Metabolic studies of human skeletal muscle by near infrared spectroscopy: possible applications in space research.
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Humans↗
Biomedical subjects
P Cerretelli
Publications and source records attributed to P Cerretelli.
Gas exchange and cardiovascular kinetics with different exercise protocols in heart transplant recipients.
Metabolic and cardiovascular adjustments to various submaximal exercises were evaluated in 82 heart transplant recipients (HTR) and in 35 control subjects (C). HTR were tested 21.5 +/- 25.3 (SD) mo (range 1.0-137.1 mo) posttransplantation. Three protocols were used: protocol A consisted of 5 min of rectangular 50-W load repeated twice, 5 min apart [5 min rest, 5 min 50 W (Ex 1), 5 min recovery, 5 min 50 W (Ex 2)]; protocol B consisted of 5 min of rectangular load at 25, 50, or 75 W; protocol C consisted of 15 min of rectangular load at 25 W. Breath-by-breath pulmonary ventilation (VE), O2 uptake (VO2), and CO2 output (VCO2) were determined. During protocol A, beat-by-beat cardiac output (Q) was estimated by impedance cardiography. The half times (t1/2) of the on- and off-kinetics of the variables were calculated. In all protocols, t1/2 values for VO2 on-, VE on-, and VCO2 on-kinetics were higher (i.e., the kinetics were slower) in HTR than in C, independently of workload and of the time post-transplantation. Also, t1/2 Q on- was higher in HTR than in C. In protocol A, no significant difference of t1/2 VO2 on- was observed in HTR between Ex 1 (48 +/- 9 s) and Ex 2 (46 +/- 8 s), whereas t1/2 Q on- was higher during Ex 1 (55 +/- 24 s) than during Ex 2 (47 +/- 15 s). In all protocols and for all variables, the t1/2 off-values were higher in HTR than in C, In protocol C, no differences of steady-state VE, VO2, and VCO2 were observed in both groups between 5, 10, and 15 min of exercise. We conclude that 1) in HTR, a "priming" exercise, while effective in speeding up the adjustment of convective O2 flow to muscle fibers during a second on-transition, did not affect the VO2 on-kinetics, suggesting that the slower VO2 on- in HTR was attributable to peripheral (muscular) factors; 2) the dissociation between Q on- and VO2 on-kinetics in HTR indicates that an inertia of muscle metabolic machinery is the main factor dictating the VO2 on-kinetics; and 3) the VO2 off-kinetics was slower in HTR than in C, indicating a greater alactic O2 deficit in HTR and, therefore, a sluggish muscle VO2 adjustment.
Adolescent↗
Cardiovascular changes during deep breath-hold dives in a pressure chamber.
Electrocardiogram, cardiac output, and blood lactate accumulation were recorded in three elite breath-hold divers diving to 40-55 m in a pressure chamber in thermoneutral (35 degrees C) or cool (25 degrees C) water. In two of the divers, invasive recordings of arterial blood pressure were also obtained during dives to 50 m in cool water. Bradycardia during the dives was more pronounced and developed more rapidly in the cool water, with heart rates dropping to 20-30 beats/min. Arrhythmias occurred, particularly during the dives in cool water, when they were often more frequent than sinus beats. Because of bradycardia, cardiac output decreased during the dives, especially in cool water (to <3 l/min in 2 of the divers). Arterial blood pressure increased dramatically, reaching values as high as 280/200 and 290/150 mmHg in the two divers, respectively. This hypertension was secondary to peripheral vasoconstriction, which also led to anaerobic metabolism, reflected in increased blood lactate concentration. The diving response of these divers resembles the one described for diving animals, although the presence of arrhythmias and large increases in blood pressure indicate a less perfect adaptation in humans.
Adult↗
In vivo human gastrocnemius architecture with changing joint angle at rest and during graded isometric contraction.
1. Human gastrocnemius medialis architecture was analysed in vivo, by ultrasonography, as a function of joint angle at rest and during voluntary isometric contractions up to the maximum force (MCV). maximum force (MVC). 2. At rest, as ankle joint angle increased from 90 to 150 deg, pennation increased from 15.8 to 27.7 deg, fibre length decreased from 57.0 to 34.0 mm and the physiological cross-sectional area (PCSA) increased from 42.1 to 63.5 cm2. 3. From rest to MVC, at a fixed ankle joint angle of 110 deg, pennation angle increased from 15.5 to 33.6 deg and fibre length decreased from 50.8 to 32.9 mm, with no significant change in the distance between the aponeuroses. As a result of these changes the PCSA increased by 34.8%. 4. Measurements of pennation angle, fibre length and distance between the aponeuroses of the gastrocnemius medialis were also performed by ultrasound on a cadaver leg and found to be in good agreement with direct anatomical measurements. 5. It is concluded that human gastrocnemius medialis architecture is significantly affected both by changes of joint angle at rest and by isometric contraction intensity. The remarkable shortening observed during isometric contraction suggests that, at rest, the gastrocnemius muscle and tendon are considerably slack. The extrapolation of muscle architectural data obtained from cadavers to in vivo conditions should be made only for matching muscle lengths.
Adult↗
Human quadriceps cross-sectional area, torque and neural activation during 6 months strength training.
Quadriceps muscle and fibre cross-sectional areas (CSA), torque and neural activation were studied in seven healthy males during 6 months of weight training on alternate days with six series of eight unilateral leg extensions at 80% of one repetition maximum. After training, the quadriceps cross-sectional area increased by 18.8 +/- 7.2% (P < 0.001) and 19.3 +/- 6.7% (P < 0.001) in the distal and proximal regions respectively, and by 13.0 +/- 7.2% (P < 0.001) in the central region of the muscle. Hypertrophy was significantly different between and within the four constituents of the quadriceps. Biopsies of the vastus lateralis at mid-thigh did not show any increase in mean fibre cross-sectional area. Maximum isometric voluntary torque increased by 29.6 +/- 7.9%-21.1 +/- 8.6% (P < 0.01-0.05) between 100 degrees and 160 degrees of knee extension, but no change in the optimum angle (110 degrees-120 degrees) for torque generation was found. A 12.0 +/- 10.8% (P < 0.02) increase in torque per unit area together with a right shift in the IEMG-torque relation and no change in maximum IEMG were observed. Time to peak isometric torque decreased by 45.8% (P < 0.03) but no change in time to maximum IEMG was observed. In conclusion, strength training of the quadriceps results in a variable hypertrophy of its components without affecting its angle-torque relation. The increase in torque per unit area, in the absence of changes in IEMG, may indicate changes in muscle architecture. An increase in muscle-tendon stiffness may account for the decrease in time to peak torque.
Adult↗
Peak blood lactate and blood lactate vs. workload during acclimatization to 5,050 m and in deacclimatization.
Peak blood lactate ([Labl]peak) and blood lactate concentration ([Labl]) vs. workload (W) relationships during acclimatization to altitude and in the deacclimatization were evaluated in 10 Caucasian lowlanders at sea level (SL0); after approximately 1 wk (Alt1wk), 3 wk (Alt3wk), and 5 wk (Alt5wk) at 5,050 m; and weekly during the first 5 wk after return to sea level (SL1wk-SL5wk). Incremental bicycle ergometer exercises (30 W added every 4 min up to exhaustion) were performed. At Alt1wk and at Alt5wk, the experiments were repeated in hypobaric normoxia (Alt1wk-O2 and Alt5wk-O2). [Labl] was determined at rest and during the last approximately 30 s of each W. [Labl]peak was taken as the highest [Labl] during recovery. Acid-base status (pH and concentration of HCO-3 in arterialized capillary blood) was determined at rest. Mean [Labl]peak values were 11.5 (SL0), 8.0 (Alt1wk), 6.4 (Alt3wk), 6.3 (Alt5wk), 8.0 (SL1wk), 9.4 (SL2wk), 10.8 (SL3wk), 11.3 (SL4wk), and 11.6 (SL5wk) mM. At Alt1wk-O2 and Alt5wk-O2, peak W increased, compared with Alt1wk and Alt5wk, whereas no changes were observed for [Labl]peak. [Labl] vs. W was shifted to the left (i.e., higher [Labl] values were found for the same W) at Alt1wk compared with SL0 and partially shifted back to the right (i.e., lower [Labl] values were found for the same W) at Alt3wk and Alt5wk. At Alt1wk-O2 and Alt5wk-O2, [Labl] vs. W values were superimposed on that at SL0. At SL1wk-SL5wk, [Labl] vs. W values were shifted to the right compared with that at SL0. At Alt1wk, a condition of respiratory alkalosis was found, which was only partially compensated for during acclimatization. At SL1wk, the acid-base status was back to normal. We conclude that 1) the reduced [Labl]peak at altitude is still present for 2-3 wk after return from altitude; is not attributable to reduced peak W nor to hypoxia per se, nor to a reduced buffer capacity; alternatively, it could be related to some central determinants of fatigue. 2) The [Labl] vs. W leftward shift at altitude was due to hypoxia per se. 3) The factor(s) responsible for the [Labl] vs. W partial rightward shift during acclimatization could still be effective during the first weeks after return to sea level.
Acclimatization↗
Muscle ultrastructure and biochemistry of lowland Tibetans.
Muscle ultrastructure and biochemistry in vastus lateralis muscle biopsies and the response to exercise of 8 lowland Tibetans (T) were compared with those of 8 Nepalese lowlanders (N). Blood hemoglobin was lower in T than in N (119 +/- 3 vs. 131 +/- 2 g/l; P < 0.05). Peak O2 consumption per kilogram of body mass was similar [37.9 +/- 2.2 (T) vs. 40.1 +/- 1.36 ml.min-1.kg body mass-1 (N)]. Maximum exercise blood lactate was the same [11.4 (T) +/- 0.5 vs. 11.3 +/- 0.6 mM (N)]. Muscle fiber type distribution was similar [type I, 58.6 +/- 3.4 (N) vs. 57.0 +/- 3.4% (T); type IIa, 24.1 +/- 3.5 vs. 27.1 +/- 1.6%; type IIb, 17.4 +/- 1.4 vs. 15.9 +/- 2.9%]. T had smaller fiber cross-sectional areas [3,413 +/- 677 (T) vs. 3,895 +/- 447 microns 2 (N); P < 0.05] but had similar number of capillaries per muscle fiber [1.35 +/- 0.23 (T) vs. 1.46 +/- 0.08 (N)] and muscle fiber area supplied per capillary [399 +/- 29 (T) vs. 382 +/- 65 mm2 (N)]. Total mitochondrial volume density was much lower in T (3.99 +/- 0.17%) than in N (5.51 +/- 0.19%) (P < 0.025). Mirroring mitochondrial volume density, citrate synthase and 3-hydroxyacyl-CoA dehydrogenase activities were lower in T than in N (P < 0.05). The activities of L-lactate dehydrogenase and hexokinase were the same in both groups. T had significantly less muscle fiber lipid droplets than did N, which correlated with the low activity of 3-hydroxyacyl-CoA dehydrogenase (r = 0.57, P = 0.02). In conclusion, lowland-born T have a low mitochondrial volume-to-specific peak O2 consumption ratio, which, based on previous measurements on altitude-born Sherpas (B. Kayser, H. Hoppeler, H. Claassen and P. Cerretelli. J. Appl. Physiol. 70: 1938-1942, 1991), appears to be an inborn feature.
Adolescent↗
Biologic effects of prolonged exposure to ELF electromagnetic fields in rats: II. 50 Hz magnetic fields.
To provide possible laboratory support to health risk evaluation associated with long-term, low-intensity magnetic field exposure, 256 male albino rats and an equal number of control animals (initial age 12 weeks) were exposed 22 h/day to a 50 Hz magnetic flux density of 5 microT for 32 weeks (a total of about 5000 h). Hematology was studied from blood samples before exposure to the field and at 12 week intervals. Morphology and histology of liver, heart, mesenteric lymph nodes, and testes as well as brain neurotransmitters were assessed at the end of the exposure period. In two identical sets of experiments, no significant differences in the investigated variables were found between exposed and sham-exposed animals. It is concluded that continuous exposure to a 50 Hz magnetic field of 5 microT from week 12 to week 44, which makes up approximately 70% of the life span of the rat before sacrifice, does not cause changes in growth rate, in the morphology and histology of liver, heart, mesenteric lymph nodes, testes, and bone marrow, in hematology and hematochemistry, or in the neurotransmitters dopamine and serotonin.
Animals↗
The role of pulmonary CO2 flow in the control of the phase I ventilatory response to exercise in humans.
To gain an insight into the origin of the phase I ventilatory response to exercise (ph I) in humans, pulmonary ventilation (VE) and end-tidal partial pressures of oxygen and carbon dioxide (PETO2 and PETCO2, respectively) were measured breath-by-breath in six male subjects during constant-intensity exercise on the cycle ergometer at 50, 100 and 150 W, with eupnoeic normocapnia (N) or hyperpnoeic hypocapnia (H) established prior to the exercise test. Cardiac output (Qc) was also determined beat-by-beat by impedance cardiography on eight subjects during moderate exercise (50 W), and the CO2 flow to the lungs (Qc.Cv-CO2 where Cv-CO2 is concentration of CO2 in mixed veneous blood) was estimated with a time resolution of one breathing cycle. In N, the initial abrupt increase of VE during ph I (delta VE approximately 18 1.min-1 above rest) was followed by a transient fall. When PETCO2 started to increase (and PETO2 decreased) VE increased again (phase II ventilatory response, ph II). In H, during ph I delta VE was similar to that of N. By contrast, during ph II delta VE kept gradually decreasing and started to increase only when PETCO2 had returned to approximately 40 mmHg (5.3 kPa). Thus, as a result of the prevailing initial conditions (N or H) a temporal shift of the time-course of VE during ph II became apparent. No correlation was found between CO2 flow to the lungs and VE during ph I. These results are interpreted as suggesting that an increased CO2 flow to the lungs does not constitute an important factor for the initial hyperventilatory response to exercise. They are rather compatible with a neural origin of ph I, and would support the "neurohumoral" theory of ventilatory control during exercise.
Adult↗
Kinetics of oxygen consumption during maximal exercise at different muscle temperatures.
The aim of this study was to test at maximal exercise the hypothesis of the temperature-dependence of the kinetics of O2 consumption (VO2), which predicts a greater O2 deficit as muscle temperature is decreased. Six male subjects underwent 3 min exercise bouts at the minimum power eliciting maximum O2 consumption (VO2max), at normal temperature (A) and after cooling the thigh muscles by water immersion (C). Breath-by-breath VO2 was measured together with muscle blood flow (Qm), blood lactate accumulation ("early lactate", eLa), heart rate and muscle temperature (Tm). The O2 deficit was calculated by standard procedure. Net VO2max was 2.92 +/- 0.85 (SD) and 3.19 +/- 0.71 l center dot min-1 in C and A respectively (P < 0.05). Correspondingly, maximum power was 20 W lower in C than in A. At exercise start, Tm was 35.0 +/- 1.2 and 27.5 +/- 1.8 degrees C in A and C respectively. O2 deficit was 2.25 +/- 0.53 and 3.05 +/- 1.12 l in A and C respectively. The corresponding eLa was 7.7 +/- 2.5 and 13.8 +/- 2.5 mM, (P < 0.05) while Qm was 376 +/- 92 and 290 +/- 50 ml center dot kg-1 center dot min-1 (P < 0.05) in A and C, respectively. The eLa increase in C is associated with an impaired muscle blood flow and decreased muscle O2 unloading, and does not completely explain the greater O2 deficit in C. The unexplained fraction of the latter is perhaps accounted for by a greater net alactic O2 deficit, in agreement with a temperature-dependent decrease of the velocity constants of oxidative reactions, as suggested by the tested hypothesis.
Adult↗
Maximal rate of blood lactate accumulation during exercise at altitude in humans.
The lower peak lactate accumulation in blood ([La(b)]p) at altitude may be associated with a reduced maximal glycolytic flux. Based on certain assumptions, the latter can be indirectly evaluated in vivo, during short supramaximal exercises, by measuring the maximal rate of lactate accumulation in blood (delta [La(b)]max). delta [La(b)]max was determined on six white subjects at sea level (SL1), after approximately 1 wk (Alt1) and 4 wk (Alt2) of a 35-day sojourn at 5,050 m, and 1 wk after return to sea level (SL2). The subjects performed exercises of increasing duration (5, 15, 25, 35, 45 s or until exhaustion) on a bicycle ergometer at loads = 200% of the individual Wmax. The latter was previously determined in each condition as the greatest work rate that could be sustained for 2-4 min during an incremental exercise. Net [La(b)] accumulation (delta [La(b)]) was measured after each exercise bout. delta [La(b)] resulted to be linearly related to exercise duration. The slopes of the individual delta [La(b)] vs. exercise duration lines were taken as delta [La(b)]max. Exhaustion times were approximately 30-45 s in all conditions. [La(b)]p (in mM) during recovery after the exhaustive load was higher at SL1 (10.22 +/- 1.09; means +/- SD) than at Alt1 (5.08 +/- 0.82), Alt2 (8.13 +/- 2.67), and SL2 (8.18 +/- 1.43). delta [La(b)]max was lower at Alt1 (0.09 +/- 0.02) and at Alt2 (0.17 +/- 0.05) than at SL1 (0.25 +/- 0.05) and SL2 (0.23 +/- 0.06). Both [La(b)]p and delta [La(b)]max increased during acclimatization.(ABSTRACT TRUNCATED AT 250 WORDS)
Acclimatization↗
Autonomic nervous control of heart rate at altitude (5050 m).
To investigate possible changes in autonomic regulation of heart rate as a result of acclimatization to high altitude, indexes of autonomic nervous activity were obtained non invasively by spectrum analysis of heart rate variability on five healthy male subjects [age, 31 (SEM 2) years] during a postural change from supine to seated, both at sea level and after 1 month of exposure to an altitude of 5050 m. Heart rate fluctuations at the respiratory frequency (high frequency, HF) are mediated by the parasympathetic system whereas fluctuations at about 0.1 Hz (low frequency, LF) are due to both sympathetic and parasympathetic nervous systems. Maximal heart rate, as measured during an incremental exercise test, decreased from 184 (SEM 5) beats.min-1 at sea level to 152 (SEM 2) beats.min-1 at 5050 m. At sea level, the change in posture from supine to seated induced an increase in LF amplitude accompanied by an increase or a decrease in HF amplitude, whereas after 1 month at altitude the HF amplitude decreased in all subjects, with little or no change in LF amplitude. These results indicate a changed strategy of heart rate regulation after acclimatization to high altitude. At sea level, the postural change induced an increase in sympathetic activity in all subjects with different individual vagal responses, whereas at altitude the postural change induced a net decrease in vagal tone in all subjects, with little or no change in sympathetic activity. These results corroborate the reported reduced sensitivity of the heart to adrenergic drive in chronic hypoxia, which may, at least in part, explain the decreased maximal heart rate in altitude-acclimatized human subjects.
Acclimatization↗
Standardisation of 31phosphorus-nuclear magnetic resonance spectroscopy determinations of high energy phosphates in humans.
A procedure is described for standardising the determination of adenosine 5'-triphosphate and phosphocreatine concentration ([ATP] and [PC], respectively, in absolute arbitrary units) in human muscle by nuclear magnetic resonance (NMR) spectroscopy. The individual 31phosphorus (31P)-NMR spectra obtained on equal hemispherical tissue volumes (muscle plus skin and fat) were corrected for the thickness of the skin and of the subcutaneous fat. The volumes investigated were standardised using an external reference. The procedure described made possible the comparison of high energy phosphate concentrations among different subjects. It was applied to the assessment of [ATP] and [PC] in four groups of sedentary subjects (children, and adults aged 20-35, 35-50 and over 50 years), and in a group of athletes (volleyball players). The [ATP] and [PC] were not statistically different in the groups investigated.
Adenosine Triphosphate↗
Determinants of peak muscle power: effects of age and physical conditioning.
The relationships between absolute peak muscle power (Wpeak), muscle cross sectional area (CSAtot, i.e. the sum of both thigh and calf CSA) and muscle high energy phosphate concentration (adenosine 5'-triphosphate [ATP] and phosphocreatine concentrations [PC]) were studied in 47 subjects classified into five groups: A, 10 sedentary (S) subjects aged 20-35 years; B, 9 S aged 35-50 years; C, 9 S aged more than 50 years; D, 13 children aged 8-13 years; and E, 6 athletes (top level volleyball players) aged 24 (SD 3) years. The Wpeak was measured during a maximal vertical high jump off both feet on a force platform. The CSAtot was measured anthropometrically. The [ATP] and [PC] were determined by 31Phosphorus nuclear magnetic resonance spectroscopy. The Wpeak decreased with age, was 65% lower in D than in A, and 43% higher in E than in A. The CSAtot did not vary with age, was 45% smaller in D than in A, and 15% greater in E than in A. The [ATP] and [PC] were essentially the same in all groups. The changes observed in Wpeak were only partially accounted for by changes in CSAtot. Therefore, in addition to the variables investigated, other factors appear to have been involved in the determination of Wpeak with increasing age and training. An important role may be played by hormonal, particularly at puberty, and neural factors.
Adenosine Triphosphate↗
The metabolic and ventilatory response to exercise in Tibetans born at low altitude.
The exercise response of 20 Tibetans (T) born and living in Kathmandu, Nepal (1300 m) was compared to that of 21 age- and sex-matched local lowlanders. The subjects carried out an incremental exercise protocol on a bicycle ergometer (30 watt steps every 4 min) until exhaustion. The kinetics of readjustment of VO2 measured as half time (t-on) upon a 90 watt constant load exercise was also determined. Breath-by-breath gas exchange, heart rate (HR) and blood lactate concentration ([La]) were measured at rest, at the end of each load and during recovery. The slope of the straight line relating VO2 to work load was 10.8 ml.watt-1 in both groups which corresponds to a mechanical efficiency of 0.26 (assuming a RQ of 0.89 and an energy equivalent of 20.9 kJ.L-1 O2). At submaximal loads T were characterized by higher VE (P < 0.05), VE.VO2(-1) (P < 0.01) and VCO2 levels (P < 0.001) than N. The found higher VE in T, resulting from a lower tidal volume coupled to a higher respiratory frequency, led to higher PETO2 (P < 0.001) and SaO2 (P < 0.001) at all work levels. Absolute VO2max in the two investigated groups were 1977 +/- 72 (T) and 2095 +/- 80 (N) ml.min-1 (NS). Specific (i.e. per kg body weight) VO2max were identical (37.0 +/- 1.1 [T] vs. 36.7 +/- 1.1 ml.kg-1.min-1 [N]). [La]max were 11.4 +/- 0.4 (T) vs. 12.3 +/- 0.4 (N) mM (NS). [La] accumulation in blood as a function of workload and its rate of disappearance during recovery were similar. t-on at 90 watt was 30.7 +/- 2.4 sec in T and 28.9 +/- 2.3 sec in N (NS). The corresponding average contracted O2 deficit were 971 ml for T and 994 ml for N (NS). In conclusion, Tibetans born at low altitude do not seem to differ from lowlanders with regard to their metabolic response whereas their ventilatory response to exercise is greater.
Adolescent↗
Ventilatory responses to hypercapnia and hypoxia in elite breath-hold divers.
It was recently hypothesized that elite breath-hold divers may display blunted ventilatory responses to hypoxia and/or hypercapnia (Ferretti et al., J. Appl. Physiol. 70: 794-802, 1991). To test this hypothesis, the following measurements were made on three elite breath-hold divers (members of the same family), and on 9 healthy untrained control subjects (C): (1) Steady-state pulmonary ventilation (VE) at rest in the supine posture while breathing room air or normoxic CO2-enriched mixtures. (2) Breath-by-breath VE changes (delta VE), with respect to baseline conditions, after 4 breaths of 100% O2, under the following conditions: normoxia (PIO2 = 146 Torr) at rest (NR); normoxic exercise (60 watt on a bicycle ergometer) (NE); hypoxia (PIO2 = 77 Torr) at rest (HR); hypoxic exercise (HE). The results were as follows: (1) In hypercapnic experiments VE (normalized per unit of body surface area) was significantly lower in the divers than in C (4.32 +/- 0.04 [mean +/- SD]L.min-1.m-2 vs. 5.31 +/- 0.62 at FICO2 = 1.5%; 5.21 +/- 0.17 vs. 7.72 +/- 1.39 at FICO2 = 3%; 8.86 +/- 0.76 vs. 13.14 +/- 2.27 at FICO2 = 5%), as well as than in subjects described by previous authors as being characterized by 'low CO2 sensitivity'. (2) The 100% O2-breathing maneuvers did not induce significant delta VE both in NR and in HR, whereas peak delta VE were -6.73 +/- 1.38 L.min-1 (divers) vs. -5.24 +/- 3.10 (C) in NE, and -17.39 +/- 4.92 (divers) vs. -17.52 +/- 6.32 (C) in HE (no significant differences). It is concluded that the divers, compared to C, had a blunted ventilatory response to hypercapnia, but not to hypoxia. The former may represent an adaptive or genetically inherited phenomenon.
Adaptation, Physiological↗
Aspirin does not affect exercise performance.
A single-blind, cross-over study was carried out to evaluate the effects of acetylsalicylic acid (ASA) on cardiorespiratory performance during exercise. Eighteen young men, 9 athletes and 9 untrained but active subjects, performed a progressive maximal exercise test on a cycle ergometer (30 watt, 3 min steps, starting at 60 watt) on three different occasions, after a single administration of plain aspirin (1000mg of ASA), chewable buffered aspirin (1000mg of ASA and 600 mg of calcium carbonate) and placebo. Continuous measurement of breath-by-breath ventilation, oxygen consumption, carbon dioxide output, respiratory frequency and heart rate was carried-out at rest and during the exercise test. Blood lactate concentration was measured just before the start of exercise and at the third minute of each step in order to detect the anaerobic threshold. The pharmacokinetics of aspirin during exercise was also investigated in ten of the eighteen participants. The analysis of all investigated variables did not show any statistically significant difference between treatments, suggesting that a single dose of 1000mg of aspirin does not affect physical performance during submaximal and maximal exercise.
Adolescent↗
Fatigue and exhaustion in chronic hypobaric hypoxia: influence of exercising muscle mass.
Exhaustive dynamic exercise with large muscle groups in chronic hypobaric hypoxia may be limited by central (nervous) rather than peripheral (metabolic) fatigue. Six males [32 +/- 4 (SD) yr] at sea level (SL) and after 1-mo acclimatization at 5,050 m (HA) performed exhaustive dynamic forearm exercise at a constant absolute load, requiring regional maximum aerobic power at SL, and exhaustive cycle exercise at prevailing maximal O2 uptake (HA approximately equal to 80% SL). Exhaustion time (t(ex)), blood O2 saturation (SaO2), and heart rate (HR) were measured during each exercise bout. Before and after both arm and leg exercise, lactate concentration ([La]), PO2, PCO2, and pH were measured in arterialized blood samples. Integrated electromyogram activity (IEMG) and mean (MPF) and centroid (CPF) power frequencies of the EMG power spectrum during exercise were calculated for forearm flexors and vastus lateralis muscle. t(ex) for forearm exercise at the same absolute load was the same at SL and HA. Similar increases of IEMG (+214% at SL vs. +172% at HA) and decreases of CPF (-13% at SL vs. -16% at HA) and MPF (-22% at SL vs. -21% at HA) were observed. By contrast, at HA, for similar t(ex), leg exercise had to be performed at the same relative (i.e., prevailing maximal O2 uptake) but lower absolute load (approximately equal to 80% of SL).(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗