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Biomedical subjects

P Cerretelli

Publications and source records attributed to P Cerretelli.

At least 55 records · Page 3Linked to original sources
PubMed1994

Bioenergetic approach to transfer function of human skeletal muscle.

A mathematical model analogous to Chance's "transfer function" was derived on the basis of the energy consumption principle, which is suitable to describe the energetics of human skeletal muscle during aerobic activity. The implications and the characteristics of this model are that 1) the half time of phosphocreatine (PCr) hydrolysis at the onset of a mechanical constant-load exercise is independent of the imposed charge, 2) the changes of O2 consumption in the muscle at steady state when changing workload are linearly related to PCr concentration, 3) the kinetics of the intracellular oxygen consumption during a rest-to-work transient are influenced by anaerobic glycolysis, 4) it may explain the PCr-time relationship of different muscles types (e.g., skeletal, heart, trained vs. untrained), 5) it allows one to interpret correctly the significance of the oxygen consumption kinetics in the rest-to-work transient at the lung level, and 6) it is conceived for in vivo applications.

Adenosine Diphosphate↗
PubMed1994

Adjustment of cardiac output to step exercise in heart transplant recipients.

The maximal rate of O2 uptake (max VO2) during constant-load exercise is markedly reduced (about 30-50%) in heart transplant recipients (HTX) compared to peak aerobic performance of healthy sedentary controls (CTL). In order to evaluate the role of central and peripheral factors for O2 transport and utilization, breath-by-breath measurements of oxygen consumption (VO2) carbon dioxide output (VCO2), and beat-by-beat determination of cardiac output (Q) by transthoracic impedance cardiography were performed during upright submaximal square-wave cycloergometric exercise (50 W, 5 min) in a group of 21 HTX (age: 44 +/- 8 years; 23 +/- 29 months after transplantation, range 1.3-137 months) and 10 CTL (age: 37 +/- 10 years). The steady-state values (+/- SD) at 50 W for HTX and CTL, respectively, were: (VO2) 1.01 L/min +/- 0.10 and 0.98 L/min +/- 0.05 (NS); (VCO2) 1.07 L/min +/- 0.14 and 0.84 L/min +/- 0.06 (P < 0.01); (Q) 15.6 L/min +/- 5.3 and 12.8 L/min +/- 3.6 (NS). Heart rate (HR) in HTX, after an initial 60-90 s delay, increased linearly with time of exercise up to 122/min +/- 11. The half-time of the readjustment of Q at the onset of exercise was, in HTX and CTL respectively: 52 s +/- 16 and 40 s +/- 17 (NS). In spite of the time lag in the readjustment of HR, the Q on-response in HTX is only moderately delayed, indicating that the increase of stroke volume by augmented preload and the Frank-Starling mechanism at the onset of exercise compensates for the lack of autonomic control of the denervated allograft.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Biologic effects of prolonged exposure to ELF electromagnetic fields in rats. I. 50 Hz electric fields.

A three-year investigation was conducted on the biological effects of high-intensity electric field exposures of rats for up to 18% of their life span. Two hundred and forty adult male rats, divided into groups of 20 animals each, were exposed at ground potential for 8 h/day at 25-kV/m and 100-kV/m 50-Hz electric fields or were sham exposed for 280, 440, and 1240 h. The corresponding ages at sacrifice were 140, 164, and 315 days. An additional group of 40 rats was investigated under similar experimental conditions after 440 h of exposure at floating potential. Independent of exposure duration, mode of grounding, and field strength, no statistical differences in body weight, morphology, and histology of the liver, heart, mesenteric lymph nodes, and blood variables (hematology and serum chemistry) were found in comparison with sham-exposed animals. Plasma levels of luteinizing hormone (LH), follicle-stimulating hormone (FSH), and testosterone (TS) at sacrifice varied widely among experimental animals in the same group but did not differ in exposed compared with sham-exposed rats. A nonsignificant tendency toward a decrease in the testes/body weight ratio was found after 1240 h of exposure. Microscopic examination of a large number of specimens showed no quantitative or qualitative statistical differences in testes alterations either among exposed animals or between exposed and their corresponding sham-exposed groups. We conclude that 50-Hz electric field exposure, even of long duration at very high field strengths, does not induce harmful effects on tissues with high cellular turnover rates and does not impair the reproductive function of rats. Moreover, after exposure, all variables investigated were well within the normal physiological range.

Animals↗
PubMed1993

Ventilatory response to exercise after heart and lung denervation in humans.

This study, aimed at investigating some aspects of breathing control at work, was conducted on 8 heart and lung transplant recipients (HLTR) (age 33 +/- 13 years, mean +/- SD; 10 +/- 6 months post-transplantation) and on two control groups, i.e. 11 heart transplant recipients (HTR) and 11 healthy untrained subjects (C). The patients performed a series of 2 to 6 1-min exercise bouts (at 25 or 50 W, corresponding to about 50% of their VO2max) on a bicycle ergometer, followed by a 5 min 25 or 50 W constant load. C exercised both at 50 W (C1) and at 50% of their VO2max (C2). Inspiratory (VI) and expiratory (VE) ventilation, tidal volume (VT), respiratory frequency (fR), end-tidal O2 and CO2 partial pressures (PETO2 and PETCO2 and gas exchange (VO2 and VCO) were measured breath-by-breath. "Phase I" ventilatory response (ph I) was determined as the mean changes of VI, VE, VT, fR, PETO2 and PETCO2, compared to rest, during the first two respiratory cycles following exercise onset. In HLTR ph I did not significantly differ from that of C1 and C2, whereas the response was lower in HTR. VE, VO2 and VCO2 responses during "phase II" (t 1/2 on-) and "phase III" (steady state exercise) were similar in HLTR and in HTR. t 1/2 on- were longer in HLTR and in HTR compared to C1. In 3 HLTR the ventilatory pattern during the 5 min constant loads was similar to that of HTR and C, whereas 4 HLTR presented higher VT and lower fR values. It is concluded that: 1) The ventilatory response to exercise, in all its phases, is substantially preserved despite lung denervation. When slight alterations are found (i.e. the slower phase II), they are presumably of peripheral origin. 2) The normal ph I in HLTR indicates that cardiac and/or pulmonary inputs to the respiratory centers are not involved in its regulation, or that their role can be subserved by other ventilatory control mechanisms.

Adolescent↗
PubMed1993

Body composition and maximum alactic anaerobic performance during a one month stay at high altitude.

Prolonged altitude exposure usually leads to considerable weight loss of which a large part is from muscle tissue. This loss reduces maximum alactic anaerobic muscle power. It was hypothesized that most of the weight loss may simply be the result of malnutrition due to lack of palatable food in an uncomfortable environment. To test this hypothesis eight healthy male subjects (age 33.7 +/- 4.6 S.C. yr), well acclimatized to prevent symptoms of acute mountain sickness, were exposed for 4 weeks to an altitude of 5050 m with access to a large choice of palatable food in comfortable conditions. Body weight (with a scale), body composition (from skinfolds), arm muscle plus bone cross-sectional area (Am + b) and muscle plus bone leg volume (Vm+b) (from skinfolds and circumferences), maximum voluntary contraction force of the elbow flexors (MVC, with a load cell) and maximum jumping height (Hmax, on a platform) were measured before departure (SL) and in the first (ALT1), second (ALT2) and fourth week (ALT4) of their altitude sojourn. Three-day dietary records were obtained at SL and at ALT4. Body mass had decreased significantly at ALT2 (-3.8%) and at ALT4 (-4.6%) likely reflecting changes in body water homeostasis. No changes were found in %fat, Am+b, Vm+b, MVC or Hmax. Average dietary intake at SL was 8.96 +/- 1.45 MJ and had increased to 13.59 +/- 3.07 MJ at ALT4. In conclusion, up to an altitude of 5050 m loss of body mass from fat and muscle tissue, and hence impairment of maximum anaerobic muscle power (alactic) appears to be avoidable by food intake matched to energy expenditure. The latter may be achieved simply by proper acclimatization, sufficient comfort and availability of palatable food.

Adipose Tissue↗
PubMed1993

Maximal lactic capacity at altitude: effect of bicarbonate loading.

The aim of the present study was to test the hypothesis that the net maximal blood lactate accumulation ([La]max) during heavy exercise in lowlanders acclimatized to chronic hypoxia may be limited by the reduced bicarbonate stores. Six men [age 32 +/- 4 (SD) yr] performed supramaximal exercise until voluntary exhaustion at sea level (204 +/- 54 W) and after sojourning for 1 mo at 5,050 m (175 +/- 23 W), without (C) and with (B) oral sodium-bicarbonate loading (0.3 g/kg body wt). Exhaustion time, arterial blood lactate concentration, arterial pH (pHa), arterial PCO2, and intramuscular pH were measured at rest and after exercise. At sea level, exhaustion time increased from 6.5 +/- 2.8 min in C to 7.5 +/- 2.7 min in B (P < 0.05). At altitude, exhaustion times were similar to the sea level C values and the same in C and B. At sea level, resting pHa increased from 7.41 +/- 0.02 in C to 7.46 +/- 0.03 in B (P < 0.001); the corresponding values at altitude were 7.46 +/- 0.04 and 7.55 +/- 0.03 (P < 0.001). Postexercise pHa at sea level was 7.22 +/- 0.02 in C and 7.25 +/- 0.08 in B (NS). After exercise at altitude, pHa was 7.32 +/- 0.04 and 7.44 +/- 0.03 in C and B, respectively (P < 0.001). [La]max increased from 12.86 +/- 1.45 mM in C to 16.63 +/- 1.76 mM in B (P < 0.01) at sea level and from 6.85 +/- 1.40 mM in C to 7.95 +/- 1.74 mM in B (NS) at altitude.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗
PubMed1993

Human red blood cell aging at 5,050-m altitude: a role during adaptation to hypoxia.

To test the hypothesis that the human red blood cell aging process participates actively in the adaptation to hypoxia, we studied some physical and biochemical hematologic variables in 10 volunteers at sea level (SL) and after 1 (1WK) or 5 wk (5WK) of exposure to 5,050-m altitude. The 2,3-diphosphoglycerate-to-hemoglobin ratio (2,3-DPG/Hb) was 0.88 +/- 0.03 (mol/mol) at SL and increased to 1.08 +/- 0.03 (P = 0.002) and 1.28 +/- 0.05 (P < 0.0001) at 1WK and 5WK, respectively. The average red blood cell density (D50), which is inversely proportional to the fraction of young red blood cells and is therefore an index of the red blood cell aging process, was 1.1053 +/- 0.0007 g/ml at SL and decreased to 1.1046 +/- 0.0008 g/ml (NS) and 1.1018 +/- 0.0008 g/ml (P < 0.001) at 1WK and 5WK, respectively. D50 was correlated with 2,3-DPG/Hb at SL (P = 0.004), only weakly at 5WK (P = 0.1), but not at all at 1WK. The arterial O2 saturation was correlated with the change of 2,3-DPG/Hb in 1WK (P = 0.02) and that of D50 in 5WK (P = 0.04). It is concluded that short-term (1WK) increase of 2,3-DPG/Hb is not associated with the erythropoietic response but is presumably due to respiratory alkalosis. By contrast, after prolonged hypoxia (5WK), erythropoiesis may provide an efficient way for increasing blood 2,3-DPG through an augmented proportion of young red blood cells.

2,3-Diphosphoglycerate↗
PubMed1992

Effects of temperature on the maximal instantaneous muscle power of humans.

The maximal instantaneous muscle power (wi,max) probably reflects the maximal rate of adenosine 5'-triphosphate (ATP) hydrolysis (ATPmax), a temperature-dependent variable, which gives rise to the hypothesis that temperature, by affecting ATPmax, may also influence wi,max. This hypothesis was tested on six subjects, whose vastus lateralis muscle temperature (Tmuscle) was monitored by a thermocouple inserted approximately 3 cm below the skin surface. The Wi,max was determined during a series of high jumps off both feet on a force platform before and after immersion up to the abdomen for 90 min in a temperature controlled (T = 20 +/- 0.1 degrees C) water bath. Control Tmuscle was 35.8 +/- 0.7 degrees C, with control Wi,max being 51.6 (SD 8.7) W.kg-1. After cold exposure, Tmuscle decreased by about 8 degrees C, whereas wi,max 27% lower. The temperature dependence of Wi,max was found to be less (Q10 less than 1.5, where Q10 is the temperature coefficient as calculated in other studies) than reported in the literature for ATPmax. Such a low Q10 may reflect an increase in the mechanical equivalent of ATP splitting, as a consequence of the reduced velocity of muscle contraction occurring at low Tmuscle.

Adenosine Triphosphate↗
PubMed1992

Effects of muscle temperature on the VO2 kinetics at the onset of exercise in man.

The kinetics (i.e. the rate of readjustment) of O2 uptake (VO2) at the mouth of muscle blood flow in the vastus lateralis muscle (Qm), and the net accumulation of lactate in the rest-to-exercise transient (early lactate) were assessed in 6 untrained men (age 31 +/- 8 (SD) yrs) during constant-load 5-min duration exercises on the cyclo ergometer of 75 and 125 W, performed at muscle temperatures (Tm) of 35.5 +/- 0.9 degrees C (N) and of 28.0 +/- 1.65 degrees C (C). VO2 was measured breath-by-breath; Qm was assessed from 133Xe clearance; early lactate was calculated as the difference between the venous lactate concentrations observed after and before exercise. At both work loads, steady-state VO2 was slightly higher in N than in C (P less than 0.05 at 75 W; NS at 125 W). The half-times of VO2 kinetics were: in N, 36.2 +/- 6.7 s at 75 W and 41.6 +/- 8.6 s at 125 W; in C, 41.4 +/- 10.0 at 75 W and 43.8 +/- 14.0 at 125 W (NS). Mean steady state Qm was 8.5 ml.min-1.100 g-1 in C, and 13.4 in N at 75 W (NS); at 125 W, Qm was 18.3 ml.min-1.100 g-1 in C vs. 25.0 in N (NS). The half-times of the Qm kinetics tended to be slower in C than in N (NS). At both work loads, early lactate was slightly greater in C than in N (NS). It is concluded that, at submaximal exercise, (a) steady state VO2 and the VO2 kinetics are not affected by Tm, and (b) at the onset of exercise Qm does not affect VO2 kinetics.

Adult↗
PubMed1992

Energy sources for muscular exercise.

The basic energy yielding mechanisms of muscle contraction are reviewed and the main structural and functional features of human muscle are compared with those of some common athletic animal species. Sex and age related muscle power (alactic) characteristics are examined in both sedentary and athletic subjects. Recent measurements of the kinetics of contraction of the O2 debt by NMR spectroscopy by the human plantar flexors are shown. The main features of anaerobic (lactic) exercise in untrained and trained subjects, as a function of sex, age and environmental conditions (high altitude), are described with particular emphasis on the so-called lactic anaerobic threshold. With regard to aerobic exercise, the main determinants of O2 transport to the tissues are reviewed and an update of the factors limiting human performance is made. The possible causes of arterial O2 desaturation in athletes, both at sea level and at altitude, are discussed. A comparative analysis between man and woman of the progress of the records of some typical competitions is made and possible implications are discussed. The potential role of some commonly used physiological and/or paraphysiological procedures for improving the performance is analyzed.

Age Factors↗
PubMed1992

Metabolic transient studies by NMR.

The time course of phosphocreatine (PC) hydrolysis in humans was measured by 31P-NMR spectroscopy (31P-NMRS) with a time resolution of 10.8 s in the gastrocnemius muscle and a relationship between muscle O2 consumption (VO2) and [PC] was derived from a bioenergetic model. This allowed a direct estimate of the half-time of the intracellular VO2 kinetics (t1/2 VO2) of the contracting human gastrocnemius in aerobic conditions. t1/2 VO2 was found to be approximately 16 s and independent of the work load. This value corresponds to the shortest t1/2 VO2 determined at the mouth of the subject in the absence of lactate accumulation in the rest to work transient. t1/2 VO2 may now be assessed in man at low muscle temperatures. To this aim a procedure was developed allowing corrections of the 31P-NMR spectra based on the muscle temperature profiles obtained by a simultaneously acquired proton image.

Adenosine Triphosphate↗
PubMed1992

Muscle carnitine after strenuous endurance exercise.

The effect of very long endurance exercise on muscle carnitine was studied. Eighteen cross-country skiers took part in a race in the Alps (average inspired partial pressure of O2 100-110 Torr) that lasted on average 13 h 26 min. Carnitine intake, evaluated for 2 wk before the event, was 50 +/- 4 (SE) mg/day. Muscle (vastus lateralis) total carnitine concentration, measured twice with a 2-yr interval on eight rested subjects, did not change with time (17 vs. 16 mumol/g dry wt, NS) but showed consistent interindividual differences (range 12-22, P = 0.001) with no correlation with intake. After exercise, total muscle carnitine was unaltered (from 17.9 +/- 1.0 at rest to 18.3 +/- 0.8 mumol/g dry wt postexercise in the 15 subjects who completed the race, NS), but muscle free carnitine decreased 20% (from 14.9 +/- 0.8 mumol/g, P = 0.01) and short-chain acylcarnitine increased 108% (from 3.5 +/- 0.4 mumol/g, P = 0.01). These results suggest that carnitine deficiency will probably not result from strenuous aerobic exercise in trained subjects who consume a moderate amount of carnitine in their food.

Adult↗
PubMed1992

Phosphocreatine hydrolysis by 31P-NMR at the onset of constant-load exercise in humans.

The kinetics of phosphocreatine (PC) breakdown in human plantar flexors at the onset of constant-load aerobic exercise was determined by high-resolution 31P-nuclear magnetic resonance spectroscopy (NMRS). The half time of the process (t1/2PC) was obtained by fitting curves (n = 13) from five subjects at various aerobic work loads for which muscle pH was not different from that at rest. Steady-state PC concentration ([PC]) was not < 70% of the resting value and was linearly related to the work load (w) ([PC] = -3.01 +/- 0.08 w + 1 (r = 0.48, 2P < 0.1)). The average t1/2PC was 16.2 s and was independent of work load. Because the half time of the muscle PC kinetics reflects the half time of the O2 uptake (MO2) kinetics (t1/2MO2), the latter is equal to that found earlier in the isolated perfused dog gastrocnemius. Whereas in the dog the above t1/2MO2 compares well with the homologous half time of the O2 uptake at the alveolar level, in humans such equivalence is found only at extremely low work loads, when the transient contribution by anaerobic glycolysis is negligible.

Adult↗
PubMed1992

Protein absorption and energy digestibility at high altitude.

To test the hypothesis that malabsorption of dietary protein is partly responsible for the weight loss observed during prolonged altitude exposure, six healthy male subjects [31.8 +/- 4.5 (SD) yr] received 15N-labeled soya protein by mouth and [15N]glycine intravenously at 122 and 5,000 m. From the subsequent 4-day total urine and fecal pools, the different fractions of the administered 15N were determined by mass spectrometry. Weight and skinfold thickness were measured at the beginning and end of the altitude exposure. In addition, the overall digestible energy of the diet at altitude was assessed by a 3-day diet control and adiabatic bomb calorimetric assessment of the energy content of the corresponding fecal pool. The average decrease of the subjects' weight during altitude exposure was 3%. Loss of fat mass at altitude estimated from the skinfold measurements was 9%. Protein absorption, calculated as 100--[fecal excretion of 15N after ingestion of 15N soya protein (% of dose given)--fecal excretion of 15N after injection of 15N glycine (% of dose given)], was not significantly impaired at altitude compared with sea level (96 vs. 97%, respectively), and overall digestible energy at altitude, calculated as 100--percent undigested gross energy in the feces, amounted to 96%. It is concluded that, at least up to an altitude of 5,000 m, malabsorption does not play a role in altitude-related weight loss.

Adult↗
PubMed1992

Muscle energetics and ultrastructure in chronic hypoxia.

High-altitude exposure impairs both maximal aerobic and anaerobic (lactic and alactic) performances. The maximal aerobic power (VO2max) decreases exponentially with increasing altitude. At 5,350 m, a sudden rise in inspired O2 pressure (PIO2) was found to raise the VO2max of acclimatized lowlanders from 70 to only 92% of the control sea-level value. Since the hemoglobin concentration was about 35% higher than that of the controls, hemoglobin O2 saturation was restored to about 100%, and maximal cardiac output was only 10-20% lower than at sea level, the above result can only be the consequence: (1) of a reduced muscle mass and/or of muscle deterioration, and (2) of impaired muscle perfusion. In muscle biopsies taken from the vastus lateralis muscles of mountaineers after a 6- to 8-week sojourn at high altitude, a reduction in the fiber cross-sectional area was found which was accompanied by a decrease in the volume density of the mitochondria and by a lower tissue oxidative capacity. In acclimatized lowlanders, the maximal blood lactate concentration after exhausting exercise was halved compared to sea-level conditions. On the other hand, the peak anaerobic power was not affected by severe hypoxia within the first 3 weeks of exposure; thereafter, it decreased by about 25%, probably as a consequence of muscle deterioration. It is concluded that, whereas in acute hypoxia VO2max is primarily reduced by a lack of O2, in chronic hypoxia muscle deterioration may become an important factor contributing to the limitation of the maximal aerobic performance.

Acclimatization↗