[Suicide prevention training for youth care professionals]. / Suïcidepreventietraining voor jeugdzorgprofessionals.

BACKGROUND: Suicidality is common in youth care and has a major impact on young people, parents and professionals. The number of suicides among young people (10-25 years) in the Netherlands has risen in recent years from 103 suicides in 2008 to 159 suicides in 2019, with a high of 169 suicides in 2017. Many youth care professionals experience timidity in dealing with suicidal behaviour. AIM: To investigate whether suicide prevention training leads to an improvement in knowledge, skills and self-confidence in dealing with suicidal behavior in young people. METHOD: Professionals working at a national youth care institution participated in suicide prevention training. Before and immediately after the training they completed questionnaires to measure their knowledge, skills and self-confidence in the field of suicide prevention. RESULTS: There was an improvement in knowledge, skills and self-confidence of youth care professionals after the training. In particular, more knowledge about suicide prevention led to more self-confidence. The change was equal in the different forms of care. Scientifically trained and higher educated professionals showed a less strong change in their competencies than secondary educated professionals. The change in knowledge and skills was less pronounced the older the professionals were. CONCLUSION: Participation in suicide prevention training led to more knowledge, skills and self-confidence of youth care professionals in dealing with suicidal behaviour.

Do upper leg compression garments aid performance and reduce exercise-induced muscle damage in recreational marathon runners?

Background: Despite the lack of scientific knowledge on the physiological and biomechanical effects of wearing compression garments (CGs), there has been an increase in the use of compression garments (CG) amongst endurance runners. Objectives: To compare marathon race performance, post-race pain, and mid-thigh circumference in marathon runners using upper leg CGs, with runners who did not use CGs in the same marathon race. Methods: The study was conducted on healthy, long-distance runners (n=18) participating in the Winelands Marathon race, Cape Town, South Africa. The CG group (n=10) participated in the race wearing upper leg CGs, while the control group (n=8) did not. Participants were tested on three occasions for various subjective markers of exercise-induced muscle damage (Visual analogue scale (VAS) pain rating score, and Likert scale for muscle pain), mid-thigh circumference for muscle swelling, and running performance (race pace). Results: VAS pain ratings for hamstring (p=0.04), knee flexion (p=0.02) and hip extension (p=0.04) were significantly lower than the ratings of the control group immediately post-race and two days post-race. No statistically significant differences were detected in race performance, mid-thigh circumferences or Likert scale for determination of muscle soreness. Discussion: Wearing of upper leg CGs while running a marathon race improved VAS pain ratings immediately post-race through to two days post-race. However, due to no placebo control, this beneficial effect may be psychological as opposed to a physiological effect of the CGs on muscle pain. Conclusion: The use of upper leg CGs reduced subjective muscle pain in runners in the first 48 hours post-race.

Swimrun race, athletes, safety and performance: A brief review.

Swimrun was established in Sweden in 2006. In competition athletes alternate between running and swimming multiple times. It has grown from only being hosted in Sweden to now being a global sport. The swimrun race exposes athletes to environments that require a unique set of skills. For example, participants have to negotiate ocean currents and waves. The environmental conditions change between the runs and the swims. Athletes may be exposed to hot temperatures when running in wetsuits (25 â€‹°C and hotter) and cold water (colder than 16 â€‹°C) when swimming. This sudden change in environmental conditions imposes a poorly defined physiological stress on the participants. Research on the demands of swimrun is scarce. More research is needed to improve athlete safety during events. Also, research is needed to provide insight into enhancing training methods and performance.

The effect of a preexercise meal on time to fatigue during prolonged cycling exercise.

PURPOSE AND METHODS: Seven subjects exercised to exhaustion on a bicycle ergometer at a workload corresponding to an intensity of 70% maximal oxygen uptake (VO2max). On one occasion (FED), subjects consumed a preexercise carbohydrate (CHO) containing breakfast (100 g CHO) 3 h before exercise. On the other occasion (FASTED), subjects exercised after an overnight fast. Exercise time to fatigue was significantly longer (P < 0.05) when subjects consumed the breakfast (136+/-14 min) compared with when they exercised in the fasted state (109+/-12 min). RESULTS: Pre- and post-exercise muscle glycogen concentrations, respiratory exchange ratio, carbohydrate and fat oxidation, and lactate and insulin concentrations were not significantly different between the two trials. Insulin concentrations decreased significantly (P < 0.05) from 4.7+/-0.05 microIU.mL(-1) to 2.8+/-0.4 microIU.mL(-1) in FED and from 6.6+/-0.6 microIU.mL(-1) to 3.7+/-0.6 microIU.mL(-1) in FASTED subjects and free fatty acid concentrations (FFA) increased significantly (P < 0.05) from 0.09+/-0.02 mmol.L(-1) to 1.4+/-0.6 mmol.L(-1) in FED and from 0.17+/-0.02 mmol.L(-) to 0.74+/-0.27 mmol.L(-1) in FASTED subjects over the duration of the trials. CONCLUSIONS: In conclusion, the important finding of this study is the increased time to fatigue when subjects ingested the CHO meal with no negative effects ascribed to increased insulin concentrations and decreased FFA concentrations after CHO ingestion.

Influence of muscle glycogen content on metabolic regulation.

Euglycemia was maintained in 13 subjects with low muscle glycogen [low glycogen, euglycemic (LGE), n = 8; low glycogen, euglycemic, hyperinsulinemic (LGEI), n = 5] and 6 subjects with normal muscle glycogen (NGE), whereas hyperglycemia was maintained in 8 low muscle glycogen subjects (LGH). All subjects cycled for 145 min at 70% of maximal oxygen uptake during the infusions. Insulin was infused in LGEI at 0.2 mU.kg-1.min-1. During exercise, respiratory exchange ratio (RER) was lower and norepinephrine higher in LGE than in NGE. In LGEI and LGH, RER at the start of exercise was the same as in LGE but did not decrease as in LGE. Free fatty acids (FFA) were higher and plasma insulin concentrations lower in LGE than NGE, LGEI, or LGH over the first 45 min of exercise. Rate of glucose infusion (Ri) and rate of glucose oxidation (Rox) were higher in LGH and LGEI than in NGE or LGE, and Ri matched Rox in all groups except LGH, in which Ri was greater than Rox. Muscle glycogen disappearance was greater in NGE than LGE, LGEI, or LGH, but the latter three groups did not differ. In conclusion, this study showed that low muscle glycogen content results in a decrease in RER, an increase in FFA, fat oxidation, and norepinephrine both at rest and during exercise, and does not affect Rox when euglycemia is maintained by infusion of glucose alone. Rox was increased only during insulin and hyperglycemia.

Preexercise muscle glycogen content affects metabolism during exercise despite maintenance of hyperglycemia.

Trained cyclists with low muscle glycogen (LGH; n = 8) or normal glycogen (NGH; n = 5) exercised for 145 min at 70% of maximal oxygen uptake during a hyperglycemic clamp. Respiratory exchange ratio was higher in NGH than LGH, and free fatty acid concentrations were lower in NGH than LGH. Areas under the curve for insulin and lactate were lower in LGH than NGH. Total glucose infusion and total glucose oxidation were not different between NGH and LGH, and total glucose oxidation amounted to 65 and 66% of total glucose infusion in NGH and LGH, respectively. Rates of glucose oxidation rose during exercise, reaching peaks of 9.2 +/- 1.7 and 8.3 +/- 1.1 mmol/min in NGH and LGH, respectively. Muscle glycogen disappearance was greater in NGH than LGH. Thus 1) low muscle glycogen content does not cause increased glucose oxidation, even during hyperglycemia; instead there is an increase in fat oxidation, 2) there is an upper limit to the rate of glucose oxidation during exercise with hyperglycemia irrespective of muscle glycogen status, and 3) net muscle glycogen utilization is determined by muscle glycogen content at the start of exercise, even during hyperglycemia.

Fuel substrate turnover and oxidation and glycogen sparing with carbohydrate ingestion in non-carbohydrate-loaded cyclists.

This study examined the effects of ingesting 500 ml/h of either a 10% carbohydrate (CHO) drink (CI) or placebo (PI) on splanchnic glucose appearance rate (endogenous + exogenous) (Ra), plasma glucose oxidation and muscle glycogen utilisation in 17, non-carbohydrate-loaded, male, endurance-trained cyclists who rode for 180 min at 70% of maximum oxygen uptake. Mean muscle glycogen content at the start of exercise was 130 +/- 6 mmol/kg ww; (mean +/- SEM). Total CHO oxidation was similar in CI and PI subjects and declined during the trial. Ra increased significantly during the trial (P < 0.05) in both groups. Plasma glucose oxidation also increased significantly during the trial, reaching a plateau in the PI subjects, but was significantly (P < 0.05) higher in CI than PI subjects at the end of exercise [(98 +/- 14 vs. 72 +/- 10 micromol/min/kg fat-free mass) (FFM) (1.34 +/- 0.19 vs. 0.93 +/- 0. 13 g/min)]. However, mean endogenous Ra was significantly (P < 0.05) lower in the CI than PI subjects throughout exercise (35 +/- 7 vs. 54 +/- 6 micromol/min/kg FFM), as was the oxidation of endogenous plasma glucose, which remained almost constant in CI subjects, and reached values at the end of exercise of 42 +/- 13 and 72 +/- 10 micromol/min/kg FFM in the CI and PI groups respectively. Of the 150 g CHO ingested during the trial, 50% was oxidised. Muscle glycogen disappearance was identical during the first 2 h of exercise in both groups and continued at the same rate in PI subjects, however no net muscle glycogen disappearance occurred during the final hour in CI subjects. We conclude that ingestion of 500 ml/h of a 10% CHO solution during prolonged exercise in non carbohydrate loaded subjects has a marked liver glycogen-sparing effect or causes a reduction in gluconeogenesis, or both, maintains plasma glucose concentration and has a muscle glycogen-sparing effect.

Fuel substrate kinetics of carbohydrate loading differs from that of carbohydrate ingestion during prolonged exercise.

This study compared fuel substrate kinetics in trained cyclists who ingested a 10% carbohydrate (CHO) drink without prior CHO-loading ([NLC] n=9) with those in cyclists who ingested a water placebo after CHO-loading ([CLP] n=7) during 180 minutes of cycling at 70% maximum oxygen consumption (Vo2 max). Muscle glycogen at the start of exercise was 194 +/- 4 and 124 +/- 8 mmol/kg wet weight (mean +/- SEM) in CLP and NLC subjects, respectively . Total CHO oxidation was similar. Total rate of appearance of glucose from endogenous (Raend) and exogenous (Raexog) origin and plasma glucose oxidation increased significantly (P<.05), with NLC subjects ending significantly higher than CLP subjects (104 +/- 17 v 79 +/- 9 and 115 +/- 16 v 74 +/- 11 micromol/min/kg fat-free mass [FFM], respectively). However, Raend was lower (P<.05) in NLC than in CLP subjects (40 +/- 10 v 79 +/- 9 micromol/min/kg FFM), as was endogenous plasma glucose oxidation (42 +/- 13 v 75 +/- 11 micromol/min kg FFM). Muscle glycogen disappearance was identical in the first hour, but declined thereafter in NLC subjects. Two NLC subjects with the lowest muscle glycogen content were unable to complete the trial despite CHO ingestion. We conclude that with respect to the groups studied (1) CHO loading before exercise reduces the relative contribution of plasma glucose oxidation to total CHO oxidation, but may prolong time to exhaustion as a function of higher muscle glycogen concentration; (2) CHO ingestion has a liver glycogen-sparing effect, causes a reduction in gluconeogenesis, or both, that should delay the onset of hypoglycemia; (3) the progressive increase in plasma glucose oxidation that occurs during prolonged exercise is related to muscle glycogen status and occurs irrespective of whether CHO is ingested: (4) the effects of CHO ingestion and CHO-loading on fuel substrate kinetics are different.

Fuel utilisation during prolonged low-to-moderate intensity exercise when ingesting water or carbohydrate.

Previously, we examined the effects of carbohydrate (CHO) ingestion on glucose kinetics during exercise at 70% of maximum O2 uptake (VO2, max). Here we repeat those studies in heavier cyclists (n = 6 per group) cycling for 3 h at a similar absolute O2 uptake but at a lower (55% of VO2, max) relative exercise intensity. During exercise, the cyclists were infused with a 2-3H-glucose tracer and ingested U-14C glucose-labelled solutions of either flavoured water (H2O) or 10 g/100 ml glucose polymer, at a rate of 600 ml/h. Two subjects in the H2O trial fatigued after 2.5 h of exercise. Their rates of glucose appearance (Ra) declined from 2.9 +/- 0.6 to 2.0 +/- 0.1 mmol/min (mean +/- SEM) and, as their plasma glucose concentration [Glu] declined from 4.7 +/- 0.2 to below 3.5 +/- 0.2 mM, their rates of glucose oxidation (Rox) and fat oxidation plateaued at 2.7 +/- 0.4 and 1.7 +/- 0.1 mmol/min respectively. In contrast, all subjects completed the CHO trial. Although CHO ingestion during exercise reduced the final endogenous Ra from 3.4 +/- 0.6 to 0.9 +/- 0.3 mmol/min at the end of exercise, it increased total Ra to 5.5 +/- 0.5 mmol/min (P < 0.05). A higher total Ra with CHO ingestion raised [Glu] from 4.3 +/- 0.3 to 5.3 +/- 0.1 mM and accelerated Rox from 3.5 +/- 0.2 to 5.9 +/- 0.2 mmol/min after 180 min of exercise (P < 0.05). The increased contribution to total energy production from glucose oxidation (34 +/- 1 vs. 20 +/- 1%) decreased energy production from fat oxidation from 51 +/- 2 to 40 +/- 5% (P = 0.08) and produced patterns of glucose, muscle glycogen (plus lactate) and fat utilisation similar to those during exercise at 70% of (V˙O2, max). Thus, CHO ingestion is necessary to sustain even prolonged, low to moderate intensity exercise and when ingested, it suppresses the higher relative rates of fat oxidation usually observed at exercise intensities less than 60% of VO2, max.

Influence of carbohydrate ingestion on fuel substrate turnover and oxidation during prolonged exercise.

This study examined effects of ingesting a 10% carbohydrate (CHO) drink (CI) or placebo (PI) at 500 ml/h on total (splanchnic) glucose appearance (endogenous+exogenous; Ra), blood glucose oxidation, and muscle glycogen utilization in 14 male endurance-trained cyclists who rode for 180 min at 70% of maximal O2 uptake after CHO loading [starting muscle glycogen 203 +/- 7 (SE) mmol/kg wet wt]. Total CHO oxidation was similar in CI and PI, but Ra increased significantly during the trial in both groups with CI reaching a plateau after 75 min. Ra was significantly greater in CI than in PI at the end of exercise. Blood glucose oxidation also increased significantly during the trial to a plateau in CI and was significantly higher in CI than in PI at the end of exercise. However, mean endogenous Ra was significantly lower in CI than in PI throughout exercise, as was oxidation of endogenous blood glucose, which remained almost constant in CI and reached 43 +/- 8 and 73 +/- 13 mumol.min-1.kg fat-free mass-1 in CI and PI, respectively, at the end of exercise. At 0.83 g/min of CHO ingestion, 0.77 +/- 0.03 g/min was oxidized. Muscle glycogen utilization was identical in both groups and was higher during the 1st h of exercise.(ABSTRACT TRUNCATED AT 250 WORDS)

Glucose kinetics during prolonged exercise in euglycaemic and hyperglycaemic subjects.

To determine the limits to oxidation of exogenous glucose by skeletal muscle, the effects of euglycaemia (plasma glucose 5 mM, ET) and hyperglycaemia (plasma glucose 10 mM, HT) on fuel substrate kinetics were evaluated in 12 trained subjects cycling at 70% of maximal oxygen uptake (VO2, max) for 2 h. During exercise, subjects ingested water labelled with traces of U-14C-glucose so that the rates of plasma glucose oxidation (Rox) could be determined from plasma 14C-glucose and expired 14CO2 radioactivities, and respiratory gas exchange. Simultaneously, 2-3H-glucose was infused at a constant rate to estimate rates of endogenous glucose turnover (Ra), while unlabelled glucose (25% dextrose) was infused to maintain plasma glucose concentration at either 5 or 10 mM. During ET, endogenous liver glucose Ra (total Ra minus the rate of infusion) declined from 22.4 +/- 4.9 to 6.5 +/- 1.4 mumol/min per kg fat-free mass [FFM] (P < 0.05) and during HT it was completely suppressed. In contrast, Rox increased to 152 +/- 21 and 61 +/- 10 mumol/min per kg FFM at the end of HT and ET respectively (P < 0.05). HT (i.e., plasma glucose 10 mM) and hyperinsulinaemia (24.5 +/- 0.9 microU/ml) also increased total carbohydrate oxidation from 203 +/- 7 (ET) to 310 +/- 3 mumol/min per kg FFM (P < 0.0001) and suppressed fat oxidation from 51 +/- 3 (ET) to 18 +/- 2 mumol/min per kg FFM (P < 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of glucose ingestion or glucose infusion on fuel substrate kinetics during prolonged exercise.

To determine if bypassing both intestinal absorption and hepatic glucose uptake by intravenous glucose infusion might increase the rate of muscle glucose oxidation above 1 g.min-1, ten endurance-trained subjects were studied during 125 min of cycling at 70% of peak oxygen uptake (VO2peak). During exercise the subjects ingested either a 15 g.100 ml-1 U-14C labelled glucose solution or H2O labelled with a U-14C glucose tracer for the determination of the rates of plasma glucose oxidation (Rox) and exogenous carbohydrate (CHO) oxidation from plasma 14C glucose and 14CO2 specific activities, and respiratory gas exchange. Simultaneously, 2-3H glucose was infused at a constant rate to measure glucose turnover, while unlabelled glucose (25% dextrose) was infused into those subjects not ingesting glucose to maintain plasma glucose concentration at 5 mmol.l-1. Despite similar plasma glucose concentrations [ingestion 5.3 (SEM 0.13) mmol.l-1; infusion 5.0 (0.09) mmol.l-1], compared to glucose infusion, CHO ingestion significantly increased plasma insulin concentrations [12.9 (1.0) vs 4.8 (0.5) mU.l-1; P < 0.05], raised total Rox values [9.5 (1.2) vs 6.2 (0.7) mmol.125 min-1 kg fat free mass-1 (FFM); P < 0.05] and rates of CHO oxidation [37.2 (2.8) vs 24.1 (3.9) mmol.125 min-1 kg FFM-1; P < 0.05]. An increased reliance on CHO metabolism with CHO ingestion was associated with a decrease in fat oxidation. Whereas the contribution from fat oxidation to energy production increased to 51 (10)% with glucose infusion, it only reached 18 (4)% with glucose ingestion (P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Superior fatigue resistance of elite black South African distance runners.

Black athletes currently dominate long-distance running events in South Africa. In an attempt to explain an apparently superior running ability of black South African athletes at distances > 3 km, we compared physiological measurements in the fastest 9 white and 11 black South African middle-to long-distance runners. Whereas both groups ran at a similar percentage of maximal O2 uptake (%VO2max) over 1.65-5 km, the %VO2max sustained by black athletes was greater than that of white athletes at distances > 5 km (P < 0.001). Although both groups had similar training volumes, black athletes reported that they completed more exercise at > 80% VO2max (36 +/- 18 vs. 14 +/- 7%: P < 0.005). When corrections were made for the black athletes' smaller body mass, their superior ability to sustain a high %VO2max could not be explained by any differences in VO2max, maximal ventilation, or submaximal running economy. Superior distance running performance of the black athletes was not due to a greater (+/- 50%) percentage of type I fibers but was associated with lower blood lactate concentrations during exercise. Time to fatigue during repetitive isometric muscle contractions was also longer in black runners (169 +/- 65 vs. 97 +/- 69 s; P < 0.05), but whether this observation explains the superior endurance or was due to the lower peak muscle strength (46.3 +/- 10.3 vs. 67.5 +/- 18.0 Nm/l lean thigh volume; P < 0.01) remains to be established.

Influence of carbohydrate loading on fuel substrate turnover and oxidation during prolonged exercise.

This study compared liver glucose turnover, blood glucose oxidation, and muscle glycogen utilization in 15 male endurance-trained cyclists who rode for 180 min at 70% of maximal O2 consumption in either a carbohydrate-(CHO) loaded (CL) or a non-CHO-loaded (NL) state. Total CHO oxidation during exercise was similar in the CL and NL subjects (492 +/- 77 vs. 448 +/- 43 g, respectively), as were blood glucose oxidation (103 +/- 19 vs. 99 +/- 7 g, respectively) and liver glucose appearance (110 +/- 15 vs. 127 +/- 16 g, respectively). However, total muscle glycogen utilization was greater in CL than NL subjects (134 +/- 11 vs. 95 +/- 12 mmol/kg wet wt; P < 0.05), the former of which had higher muscle glycogen content at the start (194 +/- 4 vs. 124 +/- 7 mmol/kg wet wt; P < 0.05) and throughout the trial. Whereas high rates of muscle glycogen breakdown were maintained throughout the trial in CL subjects, rates of muscle glycogenolysis in NL subjects decreased to 26 mmol.kg wet wt-1.h-1 after 60 min of exercise (P < 0.05) when their muscle glycogen content had declined to 70 mmol/kg wet wt. Comparable rates of blood glucose and overall CHO oxidation in CL and NL subjects, despite a slowing of muscle glycogenolysis in the NL group, could be explained by an accelerated breakdown of glycogen in the nonworking muscles to redistribute CHO (lactate) to the working muscles for oxidation.(ABSTRACT TRUNCATED AT 250 WORDS)

Ventilation and blood lactate increase exponentially during incremental exercise.

This study examined whether the ventilatory (V) compensation for metabolic acidosis with increasing O2 uptake (VO2) and CO2 output (VCO2) might be more in accord with the theoretical expectation of a progressive acceleration of proton production from carbohydrate oxidation rather than a sudden onset of blood lactate (BLa) accumulation. The interrelationships between V, VO2, VCO2 and BLa concentration, [BLa], were investigated in 10 endurance-trained male cyclists during incremental (120 +/- 15 W min-1) exercise tests to exhaustion. Regression analyses on the V, VCO2 and [BLa] vs VO2 data revealed that all were better fitted by continuous Y = A.exp.[B.VO2] + C rate laws than by threshold linear rate equations (P < 0.0001). Plots of V vs VCO2 and [BLa] were also non-linear. Ventilation increased as an exponential V = 27 +/- 4.exp.[0.37 +/- 0.03.VCO2] function of VCO2 and as a hyperbolic function of [BLa]. In opposition to the 'anaerobic (lactate) threshold' hypothesis, we suggest these data are more readily explained by a continuous development of acidosis, rather than a sudden onset of BLa accumulation, during progressive exercise.

Effects of training on lactate production and removal during progressive exercise in humans.

To determine whether the reduced blood lactate concentrations [La] during submaximal exercise in humans after endurance training result from a decreased rate of lactate appearance (Ra) or an increased rate of lactate metabolic clearance (MCR), interrelationships among blood [La], lactate Ra, and lactate MCR were investigated in eight untrained men during progressive exercise before and after a 9-wk endurance training program. Radioisotope dilution measurements of L-[U-14C]lactate revealed that the slower rise in blood [La] with increasing O2 uptake (VO2) after training was due to a reduced lactate Ra at the lower work rates [VO2 less than 2.27 l/min, less than 60% maximum VO2 (VO2max); P less than 0.01]. At power outputs closer to maximum, peak lactate Ra values before (215 +/- 28 mumol.min-1.kg-1) and after training (244 +/- 12 mumol.min-1.kg-1) became similar. In contrast, submaximal (less than 75% VO2max) and peak lactate MCR values were higher after than before training (40 +/- 3 vs. 31 +/- 4 ml.min-1.kg-1, P less than 0.05). Thus the lower blood [La] values during exercise after training in this study were caused by a diminished lactate Ra at low absolute and relative work rates and an elevated MCR at higher absolute and all relative work rates during exercise.

Oxidation of exogenous carbohydrate during prolonged exercise: the effects of the carbohydrate type and its concentration.

We studied rates of exogenous carbohydrate (CHO) oxidation during 90 min of cycling exercise in trained cyclists exercising at 70% of maximal oxygen consumption (VO2max) when they ingested glucose, sucrose, or glucose polymer solutions at concentrations of 7.5%, 10% or 15%. Drinks were labelled with [U-14C]glucose or sucrose and were ingested at a rate of 100 ml.10 min-1. Rates of oxidation of the ingested CHO were calculated from the specific radio-activity of the labelled CHO, expired 14CO2 and carbon dioxide output (VCO2). Total CHO oxidation, determined from oxygen consumption and VCO2 was not influenced by CHO type or concentration. Gastric emptying (P = 0.01) and the rate of exogenous CHO oxidation (P = 0.028) was greatest for the glucose polymer solutions, and least for glucose. Although gastric emptying (P = 0.006) decreased with increasing CHO concentration, CHO delivery to the intestine and exogenous CHO oxidation increased linearly with increasing CHO concentration. The percentage of the CHO delivered to the intestine that was oxidized ranged from 30.0% for 7.5% CHO to 38.1% for 15% CHO. Our results indicated that the rate of gastric emptying for CHO was not controlled to provide a constant rate of energy delivery as is commonly believed and that factors subsequent to gastric emptying limit the rate of exogenous CHO oxidation from the ingested solution.

High rates of exogenous carbohydrate oxidation from starch ingested during prolonged exercise.

This study compared the gastric emptying and oxidation of two 15% carbohydrate (CHO) solutions: a 22-chain-length glucose polymer (GP) and soluble starch (SS). Six endurance-trained subjects ingested 1,200 ml of either GP or SS while cycling for 90 min at 70% of maximal oxygen consumption (VO2max). Whereas the calculated total CHO oxidation (GP 266.8 +/- 41.9 g; SS 263.6 +/- 28.9 g) and the volume emptied from the stomach (GP 813 +/- 130 ml; SS 919 +/- 116 ml) were similar, the appearance of the 14C label in plasma occurred more rapidly from ingested SS than from GP (P less than 0.001). This resulted in a significantly greater rate of SS oxidation than that from GP (SS 105.9 +/- 21.9 g, GP 49.6 +/- 10.2 g; P less than 0.001). Exogenous CHO oxidation from GP accounted for 19% of total CHO oxidation, whereas the corresponding value for SS was 40%. This study suggests that the oxidation of SS and GP solutions ingested during exercise at 70% VO2max is not limited by gastric emptying. Rather, it appears to be either the rate of digestion or absorption of these solutions that determines their utilization.

Physiological differences between black and white runners during a treadmill marathon.

To determine why black distance runners currently out-perform white distance runners in South Africa, we measured maximum oxygen consumption (VO2max), maximum workload during a VO2max test (Lmax), ventilation threshold (VThr), running economy, inspiratory ventilation (VI), tidal volume (VT), breathing frequency (f) and respiratory exchange ratio (RER) in sub-elite black and white runners matched for best standard 42.2 km marathon times. During maximal treadmill testing, the black runners achieved a significantly lower (P less than 0.05) Lmax (17 km h-1, 2% grade, vs 17 km h-1, 4% grade) and VI max (6.21 vs 6.82 l kg-2/3 min-1), which was the result of a lower VT (101 vs 119 ml kg-2/3 breath-1) as fmax was the same in both groups. The lower VT in the black runners was probably due to their smaller body size. The VThr occurred at a higher percentage VO2max in black than in white runners (82.7%, SD 7.7% vs 75.6%, SD 6.2% respectively) but there were no differences in the VO2max. However, during a 42.2-km marathon run on a treadmill, the black athletes ran at the higher percentage VO2max (76%, SD 7.9% vs 68%, SD 5.3%), RER (0.96, SD 0.07 vs 0.91, SD 0.04) and f (56 breaths min-1, SD 11 vs 47 breaths min-1, SD 10), and at lower VT (78 ml kg-2/3 breath-1, SD 15 vs 85 ml kg-2/3 breath-1, SD 19). The combination of higher f and lower VT resulted in an identical VI.(ABSTRACT TRUNCATED AT 250 WORDS)