% of energy expenditure; main effect of trial, P < 0.05). Liver-derived glucose oxidation was reduced, although the rate of muscle glycogen oxidation was unaffected with CHO ingestion (males: WAT, 108 +/- 12 micromol x kg LBM(-1) x min(-1); CHO, 108 +/- 11 micromol x kg LBM(-1) x min(-1); females: WAT, 89 +/- 10 micromol x kg LBM(-1) x min(-1); CHO, 93 +/- 11 micromol x kg LBM(-1) x min(-1)). CHO ingestion reduced fat oxidation and lipolytic rate (R(a) glycerol) to a similar extent in both sexes. Finally, ingested CHO was oxidized at similar rates in men and women during exercise (peak rates of 0.70 +/- 0.08 and 0.65 +/- 0.06 g/min, respectively). The present investigation suggests that the metabolic response to CHO ingestion during exercise is largely similar in men and women.     

Metabolic and physiological response of the rabbit to continuous and intermittent treadmill exercise

Our knowledge of the effects of exercise on the heart is limited by the predominant use of rats as an animal model. The rabbit has many advantages over the rat as an animal model to study. However, little work has characterized its capacity to exercise. The purposes of the present study were to determine if the rabbit could (i) learn to run on a motor-driven treadmill at relatively high speeds using different exercise protocols, and (ii) characterize the various physiological and metabolic responses of the rabbit to acute bouts of exercise. We found that female New Zealand white rabbits had the capacity to run continuously on the treadmill for up to 21 min at 20 m/min until exhausted. Continuous, endurance-type exercise resulted in significant elevations in body temperature, heart rate, and plasma lactate levels. Plasma triglyceride concentration decreased as a function of this type of running whereas plasma glucose levels were unchanged. Twenty-four hours after a bout of running, plasma creatine phosphokinase activity was significantly elevated. The rabbits also had the capacity to learn to run using an intermittent, higher speed protocol. These physically untrained animals could achieve speeds of up to 70 m/min for 10 bouts of 15 s run/30 s rest. Their metabolic and physiological responses to this protocol were similar to those of continuous running with the following exceptions. The decrease in plasma triglyceride was less marked and the increase in plasma lactate was greater after intermittent exercise. Glycogen content of the rabbit vastus lateralis muscle was also significantly depleted after exhaustive, intermittent exercise.(ABSTRACT TRUNCATED AT 250 WORDS)     

Sympathetic response to maximal bicycle exercise before and after leg strength training

Plasma catecholamine concentrations at rest and in response to maximal exercise on the cycle ergometer (278 +/- 15 watts, 6 min duration) have been measured on seven young active male subjects (19 +/- 1 years old; 80 +/- 3 kg; 176 +/- 3 cm) prior to and after a eight week leg strength training program (5RM, squat and leg press exercise). Strength training resulted in a significant increase in performance on squat (103 +/- 3 to 140 +/- 5 kg) and leg press exercise (180 +/- 9 to 247 +/- 15 kg) associated with a small significant increase in lean body mass (64.5 +/- 2.2 to 66.3 +/- 2.1 kg) and no change in maximal oxygen consumption (47.5 +/- 1.3 to 46.9 +/- 1.2 ml X kg-1 X min-1). Plasma norepinephrine (NE) and epinephrine (E) concentrations (pg X mL-1) were not significantly different before and after training at rest (NE: 172 +/- 19 vs 187 +/- 30; E: 33 +/- 10 vs 76 +/- 16) or in response to maximal exercise (NE: 3976 +/- 660 vs 4163 +/- 1081; E: 1072 +/- 322 vs 1321 +/- 508). Plasma lactate concentrations during recovery were similar before and after training (147 +/- 5 vs 147 +/- 15 mg X dL-1). Under the assumption that the "central command" is reduced for a given absolute workload on the bicycle ergometer following leg strength training, these observations support the hypothesis that the sympathetic response to exercise is under the control of information from muscle chemoreceptors.     

Training effects on regional blood flow response to maximal exercise in foxhounds

The effect of training on the regional blood flow response to maximal exercise was investigated in the foxhound. Training consisted of 8-12 wk of treadmill running at 80% of maximal heart rate 1 h/day for 5 days/wk and resulted in a 31% increase in maximal O2 consumption, a 28% increase in maximal cardiac output, and a 23% decrease in systemic vascular resistance during maximal exercise. Blood flow to the heart, diaphragm, brain, skin, and 9 of 10 muscles investigated was similar during maximal exercise pre- and posttraining; however, blood flow to the gastrocnemius muscle was greater posttraining than it was pretraining. Blood flow to the stomach, small intestine, and pancreas decreased during maximal exercise pre- and posttraining; however, blood flow to the large intestine, spleen, liver, adrenal glands, and kidneys decreased during maximal exercise only posttraining. In addition, a larger decrease in blood flow to the stomach during maximal exercise was found posttraining compared with pretraining. These results demonstrate that blood flow to skeletal muscle, the kidneys, and the splanchnic region of the foxhound during maximal exercise can be significantly altered by dynamic exercise training.     

Metabolic changes induced by maximal exercise in human subjects following L-carnitine administration

In double-blind cross-over experiments, ten moderately trained male subjects were submitted to two bouts of maximal cycle ergometer exercise separated by a 3 day interval. Each subject was randomly given either L-carnitine (2 g) or placebo orally 1 h before the beginning of each exercise session. At rest L-carnitine supplementation resulted in an increase of plasma-free carnitine without a change in acid-soluble carnitine esters. Treatment with L-carnitine induced a significant post-exercise decrease of plasma lactate and pyruvate and a concurrent increase of acetylcarnitine. The determination of the individual carnitine esters in urine collected for 24 h after the placebo exercise trial revealed a decrease of acetyl carnitine and a parallel increase of a C4 carnitine ester, probably isobutyrylcarnitine. Conversely, acetylcarnitine was strongly increased and C4 compounds were almost suppressed in the L-carnitine loading trial. These results suggest that L-carnitine administration prior to high-intensity exercise stimulates pyruvate dehydrogenase activity, thus diverting pyruvate from lactate to acetylcarnitine formation.     

Metabolic response to green tea extract during rest and moderate-intensity exercise

BackgroundGreen tea catechins have been hypothesized to increase energy expenditure and fat oxidation by inhibiting catechol-O-methyltransferase (COMT) and thus promoting more sustained adrenergic stimulation. Metabolomics may help to clarify the mechanisms underlying their putative physiological effects.ObjectiveThe study investigated the effects of 7-day ingestion of green tea extract (GTE) on the plasma metabolite profile at rest and during exercise.MethodsIn a placebo-controlled, double-blind, randomized, parallel study, 27 healthy physically active males consumed either GTE (n=13, 1200 mg catechins, 240 mg caffeine/day) or placebo (n=14, PLA) drinks for 7 days. After consuming a final drink (day 8), they rested for 2 h and then completed 60 min of moderate-intensity cycling exercise (56%±4% VO₂max). Blood samples were collected before and during exercise. Plasma was analyzed using untargeted four-phase metabolite profiling and targeted profiling of catecholamines.ResultsUsing the metabolomic approach, we observed that GTE did not enhance adrenergic stimulation (adrenaline and noradrenaline) during rest or exercise. At rest, GTE led to changes in metabolite concentrations related to fat metabolism (3-β-hydroxybutyrate), lipolysis (glycerol) and tricarboxylic acid cycle (TCA) cycle intermediates (citrate) when compared to PLA. GTE during exercise caused reductions in 3-β-hydroxybutyrate concentrations as well as increases in pyruvate, lactate and alanine concentrations when compared to PLA.ConclusionsGTE supplementation resulted in marked metabolic differences during rest and exercise. Yet these metabolic differences were not related to the adrenergic system, which questions the in vivo relevance of the COMT inhibition mechanism of action for GTE.     

Genomic structure and expression analyses of the PYGM gene in the thoroughbred horse

Muscle glycogen Phosphorylase (PYGM) has been shown to catalyze the degradation of glycogen to glucose-1-phosphate. The PYGM gene can contribute to providing energy to the body by disassembling the glycogen in muscle. Here, we analyzed the genomic structure and expression of the PYGM gene in the thoroughbred horse. The PYGM gene, containing several transposable elements (MIRs, LINEs, and MERs), was highly conserved in mammalian genomes. In order to understand the expression of the horse PYGM gene, we performed quantitative RT-PCR using 11 thoroughbred horse tissue samples. The horse PYGM gene was broadly expressed in all tissues tested. In particular, the highest expression of the horse PYGM gene was observed in skeletal muscle tissue relative to the other tissues. Interestingly, the horse PYGM gene contains fewer mobile elements than its human ortholog, resulting in an increase in the structural stability of the PYGM gene sequence. This study provides insights into the genomic structure of the horse PYGM gene that may be useful in future studies of its association with exercise capability.     

Factors in maximal power production and in exercise endurance relative to maximal power

The relationship of muscle fiber type and mass to maximal power production and the maintenance of power (endurance time to exhaustion) at 36%, 55%, and 73% of maximal power was investigated in 18 untrained but physically active men. Power output was determined at constant pedalling rate (60 rev.min-1) on a cycle ergometer instrumented with force transducers and interfaced with a computer. Maximal power was determined for each subject as the highest one-revolution average power. Fat-free mass was determined by hydrostatic weighing, fat-free thigh volume by water displacement and skinfold measurement, and percentage and area of type II fibers from biopsy specimens taken from the vastus lateralis. Maximal power averaged 771 +/- 149 W with a range of 527-1125 W. No significant correlations were found among percentage of type II fibers, relative area of type II fibers, or fat-free thigh volume and maximal power or endurance times to exhaustion at any percentage of maximal power. Weak but significant relationships were found for fat-free mass with both maximal power (r = 0.57) and endurance time at 73% of maximal power (r = -0.47). These results show maximal power to be more dependent on factors related to body size than muscle-fiber characteristics. The low correlations for so many of the relationships, however, suggest that individuals employ either different combinations of these factors or utilize other strategies for the generation of high power.