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Biomedical subjects

S L Dodd

Publications and source records attributed to S L Dodd.

31 records · Page 2Linked to original sources
PubMed1995

Interaction of glucocorticoids and activity patterns affect muscle function.

The purpose of this study was to determine the effects of glucocorticoids on muscle mass and contractile properties of muscles of similar fiber composition but differing in activity patterns. Rats were divided into two groups and administered prednisolone (5 mg/kg per day) (P; N = 9) or served as controls (C; N = 10) for 10 days. Contractile properties were then determined in the left gastrocnemius-plantaris-soleus (GPS) muscle complex and a strip of costal diaphragm (D). An index of fatigue was also determined in both muscle preparations. Whole-body, GPS, and D weights decreased (P < 0.05) in the P animals (22%, 17%, and 15%, respectively) when compared to C. Specific tension (PO) increased (P < 0.05) in the GPS complex (21%) and decreased in the D (26%). Maximal shortening velocity (Vmax) was not different (P > 0.05) between groups in either the GPS or the D. While the index of fatigue was not different (P > 0.05) between groups in the D, there was a 30% increase (P < 0.05) in the rate of fatigue in the GPS. These data indicate that, although glucocorticoids cause decreased muscle mass in both D and GPS, a change in muscle architecture may prevent a decrease in force-generating ability in some limb muscles. However, glucocorticoids do not increase D fatigability as seen in the GPS.

Animals↗
PubMed1994

Tension development and duty cycle affect Qpeak and VO2peak in contracting muscle.

Ten canine gastrocnemius-plantaris muscle preparations were stimulated in situ to determine the interaction between tension development and the duty cycle in determining Qpeak and VO2peak. The muscle was stimulated with supramaximal voltage using four different stimulation protocols: 1) 5 twitches.s-1 (Tw), 2) 1 train.s-1-200 ms (1-200), 3) 1 train.s-1-300 ms (1-300), and 4) 2 trains.s-1-100 ms (2-100). Arterial and venous blood were sampled and Qpeak measured for determination of VO2peak. The total tension developed per second was integrated and averaged over 1 s (TDa) and used as an index of work of the muscle for each condition. The Qpeak and VO2peak were greater (P < 0.05) in the 1-200 condition compared to all other conditions. Further, Qpeak and VO2peak were greater (P < 0.05) in both the 1-300 and 2-100 conditions than during Tw: Qpeak (ml.kg-1.min-1) (mean +/- SE) for (Tw) = 928 +/- 65; (1-200) = 1368 +/- 102; (1-300) = 1150 +/- 96; (2-100) = 1189 +/- 89; VO2peak (ml.kg-1.min-1) for (Tw) = 108 +/- 8; (1-200) = 159 +/- 9; (1-300) = 135 +/- 11; (2-100) = 137 +/- 8. The TDa was significantly different among all conditions: TDa (N.kg-1) for (Tw) = 443 +/- 56; (1-200) = 606 +/- 81; (1-300) = 722 +/- 79; (2-100) = 522 +/- 41. We interpret these findings as an indication that the interaction of the duty cycle and tension development is a prime determinant of blood flow during muscle contractions.

Animals↗
PubMed1993

Effects of reduced O2 delivery with anemia, hypoxia, or ischemia on peak VO2 and force in skeletal muscle.

This investigation was designed to describe alterations in O2 uptake (VO2) and tension development in a contracting in situ gastrocnemious-plantaris muscle preparation during three conditions of reduced O2 delivery [arterial O2 concentration X blood flow (Q)]. The three conditions, hypoxemia (H), ischemia (I), and anemia (A), were matched for O2 delivery. A normoxic normal flow condition was also utilized for comparison. H was produced by respiring the animals with 9% O2 in N2; I was produced by lowering Q, and A was produced by hemodilution with 6% dextran. The stimulation pattern for the isometric tetanic contractions used was 1 train/s, and each train was 200 ms, 70 Hz, and 6 V. The muscle was maximally contracted during each of the experimental conditions, and the conditions were administered in random order. In each bout the contractions continued for 5 min with 30 min of rest between bouts. Samples of arterial and muscle venous blood were obtained during the last 30 s of each bout. VO2 during I (125 ml.kg-1.min-1) was less than during N (145 ml.kg-1.min-1; P < 0.05) and greater than during H or A (104 and 101 ml.kg-1.min-1, respectively; P < 0.05). Venous PO2 (PVO2) was significantly lower during H (17.1 Torr) compared with the other conditions; no differences existed between N, I, and A (26.8, 26.0, and 28.1 Torr, respectively). Tension development was reduced by the reduction of O2 delivery during I, H, and A compared with N. Tension developed among the reduced O2 delivery groups was not significantly different.(ABSTRACT TRUNCATED AT 250 WORDS)

Anemia↗
PubMed1993

Caffeine and exercise performance. An update.

Three principal cellular mechanisms have been proposed to explain the ergogenic potential of caffeine during exercise: (a) increased myofilament affinity for calcium and/or increased release of calcium from the sarcoplasmic reticulum in skeletal muscle; (b) cellular actions caused by accumulation of cyclic-3',5'-adenosine monophosphate (cAMP) in various tissues including skeletal muscle and adipocytes; and (c) cellular actions mediated by competitive inhibition of adenosine receptors in the central nervous system and somatic cells. The relative importance of each of the above mechanisms in explaining in vivo physiological effects of caffeine during exercise continues to be debated. However, growing evidence suggests that inhibition of adenosine receptors is one of the most important, if not the most important, mechanism to explain the physiological effects of caffeine at nontoxic plasma concentrations. Numerous animal studies using high caffeine doses have reported increased force development in isolated skeletal muscle in both in vitro and in situ preparations. In contrast, in vivo human studies have not consistently shown caffeine to enhance muscular performance during high intensity, short term exercise. Further, recent evidence supports previous work that shows caffeine does not improve performance during short term incremental exercise. Although controversy exists, the major part of published evidence evaluating performance supports the notion that caffeine is ergogenic during prolonged (> 30 min), moderate intensity (approximately 75 to 80% VO2max) exercise. The mechanism to explain these findings may be linked to a caffeine-mediated glycogen sparing effect secondary to an increased rate of lipolysis.

Animals↗
PubMed1991

The effects of caffeine on graded exercise performance in caffeine naive versus habituated subjects.

The physiological effects of caffeine on subjects habituated to caffeine is relatively unstudied compared to those of caffeine naive subjects during graded exercise. Thus, the purpose of this investigation was to determine the effects of caffeine on maximal oxygen consumption (VO2max) and the anaerobic threshold in these two populations. Seventeen moderately trained males were classified according to caffeine usage: (1) caffeine consumption 25 mg.day-1 or less (CN) (n = 8) or (2) caffeine consumption above 300 mg.day-1 (CH) (n = 9). The subjects were tested post-absorptive on the same cycle ergometer on three occasions with 7 days separating the tests. One hour before each test the subject ingested either a gelatin capsule (C); 3 mg.kg-1 body weight of caffeine (C3); or 5 mg.kg-1 body weight of caffeine (C5). The subject then performed an incremental VO2max test beginning at 50 W and the work rate was increased 30 W every 2 min until the subject could not maintain the power output. Serial venous blood samples were drawn over 30 s at the end of each stage. The CN group significantly increased resting heart rate (fc) and expired ventilation volume (VE) after C3 and C5 and VO2 after C5. No significant differences were found for exercise VE, VO2, respiratory exchange ratio, fc or time to exhaustion. There were no significant differences (P less than 0.05) in the lactate threshold or the ventilatory threshold between treatment in either group. The CH subjects showed a significant increase (P less than 0.05) in resting plasma free fatty acid (FFA) concentration only during the C3 and C5 treatments.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1989

Exercise performance following intense, short-term ventilatory work.

Evidence exists to indicate that prolonged ventilatory work fatigues respiratory muscles and may limit exercise tolerance. However, the effects of short-duration, high-intensity ventilatory work on subsequent exercise remains in question. We tested the hypothesis that intense short-term volitional hyperpnea would result in respiratory muscle fatigue and would therefore hinder subsequent exercise tolerance. Pulmonary function was determined in ten healthy, male subjects before and after two constant load exercise tests to exhaustion on a cycle ergometer. Test 1 was a preliminary test to determine VO2max, peak exercise VE, and peak exercise power output. Test 2 was a constant load (85% peak power output) exercise test to exhaustion. Test 3 was identical to test 2 but was preceded by 10 min of volitional, isocapnic hyperpnea (85% of peak exercise V.E) at a controlled frequency and tidal volume. Pulmonary function measures (FVC, FEV1, FEV1/FVC, and peak flow) were not significantly (P less than 0.05) altered by the volitional hyperpnea. Ventilation and gas exchange variables (VO2, VE, f, end-tidal PO2 and PCO2, VE/VO2, VE/VCO2, %SaO2) during exercise and time to exhaustion were not significantly (P less than 0.05) different between treatments. These experiments failed to show any effect of short-term ventilatory work on pulmonary function or subsequent exercise performance.

Adult↗
PubMed1989

Regional hemodynamic responses to hypoxia and hypermetabolism in polycythemic dogs.

Normovolemic polycythemia did not improve the ability of either resting muscle or gut to maintain O2 uptake (VO2) during severe hypoxia because of the adverse effects of increased viscosity on blood flow to those regions. The present study tested whether increased metabolic demand would promote vasodilation sufficiently to overcome those effects. We measured whole body, muscle, and gut blood flow, O2 extraction, and VO2 in anesthetized dogs after increasing hematocrit to 65% and raising O2 demand with 2,4-dinitrophenol (n = 8). We also tested whether regional denervation (n = 8) and hypervolemia (n = 6) affected these responses. After raising hematocrit and metabolism, the dogs were ventilated with air, with 9% O2-91% N2, and again with air for 30-min periods. Reduced blood flow and increased O2 demand, caused by increased blood viscosity and 2,4-dinitrophenol, respectively, increased O2 extraction so that muscle VO2 was nearly supply limited in normoxia. Denervation showed that vasoconstriction had increased in gut and muscle with hypoxia onset but this was overcome after 15 min. By then, muscle was receiving a major portion of cardiac output, whereas gut showed little change. With hypervolemia cardiac output increased in hypoxia but neither gut nor muscle increased blood flow in those experiments. Because regional and whole body VO2 fell in all groups during hypoxia to the same extent found earlier in normocythemic dogs, any real benefit of polycythemia under the conditions of these experiments was dubious at best.

Animals↗
PubMed1987

Responses of innervated and denervated gut to whole-body hypoxia.

As a significant user of O2 at rest (20% of whole body), the gut may be subject to more severe limitation of O2 supply during global hypoxia than more vital areas because of preferential redistribution of blood flow. Accordingly, its accumulation of O2 deficit during hypoxia and its excess O2 use during normoxic recovery might be altered by extrinsic neural activity. We measured blood flow and O2 uptake in whole body (WB) and gut segments while anesthetized dogs were ventilated with 9% O2-91% N2 for 30 min followed by 30-min normoxic recovery. In six dogs extrinsic innervation to the gut segment was left intact and it was severed in another six animals. O2 deficit and excess were the accumulated differences from the normoxic O2 uptake for both gut and WB corrected for O2 stores changes. The intact gut, although only 4% body wt, incurred 22% of WB O2 deficit but contributed only 8% to WB O2 excess. The imbalance (gut excess was only 44% of gut deficit) implied that O2 using functions were curtailed during hypoxia without obligating an energy stores deficit. Denervation did not alter these quantitative relationships. Blood flow responses to transition between normoxia and hypoxia were only transiently altered. Extrinsic innervation apparently plays no major role in gut responses to WB hypoxia.

Animals↗
PubMed1987

Muscle O2 deficit during hypoxia and two levels of O2 demand.

We have examined the relative deficits in tension development and O2 uptake in contracting skeletal muscle during severe hypoxic hypoxia. Anesthetized mongrel dogs were ventilated to maintain an end-tidal PCO2 between 35 and 40 Torr. Venous outflow from the gastrocnemius muscle was measured using an electromagnetic flow probe. The tendon was cut and attached to a strain gauge. The muscle was stimulated to contract isometrically at 2 or 4 Hz for 20 min. Hypoxia (9% O2 in N2) was then imposed for 30 min, followed by 30 min of normoxia. Blood flow first increased in proportion to the contraction frequency and then increased further a similar amount in both groups during hypoxia. O2 extraction and blood flow reached maximal levels during hypoxia in the 2-Hz group. The further O2 deficit that was accumulated during 4 Hz and hypoxia was, therefore, a result of the greater discrepancy between O2 supply and demand. O2 uptake decreased more in hypoxia than did developed tension. These results are best explained by ATP supplementation from nonaerobic energy sources that was promoted by the free-flow condition of hypoxic hypoxia.

Animals↗
PubMed1987

Systemic and intestinal limits of O2 extraction in the dog.

When systemic delivery of O2 (QO2 = QT X CaO2, where QT is cardiac output and CaO2 is arterial O2 content) is reduced by bleeding, the systemic O2 extraction ratio [ER = (CaO2 - CVO2)/CaO2, where CVO2 is venous O2 content] increases until a critical limit is reached below which O2 uptake (VO2) becomes limited by O2 delivery. During hypovolemia, reflex increases in mesenteric arterial tone may preferentially reduce gut blood flow so that the onset of O2 supply dependence occurs in the gut before other regions. We compared the critical O2 delivery (QO2c) and critical extraction ratio (ERc) of whole body and an isolated segment (30-50 g) of small bowel in seven anesthetized paralyzed dogs ventilated with room air. Systemic QO2 was reduced in stages by controlled hemorrhage as arterial O2 content was maintained, and systemic and gut VO2 and QO2 were measured at each stage. Body QO2c was 7.9 +/- 1.9 ml X kg-1 X min-1 (ERc = 0.69 +/- 0.12), whereas gut O2 supply dependency occurred when gut QO2 was 34.3 +/- 11.3 ml X min-1 X kg gut wt-1 (ERc = 0.63 +/- 0.09). O2 supply dependency in the gut occurred at a higher systemic QO2 (9.7 +/- 2.7) than whole-body QO2c (P less than 0.05). The extraction ratio at the final stage (maximal ER) was less in the gut (0.80 +/- 0.05) than whole body (0.87 +/- 0.06). Thus during reductions in systemic QO2, gut VO2 was maintained by increases in gut extraction of O2.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

O2 delivery to contracting muscle during hypoxic or CO hypoxia.

The consequences of a decreased O2 supply to a contracting canine gastrocnemius muscle preparation were investigated during two forms of hypoxia: hypoxic hypoxia (HH) (n = 6) and CO hypoxia (COH) (n = 6). Muscle O2 uptake, blood flow, O2 extraction, and developed tension were measured at rest and at 1 twitch/s isometric contractions in normoxia and in hypoxia. No differences were observed between the two groups at rest. During contractions and hypoxia, however, O2 uptake decreased from the normoxic level in the COH group but not in the HH group. Blood flow increased in both groups during hypoxia, but more so in the COH group. O2 extraction increased further with hypoxia (P less than 0.05) during concentrations in the HH group but actually fell (P less than 0.05) in the COH group. The O2 uptake limitation during COH and contractions was associated with a lesser O2 extraction. The leftward shift in the oxyhemoglobin dissociation curve during COH may have impeded tissue O2 extraction. Other factors, however, such as decreased myoglobin function or perfusion heterogeneity must have contributed to the inability to utilize the O2 reserve more fully.

Animals↗