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Biomedical subjects

B J Martin

Publications and source records attributed to B J Martin.

At least 163 records · Page 9Linked to original sources
PubMed1981

Control of breathing during prolonged exercise.

Ventilation (VE) climbs steadily throughout prolonged heavy exercise. While this VE "drift" has implications for the adequacy of gas exchange in long-term exercise, its mechanism remains unknown. We examined the behavior of previously proposed mediators of VE drift during one hour of cycle ergometer exercise at constant work rate requiring 2/3 VO2 max in 10 subjects. VE increased 13% from 12 to 61 min of exercise (P less than 0.05). Although body core temperature rose as VE rose, equal elevation of core temperature by passive means failed to increase exercise VE. Rising VE during the hour of exercise occurred despite unchanged arterial pH, PCO2, and lactate and despite unchanged VCO2. Thus, all of the VE increase was calculated to be due to increased dead space ventilation (VD). Tidal volume (VT) was unchanged, while VD/VT rose from 0.16 to 0.24 from 12 to 61 min of work (P less than 0.05). These results show that increased body core temperature does not mediate VE drift, and that changes in previously proposed mediators (arterial pH, arterial lactate, and VCO2) are not necessary for a slow VE rise to occur in prolonged heavy exercise.

Body Temperature↗
PubMed1981

Phosphorylation and adenosine triphosphatase activity of myofibrils from thyrotoxic rabbit hearts.

Cardiac hypertrophy induced by thyrotoxic stress leads to an increase in the rate of force development, velocity of shortening, tension-dependent heat generation, and myosin ATPase activity. We did studies to see whether alterations in covalent phosphorylation of myofibrillar proteins correlate with these changes. The protein preparations were isolated from control and thyrotoxic hearts of male albino rabbits freeze-clamped in situ. We measured myofibrillar ATPase, and the covalent phosphate content of ventricular myosin 19,000 (mol wt) light chain (P-light chain) and troponin I (TnI). The myofibrillar ATPase activity was increased 2-fold in the thyrotoxic preparations with no change in the level of myofibrillar phosphorylation. The covalent phosphate content of TnI was 1.21 +/- 0.09 mol P/mol TnI in control hearts and 1.14 +/- 0.04 mol P/mol TnI in thyrotoxic hearts. The covalent phosphate content of the light chain fraction was 0.41 +/- 0.06 mol P/mol P-light chain in control hearts and 0.37 +/- 0.04 mol P/mol P-light chain in thyrotoxic hearts. The dependence of the normalized myofibrillar ATPase on free calcium concentration was the same in control and thyrotoxic preparations. Thus the mechanical, thermal, and biochemical changes found in hearts from thyrotoxic animals probably occur with no change in phosphorylation of TnI or myosin light chains.

Adenosine Triphosphatases↗
PubMed1981

Exercise after sleep deprivation.

The influence of acute sleep loss on subsequent exercise remains poorly defined. To investigate this question, six subjects performed cycle ergometer exercise daily in a 3-d series that included 30 h without sleep before day 2, and then unlimited sleep before day 3. Each day 8 min of exercise was performed at each of three constant external work loads that required approximately 25%, 50%, and 75% of the VO2max. On days 2 and 3 after sleep loss, exercise at all work loads resulted in unchanged O2 uptake (VO2), CO2 production (VO2), CO2 production (VCO2), ventilation (VE), heart rate, and arterial blood perssure, when compared with the equivalent day in a control series. Despite these unchanged physiological variables, ratings of preceived exertion were increased significantly during moderate and heavy exercise on day 2 (P less than 0.05), but returned to control levels on day 3. In further experiments on six additional subjects, sleep loss failed to alter VO2max, while it significantly reduced peak exercise heart rate (P less than 0.05). These results suggest that acute sleep deprivation primarily alters the psychological responses to moderate and heavy exercise.

Adult↗
PubMed1981

Ventilatory endurance in athletes and non-athletes.

Do the ventilatory muscles (VM) of normal persons become fatigued while high ventilation is maintained during strenuous exercise? If so, then one effect of the intense training performed by endurance athletes should be an increase in VM endurance. To investigate this possibility, eight female endurance-athletes and eight female non-athletes were compared in studies of both short-term and long-term maximal ventilation. The two groups were matched for age, body size, and vital capacity. While athletes and non-athletes had similar short-term maximal ventilation (12-s MVV), the athletes displayed greater ventilatory endurance on two-long-term breathing tests. In the first, ventilation was increased 30 1/min every 4 min. Before exhaustion, athletes reached a ventilation that was a significantly greater fraction of their 12-s MVV (75% vs 67%, P less than 0.01), than did non-athletes. Although the energy cost (VO2) of submaximal levels of ventilation was identical in the two groups, athletes reached a significantly greater peak VO2 during this progressive test (P less than 0.05). In the second test of ventilatory endurance, 80% of the 12-s MVV was sustained until exhaustion. Endurance times averaged 11 min for athletes and 3 min for non-athletes (P less than 0.01). While these results do not rule out the possibility of genetic predisposition to high VM endurance in athletes, they are consistent with the possibility that VM training may occur in normal persons during forms of endurance exercise training.

Female↗
PubMed1980

Relative selective action of propranolol on cardiovascular and respiratory responses to isoproterenol.

Organ selectivity of beta sympathetic blockade with propranolol was studied in 6 normal men by comparing the cardiovascular and respiration responses during isoproterenol infusions before and after propranolol. Beta sympathetic blockade was achieved with propranolol and was considered present when there was no heart rate (HR) response to isoproterenol during an infusion tenfold greater than that which raised HR 25% during a control period. During blockade there was no change in HR or systolic or diastolic blood pressure during isoproterenol infusions. There was a consistent (p less than 0.05) rise in resting ventilation (+17%), oxygen consumption (+9%), and carbon dioxide production (+15%) with low-dose (raised HR 10% before blockade) isoproterenol infusion during blockade. These respiratory effects of low-dose isoproterenol during cardiovascular blockade were quantitatively similar to that before blockade. With infusion that raised HR 25%, there was a further increase in VE, VO2, and VCO2 before blockade but no further increase during beta blockade. Changes in acid-base status did not explain the increase in VE during blockade. We conclude that there are differences between effectiveness of propranolol blockade of the cardiovascular system and of the respiratory system.

Blood Gas Analysis↗
PubMed1980

Enhanced thrombin and plasmin activity with exercise in man.

We measured products of thrombin and plasmin action and of the platelet release reaction during exercise to determine if the well-known effect of exercise on in vitro coagulation and fibrinolytic tests reflects activity of these systems in vivo. Plasma fibrinopeptide A, produced by thrombin-mediated proteolysis of fibrinogen, increased with graded treadmill and cycle exercise to postexercise levels of 20--30 times resting values. Fibrin/fibrinogen-related D antigen increased in a similar fashion with peak levels at maximal O2 uptake. Plasma-activated partial thromboplastin times fell as fibrinopeptide A levels increased. Unheated fibrin plate lysis areas increased as D antigen concentrations rose, indicating increased release of plasminogen activator. In contrast to activation of the soluble coagulation and fibrinolytic systems, platelet counts and plasma levels of beta-thromboglobulin, a platelet release protein, did not change significantly with exercise. The effect of exercise on thrombin and plasmin was not influenced by prior physical training, but appeared to be less with cycle exercise than with treadmill exercise.

Blood Coagulation↗
PubMed1980

Morphine reduces ventilation without changing metabolic rate in exercise.

Morphine reduces ventilation (VE) in exercising man. The mechanism of this ventilatory depression remains unclear. Recent evidence suggests that morphine may reduce exercise VE by simultaneously reducing exercise metabolic rate. We measured exercise VE in six normal subjects after intravenous injection of either saline or 0.1 mg/kg morphine sulfate. During treadmill walks requiring 1/3 and 2/3 of the maximal oxygen uptake, morphine reduced VE (P < 0.05), while it left metabolic rate unchanged. Morphine treatment elevated end-tidal PCO2 at both work levels (P < 0.05). Lower VE and higher PETCO2 in exercise after morphine persisted after elevation of alveolar PO2 to 200 torr. Thus, morphine left unchanged the contribution of the hypoxic chemoreflex to normoxic exercise VE. In addition, morphine failed to alter the ventilatory responses to hypercapnia measured at each exercise level. These results suggest that analgesic dosages of morphine reduce the ventilatory response to exercise through a mechanism other than alterations in metabolic rate or chemical ventilatory responses.

Carbon Dioxide↗
PubMed1979

Cesarean hysterectomy: a twenty-five-year review.

This article analyzes cesarean hysterectomies performed at Louisville General Hospital on clinic patients for the 25 year period 1953 through 1977. During this time there were 63,259 deliveries, of which 2417 were cesarean sections and 149 were cesarean hysterectomies. Twenty-six of the latter were classified as emergency operations done for urgent medical indications; in the remaining 123 patients the indications were elective to some degree. Operative and postoperative complications and morbidity are discussed, and changing trends regarding the place of cesarean hysterectomy in obstetrics over the years are evaluated.

Adolescent↗
PubMed1979

CO2 and exercise tidal volume.

In progressive exercise increased tidal volume (VT) accompanies increased ventilation (VE) until a VT plateau is reached. We observed in 13 subjects a correspondence between the arrival of the VT plateau and the anaerobic threshold (AT). To examine this association between a mechanical event (the VT plateau) and a metabolic event (the AT), we changed those variables that change at the AT and looked for changes in VT. We found in 13 subjects that CO2 addition to prevent alveolar hypocapnia during cycle ergometer exercise progressing to exhaustion in 12-15 min significantly elevated the VT plateau (mean increase 4.4%; P less than 0.01) as compared with a spontaneous test that induced a mean end-tidal carbon dioxide tension fall of 5.5 Torr. This VT increase was mediated by a significant increase in inspiratory time (TI; P less than 0.02); both the ratio of TI to the total breath duration (TI/Ttot) and the mean rate of inspired airflow (VT/TI) were unchanged at matched VE. Changing other variables known to change at the AT--blood lactate ion concentration and alveolar oxygen tension--left ventilatory pattern unchanged. These results suggest that hypocapnia in severe exercise measurably lowers the VT plateau in normal man.

Carbon Dioxide↗
PubMed1979

Influence of exercise hyperthermia on exercise breathing pattern.

Passive elevation of the body core temperature (Tc) induces rapid, shallow breathing in resting man. We wondered if exercise-induced Tc elevation would also lead to decreased tidal volume (VT) and increased breathing frequency (f) during exercise. To investigate this question, 10 subjects each performed 47 min of cycle ergometer exercise at 50--60% of the maximal aerobic capacity, with the work rate adjusted to maintain ventilation (VE) constant. This long ride raised mean Tc (rectal) 0.8 degrees C. Before and immediately after the long ride, ranges of VE and VT were obtained from short 6-min rides that progressed from unloaded pedaling to the anaerobic threshold. At the constant VE of the long ride, f rose and VT fell as Tc rose (P less than 0.05). The fall in VT was associated with a fall in inspiratory time (TI); drive (VT/TI) and timing (TI/Ttot)components of VE were unchanged. These effects were consistent over the entire range of VE obtained from the short 6-min rides. Passive heating in warm water to produce equal Tc elevation in the same subjects yielded similar exercise breathing-pattern changes. These findings suggest that increased Tc mediates the VT fall during prolonged exercise, possibly through stimulation of the central respiratory pacemaker.

Body Temperature↗
PubMed1979

Low exercise ventilation in endurance athletes.

Previous studies have shown that endurance athletes are endowed with low ventilatory responses to chemical stimuli. The implications of this association have never been clear. Although recent evidence shows that exercise ventilation (VE) correlates with ventilatory chemoresponsiveness in a group of athletes, the extent to which non-athletes may differ from athletes in this regard is unknown. We have examined the relationship between ventilatory chemoresponsiveness and exercise VE in a group of 7 non-athletes, and contrasted these findings with those obtained previously from 8 endurance and 8 non-endurance athletes. Correlation lines of exercise VE with chemical responses were similar in slope and intercept for both athletes and non-athletes. However, we found that non-athletes had greater exercise VE per unit metabolic rate (VO2 or VCO2), and greater ventilatory responses to O2 and CO2, when compared with endurance athletes at equal relative work loads (P less than 0.05). The lower exercise VE/VCO2 of endurance athletes as compared with non-athletes persisted in hyperoxia, indicating that factors other than differences in hypoxic sensitivity explain the lower exercise VE of endurance athletes. Low exercise VE may be the link between low ventilatory chemosensitivity and outstanding endurance athletic performance.

Adult↗
PubMed1978

Exercise ventilation correlates positively with ventilatory chemoresponsiveness.

To determine the relationship of ventilatory responsiveness to hypoxia and hypercapnia to exercise hyperpnea, these responses and steady-state exercise ventilation (VE) were measured in 16 athletes during light (1/3 VO2 max) and heavy (2/3 VO2 max) exercise. Both the hypoxic and hypercapnic ventilatory responses correlated positively with VE per unit metabolic rate (VE/VCO2) at both exercise levels (P less than 0.05). The contribution of the hypoxic response to normoxic exercise VE was quantified by comparing VE in normoxia to VE during a brief (1 min) exposure to high O2 (PAO2 = 200 Torr). High O2 reduced normoxic exercise VE by a mean of 20% at either exercise intensity. Among individuals this reduction was directly dependent upon the intensity of the hypoxic response, and ranged from 7 to 42% of normoxic VE. After the variable reduction of normoxic VE by hyperoxia, all correlations of ventilatory response with exercise VE were lost except for the correlation of hypercapnic response with heavy exercise VE/VCO2. These findings indicate that the extent of VE in light or heavy exercise is modified by the strength of the hypoxic ventilatory response, and that the hypercapnic response independently correlates with VE during heavy exercise.

Adult↗
PubMed1975

Effect of warm-up on metabolic responses to strenuous exercise.

Aerobic and anaerobic energy transformations were measured in two trained runners during 90-sec treadmill runs at 23.6 km/hr (2% grade). The runs were preceded by rest or either of two warm-ups: 1) 15-min run at 10 km/hr, or 2) 15-min run at 10 km/hr followed by 3-min standing. Compared with runs without warm-up, during the third half minute of runs following both types of warm-up 11% greater heart rates (HR), 8% greater oxygen consumption (Vo2), and unchanged ventilation were recorded. The rate constant of the approach of Vo2 to O2 in the first minute of work was unaffected by warm-up. Runs following either warm-up resulted in 25% lower lactate production; during these runs 3 to 4 degrees C higher gastrocnemius muscle temperatures (Tm) were maintained. The differences in HR, Vo2, and Tm continued throughout exhausting 5-min runs at 20.9 km/hr (2% grade). An elevated muscle temperature may therefore be requisite for the maximal aerobic response to a short exhausting run.

Adaptation, Physiological↗