Intense Exercise In Humans Research Articles

Enhanced pyruvate dehydrogenase activity does not affect muscle O2 uptake at onset of intense exercise in humans.

It has been proposed that the activation state of pyruvate dehydrogenase (PDH) may influence the rate of skeletal muscle O2 uptake during the initial phase of exercise; however, this has not been directly tested in humans. To remedy this, we used dichloroacetate (DCA) infusion to increase the active form of PDH (PDH(a)) and, subsequently, measured leg O2 uptake and markers of anaerobic ATP provision during conditions of intense dynamic exercise, when the rate of muscle O2 uptake would be very high. Six subjects performed brief bouts of one-legged knee-extensor exercise at approximately 110% of thigh peak O2 uptake (65.3 +/- 3.7 W) on several occasions: under noninfused control (Con) and DCA-supplemented conditions. Needle biopsy samples from the vastus lateralis muscle were obtained at rest and after 5 s, 15 s, and 3 min of exercise during both experimental conditions. In addition, thigh blood flow and femoral arteriovenous differences for O2 and lactate were measured repeatedly during the 3-min work bouts (Con and DCA) to calculate thigh O2 uptake and lactate release. After DCA administration, PDH(a) was four- to eightfold higher (P < 0.05) than Con at rest, and PDH(a) remained approximately 130% and 100% higher (P < 0.05) after 5 and 15 s of exercise, respectively. There was no difference between trials after 3 min. Despite the marked difference in PDH(a) between trials at rest and during the initial phase of exercise, thigh O2 uptake was the same. In addition, muscle phosphocreatine utilization and lactate production were similar after 5 s, 15 s, and 3 min of exercise in DCA and Con. The present findings demonstrate that increasing PDH(a) does not alter muscle O2 uptake and anaerobic ATP provision during the initial phase of intense dynamic knee-extensor exercise in humans.

Muscle oxygen kinetics at onset of intense dynamic exercise in humans.

The present study examined the onset and the rate of rise of muscle oxidation during intense exercise in humans and whether oxygen availability limits muscle oxygen uptake in the initial phase of intense exercise. Six subjects performed 3 min of intense one-legged knee-extensor exercise [65.3 +/- 3.7 (means +/- SE) W]. The femoral arteriovenous blood mean transit time (MTT) and time from femoral artery to muscle microcirculation was determined to allow for an examination of the oxygen uptake at capillary level. MTT was 15.3 +/- 1.8 s immediately before exercise, 10.4 +/- 0.7 s after 6 s of exercise, and 4.7 +/- 0.5 s at the end of exercise. Arterial venous O(2) difference (a-v(diff) O(2)) of 18 +/- 5 ml/l before the exercise was unchanged after 2 s, but it increased (P < 0.05) after 6 s of exercise to 43 +/- 10 ml/l and reached 146 +/- 4 ml/l at the end of exercise. Thigh oxygen uptake increased (P < 0.05) from 32 +/- 8 to 102 +/- 28 ml/min after 6 s of exercise and to 789 +/- 88 ml/min at the end of exercise. The time to reach half-peak a-v(diff) O(2) and thigh oxygen uptake was 13 +/- 2 and 25 +/- 3 s, respectively. The difference between thigh oxygen delivery (blood flow x arterial oxygen content) and thigh oxygen uptake increased (P < 0.05) after 6 s and returned to preexercise level after 14 s. The present data suggest that, at the onset of exercise, oxygen uptake of the exercising muscles increases after a delay of only a few seconds, and oxygen extraction peaks after approximately 50 s of exercise. The limited oxygen utilization in the initial phase of intense exercise is not caused by insufficient oxygen availability.

Effect of high-intensity exercise training on lactate/H+ transport capacity in human skeletal muscle.

The present study examined the effect of high-intensity exercise training on muscle sarcolemmal lactate/H+ transport and the monocarboxylate transporters (MCT1 and MCT4) as well as lactate and H+ release during intense exercise in humans. One-legged knee-extensor exercise training was performed for 8 wk, and biopsies were obtained from untrained and trained vastus lateralis muscle. The rate of lactate/H+ transport determined in sarcolemmal giant vesicles was 12% higher (P < 0.05) in the trained than in untrained muscle (n = 7). The content of MCT1 and MCT4 protein was also higher (76 and 32%, respectively; n = 4) in trained muscle. Release of lactate and H+ from the quadriceps muscle at the end of intense exhaustive knee-extensor exercise was similar in the trained and untrained leg, although the estimated muscle intracellular-to-interstitial gradients of lactate and H+ were lower (P < 0.05) in the trained than in the untrained muscle. The present data show that intense exercise training can increase lactate/H+ transport capacity in human skeletal muscle as well as improve the ability of the muscle to release lactate and H+ during contractions.

Noninvasive skeletal muscle lactate detection between periods of intense exercise in humans.

We investigated whether localized 1H nuclear magnetic resonance spectroscopy (NMRS) using stimulated echoes (STEAM) with a long mixing time (t(m)) allowed the suppression of the fat signal and detection of lactate in skeletal muscle. The 1H NMRS sequence was first validated in three isolated and perfused rabbit biceps brachii muscles. Spectra were obtained on a wide-bore spectrometer using a dual-tuned probe (1H and 31P). Death was simulated by ceasing the muscle perfusion, which allowed post-mortem changes to be followed. During and after the simulated death, changes in levels of pH and in content of energy-rich compounds were observed with 31P NMRS. Our results showed an inverse linear relationship between pH and lactate in each of the three rabbits (r = 0.93, P < 0.001; r = 0.92, P < 0.01; r = 0.89, P < 0.01) and a decrease in phosphocreatine and concomitant increase in lactate. We then investigated whether this sequence allowed repeated detection of lactate in human soleus muscle during the recovery between periods of intense exercise (force-velocity test, F-v test). Seven subjects mean age 25.1 (SEM 0.8) years participated in this study. Soleus muscle lactate was detected at rest and for 3 min 30 s of the 5-min recovery between periods using a 2.35-T 40-cm bore magnet spectrometer. Arm venous plasma lactate concentration was measured at rest, during the F-v test when the subject stopped pedalling (S1), and at the end of each 5-min recovery between periods (S2). Results showed that the venous plasma lactate concentration at S1 and S2 increased significantly from the beginning of the F-v test to peak anaerobic power (W(an,peak)) (P < 0.001). The spectra showed that muscle lactate resonance intensity rose markedly when W(an,peak) was achieved. The muscle lactate resonance intensity plotted as a percentage of the resting value increased significantly at W(an,peak) compared with submaximal braking forces (P < 0.05). We concluded from these results that localized 1H NMRS using STEAM with a long t(m) allows suppression of the fat signal and repeated detection of lactate on isolated perfused skeletal muscle in animals and between periods of intense exercise in humans.

Muscle glycogen synthesis in recovery from intense exercise in humans.

The present study examined the role of lactate and glucose as substrates for glyconeogenesis in muscle in recovery from high-intensity exercise in humans. Seven subjects performed approximately 100 min of intense intermittent one-legged knee extensor exercise on two occasions: with [high lactate (HL)] and without [control (C)] intense arm exercise between the leg exercise bouts, leading to end exercise arterial plasma lactate concentrations of 16.0 +/- 1.6 and 9.2 +/- 1.6 mmol/l, respectively (P < 0.05). At the end of exercise, muscle lactate and glycogen were similar in HL and C (20.5 +/- 1.3 vs. 17.3 +/- 2.0 mmol/kg wet wt and 48.1 +/- 11.3 vs. 56.3 +/- 8.6 mmol/kg wet wt, respectively). Muscle glycogen increased (P < 0.05) during the first 5 min of recovery only in HL, but after 90 min of recovery the muscle glycogen concentration was the same in C and HL (61.2 +/- 12.0 vs. 71.5 +/- 10.9 mmol/kg wet wt). Muscle lactate not released to the blood could maximally account for 28 (C) and 54% (HL) of the increase in muscle glycogen during 90 min of recovery or < 10% of glycogen synthesis after full recovery. The total net glucose uptake corresponded to 84 (C) and 57% (HL) of the glycogen synthesized. Apparently, muscle glyconeogenesis may occur in humans, but the role of lactate as a substrate is minor. Instead, blood glucose appears to be the most important precursor for muscle glycogen synthesis after intense exercise.

Effects of creatine loading and training on running performance and biochemical properties of rat skeletal muscle

Several reports have shown that the use of oral creatine (Cr) supplementation can increase performance during brief high intensity exercise in humans. The purpose of this study was to examine the separate and combined effects of Cr supplementation and high intensity run training on the performance capacity and biochemical properties of rodent skeletal muscle. Running performance was assessed following acute (10-d) and chronic (4-wk) Cr supplementation. Results indicate that Cr supplementation alone has ergogenic effects and the combination of run training plus Cr results in a more pronounced enhancement of performance than either intervention alone. The benefits of Cr supplementation were seen most clearly during repetitive bouts of high intensity interval running. Cr concentrations increased in both the slow soleus and fast plantaris muscles (P < 0.05) in response to Cr supplementation. Increased creatine concentrations appeared to be reflected in increased phosphorylated creatine (PCr). Citrate synthase (CS) activity was increased in both the soleus and plantaris muscles following training (P < 0.05). CS activity of the untrained soleus but not the plantaris responded to the dietary stimulus. There were no significant changes in either creatine phosphokinase activity or myosin heavy chain isoform distribution following training or supplementation. These results indicate that the gains in high intensity running performance seen following Cr loading are a combined result of increased aerobic (CS) and anaerobic (Cr and PCr) energy buffering capacity of the muscle.

Haemodynamic and metabolic responses of the lower limb after high intensity exercise in humans.

This study assessed blood flow in the common femoral, superficial femoral and profunda femoris arteries, the effects of vasodilator metabolites and changes in blood pressure and pulse during recovery after high intensity exercise (Wingate test). Mean common femoral artery flow increased sevenfold in response to the exercise. The subsequent decline in mean common femoral artery flow was mono-exponential with a mean time constant of 19 min. The post-exercise increase in profunda femoris artery flow (ninefold) was significantly greater than the superficial femoral artery flow (fourfold, P < 0.05). Systolic blood pressure and heart rate decreased monotonically throughout recovery. In contrast, diastolic blood pressure showed a significant fall below baseline at 3 min (P < 0.05) with a return to baseline at 60 min. The greatest drop below baseline (approximately 20 mmHg) occurred around 7 min. Lactate reached a maximum of 13.6 +/- 2.3 mmol -1 at 8 min (P < 0.05) and was still significantly above baseline at 60 min. pH remained below 7.2 until 20 min of recovery. The results demonstrate that following high intensity exercise, blood flow to the limbs appears to be controlled by complex interactions of various vaso-active metabolites, each contributing proportionally more at different times during recovery.

IMP metabolism in human skeletal muscle after exhaustive exercise

This study addressed whether AMP deaminase (AMPD)myosin binding occurs with deamination during intense exercise in humans and the extent of purine loss from muscle during the initial minutes of recovery. Male subjects performed cycle exercise (265 +/- 2 W for 4.39 +/- 0.04 min) to stimulate muscle inosine 5'-monophosphate (IMP) formation. After exercise, blood flow to one leg was occluded. Muscle biopsies (vastus lateralis) were taken before and 3.6 +/- 0.2 min after exercise from the occluded leg and 0.7 +/- 0.0, 1.1 +/- 0.0, and 2.9 +/- 0.1 min postexercise in the nonoccluded leg. Exercise activated AMPD; at exhaustion IMP was 3.5 +/- 0.4 mmol/kg dry muscle. Before exercise, 16.0 +/- 1.6% of AMPD cosedimented with the myosin fraction; the extent of AMPD:myosin binding was unchanged by exercise. Inosine content increased about threefold during exercise and twofold more during recovery; by 2.9 min postexercise it was 0.43 +/- 0.02 mmol/kg dry muscle. IMP decreased 2.1 +/- 0.3 mmol/kg dry muscle with no change in total adenylates. Total purines declined significantly (P < 0.05) during the recovery period in the nonoccluded leg, consistent with a loss of purines to the circulation, whereas total purines were unchanged in the occluded leg. Regulation of muscle purine content is a dynamic process that must accommodate rapid changes due to degradation and efflux.

Skeletal muscle ammonia production and repeated, intense exercise in humans.

We investigated the impact of repeated, high-intensity exercise on NH3 metabolism using the single-leg knee extensor model. The muscle glycogen level would be lowered by the initial exercise and low glycogen may stimulate NH3 production independent of any other effects of previous exercise. Therefore a high muscle glycogen condition was included in the protocol so that the pre-exercise glycogen concentration would be at least at a normal resting level for the second exercise. The subjects (n = 6) used previous exercise and (or) diet to begin the exercise with either normal (87.0 +/- 14.4 mmol/kg wet weight) or high (176.8 +/- 22.9 mmol/kg wet weight) glycogen (C and HG, respectively) in the quadriceps. They exercised (Ex1) one leg to exhaustion (140% leg VO2 max), rested 1 h, repeated the exercise (Ex2), and then repeated the protocol with the opposite leg. The exercise durations of Ex1 and Ex2, respectively, for C were 2.82 +/- 0.51 and 2.47 +/- 0.47 min (p < 0.05) and for HG were 2.92 +/- 0.57 and 2.77 +/- 0.50 min. The NH3 efflux was reduced (p < 0.05) from Ex1 to Ex2 in both C (516 +/- 159 and 250 +/- 69 mumol, respectively) and HG (618 +/- 233 and 275 +/- 124 mumol, respectively). While NH3 efflux was virtually identical between C and HG in both Ex1 and Ex2, HG consistently had a greater arterial NH3 concentration (p < 0.05). The decreased efflux in Ex2 compared with Ex1 was not due to greater accumulation of muscle NH3.(ABSTRACT TRUNCATED AT 250 WORDS)

AMMONIA PRODUCTION, MUSCLE GLYCOGEN AND REPEATED, INTENSE EXERCISE IN HUMANS

AMMONIA PRODUCTION, MUSCLE GLYCOGEN AND REPEATED, INTENSE EXERCISE IN HUMANS

Influence of active muscle mass on glucose homeostasis during exercise in humans

To study the effect of increasing amounts of exercising muscle mass on the relationship between glucose mobilization and peripheral glucose uptake, seven young men (23-28 yr) bicycled for 70 min at a work load of 55-60% VO2max. From minute 30 to 50, arm cranking was added and total work load increased to 82 +/- 4% VO2max. During leg exercise, hepatic glucose production (Ra) increased in parallel with peripheral glucose uptake (Rd) and euglycemia was maintained. During arm + leg exercise, Ra increased more than Rd and accordingly plasma glucose increased from 5.11 +/- 0.22 to 8.00 +/- 0.66 mmol/l (P less than 0.05). Plasma catecholamines increased three- to four-fold more during arm + leg exercise than during leg exercise. Leg glucose uptake increased with time regardless of arm cranking. Net leg lactate release during leg exercise was reverted to a net leg lactate uptake during arm + leg exercise. The rate of glycogen breakdown in exercising leg muscle was not altered by addition of arm cranking. In conclusion, when large amounts of muscle mass are active, plasma catecholamines increase sharply and mobilization of glucose exceeds peripheral glucose uptake. This indicates that mechanisms other than feedback regulation to maintain euglycemia are involved in hormonal and substrate mobilization during intense exercise in humans.

Myocardial substrate utilization during exercise in humans. Dual carbon-labeled carbohydrate isotope experiments.

The purpose of this study was to investigate myocardial substrate utilization during moderate intensity exercise in humans. Coronary sinus and arterial catheters were inserted in nine healthy trained male subjects (mean age, 25 +/- 6 (SD) years). Dual carbon-labeled isotopes were infused, and substrate oxidation was quantitated by measuring myocardial production of 14CO2. Supine cycle ergometer exercise was performed at 40% of the subject's maximal O2 uptake. With exercise there was a significant increase in the arterial lactate level (P less than 0.05). A highly significant positive correlation was observed between the lactate level and the isotopic lactate extraction (r = 0.93; P less than 0.001). The myocardial isotopic lactate uptake increased from 34.9 +/- 6.5 mumol/min at rest to 120.4 +/- 36.5 mumol/min at 5 min of exercise (P less than 0.005). The 14CO2 data demonstrated that 100.4 +/- 3.5% of the lactate extracted as determined by isotopic analysis underwent oxidative decarboxylation. Myocardial glucose uptake also increased significantly with exercise (P less than 0.04). The [14C]glucose data showed that only 26.0 +/- 8.5% of the glucose extracted underwent immediate oxidation at rest, and during exercise the percentage being oxidized increased to 52.6 +/- 7.3% (P less than 0.01). This study demonstrates for the first time in humans an increase in myocardial oxidation of exogenous glucose and lactate during moderate intensity exercise.

Muscle fiber composition and blood ammonia levels after intense exercise in humans.

The relationship between fiber type composition and the increase in blood ammonia was examined following a maximal O2 consumption (VO2max) test. Muscle biopsies were taken from the middle portion of the vastus lateralis for determination of fiber type percentages. Two subject groups were selected on the basis of a high (HST) or low (LST) percentage of slow-twitch fibers and compared for blood ammonia and lactate levels after exercise at work loads of approximately 85 and 110% of VO2max. An inverse relationship was found between the percentage of slow-twitch fibers and the increase in blood ammonia. Blood ammonia increased after exercise at both 85 and 110% of VO2max. However, the increase was twofold greater for the LST group following the 110% work effort. The increases in blood ammonia and lactate were positively correlated for both groups following exercise. The results suggest that the proportion of slow-twitch fibers plays an important role in determining the magnitude of the increase in blood ammonia after intense exercise.