Untrained Humans Research Articles

Story Generation with Crowdsourced Plot Graphs

Story generation is the problem of automatically selecting a sequence of events that meet a set of criteria and can be told as a story. Story generation is knowledge-intensive; traditional story generators rely on a priori defined domain models about fictional worlds, including characters, places, and actions that can be performed. Manually authoring the domain models is costly and thus not scalable. We present a novel class of story generation system that can generate stories in an unknown domain. Our system (a) automatically learns a domain model by crowdsourcing a corpus of narrative examples and (b) generates stories by sampling from the space defined by the domain model. A large-scale evaluation shows that stories generated by our system for a previously unknown topic are comparable in quality to simple stories authored by untrained humans

Distributed Medical Image Analysis and Diagnosis through Crowd-Sourced Games: A Malaria Case Study

In this work we investigate whether the innate visual recognition and learning capabilities of untrained humans can be used in conducting reliable microscopic analysis of biomedical samples toward diagnosis. For this purpose, we designed entertaining digital games that are interfaced with artificial learning and processing back-ends to demonstrate that in the case of binary medical diagnostics decisions (e.g., infected vs. uninfected), with the use of crowd-sourced games it is possible to approach the accuracy of medical experts in making such diagnoses. Specifically, using non-expert gamers we report diagnosis of malaria infected red blood cells with an accuracy that is within 1.25% of the diagnostics decisions made by a trained medical professional.

Manual dexterity correlating with right lobule VI volume in right-handed 14-year-olds

Dexterity is a fundamental skill in our everyday life. Particularly, the fine-tuning of reaching for objects is of high relevance and crucially coordinated by the cerebellum. Although neuronal cerebellar structures mediate dexterity, classical whole brain voxel-based morphometry (VBM) has not identified structural correlates of dexterity in the cerebellum. Clusters of gray matter (GM) volume associated with the Purdue Pegboard Dexterity Test, a test of fine motor skills and complex upper limb movements, were identified in a cerebellum-optimized VBM analysis using the Spatially Unbiased Infratentorial (SUIT) toolbox in 65 healthy, right-handed 14-year-olds. For comparison, classical whole brain VBM was performed. The cerebellum-optimized VBM indicated a significant positive correlation between manual dexterity and GM volume in the right cerebellum Lobule VI, corrected for multiple comparisons and non-stationary smoothness. The classical whole brain VBM revealed positive associations (uncorrected) between dexterity performance and GM volume in the left SMA (BA 6), right fusiform gyrus (BA 20) and left cuneus (BA 18), but not cerebellar structures. The results indicate that cerebellar GM volumes in the right Lobule VI predict manual dexterity in healthy untrained humans when cerebellum-optimized VBM is employed. Although conventional VBM identified brain motor network areas it failed to detect cerebellar structures. Thus, previous studies might have underestimated the importance of cerebellum in manual dexterity.

Sweat sodium concentration during exercise in the heat in aerobically trained and untrained humans

The purpose of this study was to determine whether sweat sodium concentration ([Na(+)](sweat)) during exercise in the heat differs between aerobically trained and untrained individuals. On three occasions, ten endurance-trained (Tr) and ten untrained (UTr) subjects (VO2peak = 4.0 ± 0.8 vs. 3.4 ± 0.7 L min(-1), respectively; P < 0.05) cycled in a hot-ventilated environment (36 ± 1°C; 25 ± 2% humidity, airflow 2.5 m s(-1)) at three workloads (i.e., 40, 60, and 80% VO2peak). Whole-body (SR(WB)) and back sweat rates (SR(BACK)) were measured. At the conclusion of the study, Na(+) in sweat and blood samples was analyzed to calculate Na(+) secretion and reabsorption rates. SR(WB) and SR(BACK) were highly correlated in Tr and UTr (r = 0.74 and 0.79, respectively; P < 0.0001). In both groups, SR(BACK) increased with the increases in exercise intensity (P < 0.05). Likewise, [Na(+)](sweat) increased with the exercise intensity in both groups (P < 0.05) and it tended to be higher in Tr than in UTr at 60 and 80% VO2peak (~22 mmol L(-1) higher; P = 0.06). However, when normalized for SR(BACK), [Na(+)](sweat) was not different between groups. In both groups, Na(+) secretion and reabsorption rates increased with the increases in SR(BACK) (P < 0.05). However, Na(+) reabsorption rate was lower in the Tr than in the UTr (mean slope = 48 vs. 82 ηmol cm(-2) min(-1); P = 0.03). In conclusion, using a cross-sectional study design, our data suggest that aerobic fitness level does not reduce sweat Na(+) secretion or enhance Na(+) reabsorption during prolonged exercise in the heat that induced high sweat rates.

Athletic humans and horses: Comparative analysis of interleukin-6 (IL-6) and IL-6 receptor (IL-6R) expression in peripheral blood mononuclear cells in trained and untrained subjects at rest

BackgroundHorses and humans share a natural proclivity for athletic performance. In this respect, horses can be considered a reference species in studies designed to optimize physical training and disease prevention. In both species, interleukin-6 (IL-6) plays a major role in regulating the inflammatory process induced during exercise as part of an integrated metabolic regulatory network. The aim of this study was to compare IL-6 and IL-6 receptor (IL-6R) mRNA expression in peripheral blood mononuclear cells (PBMCs) in trained and untrained humans and horses.ResultsNine highly trained male swimmers (training volume: 21.6 ± 1.7 h/wk in 10-12 sessions) were compared with two age-matched control groups represented by eight lightly trained runners (training volume: 6.4 ± 2.6 h/wk in 3-5 sessions) and nine untrained subjects. In addition, eight trained horses (training volume: 8.0 ± 2.1 h/wk in 3-4 sessions) were compared with eight age-matched sedentary mares. In humans, IL-6 mRNA levels in PBMCs determined by quantitative reverse transcription-polymerase chain reaction were significantly higher in highly trained subjects, whereas IL-6R expression did not differ among groups. In horses, transcripts of both IL-6 and IL-6R were significantly up-regulated in the trained group.ConclusionsUp-regulation of IL-6R expression in PBMCs in horses could reflect a mechanism that maintains an adequate anti-inflammatory environment at rest through ubiquitous production of anti-inflammatory cytokines throughout the body. These findings suggest that the system that controls the inflammatory response in horses is better adapted to respond to exercise than that in humans.

Cardiorespiratory and cerebrovascular responses to head-up tilt I: Influence of age and training status

The purpose of this study was to examine the combined cardiorespiratory and cerebrovascular responses to head-up tilt (HUT) in young (27 ± 4 years) and older (65 ± 5 years) trained and untrained humans. Middle cerebral artery blood velocity (MCAv; transcranial Doppler ultrasound), blood pressure (BP; Finometer) and cardiac output (Q̇) were measured continuously whilst supine and during 60° HUT for 15 min or to pre-syncope in 41 participants [nine young trained; eleven young untrained; twelve older trained; nine older untrained]. Thirty seven of forty one participants completed 15 min HUT, and orthostatic tolerance did not differ with age or fitness ( P = 0.66). Supine MCAv was 30% lower in the older participants but the HUT-induced drop in MCAv was not altered by age [− 18% (young) vs. − 17% (older)], or fitness. Mean arterial BP was maintained during HUT and not altered by age or fitness. In the untrained, peripheral resistance was elevated [11% vs. − 2% (trained); P = 0.01], and Q̇ was reduced [− 10% vs. − 5% (trained); P = 0.04] with HUT. Despite these age- and fitness-associated differences in some cardiovascular responses to HUT, orthostatic tolerance was similar across groups. Thus, at least in this healthy population, neither age nor fitness impacts on the ability to adapt to postural change.

Cardiorespiratory and cerebrovascular responses to head-up tilt II: Influence of age, training status and acute exercise

The purpose of this study was to examine the combined cardiorespiratory and cerebrovascular responses to head-up tilt (HUT) in young and older trained and untrained humans following moderate-duration exercise. Middle cerebral artery blood flow velocity (MCAv; transcranial Doppler ultrasound), blood pressure (BP; Finometer), and stroke volume (SV) were measured continuously whilst supine and during 60° HUT for 15 min or to pre-syncope in 41 participants [nine young trained; eleven young untrained; twelve older trained; nine older untrained] prior to and following 30 min of treadmill exercise at 70–80% maximal HR. Orthostatic tolerance was not reduced following exercise [Mean (all groups) 14:45 ± 1:19, vs. 14:47 ± 0:43 min:s (before exercise); P = 0.73], and did not differ with age or fitness. Mean MCAv was elevated [~ 5 ± 11%] whilst supine after exercise in the older participants but reduced [~−4 ± 12%] in the young [ P = 0.03]. The postural reductions in MCAv [~−22% vs. –17%; P = 0.02], MAP [~−8% vs. −3%; P = 0.04] and SV [~−28% vs. −23%; P = 0.03] were increased after exercise (vs. pre-exercise). Orthostatic tolerance was not reduced following 30 min of exercise, and did not differ with age or fitness, despite more pronounced post-exercise reductions in MCAv, MAP and SV with postural change.

Roles of nitric oxide synthase and cyclooxygenase in leg vasodilation and oxygen consumption during prolonged low-intensity exercise in untrained humans

The vasodilator signals regulating muscle blood flow during exercise are unclear. We tested the hypothesis that in young adults leg muscle vasodilation during steady-state exercise would be reduced independently by sequential pharmacological inhibition of nitric oxide synthase (NOS) and cyclooxygenase (COX) with NG-nitro-L-arginine methyl ester (L-NAME) and ketorolac, respectively. We tested a second hypothesis that NOS and COX inhibition would increase leg oxygen consumption (VO2) based on the reported inhibition of mitochondrial respiration by nitric oxide. In 13 young adults, we measured heart rate (ECG), blood pressure (femoral venous and arterial catheters), blood gases, and venous oxygen saturation (indwelling femoral venous oximeter) during prolonged (25 min) steady-state dynamic knee extension exercise (60 kick/min, 19 W). Leg blood flow (LBF) was determined by Doppler ultrasound of the femoral artery. Whole body VO2 was measured, and leg VO2 was calculated from blood gases and LBF. Resting intra-arterial infusions of acetylcholine (ACh) and nitroprusside (NTP) tested inhibitor efficacy. Leg vascular conductance (LVC) to ACh was reduced up to 53±4% by L-NAME+ketorolac infusion, and the LVC responses to NTP were unaltered. Exercise increased LVC from 4±1 to 33.1±2 ml.min(-1).mmHg(-1) and tended to decrease after L-NAME infusion (31±2 ml.min(-1).mmHg(-1), P=0.09). With subsequent administration of ketorolac LVC decreased to 29.6±2 ml.min(-1).mmHg(-1) (P=0.02; n=9). While exercise continued, LVC returned to control values (33±2 ml.min(-1).mmHg(-1)) within 3 min, suggesting involvement of additional vasodilator mechanisms. In four additional subjects, LVC tended to decrease with L-NAME infusion alone (P=0.08) but did not demonstrate the transient recovery. Whole body and leg VO2 increased with exercise but were not altered by L-NAME or L-NAME+ketorolac. These data indicate a modest role for NOS- and COX-mediated vasodilation in the leg of exercising humans during prolonged steady-state exercise, which can be restored acutely. Furthermore, NOS and COX do not appear to influence muscle VO2 in untrained healthy young adults.

Contraction‐induced changes in skeletal muscle Na+,K+ pump mRNA expression – importance of exercise intensity and Ca2+‐mediated signalling

To investigate if exercise intensity and Ca(2+) signalling regulate Na(+),K(+) pump mRNA expression in skeletal muscle. The importance of exercise intensity was evaluated by having trained and untrained humans perform intense intermittent and prolonged exercise. The importance of Ca(2+) signalling was investigated by electrical stimulation of rat soleus and extensor digitorum longus (EDL) muscles in combination with studies of cell cultures. Intermittent cycling exercise at approximately 85% of VO(2peak) increased (P < 0.05) alpha1 and beta1 mRNA expression approximately 2-fold in untrained and trained subjects. In trained subjects, intermittent exercise at approximately 70% of VO(2peak) resulted in a less (P < 0.05) pronounced increase ( approximately 1.4-fold; P < 0.05) for alpha1 and no change in beta1 mRNA. Prolonged low intensity exercise increased (P < 0.05) mRNA expression of alpha1 approximately 3.0-fold and alpha2 approximately 1.8-fold in untrained but not in trained subjects. Electrical stimulation of rat soleus, but not EDL, muscle increased (P < 0.05) alpha1 mRNA expression, but not when combined with KN62 and cyclosporin A incubation. Ionomycin incubation of cultured primary rat skeletal muscle cells increased (P < 0.05) alpha1 and reduced (P < 0.001) alpha2 mRNA expression and these responses were abolished (P < 0.05) by co-incubation with cyclosporin A or KN62. (1) Exercise-induced increases in Na(+),K(+) pump alpha1 and beta1 mRNA expression in trained subjects are more pronounced after high- than after moderate- and low-intensity exercise. (2) Both prolonged low and short-duration high-intensity exercise increase alpha1 mRNA expression in untrained subjects. (3) Ca(2+)(i) regulates alpha1 mRNA expression in oxidative muscles via Ca(2+)/calmodulin-dependent protein kinase (CaMK) and calcineurin signalling pathways.

Short-duration Quercetin Supplementation Does Not Alter Substrate Utilization, Cycling Economy, Or Rpe In Untrained Men

Quercetin is a naturally-occurring dietary flavonoid found in fruits and vegetables. Quercetin feedings for 7 d in sedentary mice have increased skeletal muscle mitochondrial enzyme activity by 20-30%. Increased mitochondrial enzyme activity might alter movement economy and substrate utilization during submaximal exercise. In in vitro tests, quercetin has been shown to be an adenosine A-1 receptor antagonist and, thus, may have analgesic effects that alter perception of effort. Dietary quercetin supplementation for 3-6 wk has not increased muscle mitochondrial enzyme activity, substrate utilization, movement economy, or RPE in trained cyclists, but the effects of quercetin supplementation in untrained humans are unknown. PURPOSE: To investigate the effects of short-duration quercetin supplementation on substrate utilization, movement economy, and RPE measured during submaximal cycling in untrained men. METHODS: Using a double-blind, pretest-posttest, control-group design, 30 recreationally-active, but not endurance-trained, young men were randomly assigned to Quercetin (Q) and Placebo (P) groups. Measurements during min 58-60 of submaximal cycling at 50% VO2max were performed before and after 9-16 d of supplementation with 1 g/d of quercetin in a fruit punch beverage or a placebo beverage. RESULTS: Pretest-to-posttest changes in respiratory quotient (Q: 0.89 ± 0.03 vs 0.92 ± 0.03; P: 0.89 ± 0.03 vs 0.90 ± 0.04), plasma glucose (Q: 4.5 ± 1.0 vs 4.7 ± 1.2 mmol/L; P: 4.8 ± 0.9 vs 4.8 ± 0.6 mmol/L), plasma non-esterified fatty acids (Q: 0.52 ± 0.19 vs 0.41 ± 0.13 mmol/L; P: 0.42 ± 0.18 vs 0.49 ± 0.19 mmol/L), plasma glycerol (Q: 0.09 ± 0.12 vs 0.06 ± 0.06 mmol/L; P: 0.07 ± 0.06 vs 0.07 ± 0.07 mmol/L), and beta hydroxybuterate (Q: 0.13 ± 0.10 vs 0.09 ± 0.03 mmol/L; P: 0.08 ± 0.04 vs 0.09 ± 0.05 mmol/L) were not significantly different (p > 0.05) in Q and P. Changes in VO2 (Q: 21.7 ± 4.2 vs 20.3 ± 3.3 ml/kg·min; P: 19.9 ± 2.8 vs 19.6 ± 3.4 ml/kg·min) and RPE (Q: 12.7 ± 1.4 vs 11.8 ± 1.6; P: 11.2 ± 2.7 vs 11.4 ± 2.4) also were not significant (p > 0.05). CONCLUSIONS: Dietary quercetin supplementation with 1 g/d for 9-16 d does not alter substrate utilization, cycling economy, or RPE in untrained men. Supported by the Beverage Institute for Health and Wellness, The Coca-Cola Company.

Short-duration Quercetin Supplementation Does Not Improve Vo2peak Or Cycling Performance In Untrained Men

Quercetin is a naturally-occurring dietary flavonoid found in fruits and vegetables. Quercetin feedings for 7 d in sedentary mice have increased skeletal muscle mitochondrial enzyme activity and treadmill run time to fatigue by 20-30%. Dietary quercetin supplementation for 3-6 wk has not increased skeletal muscle mitochondrial enzyme activity, VO2peak, or cycling performance in trained cyclists, but the effects of quercetin supplementation in untrained humans are unknown. PURPOSE: To investigate the effects of short-duration quercetin supplementation on a non-invasive measure of muscle oxidative capacity (PCr recovery), VO2peak, and cycling performance in untrained men. METHODS: Using a double-blind, pretest-posttest, control-group design, 30 recreationally-active, but not endurance-trained, young men were randomly assigned to Quercetin (Q) and Placebo (P) groups. Measurements of PCr recovery rate following brief (39 s) isometric quadriceps exercise from magnetic resonance spectroscopy (MRS) with a 3-Tesla GE magnet, VO2peak, and cycling performance on a maximal-effort 10-min ride following 60 min of submaximal cycling at 50% VO2peak were performed before and after 7-16 d of supplementation with 1 g/d of quercetin with vitamins in a fruit punch beverage or a placebo beverage. RESULTS: Pretest-to-posttest changes in PCr recovery time constant (Q: 32.3 ± 8.9 vs 35.2 ± 9.4 s; P: 29.7 ± 7.6 vs 33.7 ± 7.8 s), VO2peak (Q: 42.7 ± 5.3 vs 43.7 ± 6.0 ml/kg·min; P: 40.5 ± 5.4 vs 40.2 ± 5.3 ml/kg·min) or total work done during the 10-min maximal effort cycling trial (Q: 122 ± 13 vs 124 ± 13 kJ; P: 122 ± 17 vs 121 ± 14 kJ) were not significantly different (p > 0.05) in Q and P. CONCLUSION: Dietary quercetin supplementation with 1 g/d for 7-16 d does not increase skeletal muscle oxidative capacity, VO2peak, or cycling performance in untrained men. Supported by the Beverage Institute for Health and Wellness, The Coca-Cola Company

Carnosine loading and washout in human skeletal muscles

Carnosine (beta-alanyl-L-histidine) is present in high concentrations in human skeletal muscles. The oral ingestion of beta-alanine, the rate-limiting precursor in carnosine synthesis, has been shown to elevate the muscle carnosine content both in trained and untrained humans. Little human data exist about the dynamics of the muscle carnosine content, its metabolic regulation, and its dependence on muscle fiber type. The present study aimed to investigate in three skeletal muscle types the supplementation-induced amplitude of carnosine synthesis and its subsequent elimination on cessation of supplementation (washout). Fifteen untrained males participated in a placebo-controlled double-blind study. They were supplemented for 5-6 wk with either 4.8 g/day beta-alanine or placebo. Muscle carnosine was quantified in soleus, tibialis anterior, and medial head of the gastrocnemius by proton magnetic resonance spectroscopy (MRS), before and after supplementation and 3 and 9 wk into washout. The beta-alanine supplementation significantly increased the carnosine content in soleus by 39%, in tibialis by 27%, and in gastrocnemius by 23% and declined post-supplementation at a rate of 2-4%/wk. Average muscle carnosine remained increased compared with baseline at 3 wk of washout (only one-third of the supplementation-induced increase had disappeared) and returned to baseline values within 9 wk at group level. Following subdivision into high responders (+55%) and low responders (+15%), washout period was 15 and 6 wk, respectively. In the placebo group, carnosine remained relatively constant with variation coefficients of 9-15% over a 3-mo period. It can be concluded that carnosine is a stable compound in human skeletal muscle, confirming the absence of carnosinase in myocytes. The present study shows that washout periods for crossover designs in supplementation studies for muscle metabolites may sometimes require months rather than weeks.

運動鍛錬者における急性メンタルストレス中の無毛部と有毛部の皮膚血管反応

Acute mental stress induces sympathetic activation and influences vasomotor control in various organs. In the present study, to better understand the effect of physical training on peripheral vasomotor control during acute mental stress, we compared the skin vascular responses to mental arithmetic (MA) in physically trained and untrained humans. Eight physically trained (T group) and eight untrained (UT group) healthy volunteers performed 2 min of MA aloud in the supine position under a thermoneutral condition (28 degrees C). Skin blood flow (laser-Doppler flowmetry) and local temperature were monitored at the glabrous (palm, sole) and nonglabrous (forearm, calf) sites. Cutaneous vascular conductance (CVC) was evaluated from the ratio of blood flow to mean arterial pressure (tonometry). Local sweating rate (SR) was measured in the sole and calf by the ventilated capsule method. In the T group, the CVC at glabrous sites consistently decreased (P < 0.05) during MA, while in the UT group, the stress-induced decreases in CVC were transient and gradually recovered during MA. The patterns of changes in CVC at the nonglabrous sites were substantially similar to those at the glabrous sites, but the decreases in CVC at the nonglabrous sites were smaller (P < 0.05) than those at the glabrous sites in both groups. Local temperature at the glabrous sites (especially in the sole) showed higher (P < 0.05) values in the T group compared with the UT group. The SR in the sole and calf were increased (P < 0.05) during MA but did not differ between the two groups. These findings suggest that physical training acts to heighten skin temperature at the glabrous sites but not at the nonglabrous sites. It is also suggested that the change of skin temperature by physical training modifies sympathetic vasomotor control in glabrous and nonglabrous skin during acute mental stress in the peripheral level.

Trained Men Display Increased Basal Heat Shock Protein Content of Skeletal Muscle

1) To compare the baseline levels of heat shock and antioxidant protein content in the skeletal muscle of trained and untrained humans and 2) to characterize the exercise-induced stress response of aerobically trained human skeletal muscle to an acute exercise challenge. Resting muscle biopsies were obtained from the vastus lateralis muscle of six untrained and six aerobically trained young males. To characterize the stress response of a trained population, the trained subjects also performed a 45-min nondamaging running exercise protocol at an intensity corresponding to 75% of V O2max. Muscle biopsies were obtained from the vastus lateralis muscle at 48 h and 7 d after exercise. Trained subjects displayed significantly higher (P<0.05) resting levels of heat shock protein 60 (HSP60, 25%), alphaB-crystallin (43%), and manganese superoxide (MnSOD, 45%) protein content compared with untrained subjects. Trained subjects also exhibited no significant change (P > 0.05) in resting levels of HSP70 (16%), HSC70 (13%), and total superoxide dismutase (SOD) activity (46%) compared with untrained subjects. Resting HSP27 levels were unaffected by exercise training (P > 0.05). In the trained subjects, exercise failed to induce significant increases (P>0.05)in muscle content of HSP70, HSC70, HSP60, HSP27, alphaB-crystallin, and MnSOD protein content or in the activity of SOD at any time point after exercise. This study demonstrates for the first time that trained men display a selective up-regulation of basal heat shock and antioxidant protein content and do not exhibit a stress response to customary running exercise. It is suggested that an increase in these protective systems functions to maintain homeostasis during the stress of exercise by protecting against disruptions to the cytoskeleton/contractile machinery, by maintaining redox balance, and by facilitating mitochondrial biogenesis.

Exercise Training Improves Nitric Oxide (NO)-Dependent Skin Vasodilation In Response To Acetylcholine In Older Subjects

PURPOSE: We constructed incremental dose-response curves to acetylcholine infusion in the skin (ACh) in the presence and absence of nitric oxide(NO)-blockade in young, old untrained and old fit subjects. METHODS: Twelve young (6F/6M;27±1yrs,VO2max:49±3ml.kg-1.min1) subjects were recruited along with 16 older untrained(10F/6M;60±1yrs;29±1ml.kg-1.min-1) subjects and 12 masters athletes (59±1yrs;6F,6M;45±2ml.kg-1.min-1). Eight of the older (5F,3M) untrained group volunteered to undertake a 6 month exercise training program. Two microdialysis fibres were embedded into the skin of the ventral forearm and Doppler probes placed over these sites. A dose-response curve was constructed for 3 incremental doses of ACh for delivery through one probe, whilst the 2nd probe had a co-infusion of ACh+LNAME, a NO antagonist. At the end of the protocol, sodium nitroprusside (56mM) was infused through both probes in combination with localised heating at 42°C to assess maximal cutaneous vascular conductance (%CVCmax). RESULTS: The NO contribution of each ACh dose was impaired in the older untrained subjects (3±1, 11±2, 35±6%CVCmax), compared to younger (12±3, 22±4, 53±6%, P<0.05) and older fit subjects (7±1, 22±5, 53±8%, P<0.05) at the 2nd dose of ACh. Exercise training in the older unfit subjects enhanced the NO component of ACh-mediated vasodilator function at 12 and 24 weeks (12±4, 25±6, 53±5%CVCmax) and 24 weeks (8±3, 25±6, 54±6 %CVCmax, P<0.05 2-way ANOVA). CONCLUSIONS: This study characterised the contribution of NO to ACh-mediated skin blood flow responses in trained and untrained humans. Both chronic and shortterm exercise improves NO-vasodilator function in humans, a finding with potentially important clinical implications for patients with microvascular disease.

Contribution of intramuscular TG and plasma FFA to the long chain acyl‐carnitine pool: effects of insulin in trained and untrained humans

This study examined the plasma FFA, intramuscular long chain acylcarnitine (LCAC) fatty acids and imTG stores during basal and hyperinsulinemic conditions.Methods:Endurance trained (TR, n=8) and sedentary individuals (SED, n=15) were studied under overnight postabsorptive and euglycemic hyperinsulinemic clamp (1.0mU·kg FFM−1·min−1) conditions. FFA kinetics were measured using a 5‐h infusion of [U‐13C]oleate, for labeling of imTG and LCAC pools. Muscle biopsies were performed to measure imTG and imLCAC enrichment at 1400 h after 5‐h of infusion.imTG concentrations were greater in TR than SED individuals (P&lt;0.01).Table SED Trained Saline** Clamp Saline** Clamp plasma oleate FFA (mpe) 0.210±0.018* 0.271±0.036* 0.189±0.026* 0.361±0.050* imLCAC (mpe) 0.025±0.003 0.005±0.002 0.016±0.005 0.002±0.002 imTG (mpe) 0.018±0.003† 0.011±0.001† 0.024±0.004† 0.013±0.001† P&lt;0.001 saline vs. clamp; *P&lt;0.000 between compartment (plasma vs. imLCAC vs. imTG); †P&lt;0.000 imLCAC and imTG Methods:Endurance trained (TR, n=8) and sedentary individuals (SED, n=15) were studied under overnight postabsorptive and euglycemic hyperinsulinemic clamp (1.0mU·kg FFM−1·min−1) conditions. FFA kinetics were measured using a 5‐h infusion of [U‐13C]oleate, for labeling of imTG and LCAC pools. Muscle biopsies were performed to measure imTG and imLCAC enrichment at 1400 h after 5‐h of infusion.Conclusion:The imTG contributes more to the imLCAC pools than plasma FFA both in the basal and hyperinsulinemic state, and hyperinsulinemia suppressed oleate FFA entry into the imLCAC pools, more so in trained than untrained adults. Muscle fatty acid oxidation is largely via obligatory cycling of fatty acids through imTG or other intracellular complex lipid pools.

Myocardial perfusion during exercise in endurance-trained and untrained humans

Because of technical challenges very little is known about absolute myocardial perfusion in humans in vivo during physical exercise. In the present study we applied positron emission tomography (PET) in order to 1) investigate the effects of dynamic bicycle exercise on myocardial perfusion and 2) clarify the possible effects of endurance training on myocardial perfusion during exercise. Myocardial perfusion was measured in endurance-trained and healthy untrained subjects at rest and during absolutely the same (150 W) and relatively similar [70% maximal power output (W(max))] bicycle exercise intensities. On average, the absolute myocardial perfusion was 3.4-fold higher during 150 W (P < 0.001) and 4.9-fold higher during 70% W(max) (P < 0.001) than at rest. At 150 W myocardial perfusion was 46% lower in endurance-trained than in untrained subjects (1.67 +/- 0.45 vs. 3.00 +/- 0.75 ml x g(-1) x min(-1); P < 0.05), whereas during 70% W(max) perfusion was not significantly different between groups (P = not significant). When myocardial perfusion was normalized with rate-pressure product, the results were similar. Thus, according to the present results, myocardial perfusion increases in parallel with the increase in working intensity and in myocardial work rate. Endurance training seems to affect myocardial blood flow pattern during submaximal exercise and leads to more efficient myocardial pump function.

Effect of training on insulin-mediated glucose uptake in human muscle.

During insulin stimulation whole body glucose uptake is increased in trained compared with untrained humans. However, it is not known which tissue is responsible. Seven young male subjects bicycle trained one leg for 10 wk at 70% of maximal O2 consumption (VO2max). Sixteen hours after last exercise bout, a three-step euglycemic hyperinsulinemic clamp (clamp 1) was performed (insulin levels, means +/- SE: 9 +/- 1, 53 +/- 3, 174 +/- 5, and 2,323 +/- 80 was microU/ml), with measurement of arteriovenous differences and blood flow in both legs. After 6 days of detraining subjects were restudied, having exercised the untrained leg 16 h before. VO2max for trained (T) and untrained (UT) legs was 52 +/- 2 vs. 44 +/- 2 ml.min-1.kg-1 (P < 0.05). In clamp 1 glucose uptake in T and UT legs was 1.0 +/- 0.2 vs. 0.5 +/- 0.1 mg.min-1.kg-1 (basal), 9.7 +/- 2.3 vs. 6.7 +/- 1.7 (P < 0.05) (step I), 19.2 +/- 2.8 vs. 14.3 +/- 2.0 (P < 0.05) (step II), and 22.8 +/- 2.3 vs. 18.6 +/- 2.2 (P < 0.05) (step III). During insulin infusion lactate release (P < 0.05) [8.9 +/- 1.8 vs. 2.9 +/- 0.9 mumol.min-1.kg-1 (step I), 24.6 +/- 3.1 vs. 12.5 +/- 2.6 (step III)] and glycogen storage (P < 0.1) calculated by indirect calorimetry [6.7 +/- 2.3 vs. 5.0 +/- 1.7 mg.min-1.kg-1 (step I), 16.8 +/- 2.1 vs. 14.1 +/- 1.8 (step III)] were always higher in T than in UT legs. Release of glycerol, free fatty acids, and tyrosine and clearance of insulin were not influenced by training. Insulin-mediated glucose uptake was not increased after detraining or a single bout of exercise. In conclusion, training increases sensitivity and responsiveness of insulin-mediated glucose uptake in human muscle by local mechanisms. Glycolysis and glycogen storage are equally enhanced. The training effect represents a genuine adaptation to repeated exercise but is short lived. Insulin clearance in muscle is not influenced by training.

Increase of Hemoglobin Concentration After Maximal Apneas in Divers, Skiers, and Untrained Humans

Human splenic contraction occurs both during apnea and maximal exercise, increasing the circulating erythrocyte volume. We investigated the hematological responses to 3 maximal apneas performed by elite apneic divers, elite cross-country skiers, and untrained subjects. Post-apnea hemoglobin concentration had increased in all groups, but especially in divers. The increases disappeared within 10 min of recovery. Apneic duration across apneas also increased the most in divers. Responses in divers could be more pronounced as a result of apnea training.

Sensitivity of CPT I to malonyl-CoA in trained and untrained human skeletal muscle.

The present study examined the sensitivity of carnitine palmitoyltransferase I (CPT I) activity to its inhibitor malonyl-CoA (M-CoA), and simulated metabolic conditions of rest and exercise, in aerobically trained and untrained humans. Maximal CPT I activity was measured in mitochondria isolated from resting human skeletal muscle. Mean CPT I activity was 492.8 +/- 72.8 and 260.8 +/- 33.6 micromol. min(-1). kg wet muscle(-1) in trained and untrained subjects, respectively (pH 7.0, 37 degrees C). The sensitivity to M-CoA was greater in trained muscle; the IC(50) for M-CoA was 0.17 +/- 0.04 and 0.49 +/- 0.17 microM in trained and untrained muscle, respectively. The presence of acetyl-CoA, free coenzyme A (CoASH), and acetylcarnitine, in concentrations simulating rest and exercise conditions did not release the M-CoA-induced inhibition of CPT I activity. However, CPT I activity was reduced at pH 6.8 vs. pH 7.0 in both trained and untrained muscle in the presence of physiological concentrations of M-CoA. The results of this study indicate that aerobic training is associated with an increase in the sensitivity of CPT I to M-CoA. Accumulations of acetyl-CoA, CoASH, and acetylcarnitine do not counteract the M-CoA-induced inhibition of CPT I activity. However, small decreases in pH produce large reductions in the activity of CPT I and may contribute to the decrease in fat metabolism that occurs during moderate and intense aerobic exercise intensities.