Performance and metabolic responses to a high caffeine dose during prolonged exercise.

The present study examined whether a high caffeine dose improved running and cycling performance and altered substrate metabolism in well-trained runners. Seven trained competitive runners [maximal O2 uptake (VO2max) 72.6 +/- 1.5 ml.kg-1.min-1] completed four randomized and double-blind exercise trials at approximately 85% VO2max; two trials running to exhaustion and two trials cycling to exhaustion. Subjects ingested either placebo (PL, 9 mg/kg dextrose) or caffeine (CAF, 9 mg/kg) 1 h before exercise. Endurance times were increased (P less than 0.05) after CAF ingestion during running (PL 49.2 +/- 7.2 min, CAF 71.0 +/- 11.0 min) and cycling (PL 39.2 +/- 6.5 min, CAF 59.3 +/- 9.9 min). Plasma epinephrine concentration [EPI] was increased (P less than 0.05) with CAF before running (0.22 +/- 0.02 vs. 0.44 +/- 0.08 nM) and cycling (0.31 +/- 0.06 vs. 0.45 +/- 0.06 nM). CAF ingestion also increased [EPI] (P less than 0.05) during exercise; PL and CAF values at 15 min were 1.23 +/- 0.13 and 2.51 +/- 0.33 nM for running and 1.24 +/- 0.24 and 2.53 +/- 0.32 nM for cycling. Similar results were obtained at exhaustion. Plasma norepinephrine was unaffected by CAF at rest and during exercise. CAF ingestion also had no effect on respiratory exchange ratio or plasma free fatty acid data at rest or during exercise. Plasma glycerol was elevated (P less than 0.05) by CAF before exercise and at 15 min and exhaustion during running but only at exhaustion during cycling. Urinary [CAF] increased to 8.7 +/- 1.2 and 10.0 +/- 0.8 micrograms/ml after the running and cycling trials.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of carbohydrate ingestion on metabolism during running and cycling.

The effects of carbohydrate or water ingestion on metabolism were investigated in seven male subjects during two running and two cycling trials lasting 60 min at individual lactate threshold using indirect calorimetry, U-14C-labeled tracer-derived measures of the rates of oxidation of plasma glucose, and direct determination of mixed muscle glycogen content from the vastus lateralis before and after exercise. Subjects ingested 8 ml/kg body mass of either a 6.4% carbohydrate-electrolyte solution (CHO) or water 10 min before exercise and an additional 2 ml/kg body mass of the same fluid after 20 and 40 min of exercise. Plasma glucose oxidation was greater with CHO than with water during both running (65 +/- 20 vs. 42 +/- 16 g/h; P < 0.01) and cycling (57 +/- 16 vs. 35 +/- 12 g/h; P < 0.01). Accordingly, the contribution from plasma glucose oxidation to total carbohydrate oxidation was greater during both running (33 +/- 4 vs. 23 +/- 3%; P < 0.01) and cycling (36 +/- 5 vs. 22 +/- 3%; P < 0.01) with CHO ingestion. However, muscle glycogen utilization was not reduced by the ingestion of CHO compared with water during either running (112 +/- 32 vs. 141 +/- 34 mmol/kg dry mass) or cycling (227 +/- 36 vs. 216 +/- 39 mmol/kg dry mass). We conclude that, compared with water, 1) the ingestion of carbohydrate during running and cycling enhanced the contribution of plasma glucose oxidation to total carbohydrate oxidation but 2) did not attenuate mixed muscle glycogen utilization during 1 h of continuous submaximal exercise at individual lactate threshold.     

Magnesium homeostasis during high-intensity anaerobic exercise in men

This study was conducted to determine whether short-term, high-intensity anaerobic exercise alters Mg homeostasis. Thirteen men performed intermittent bouts of treadmill running at 90% of their predetermined maximum O2 uptake until exhaustion on one occasion during a week in which all men were consuming a standard diet (115 mg Mg/1,000 kcal). Plasma and erythrocyte Mg concentrations and peripheral blood mononuclear cell Mg content were measured before and after the exercise. Complete 24-h urine collections were obtained on control days, on the day of exercise, and on the day after exercise. Exercise induced a transient but significant decrease in plasma Mg content (-6.8%; P less than 0.01); over 85% of the loss could be accounted for by a shift to the erythrocytes. Significant increases in urinary excretion of Mg were observed on the day of exercise (131.5 +/- 6.8 mg/day) compared with control days (108 +/- 6.6 mg/day), with the percent increase correlating with postexercise blood lactate concentration (r = 0.68; P less than 0.01) and oxygen consumption during recovery (r = 0.84; P less than 0.001). The data indicate that high-intensity anaerobic exercise induces intercompartmental Mg shifts in blood that return to preexercise values within 2 h and urinary losses on the day of exercise that return to base line the day after exercise. It is postulated that the exercise-induced increase in Mg excretion may depend on the intensity of the exercise, and the relative contribution of anaerobic metabolism to the total energy expended during exercise.     

Exercise-Induced Blood Lactate Increase Does Not Change Red Blood Cell Deformability in Cyclists

Background

The effect of exercise-induced lactate production on red blood cell deformability and other blood rheological changes is controversial, given heavy-exercise induces biochemical processes (e.g., oxidative stress) known to perturb haemorheology. The aim of the present study was to examine the haemorheological response to a short-duration cycling protocol designed to increase blood lactate concentration, but of duration insufficient to induce significant oxidative stress.

Methods

Male cyclists and triathletes (n = 6; 27±7 yr; body mass index: 23.7±3.0 kg/m²; peak oxygen uptake 4.02±0.51 L/min) performed unloaded (0 W), moderate-intensity, and heavy-intensity cycling. Blood was sampled at rest and during the final minute of each cycling bout. Blood chemistry, blood viscosity, red blood cell aggregation and red blood cell deformability were measured.

Results

Blood lactate concentration increased significantly during heavy-intensity cycling, when compared with all other conditions. Methaemoglobin fraction did not change during any exercise bout when compared with rest. Blood viscosity at native haematocrit increased during heavy-intensity cycling at higher-shear rates when compared with rest, unloaded and moderate-intensity cycling. Heavy-intensity exercise increased the amplitude of red blood cell aggregation in native haematocrit samples when compared with all other conditions. Red blood cell deformability was not changed by exercise.

Conclusion

Acute exercise perturbs haemorheology in an intensity dose-response fashion; however, many of the haemorheological effects appear to be secondary to haemoconcentration, rather than increased lactate concentration.     

Plasma hemoglobin determination in beagle dogs. An adaptation of the method of Crosby and Furth.

The plasma hemoglobin concentration of beagle dogs was measured following an improved bleeding technic which minimized trauma of the red cells. The benzidine reaction (benzidine dihydrochloride) was used to measure the hemoglobin present. Plasma hemoglobin values of the first 2 ml of blood collected were statistically significantly higher (P less than 0.01) than values of the next 2-3 ml of blood. Plasma hemoglobin values of normal beagles were 0.5-2.5 mg/dl in minimally hemolyzed samples. Recovery rates of up to 92% of hemoglobin added to plasma were possible with this method.     

Alterations in blood volume following short-term supramaximal exercise

To investigate the role of high-intensity intermittent exercise on adaptations in blood volume and selected hematological measures, four male subjects aged 19-23 yr [peak O2 consumption (VO2max) = 53 ml X min-1 X kg-1] performed supramaximal (120% VO2max) cycle exercise on 3 consecutive days. Each exercise session consisted of intermittent work performed as bouts of 1-min work to 4-min rest until fatigue or until a maximum of 24 repetitions had been completed. Measurements on blood samples were made before the exercise period and 24 h after the last exercise session. Plasma volume (PV) estimated using 131I-human serum albumin increased by 11.6% (3,504 vs. 3,912 ml; P less than 0.05). Total blood volume (TBV) based on PV and hematocrit (Hct) values increased by 4.5% (5,798 vs. 6,059 ml; P less than 0.05), whereas red cell volume (RCV) decreased by 6.4% (2,294 vs. 2,147 ml; P less than 0.05). Measurements of hematological indices indicated significant reductions (P less than 0.05) in whole-blood Hct (39.7 vs. 35.5%), hemoglobin concentration (15.5 vs. 13.9 g/100 ml), hemoglobin content (897 vs. 839 g), and red blood cell count (5.15 vs. 4.55 X 10(6) X mm-3). The findings of this study suggest that exercise intensity is a major factor in promoting exercise-induced hypervolemia and that rapid elevations in PV can be induced early in training.     

Endurance training decreases plasma glucose turnover and oxidation during moderate-intensity exercise in men

To assess the effects of endurance training on plasma glucose kinetics during moderate-intensity exercise in men, seven men were studied before and after 12 wk of strenuous exercise training (3 days/wk running, 3 days/wk cycling). After priming of the glucose and bicarbonate pools, [U-13C] glucose was infused continuously during 2 h of cycle ergometer exercise at 60% of pretraining peak O2 uptake (VO2) to determine glucose turnover and oxidation. Training increased cycle ergometer peak VO2 by 23% and decreased the respiratory exchange ratio during the final 30 min of exercise from 0.89 +/- 0.01 to 0.85 +/- 0.01 (SE) (P less than 0.001). Plasma glucose turnover during exercise decreased from 44.6 +/- 3.5 mumol.kg fat-free mass (FFM)-1.min-1 before training to 31.5 +/- 4.3 after training (P less than 0.001), whereas plasma glucose clearance (i.e., rate of disappearance/plasma glucose concentration) fell from 9.5 +/- 0.6 to 6.4 +/- 0.8 ml.kg FFM-1.min-1 (P less than 0.001). Oxidation of plasma-derived glucose, which accounted for approximately 90% of plasma glucose disappearance in both the untrained and trained states, decreased from 41.1 +/- 3.4 mumol.kg FFM-1.min-1 before training to 27.7 +/- 4.8 after training (P less than 0.001). This decrease could account for roughly one-half of the total reduction in the amount of carbohydrate utilized during the final 30 min of exercise in the trained compared with the untrained state.     

Effect of exercise modality on oxygen uptake kinetics during heavy exercise

The mechanisms responsible for the oxygen uptake (VO2) slow component during high-intensity exercise have yet to be established. In order to explore the possibility that the VO2 slow component is related to the muscle contraction regimen used, we examined the pulmonary VO2 kinetics during constant-load treadmill and cycle exercise at an exercise intensity that produced the same level of lactacidaemia for both exercise modes. Eight healthy subjects, aged 22-37 years, completed incremental exercise tests to exhaustion on both a cycle ergometer and a treadmill for the determination of the ventilatory threshold (defined as the lactate threshold, Th1a) and maximum VO2 (VO2max). Subsequently, the subjects completed two "square-wave" transitions from rest to a running speed or power output that required a VO2 that was halfway between the mode-specific Th1a and VO2max. Arterialised blood lactate concentration was determined immediately before and after each transition. The VO2 responses to the two transitions for each exercise mode were time-aligned and averaged. The increase in blood lactate concentration produced by the transitions was not significantly different between cycling [mean (SD) 5.9 (1.5) mM] and running [5.5 (1.6) mM]. The increase in VO2 between 3 and 6 min of exercise; (i.e. the slow component) was significantly greater in cycling than in running, both in absolute terms [290 (102) vs 200 (45) ml x min(-1); P<0.05] and as a proportion of the total VO2 response above baseline [10 (3)% vs 6 (1)%; P < 0.05]. These data indicate that: (a) a VO2 slow component does exist for high-intensity treadmill running, and (b) the magnitude of the slow component is less for running than for cycling at equivalent levels of lactacidaemia. The greater slow component observed in cycling compared to running may be related to differences in the muscle contraction regimen that is required for the two exercise modes.     

Iron status in runners of various running specialties.

The blood iron status of 44 male runners of various running specialties (18 sprinters, 13 middle- and 13 long-distance runners) is evaluated by measuring serum ferritin (SF), serum iron (Si), hemoglobin concentration (Hb), hematocrit (Ht), red blood cells content (RBC) and haptoglobin concentration (Hp). The results of these analyses (except Hp) are compared to those obtained in sedentary male subjects (control group) of the same mean age. Mean SF, SI, Hb and Ht measured in athletes are significantly lower than in control group. The remarkably low Hp values obtained in athletes suggests the occurrence of hemolysis. Using unpaired t test, it appears that the blood iron status of these runners does not depend on their running specialty.     

Regional differences in blood flow and oxygen consumption in resting muscle and their relationship during recovery from exhaustive exercise.

This investigation evaluated regional differences in blood flow and oxygen consumption and their relationship in exercised muscle during recovery from exhaustive exercise. Five healthy men performed exhaustive one-legged cycling exercise. Positron emission tomography was used to measure blood flow, oxygen uptake, and oxygen extraction in the quadriceps femoris muscle before and after exercise. Regions of interest included five areas of the muscle (two proximal, one central, and two distal), which were evenly spaced across the muscle. Before exercise, blood flow and oxygen consumption decreased significantly (P < 0.05) in the direction from the proximal to the distal portions; blood flow declined from 2.0 +/- 0.5 to 1.4 +/- 0.3 ml x 100 g-1 x min-1, and oxygen consumption decreased from 0.21 +/- 0.04 to 0.17 +/- 0.02 ml.100 g-1x min-1. In contrast, these gradients in blood flow and oxygen consumption diminished during recovery after exercise. Consequently, there was a positive relationship between changes in blood flow and oxygen consumption in an exercised muscle during recovery after exercise (r = 0.963, P < 0.01). These changes became larger in the direction from proximal to distal portions: blood flow increased from 2.9 +/- 0.7 to 3.9 +/- 0.8 and oxygen consumption from 1.4 +/- 0.1 to 1.8 +/- 0.4 times resting values. These results suggest that hemodynamic variables are heterogeneous within a muscle both at rest and during recovery from exercise and that there is a systematic difference in these variables in the direction from proximal to distal regions within the quadriceps femoris muscle.     

Decreased exercise blood lactate concentrations after respiratory endurance training in humans

For many years, it was believed that ventilation does not limit performance in healthy humans. Recently, however, it has been shown that inspiratory muscles can become fatigued during intense endurance exercise and decrease their exercise performance. Therefore, it is not surprising that respiratory endurance training can prolong intense constant-intensity cycling exercise. To investigate the effects of respiratory endurance training on blood lactate concentration and oxygen consumption (VO2) during exercise and their relationship to performance, 20 healthy, active subjects underwent 30 min of voluntary, isocapnic hyperpnoea 5 days a week, for 4 weeks. Respiratory endurance tests, as well as incremental and constant-intensity exercise tests on a cycle ergometer, were performed before and after the 4-week period. Respiratory endurance increased from 4.6 (SD 2.5) to 29.1 (SD 4.0) min (P < 0.001) and cycling endurance time was prolonged from 20.9 (SD 5.5) to 26.6 (SD 11.8) min (P < 0.01) after respiratory training. The VO2 did not change at any exercise intensity whereas blood lactate concentration was lower at the end of the incremental [10.4 (SD 2.1) vs 8.8 (SD 1.9) mmol x l(-1), P < 0.001] as well as at the end of the endurance exercise [10.4 (SD 3.6) vs 9.6 (SD 2.7) mmol x l(-1), P < 0.01] test after respiratory training. We speculate that the reduction in blood lactate concentration was most likely caused by an improved lactate uptake by the trained respiratory muscles. However, reduced exercise blood lactate concentrations per se are unlikely to explain the improved cycling performance after respiratory endurance training.     

Rate of nitric oxide scavenging by hemoglobin bound to haptoglobin

Cell-free hemoglobin, released from the red cell, may play a major role in regulating the bioavailability of nitric oxide. The abundant serum protein haptoglobin, rapidly binds to free hemoglobin forming a stable complex accelerating its clearance. The haptoglobin gene is polymorphic with two classes of alleles denoted 1 and 2. We have previously demonstrated that the haptoglobin 1 protein–hemoglobin complex is cleared twice as fast as the haptoglobin 2 protein–hemoglobin complex. In this report, we explored whether haptoglobin binding to hemoglobin reduces the rate of nitric oxide scavenging using time-resolved absorption spectroscopy. We found that both the haptoglobin 1 and haptoglobin 2 protein complexes react with nitric oxide at the same rate as unbound cell-free hemoglobin. To confirm these results we developed a novel assay where free hemoglobin and hemoglobin bound to haptoglobin competed in the reaction with NO. The relative rate of the NO reaction was then determined by examining the amount of reacted species using analytical ultracentrifugation. Since complexation of hemoglobin with haptoglobin does not reduce NO scavenging, we propose that the haptoglobin genotype may influence nitric oxide bioavailability by determining the clearance rate of the haptoglobin–hemoglobin complex. We provide computer simulations showing that a twofold difference in the rate of uptake of the haptoglobin–hemoglobin complex by macrophages significantly affects nitric oxide bioavailability thereby providing a plausible explanation for why there is more vasospasm after subarachnoid hemorrhage in individuals and transgenic mice homozygous for the Hp 2 allele.     

Cardiovascular and splenic responses to exercise in humans.

To investigate splenic erythrocyte volume after exercise and the effect on hematocrit- and hemoglobin-based plasma volume equations, nine men cycled at an intensity of 60% maximal O(2) uptake for 5-, 10-, or 15-min duration, followed by an incremental ride to exhaustion. The reduction in spleen volume, calculated using (99m)Tc-labeled erythrocytes, was not significantly different among the three submaximal rides (5 min = 28%, 10 min = 30%, 15 min = 36%; P = 0.26). The incremental ride to exhaustion resulted in a 56% reduction in spleen volume, which recovered to baseline levels within 20 min. Plasma catecholamines were inversely related to spleen volume after exercise (r = 0.70-0.84; P < 0.0001). There were no differences in red cell or total blood volume pre- to postexercise; however, a significant reduction in plasma volume was observed (18.9%; P < 0.01). There was no difference between the iodinated albumin and the hematocrit and hemoglobin methods of assessing plasma volume changes. These results suggest that the spleen regulates its volume in response to an intensity-dependent signal, and plasma catecholamines appear partially responsible. Splenic release of erythrocytes has no effect on indirect measures of plasma volume.     

Effect of glucose polymer diet supplement on responses to prolonged successive swimming, cycling and running

Fifteen male endurance athletes were studied to determine the effect of a glucose polymer (GP) diet supplement on physiological and perceptual responses to successive swimming, cycling and running exercise. Thirty min of swimming, cycling and running at 70% VO2max, followed by a run to exhaustion at 90% VO2max was performed after one week of training under two dietary conditions: 1) GP (230 g of GP consumed daily) and 2) placebo (P, saccharin-sweetened supplement consumed daily). During GP, daily carbohydrate (CHO) intake was higher (p less than 0.05) by 173 g or 14% of energy intake than during P, but total energy intake was not significantly different. During 90 min of exercise, CHO utilization and blood glucose were significantly higher under GP than P by an average of 20.2% and 14.5%, respectively, but heart rate, ventilation, oxygen uptake, ratings of perceived exertion, and plasma lactate were not different. Run time to exhaustion at 90% VO2max was significantly longer by 1.2 min (23%) under GP. The results suggest that a GP diet supplement may be of value during endurance exercise by increasing the availability of CHO.     

Exercise metabolism at different time intervals after a meal

To determine how long a meal will affect the metabolic response to exercise, nine endurance-trained and nine untrained subjects cycled for 30 min at 70% of peak O2 consumption (VO2 peak) 2, 4, 6, 8, and 12 h after eating 2 g carbohydrate/kg body wt. In addition, each subject completed 30 min of cycling 4 h after the meal at an intensity that elicited a respiratory exchange ratio (RER) of 0.94-0.95. During exercise after 2 and 4 h of fasting, carbohydrate oxidation was elevated 13-15% compared with the response to exercise after an 8- and 12-h fast (P less than 0.01). The increase in blood glycerol concentration during exercise (30 to 0 min) was linearly related to the length of fasting (r = 0.99; P less than 0.01). In all subjects, plasma glucose concentration declined 17-21% during exercise after 2 h of fasting (P less than 0.01). Plasma glucose concentration also declined (15-25%) during exercise in the trained subjects after 4 and 6 h of fasting (P less than 0.05) but did not change in the untrained subjects. However, the decline in plasma glucose concentration was similar (14%) in the two groups when the exercise intensity was increased in the trained subjects (i.e., 78 +/- 1% VO2 peak) and decreased in the untrained subjects (i.e., 65 +/- 3% VO2 peak) to elicit a similar RER.(ABSTRACT TRUNCATED AT 250 WORDS)     

Metabolic and cardioventilatory responses during a graded exercise test before and 24 h after a triathlon

Previous studies have reported respiratory, cardiac and muscle changes at rest in triathletes 24 h after completion of the event. To examine the effects of these changes on metabolic and cardioventilatory variables during exercise, eight male triathletes of mean age 21.1 (SD 2.5) years (range 17-26 years) performed an incremental cycle exercise test (IET) before (pre) and the day after (post) an official classic triathlon (1.5-km swimming, 40-km cycling and 10-km running). The IET was performed using an electromagnetic cycle ergometer. Ventilatory data were collected every minute using a breath-by-breath automated system and included minute ventilation (V(E)), oxygen uptake (VO2), carbon dioxide production (VCO2), respiratory exchange ratio, ventilatory equivalent for oxygen (V(E)/VO2) and for carbon dioxide (V(E)/VCO2), breathing frequency and tidal volume. Heart rate (HR) was monitored using an electrocardiogram. The oxygen pulse was calculated as VO2/HR. Arterialized blood was collected every 2 min throughout IET and the recovery period, and lactate concentration was measured using an enzymatic method. Maximal oxygen uptake (VO2max) was determined using conventional criteria. Ventilatory threshold (VT) was determined using the V-slope method formulated earlier. Cardioventilatory variables were studied during the test, at the point when the subject felt exhausted and during recovery. Results indicated no significant differences (P > 0.05) in VO2max [62.6 (SD 5.9) vs 64.6 (SD 4.8) ml x kg(-1) x min(-1)], VT [2368 (SD 258) vs 2477 (SD 352) ml x min(-1)] and time courses of VO2 between the pre- versus post-triathlon sessions. In contrast, the time courses of HR and blood lactate concentration reached significantly higher values (P < 0.05) in the pre-triathlon session. We concluded that these triathletes when tested 24 h after a classic triathlon displayed their pre-event aerobic exercise capacity, bud did not recover pretriathlon time courses in HR or blood lactate concentration.     

Prior exercise and postprandial substrate extraction across the human leg

Prior exercise decreases postprandial plasma triacylglycerol (TG) concentrations, possibly through changes to skeletal muscle TG extraction. We measured postprandial substrate extraction across the leg in eight normolipidemic men aged 21-46 yr. On the afternoon preceding one trial, subjects ran for 2 h at 64 +/- 1% of maximal oxygen uptake (exercise); before the control trial, subjects had refrained from exercise. Samples of femoral arterial and venous blood were obtained, and leg blood flow was measured in the fasting state and for 6 h after a meal (1.2 g fat, 1.2 g carbohydrate/kg body mass). Prior exercise increased time averaged postprandial TG clearance across the leg (total TG: control, 0.079 +/- 0.014 ml.100 ml tissue(-1).min(-1) ; exercise, 0.158 +/- 0.023 ml.100 ml tissue(-1).min(-1), P <0.01), particularly in the chylomicron fraction, so that absolute TG uptake was maintained despite lower plasma TG concentrations (control, 1.53 +/- 0.13 mmol/l; exercise, 1.01 +/- 0.16 mmol/l, P < 0.001). Prior exercise increased postprandial leg blood flow and glucose uptake (both P < 0.05). Mechanisms other than increased leg TG uptake must account for the effect of prior exercise on postprandial lipemia.     

Haptoglobin and CD163: captor and receptor gating hemoglobin to macrophage lysosomes

Abstract

The plasma protein haptoglobin and the endocytic hemoglobin receptor HbSR/CD163 are key molecules in the process of removing hemoglobin released from ruptured erythrocytes. Hemoglobin in plasma is instantly bound with high affinity to haptoglobin – an interaction leading to the recognition of the complex by HbSR/CD163 and endocytosis in macrophages. The haptoglobin-dependent HbSR/CD163 scavenging system for hemoglobin clearance prevents toxic effects of hemoglobin in plasma and kidney and explains the decrease in the haptoglobin plasma concentration in patients with accelerated hemolysis. The HbSR/CD163 activity may be of quantitative importance for iron uptake in macrophages in general and for some iron-associated pathological processes, e.g. the atherogenesis-promoting oxidation of LDL leading to foam cell formation and apoptosis in the vessel wall.     

Resistance exercise enhances the molecular signaling of mitochondrial biogenesis induced by endurance exercise in human skeletal muscle

Combining endurance and strength training (concurrent training) may change the adaptation compared with single mode training. However, the site of interaction and the mechanisms are unclear. We have investigated the hypothesis that molecular signaling of mitochondrial biogenesis after endurance exercise is impaired by resistance exercise. Ten healthy subjects performed either only endurance exercise (E; 1-h cycling at ～65% of maximal oxygen uptake), or endurance exercise followed by resistance exercise (ER; 1-h cycling + 6 sets of leg press at 70-80% of 1 repetition maximum) in a randomized cross-over design. Muscle biopsies were obtained before and after exercise (1 and 3 h postcycling). The mRNA of genes related to mitochondrial biogenesis [(peroxisome proliferator-activated receptor-γ coactivator-1 (PGC-1)α, PGC-1-related coactivator (PRC)] related coactivator) and substrate regulation (pyruvate dehydrogenase kinase-4) increased after both E and ER, but the mRNA levels were about twofold higher after ER (P < 0.01). Phosphorylation of proteins involved in the signaling cascade of protein synthesis [mammalian target of rapamycin (mTOR), ribosomal S6 kinase 1, and eukaryotic elongation factor 2] was altered after ER but not after E. Moreover, ER induced a larger increase in mRNA of genes associated with positive mTOR signaling (cMyc and Rheb). Phosphorylation of AMP-activated protein kinase, acetyl-CoA carboxylase, and Akt increased similarly at 1 h postcycling (P < 0.01) after both types of exercise. Contrary to our hypothesis, the results demonstrate that ER, performed after E, amplifies the adaptive signaling response of mitochondrial biogenesis compared with single-mode endurance exercise. The mechanism may relate to a cross talk between signaling pathways mediated by mTOR. The results suggest that concurrent training may be beneficial for the adaptation of muscle oxidative capacity.     

Glutathione peroxidase and oxidative hemolysis in trout red blood cells

Red blood cells from the trout Salmo irideus contain several hemoglobin components that are prone to oxidation with production of oxygen radicals. The rate of hemolysis has been correlated to the extent of methemoglobin formation. A difference in the rate of hemolysis between red blood cells saturated with either CO or O2 was evident only when diminished glutathione peroxidase activity was observed. These results confirm the important role of this enzyme in providing protection against or repair of oxidative damage to the red cell membrane.