Effect of exercise timing on postprandial lipemia and HDL cholesterol subfractions

The purpose ofthe study was to examine the effect of exercise timing on postprandiallipemia responses. Subjects were 21 recreationally trained men (ages 27 ± 1.7 yr). Each subject performed four trials:1) Control (fat meal only),2) Post (exercise 1 h after a fat meal), 3) 1 h-Pre(exercise 1 h before a fat meal), and4) 12 h-Pre (exercise 12 h before afat meal). In each trial, subjects had a standard fat meal to inducepostprandial hypertriglyceridemia. Blood samples were taken at 0 h(immediately before the fat meal) and at 2, 4, 6, 8, and 24 h after themeal. In the exercise trials, each subject exercised at 60% of maximalO₂ consumption for 1 h. Theresults indicated that triglyceride area under the curve scores inpremeal-exercise trials were lower (P < 0.05) than those in Post and Control. At 24 h, total high-densitylipoprotein (HDL)-cholesterol in the premeal-exercise trials was higher(P < 0.05) than that at 0 h, whereastotal HDL-cholesterol was not changed in Control and Post. At 24 h, HDLsubtype 2-cholesterol was higher (P < 0.05) in the premeal-exercise trials than in Control, which did not differ from Post. These results suggest that exercising before a fatmeal may have a beneficial effect on the triglyceride response and HDLmetabolism, which may blunt atherosclerotic process induced by the fatmeal.

     

Neuromuscular fatigue after maximal stretch-shortening cycle exercise

Strojnik, V., and P. V. Komi. Neuromuscular fatigueafter maximal stretch-shortening cycle exercise. J. Appl. Physiol. 84(1): 344-350, 1998.To examinesome possible sites of fatigue during short-lasting maximally intensivestretch-shortening cycle exercise, drop jumps on an inclined sledgeapparatus were analyzed. Twelve healthy volunteers performed jumpsuntil they were unable to maintain jumping height >90% of theirmaximum. After the workout, the increases in the blood lactateconcentration and serum creatine kinase activation were statisticallysignificant (P < 0.001 and P < 0.05, respectively) but rathersmall in physiological terms. The major changes after the workout wereas follows: the single twitch was characterized by smaller peak torque(P < 0.05) and shorter time to peak(P < 0.05) and half-relaxation time(P < 0.01). The double-twitch torqueremained at the same level (P > 0.05), but with a steeper maximal slope of torque rise(P < 0.05); during 20- and 100-Hzstimulation the torque declined (both P < 0.01) and the maximal voluntarytorque changed nonsignificantly but with a smaller maximal slope oftorque rise (P < 0.01) and a higheractivation level (P < 0.05),accompanied by an increased electromyogram amplitude. These findingsindicate that the muscle response after the short-lasting consecutivemaximum jumps on the sledge apparatus may involve two distinctmechanisms acting in opposite directions:1) The contractile mechanism seemsto be potentiated through a shorterCa²⁺ transient and fastercross-bridge cycling, as implied by twitch changes.2) High-frequency action potentialpropagation shows an impairment, which is suggested as the possibledominant reason for fatigue in exercise of this type.

     

Augmented sympathetic tone alters muscle metabolism with exercise: lack of evidence for functional sympatholysis

Shoemaker, J. Kevin, Prasant Pandey, Michael D. Herr, DavidH. Silber, Qing X. Yang, Michael B. Smith, Kristen Gray, and LawrenceI. Sinoway. Augmented sympathetic tone alters muscle metabolismwith exercise: lack of evidence for functional sympatholysis. J. Appl. Physiol. 82(6):1932-1938, 1997.It is unclear whether sympathetic tone opposesdilator influences in exercising skeletal muscle. We examined highlevels of sympathetic tone, evoked by lower body negative pressure(LBNP, 60 mmHg) on intramuscular pH and phosphocreatine (PCr)levels (³¹P-nuclear magnetic resonance spectroscopy) duringgraded rhythmic handgrip (30 contractions/min; ~17, 34, 52 and 69%maximal voluntary contraction). Exercise was performedwith LBNP and without LBNP (Control). At the end of exercise, LBNPcaused lower levels of muscle pH (6.59 ± 0.09) comparedwith Control (6.78 ± 0.05; P < 0.05). PCr recovery, an index of mitochondrial respiration, was lessduring the recovery phase of the LBNP trial. Exercise mean arterialpressure was not altered by LBNP. The protocols were repeated withmeasurements of forearm blood flow velocity and deep venous samples(active forearm) of hemoglobin (Hb) saturation, pH, and lactate. WithLBNP, mean blood velocity was reduced at rest, during exercise, andduring recovery compared with Control (P < 0.05). Also, venous Hbsaturation and pH levels during exercise and recovery were lower withLBNP and lactate was higher compared with Control(P < 0.05). We concludethat LBNP enhanced sympathetic tone and reduced oxygen transport. Athigh workloads, there was a greater reliance on nonoxidativemetabolism. In other words, sympatholysis did not occur.

     

Hyperhydration: tolerance and cardiovascular effects during uncompensable exercise-heat stress

This study examined the efficacy of glycerol andwater hyperhydration (1 h before exercise) on tolerance andcardiovascular strain during uncompensable exercise-heat stress. Theapproach was to determine whether 1-h preexercise hyperhydration (29.1 ml H₂O/kg lean body mass with orwithout 1.2 g/kg lean body mass of glycerol) provided a physiologicaladvantage over euhydration. Eight heat-acclimated men completed threetrials (control euhydration before exercise, and glycerol and waterhyperhydrations) consisting of treadmill exercise-heat stress (ratio ofevaporative heat loss required to maximal capacity of climate = 416).During exercise (~55% maximalO₂ uptake), there was nodifference between glycerol and water hyperhydration methods forincreasing (P < 0.05) total bodywater. Glycerol hyperhydration endurance time (33.8 ± 3.0 min) waslonger (P < 0.05) than for control(29.5 ± 3.5 min), but was not different(P > 0.05) from that of waterhyperhydration (31.3 ± 3.1 min). Hyperhydration didnot alter (P > 0.05) core temperature, whole body sweating rate, cardiac output, blood pressure, total peripheral resistance, or core temperature tolerance. Exhaustion from heat strain occurred at similar core and skin temperatures andheart rates in each trial. Symptoms at exhaustion included syncope andataxia, fatigue, dyspnea, and muscle cramps(n = 11, 10, 2, and 1 cases,respectively). We conclude that 1-h preexercise glycerolhyperhydration provides no meaningful physiological advantage overwater hyperhydration and that hyperhydration per se only provides theadvantage (over euhydration) of delaying hypohydration duringuncompensble exercise-heat stress.

     

Effects of isoproterenol on myocardial structure and function in septic rats

In this study wesought to determine the effect of sepsis on two sequelae of prolonged(24-h) -agonist administration, myocardial hypertrophy andcatecholamine-induced cardiotoxicity. Sprague-Dawley rats wererandomized to cecal ligation and perforation (CLP) or sham study groupsand then further randomized to receive isoproterenol (2.4 mg · kg¹ · day¹ iv) or placebotreatment. At 24 h, myocardial function was assessed by using theLangendorff isolated-heart technique or the heart processed for plainlight microscopy. We found that 1)sepsis reduced contractile function, indicated by a rightward shift in the Starling curve (ANOVA with repeated measures, sepsis effect, P < 0.002);2) sepsis-induced myocardialdepression was reversed by isoproterenol treatment (isoproterenoleffect, P < 0.0001); 3) sepsis reduced, but did notblock, isoproterenol-induced myocardial hypertrophy (isoproterenoleffect, P < 0.0001);4) sepsis did not protect the heartfrom catecholamine-induced tissue injury; 5) the septic heart was protectedagainst the effects of ischemiareperfusion (decreasedpostreperfusion resting tension, ANOVA with repeated measures,P < 0.01), an effect attenuated byisoproterenol treatment (P < 0.005);and 6) sepsis reduced the incidenceof sustained asystole or ventricular fibrillation afterischemia-reperfusion (P < 0.05), an effect also attenuated by isoproterenol treatment (P < 0.01). We conclude that, insepsis, -agonists induce changes in myocardial weight and functionconsistent with acute myocardial hypertrophy. These changes occur atthe expense of significant tissue injury and increased sensitivity toischemia-reperfusion-induced tissue injury.     

Effect of tryptophan and of glucose on exercise capacity of horses

We hypothesized that central fatigue may have a role in limitingthe endurance capacity of horses. Therefore, we tested the effect ofinfusing tryptophan and/or glucose on endurance time and plasmaconcentrations of free tryptophan and other substrates thought toaffect tryptophan uptake into the brain of seven mares (3-4 yr ofage, 353-435 kg) that ran on a treadmill at 50% of maximalO₂ consumption to fatigue. Withuse of a counterbalanced crossover design, the horses were infused withtryptophan (100 mg/kg in saline solution) or a similar volume of salinesolution (placebo) before exercise. During exercise, horses receivedinfusions of glucose (2 g/min, 50% wt/vol) or a similar volume ofsaline. Thus the treatments were 1)tryptophan and glucose (T & G), 2) tryptophan and placebo (T & P), 3)placebo and glucose (P & G), and 4)placebo and placebo (P & P). Mean heart rate, hematocrit, andconcentration of plasma total solids before and during exercise weresimilar for all trials. Mean time to exhaustion was reduced (P < 0.05) for T & P and T & Gcompared with P & P [86.1 ± 6.9 and 87.1 ± 6.8 vs. 102.3 ± 10.3 (SE) min], whereas endurance for P & G(122.4 ± 11.9 min) was greater than for all other trials (P < 0.05). Compared withnontryptophan trials, during the tryptophan trials plasma prolactinincreased (P < 0.05) nearlythreefold before exercise and almost twofold early in exercise. Muscleglycogen concentrations were reduced(P < 0.05) below preexercise values in the P & G and P & P trials only. However, glucose infusions (P & G)did not affect (P > 0.05)concentrations of plasma free fatty acids or ratios of branched-chainamino acids to free tryptophan. In conclusion, tryptophan infusionreduced endurance time, which was consistent with the central fatiguehypothesis. The failure of glucose infusion to alleviate the effects oftryptophan and the absence of significant muscle glycogen reduction inthe tryptophan trials suggest that the early onset of fatigue in thetryptophan trials is not due to a lack of readily available substrate.

     

Progressive decrease of intramyocellular accumulation of H+ and Pi in human skeletal muscle during repeated isotonic exercise

The purpose of this study was to evaluatethe hypotheses that accumulation of hydrogen ions and/or inorganicphosphate (Pi) in skeletal muscle increases with repeated bouts ofisotonic exercise. ³¹P-Magnetic resonance spectroscopy wasused to examine the gastrocnemius muscle of seven highly aerobicallytrained females during four bouts of isotonic plantar flexion. Theexercise bouts (EX1-4) of 3 min and 18 swere separated by 3 min and 54 s of complete rest. Muscle ATP did notchange during the four bouts. Phosphocreatine (PCr) degradation duringEX1 (13.3 ± 2.4 mmol/kg wet weight) was higher(P < 0.01) compared with EX3-4(9.7 ± 1.6 and 9.6 ± 1.8 mmol/kg wet weight, respectively).The intramyocellular pH at the end of EX1 (6.87 ± 0.05) was significantly lower (P < 0.001) than thoseof EX2 (6.97 ± 0.02), EX3 (7.02 ± 0.01), and EX4 (7.02 ± 0.02). Total Pi anddiprotonated Pi were significantly higher (P < 0.001)at the end of EX1 (17.3 ± 2.7 and 7.8 ± 1.6 mmol/kg wet weight, respectively) compared with the values at the end of EX3 and EX4. The monoprotonated Pi at the endof EX1 (9.5 ± 1.2 mmol/kg wet weight) was alsosignificantly higher (P < 0.001) than that afterEX4 (7.5 ± 1.1 mmol/kg wet weight). Subjects' ratingof perceived exertion increased (P < 0.001) towardexhaustion as the number of exercises progressed (7.1 ± 0.4, EX1; 8.0 ± 0.3, EX2; 8.5 ± 0.3, EX3; and 9.0 ± 0.4, EX4; scale from 0 to10). The present results indicate that human muscle fatigue during repeated intense isotonic exercise is not due to progressive depletion of high energy phosphates nor to intracellular accumulation of hydrogenions, total, mono-, or diprotonated Pi.

     

Training intensity-dependent and tissue-specific increases in lactate uptake and MCT-1 in heart and muscle

We investigatedthe effects of 3 wk of moderate- (21 m/min, 8% grade) andhighintensity treadmill training (31 m/min, 15% grade) on1) monocarboxylate transporter 1 (MCT-1) content in rat hindlimb muscles and the heart and2) lactate uptake in isolated soleus(Sol) muscles and perfused hearts. In the moderately trained groupMCT-1 was not increased in any of the muscles [Sol, extensor digitorum longus (EDL), and red (RG) and white gastrocnemius(WG)] (P > 0.05). Similarly,lactate uptake in Sol strips was also not increased(P > 0.05). In contrast, in theheart, MCT-1 (+36%, P < 0.05) andlactate uptake (+72%, P < 0.05)were increased with moderate training. In the highly trained group,MCT-1 (+70%, P < 0.05) and lactateuptake (+79%, P < 0.05) wereincreased in Sol. MCT-1 was also increased in RG (+94%,P < 0.05) but not in WG and EDL(P > 0.05). In the highly trainedgroup, heart MCT-1 (+44%, P < 0.05)and lactate uptake (+173%, P < 0.05) were increased. In conclusion, it has been shown that1) in both heart and skeletal musclelactate uptake is increased only when MCT-1 is increased; 2) training-induced increases inMCT-1 occurred at a lower training intensity in the heart than inskeletal muscle; 3) in the heart, lactate uptake was increased much more after high-intensity training than after moderate-intensity training, despite similar increases inheart MCT-1 with these two training intensities; and4) the increases in MCT-1 occurredindependently of any changes in the heart's oxidative capacity (asmeasured by citrate synthase activity).

     

Thermal and metabolic responses to cold-water immersion at knee, hip, and shoulder levels

Lee, Dae T., Michael M. Toner, William D. McArdle, IoannisS. Vrabas, and Kent B. Pandolf. Thermal and metabolic responses tocold-water immersion at knee, hip, and shoulder levels.J. Appl. Physiol. 82(5):1523-1530, 1997.To examine the effect of cold-water immersion atdifferent depths on thermal and metabolic responses, eight men (25 yrold, 16% body fat) attempted 12 tests: immersed to the knee (K), hip(H), and shoulder (Sh) in 15 and 25°C water during both rest (R) orleg cycling [35% peak oxygen uptake; (E)] for up to 135 min. At 15°C, rectal (T_re)and esophageal temperatures(T_es) between R and E were notdifferent in Sh and H groups (P > 0.05), whereas both in K group were higher during E than R(P < 0.05). At 25°C,T_re was higher(P < 0.05) during E than R at alldepths, whereas T_es during E washigher than during R in H and K groups.T_re remained at control levels inK-E at 15°C, K-E at 25°C, and in H-E groups at 25°C,whereas T_es remained unchanged inK-E at 15°C, in K-R at 15°C, and in all 25°C conditions (P > 0.05). During R and E, themagnitude of T_re change wasgreater (P < 0.05) than themagnitude of T_es change in Sh andH groups, whereas it was not different in the K group(P > 0.05). Total heat flow wasprogressive with water depth. During R at 15 and 25°C, heatproduction was not increased in K and H groups from control level(P > 0.05) but it did increase in Shgroup (P < 0.05). The increase inheat production during E compared with R was smaller(P < 0.05) in Sh (121 ± 7 W/m² at 15°C and 97 ± 6 W/m² at 25°C) than in H (156 ± 6 and 126 ± 5 W/m²,respectively) and K groups (155 ± 4 and 165 ± 6 W/m², respectively). These datasuggest that T_re andT_es respond differently duringpartial cold-water immersion. In addition, water levels above knee in15°C and above hip in 25°C cause depression of internal temperatures mainly due to insufficient heat production offsetting heatloss even during light exercise.

     

Changes in leg vein filling and emptying characteristics and leg volumes during long-term head-down bed rest

Louisy, Francis, Philippe Schroiff, and Antonio Güell.Changes in leg vein filling and emptying characteristics and legvolumes during long-term head-down bed rest. J. Appl.Physiol. 82(6): 1726-1733, 1997.Leg venoushemodynamics [venous distensibility index (VDI), arterial flowindex (AFI), half-emptying time(T_1/2)], and leg volumes(LV) were assessed by mercury strain-gauge plethysmography with venousocclusion and volometry, respectively, in seven men before, during, andafter 42 days of 6° head-down bed rest. Results showed a highincrease in VDI up to day 26 of bedrest (+50% vs. control at day 26,P < 0.05), which tended to subsidethereafter (+20% increase vs. control value at day41, P < 0.05). VDIchanges were associated with parallel changes inT_1/2 (+54% vs. control atday 26 of bed rest,P < 0.05, and +25% vs.control at day 41, P < 0.05) and with a decrease in AFI(49% at day 41 vs. control, P < 0.05). LV continuously decreasedthroughout bed rest (13% vs. control at day41, P < 0.05) but was correlated with VDI only during the first month ofbed rest. These results show that during long-term 6° head-down bedrest alterations of leg venous compliance are associated withimpairment of venous emptying capacities and arterial flow. Changes inskeletal muscle mass and fluid shifts may account for venous changesduring the first month of bed rest but, subsequently, otherphysiological factors, to be determined, may also be involved in legvenous hemodynamic alterations.

     

Thermoregulatory reflexes and cutaneous active vasodilation during heat stress in hypertensive humans

During dynamic exercise in the heat, increasesin skin blood flow are attenuated in hypertensive subjects whencompared with normotensive subjects. We studied responses to passiveheat stress (water-perfused suits) in eight hypertensive and eightnormotensive subjects. Forearm blood flow was measured byvenous-occlusion plethysmography, mean arterial pressure (MAP) wasmeasured by Finapres, and forearm vascular conductance (FVC) wascalculated. Bretylium tosylate (BT) iontophoresis was used to blockactive vasoconstriction in a small area of skin. Skin blood flow was indexed by laser-Doppler flowmetry at BT-treated and untreated sites,and cutaneous vascular conductance was calculated. In normothermia, FVCwas lower in hypertensive than in normotensive subjects(P < 0.01). During heat stress, FVCrose to similar levels in both groups(P > 0.80); concurrent cutaneousvascular conductance increases were unaffected by BT treatment(P > 0.60). MAP was greater in hypertensive than in normotensive subjects during normothermia (P < 0.05, hypertensive vs.normotensive subjects). During hyperthermia, MAP fell in hypertensivesubjects but showed no statistically significant change in normotensivesubjects (P < 0.05, hypertensive vs.normotensive subjects). The internal temperature at which vasodilationbegan did not differ between groups (P > 0.80). FVC is reduced during normothermia in unmedicatedhypertensive subjects; however, they respond to passive heat stress ina fashion no different from normotensive subjects.

     

Caffeine ingestion and metabolic responses of tetraplegic humans during electrical cycling

Normally, caffeineingestion results in a wide spectrum of neural and hormonal responses,making it difficult to evaluate which are critical regulatory factors.We examined the responses to caffeine (6 mg/kg) ingestion in a group ofspinal cord-injured subjects [7 tetraplegic(C_5-7) and 2 paraplegic(T₄) subjects] at rest andduring functional electrical stimulation of their paralyzed limbs tothe point of fatigue. Plasma insulin did not change, caffeine had noeffect on plasma epinephrine, and there was a slight increase(P < 0.05) in norepinephrine after15 min of exercise. Nevertheless, serum free fatty acids were increased (P < 0.05) after caffeine ingestionafter 60 min of rest and throughout the first 15 min of exercise, butthe respiratory exchange ratio was not affected. The exercise time wasincreased (P < 0.05) by 6% or 1.26 ± 0.57 min. These data suggest that caffeine had direct effects onboth the adipose tissue and the active muscle. It is proposed that theergogenic action of caffeine is occurring, at least in part, by adirect action of the drug on muscle.

     

Effects of resistance training and chromium picolinate on body composition and skeletal muscle in older men

The effects of chromium picolinate (CrPic)supplementation and resistance training (RT) on skeletal muscle size,strength, and power and whole body composition were examined in 18 men(age range 56-69 yr). The men were randomly assigned(double-blind) to groups (n = 9) thatconsumed either 17.8 µmol Cr/day (924 µg Cr/day) as CrPic or alow-Cr placebo for 12 wk while participating twice weekly in ahigh-intensity RT program. CrPic increased urinary Cr excretion~50-fold (P < 0.001). RT-inducedincreases in muscle strength (P < 0.001) were not enhanced by CrPic. Arm-pull muscle power increased withRT at 20% (P = 0.016) but not at 40, 60, or 80% of the one repetition maximum, independent of CrPic.Knee-extension muscle power increased with RT at 20, 40, and 60%(P < 0.001) but not at 80% of onerepetition maximum, and the placebo group gained more muscle power thandid the CrPic group (RT by supplemental interaction,P < 0.05). Fat-free mass(P < 0.001), whole body muscle mass(P < 0.001), and vastus lateralistype II fiber area (P < 0.05)increased with RT in these body-weight-stable men, independent ofCrPic. In conclusion, high-dose CrPic supplementation did not enhancemuscle size, strength, or power development or lean body mass accretionin older men during a RT program, which had significant, independenteffects on these measurements.

     

Age-dependent response of the electrocardiogram to K(+) channel blockers in mice

Developmental changes in electrocardiogram (ECG) andresponse to selective K⁺ channelblockers were assessed in conscious, unsedated neonatal (days 1, 7, 14) and adult male mice(>60 days of age). Mean sinus R-R interval decreased from 120 ± 3 ms in day 1 to 110 ± 3 ms inday 7, 97 ± 3 ms inday 14, and 81 ± 1 ms in adultmice (P < 0.001 by ANOVA; all 3 groups different from day 1). Inparallel, the mean P-R interval progressively decreased duringdevelopment. Similarly, the mean Q-T interval decreased from 62 ± 2 ms in day 1 to 50 ± 2 ms inday 7, 47 ± 8 ms inday 14 neonatal mice, and 46 ± 2 ms in adult mice (P < 0.001 byANOVA; all 3 groups are significantly different fromday 1).Q-T_c was calculated asQ- interval.Q-T_c significantly shortened from179 ± 4 ms in day 1 to 149 ± 5 ms in day 7 mice(P < 0.001). In addition, the J junction-S-T segment elevation observed in day1 neonatal mice resolved by day14. Dofetilide (0.5 mg/kg), the selective blocker ofthe rapid component of the delayed rectifier(I_Kr) abolished S-T segment elevation and prolonged Q-T andQ-T_c intervals in day 1 neonates but not in adult mice.In contrast, 4-aminopyridine (4-AP, 2.5 mg/kg) had no effect onday 1 neonates but in adults prolongedQ-T and Q-T_c intervals andspecifically decreased the amplitude of a transiently repolarizingwave, which appears as an r' wave at the end of the apparent QRSin adult mice. In conclusion, ECG intervals and configuration changeduring normal postnatal development in the mouse.K⁺ channel blockers affect themouse ECG differently depending on age. These data are consistent withthe previous findings that the dofetilide-sensitiveI_Kr is dominantin day 1 mice, whereas 4-AP-sensitivecurrents, the transiently repolarizingK⁺ current, and the rapidlyactivating, slowly inactivating K⁺current are the dominant K⁺currents in adult mice. This study provides background information useful for assessing abnormal development in transgenic mice.

     

Task failure with lack of diaphragm fatigue during inspiratory resistive loading in human subjects

McKenzie, D. K., G. M. Allen, J. E. Butler, and S. C. Gandevia. Task failure with lack of diaphragm fatigue during inspiratory resistive loading in human subjects. J. Appl. Physiol. 82(6): 2011-2019, 1997.Taskfailure during inspiratory resistive loading is thought to beaccompanied by substantial peripheral fatigue of the inspiratorymuscles. Six healthy subjects performed eight resistive breathingtrials with loads of 35, 50, 75 and 90% of maximal inspiratorypressure (MIP) with and without supplemental oxygen. MIP measuredbefore, after, and at every minute during the trial increased slightlyduring the trials, even when corrected for lung volume (e.g., for 24 trials breathing air, 12.5% increase, P < 0.05). In some trials, taskfailure occurred before 20 min (end point of trial), and in thesetrials there was an increase in end-tidalPCO₂(P < 0.01), despite the absence of peripheral muscle fatigue. In four subjects (6 trials with task failure), there was no decline in twitch amplitude with bilateral phrenic stimulation or in voluntary activation of the diaphragm, eventhough end-tidal PCO₂ rose by 1.6 ± 0.9%. These results suggest that hypoventilation,CO₂ retention, and ultimate taskfailure during resistive breathing are not simply dependent on impairedforce-generating capacity of the diaphragm or impaired voluntaryactivation of the diaphragm.

     

Aerosol probes of lung injury in a 28-wk longitudinal study of mild experimental emphysema in dogs

After baseline measurements of lung mechanics,effective air space diameter (EAD), and aerosol dispersion (AD), threedogs were exposed to two treatments of aerosolized papain (3 ml of a4% solution), and measurements were repeated during a 28-wk follow-upperiod. EAD and AD were measured with boluses of 0.7-µm particles ofdi-2-ethylhexl sebacate, with Pen (i.e., volumetric boluspenetration/total lung capacity) between 0.1 and 0.4. After papainexposure, EAD increased a mean of 28%(P < 0.0001) and AD (Pen = 0.3, 0.4)increased 4-7% (P < 0.03). Theprogression of injury was indicated by increasing trends in total lungcapacity (P < 0.05), residual volume(P < 0.05), and EAD(P = 0.06) through week 18. There was no evidence ofdisease progression between weeks 18 and 28, whereas some of the data forindividual dogs suggested partial recovery from lung injury atweek 28. The results show that aerosolprobes can detect and characterize mild lung injury in experimental emphysema.     

Prolonged exercise increases peripheral plasma ACTH, CRH, and AVP in male athletes

We wished to determine whether the increased ACTH duringprolonged exercise was associated with changes in peripheralcorticotropin-releasing hormone (CRH) and/or argininevasopressin (AVP). Six male triathletes were studied during exercise: 1 h at 70% maximal oxygen consumption, followed by progressivelyincreasing work rates until exhaustion. Data obtained during theexercise session were compared with a nonexercise control session.Venous blood was sampled over a 2-h period for cortisol, ACTH, CRH,AVP, renin, glucose, and plasma osmolality. There were significantincreases by ANOVA on log-transformed data in plasma cortisol(P = 0.002), ACTH(P < 0.001), CRH(P < 0.001), and AVP(P < 0.03) during exercise comparedwith the control day. A variable increase in AVP was observed after the period of high-intensity exercise. Plasma osmolality rose with exercise(P < 0.001) and was related toplasma AVP during submaximal exercise(P < 0.03) but not with theinclusion of data that followed the high-intensity exercise. Thisindicated an additional stimulus to the secretion of AVP. The mechanismby which ACTH secretion occurs during exercise involves both CRH andAVP. We hypothesize that high-intensity exercise favors AVP release andthat prolonged duration favors CRH release.

     

Resistance exercise training reduces hypertriglyceridemia in HIV-infected men treated with antiviral therapy

Hypertriglyceridemia, peripheral insulin resistance,and trunk adiposity are metabolic complications recently recognized in people infected with human immunodeficiency virus (HIV) and treated with highly active antiretroviral therapy (HAART). These complications may respond favorably to exercise training. Using a paired design, wedetermined whether 16 wk of weight-lifting exercise increased musclemass and strength and decreased fasting serum triglycerides and adiposetissue mass in 18 HIV-infected men. The resistance exercise regimenconsisted of three upper and four lower body exercises done for1-1.5 h/day, 4 days/wk for 64 sessions. Dual-energy X-rayabsorptiometry indicated that exercise training increased whole bodylean mass 1.4 kg (P = 0.005) but did not reduce adipose tissue mass (P = NS). Axial proton-magnetic resonanceimaging indicated that thigh muscle cross-sectional area increased5-7 cm² (P < 0.005). Muscle strengthincreased 23-38% (P < 0.0001) on all exercises.Fasting serum triglycerides were decreased at the end of training(281-204 mg/dl; P = 0.02). These findings imply that resistance exercise training-induced muscle hypertrophy may promote triglyceride clearance from the circulation ofhypertriglyceridemic HIV-infected men treated with antiviral therapy.

     

Preventive effects of supplemental dietary zinc on heat-induced damage in the epididymis of boars

Hyperthermia in boars reduces growth performance and sperm production. Zinc is an essential trace element in animal nutrition. Here we investigate the effects of dietary zinc on epididymal structure and function in Bama miniature pigs treated with heat exposure and investigate approaches to improve the reproductive performance in summer. Male Bama miniature pigs (n=18; aged 6 months; bodyweight=10.79±0.06 kg) were randomly allocated to 3 groups: control group (Control), heat treatment group (HT), and the diet-supplemented and heat treatment group (H+Zn). The Control and HT groups were fed with basal diet and the H+Zn group were fed with basal diet plus 1500 mg/kg zinc daily. After being fed with these 2 different diets for 30 days, pigs in the HT and H+Zn groups were exposed to 5 h of 40 °C heat treatment for 8 days. Rectal temperature and jugular venous blood were collected 3 h after onset of heat exposure on days 1, 4 and 8. Pigs were sacrificed after the termination of heat exposure. Heat treatment increased serum testosterone concentration on day 1 and 4 (P<0.01). In addition, the HT group displayed an increase in the clear cell count and a decrease in epithelium thickness in the caput epithelium (P<0.01, P<0.05), and dietary zinc protected the boars from these impairments (P<0.01, P=0.29). Evaluation of oxidative states showed that heat exposure increased the levels of malondialdehyde (MDA) and glutathione (GSH) in the epididymis (P<0.01, P<0.05), while dietary zinc reduced this elevation (P<0.01, P<0.01). Heat exposure enhanced the glucocorticoid receptor (GR) expression in the nuclei of principal and basal cells (P<0.01, P<0.01) while dietary zinc attenuated the GR immunoreactivity intensity (P<0.01, P<0.01). These results demonstrate that dietary zinc protects the epididymis from high temperature-induced impairment, alleviates oxidative stress, restores the integrity of the caput epithelium and decreases the stress response.     

Thermoregulatory responses to cold transients: effects of menstrual cycle in resting women

Effects of themenstrual cycle on heat loss and heat production(M) and core and skin temperatureresponses to cold were studied in six unacclimatized female nonsmokers(18-29 yr of age). Each woman, resting supine, was exposed to acold transient (ambient temperature = mean radiant temperature = 20 to5°C at 0.32°C/min, relative humidity = 50 ± 2%, wind speed = 1 m/s) in the follicular (F) phase(days 2-6) and midluteal (L)phase (days 19-23) of her menstrual cycle. Clothed in each of two ensembles with different thermal resistances, women performed multiple experiments in the F andL phases. Thermal resistance was 0.2 and 0.4 m² · K · W¹for ensembles A andB, respectively. Esophagealtemperature (T_es), mean weightedskin temperature(_sk),finger temperature (T_fing), andarea-weighted heat flux were recorded continuously. Rate of heat debt(S) and integrated mean bodytemperature(_b,i)were calculated by partitional calorimetry throughout the cold ramp. Extensive peripheral vasoconstriction in the F phase during early periods of the ramp elevated T_esabove thermoneutral levels. Shivering thermogenesis(M = M  M_basal,W /m²) was highly correlated withdeclines in_sk andT_fing(P <0.0001). There was a reducedslope in M as a function of_b,i inthe L phase with ensembles A(P < 0.02) andB (P < 0.01). Heat flux was higher andS was less in the L phases withensemble A(P < 0.05). An analytic modelrevealed that_sk andT_es contribute as additive inputsand T_fing has a multiplicativeeffect on the total control of Mduring cold transients(R² = 0.9).Endogenous hormonal levels at each menstrual cycle phase, coretemperature and_skinputs, vascular responses, and variations in body heat balance must beconsidered in quantifying thermoregulatory responses in women duringcold stress.