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Biomedical subjects

C Marconi

Publications and source records attributed to C Marconi.

At least 19 recordsLinked to original sources
PubMed2005

Handgrip impairment in Charcot-Marie-Tooth disease.

AIM: Charcot-Marie-Tooth disease (CMT) is a genetic neuropathy causing muscle weakening in the feet, legs and hands, with consequent impairment of ambulation and handgrip. For fast clinical evaluation and rehabilitation management of handgrip deficits, a functional classification in 4 stages or levels of clinical severity, based on the loss of handgrip types from the finest to the roughest, has been recently proposed. The aim of this study is to evaluate the prevalence of each level of handgrip impairment in a wide population of patients affected with demyelinating and axonal CMT. METHODS: Two-hundred and forty-eight non-operated hands were examined to evaluate if and how the pinch between the pulp of the thumb and the pulp of the second or third finger was made, starting from the palm-up position with the fingers abducted or, in case of impossibility to do so, if a lateral pinch or only a grasp was possible. Following to this observation, each hand was fitted in 1 of the 4 stages described in the above-mentioned classification and then the frequency of each stage was determined. RESULTS: As a whole, 75.4% hands were at stage 1; 9.7 were at stage 2; 10.9% at stage 3; 4% at stage 4. CONCLUSIONS: The results of this survey reveal that, in the majority of the CMT cases, handgrip is affected mildly so that only simple recommendations to prevent further muscle and joint damage are required; however, in more than 1 out 5 cases, the handrip impairment is quite severe and requires a detailed rehabilitative program with daily exercises, and, in a small number of cases, is so severe that independence in the daily living activities is lost or very reduced.

Adolescent↗
PubMed2001

Power and peak blood lactate at 5050 m with 10 and 30 s 'all out' cycling.

Anecdotal observations suggest that the reduction in peak lactate accumulation in blood ([La]b peak) after exhausting exercise, in chronic hypoxia vs. normoxia, may be related to the duration of the exercise protocol, being less pronounced after short supramaximal exercise than after incremental exercise (IE) lasting several minutes. To test this hypothesis, six healthy male Caucasians (age 36.8 +/- 7.3, X +/- SD) underwent three exercise protocols on a cycle ergometer, at sea level (SL) and after 21 +/- 10 days at 5050 m altitude (ALT): (1) 10 s, (2) 30 s 'all out' exercise and (3) IE leading to exhaustion in approximately 20-25 min. 'Average' power output (P) was calculated for 10 or 30 s 'all out'; maximal power output (Pmax) was determined for IE. Lactate concentration in arterialized capillary blood ([La]b) was measured at rest and at different times during recovery; the highest [La]b during recovery was taken as [La]b peak. No significant differences in P were observed between SL and ALT, for either 10 or 30 s 'all out' exercise; Pmax during IE was significantly lower at ALT than at SL. [La]b peak after 10 s 'all out' was unaffected by chronic hypoxia (7.0 +/- 0.9 at ALT vs. 6.3 +/- 1.8 mmol x L(-1) at SL). After 30 s 'all out' the [La]b peak decrease, at ALT (10.6 +/- 0.6 mmol x L(-1)) vs. SL (12.9 +/- 1.4 mmol x L(-1)), was only approximately 50% of that observed for IE (6.7 +/- 1.6 mmol x L(-1) vs. 11.3 +/- 2.8 mmol x L(-1)). Muscle power output and blood lactate accumulation during short supramaximal exercise are substantially unaffected by chronic hypoxia.

Adult↗
PubMed2000

Pathophysiology of cardiac transplantation and the challenge of exercise.

Heart transplantation is now currently performed in adult (A-HTR) as well as in pediatric cardiac patients (P-HTR). In A-HTR, heart denervation results in a delayed, blunted heart rate (HR) response to exercise onset, mainly sustained by the level of circulating catecholamines. At the offset of exercise HR resumes the pre-exercise level in 5-25 min, depending on the absolute work intensity. Peak HR is approximately 140 beats/min. Maximal aerobic power is 19 O2/kg x min, i.e., approximately 60% than that of healthy age-matched sedentary subjects and exercise tolerance is therefore reduced. A functional impairment at the muscle level may also be present, as suggested by the slow kinetics of the VO2 readjustment (phase II) at the onset of submaximal aerobic exercise. P-HTR generally behave as A-HTR. However, recently, in a few P-HTR a fast HR response to exercise and greater peak HR values (172 +/- 22 beats/min) were demonstrated. Maximal aerobic power of P-HTR was 32 +/- 7 ml O2/kg x min, greater than that of A-HTR, but yet approximately 60% of that of healthy age-matched controls. It may be concluded that occasionally P-HTR may resume an almost normal cardiovascular response to exercise; nevertheless, their exercise tolerance is limited, likely by functional impairment at the muscle level, whose origin is still unknown.

Child↗
PubMed1999

Blood lactate accumulation and muscle deoxygenation during incremental exercise.

Near-infrared spectroscopy (NIRS) could allow insights into controversial issues related to blood lactate concentration ([La](b)) increases at submaximal workloads (). We combined, on five well-trained subjects [mountain climbers; peak O(2) consumption (VO(2peak)), 51.0 +/- 4.2 (SD) ml. kg(-1). min(-1)] performing incremental exercise on a cycle ergometer (30 W added every 4 min up to voluntary exhaustion), measurements of pulmonary gas exchange and earlobe [La](b) with determinations of concentration changes of oxygenated Hb (Delta[O(2)Hb]) and deoxygenated Hb (Delta[HHb]) in the vastus lateralis muscle, by continuous-wave NIRS. A "point of inflection" of [La](b) vs. was arbitrarily identified at the lowest [La](b) value which was >0.5 mM lower than that obtained at the following. Total Hb volume (Delta[O(2)Hb + HHb]) in the muscle region of interest increased as a function of up to 60-65% of VO(2 peak), after which it remained unchanged. The oxygenation index (Delta[O(2)Hb - HHb]) showed an accelerated decrease from 60- 65% of VO(2 peak). In the presence of a constant total Hb volume, the observed Delta[O(2)Hb - HHb] decrease indicates muscle deoxygenation (i.e., mainly capillary-venular Hb desaturation). The onset of muscle deoxygenation was significantly correlated (r(2) = 0.95; P < 0.01) with the point of inflection of [La](b) vs., i.e., with the onset of blood lactate accumulation. Previous studies showed relatively constant femoral venous PO(2) levels at higher than approximately 60% of maximal O(2) consumption. Thus muscle deoxygenation observed in the present study from 60-65% of VO(2 peak) could be attributed to capillary-venular Hb desaturation in the presence of relatively constant capillary-venular PO(2) levels, as a consequence of a rightward shift of the O(2)Hb dissociation curve determined by the onset of lactic acidosis.

Acidosis, Lactic↗
PubMed1997

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↗
PubMed1996

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↗
PubMed1996

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↗
PubMed1995

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↗
PubMed1995

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↗
PubMed1994

Subclinical impairment of lung airways in patients with panic disorder.

Lung function was assessed in 17 panic patients and 20 healthy controls. Panic patients had abnormal values for some dynamic lung volumes, namely Peak Expiratory Flow Rate (PEFR), Expiratory Flow at 75% of Vital Capacity (FEF75) and Maximum Mid-Expiratory Flow Rate (MMEF). Such functional abnormalities might indicate subclinical obstruction of lung airways, possibly relevant to the mechanisms related to panic disorder (PD).

Adult↗
PubMed1994

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↗
PubMed1994

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↗
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

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↗
PubMed1992

Gas exchange kinetics in heart transplant recipients.

Submaximal and/or peak levels of oxygen consumption (VO2), pulmonary ventilation (VE), heart rate (HR), stroke volume of heart (SV), cardiac output (Q), muscle blood flow (qm), as well as the kinetics of readjustment of gas exchange, Q and qm (t1/2 VO2on-, t1/2 Qon-, t1/2 qmon-) were determined in 44 heart transplant recipients (HTRs) and in a group of age-, sex-, and physical activity-matched control subjects (CTL) when carrying out rectangular loads (25 to 125 W) on a bicycle ergometer. The increase of SV occurring at work onset appears to compensate in HTRs for the sluggish readjustment of HR so that the rate of readjustment of Q is kept within normal limits. As a consequence, qm, t1/2 q mon-, and t1/2 VO2on- appear to be similar or only moderately delayed in HTRs compared with CTLs. It is concluded that in HTRs, because of constrained maximum HR, only work loads up to 60% of the VO2max of CTLs may be attained; also, owing to the fast readjustment of Q, up to work loads of 75 to 100 W, the rest to work transition phase is not impaired.

Electrocardiography↗
PubMed1991

Peak anaerobic power in master athletes.

The age-related decline in maximal physical performance of healthy subjects may be attributed both to the aging process per se and/or to a progressive reduction in physical activity. In two groups of master athletes, power (P) or endurance (E) trained (n = 115; aged 40-78 years), the degree and rate of the age-related deterioration of the maximal instantaneous muscle power (peak power, Wpeak), and the relative contribution of quantitative (muscle mass) and qualitative factors possibly underlying such deterioration were determined. Two groups of young athletes (n = 20; 17-26 years) and healthy untrained subjects (U, n = 37; 22-67 years) were also tested for comparison. The following two variables were assessed, firstly the lower limb muscle plus bone volume (LMV) by anthropometry, and secondly Wpeak, by means of a standardized vertical jump off both feet, performed on a force platform. The results obtained were that LMV of E and P, as well as of U, was about the same between age 20 and 45 years, whereas at older ages a progressive reduction was observed; the LMV values were higher in P than in E and U.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1991

Energetics of locomotion in African pygmies.

The energy cost of walking (Cw) and running (Cr), and the maximal O2 consumption (VO2max) were determined in a field study on 17 Pygmies (age 24 years, SD 6; height 160 cm, SD 5; body mass 57.2 kg, SD 4.8) living in the region of Bipindi, Cameroon. The Cw varied from 112 ml.kg-1.km-1, SD 25 [velocity (v), 4 km.h-1] to 143 ml.kg-1.km-1, SD 16 (v, 7 km.h-1). Optimal walking v was 5 km.h-1. The Cr was 156 ml.kg-1.km-1, SD 14 (v, 10 km.h-1) and was constant in the 8-11 km.h-1 speed range. The VO2max was 33.7 ml.kg-1.min-1, i.e. lower than in other African populations of the same age. The Cr and Cw were lower than in taller Caucasian endurance runners. These findings, which challenge the theory of physical similarity as applied to animal locomotion, may depend either on the mechanics of locomotion which in Pygmies may be different from that observed in Caucasians, or on a greater mechanical efficiency in Pygmies than in Caucasians. The low Cr values observed enable Pygmies to reach higher running speeds than would be expected on the basis of their VO2max.

Africa↗