Biomedical subjects

A W Sheel

Publications and source records attributed to A W Sheel.

10 recordsLinked to original sources

PubMed2005

The human diving response, its function, and its control.

The purpose of this review is to outline the physiological responses associated with the diving response, its functional significance, and its cardiorespiratory control. This review is separated into four major sections. Section one outlines the diving response and its physiology. Section two provides support for the hypothesis that the primary role of the diving response is the conservation of oxygen. The third section describes how the diving response is controlled and provides a model that illustrates the cardiorespiratory interaction. Finally, the fourth section illustrates potential adaptations that result after regular exposure to an asphyxic environment. The cardiovascular and endocrine responses associated with the diving response and apnea are bradycardia, vasoconstriction, and an increase in secretion of suprarenal catecholamines. These responses require the integration of both the cardiovascular system and the respiratory system. The primary role of the diving response is likely to conserve oxygen for sensitive brain and heart tissue and to lengthen the time before the onset of serious hypoxic damage. We suggest that future research should be focused towards understanding the role of altered ventilatory responses in human breath-hold athletes as well as in patients suffering from sleep-disordered breathing.

Bradycardia↗

PubMed2004

Physiology of sport rock climbing.

Rock climbing has increased in popularity as both a recreational physical activity and a competitive sport. Climbing is physiologically unique in requiring sustained and intermittent isometric forearm muscle contractions for upward propulsion. The determinants of climbing performance are not clear but may be attributed to trainable variables rather than specific anthropometric characteristics.

Anthropometry↗

PubMed2001

Fatiguing inspiratory muscle work causes reflex reduction in resting leg blood flow in humans.

1. We recently showed that fatigue of the inspiratory muscles via voluntary efforts caused a time-dependent increase in limb muscle sympathetic nerve activity (MSNA) (St Croix et al. 2000). We now asked whether limb muscle vasoconstriction and reduction in limb blood flow also accompany inspiratory muscle fatigue. 2. In six healthy human subjects at rest, we measured leg blood flow (.Q(L)) in the femoral artery with Doppler ultrasound techniques and calculated limb vascular resistance (LVR) while subjects performed two types of fatiguing inspiratory work to the point of task failure (3-10 min). Subjects inspired primarily with their diaphragm through a resistor, generating (i) 60 % maximal inspiratory mouth pressure (P(M)) and a prolonged duty cycle (T(I)/T(TOT) = 0.7); and (ii) 60 % maximal P(M) and a T(I)/T(TOT) of 0.4. The first type of exercise caused prolonged ischaemia of the diaphragm during each inspiration. The second type fatigued the diaphragm with briefer periods of ischaemia using a shorter duty cycle and a higher frequency of contraction. End-tidal P(CO2) was maintained by increasing the inspired CO(2) fraction (F(I,CO2)) as needed. Both trials caused a 25-40 % reduction in diaphragm force production in response to bilateral phrenic nerve stimulation. 3. .Q(L) and LVR were unchanged during the first minute of the fatigue trials in most subjects; however, .Q(L) subsequently decreased (-30 %) and LVR increased (50-60 %) relative to control in a time-dependent manner. This effect was present by 2 min in all subjects. During recovery, the observed changes dissipated quickly (< 30 s). Mean arterial pressure (MAP; +4-13 mmHg) and heart rate (+16-20 beats min(-1)) increased during fatiguing diaphragm contractions. 4. When central inspiratory motor output was increased for 2 min without diaphragm fatigue by increasing either inspiratory force output (95 % of maximal inspiratory pressure (MIP)) or inspiratory flow rate (5 x eupnoea), .Q(L), MAP and LVR were unchanged; although continuing the high force output trials for 3 min did cause a relatively small but significant increase in LVR and a reduction in .Q(L). 5. When the breathing pattern of the fatiguing trials was mimicked with no added resistance, LVR was reduced and .Q(L) increased significantly; these changes were attributed to the negative feedback effects on MSNA from augmented tidal volume. 6. Voluntary increases in inspiratory effort, in the absence of diaphragm fatigue, had no effect on .Q(L) and LVR, whereas the two types of diaphragm-fatiguing trials elicited decreases in .Q(L) and increases in LVR. We attribute these changes to a metaboreflex originating in the diaphragm. Diaphragm and forearm muscle fatigue showed very similar time-dependent effects on LVR and .Q(L).

Adult↗

PubMed2001

Influence of inhaled nitric oxide on gas exchange during normoxic and hypoxic exercise in highly trained cyclists.

This study tested the effects of inhaled nitric oxide [NO; 20 parts per million (ppm)] during normoxic and hypoxic (fraction of inspired O(2) = 14%) exercise on gas exchange in athletes with exercise-induced hypoxemia. Trained male cyclists (n = 7) performed two cycle tests to exhaustion to determine maximal O(2) consumption (VO(2 max)) and arterial oxyhemoglobin saturation (Sa(O(2)), Ohmeda Biox ear oximeter) under normoxic (VO(2 max) = 4.88 +/- 0.43 l/min and Sa(O(2)) = 90.2 +/- 0.9, means +/- SD) and hypoxic (VO(2 max) = 4.24 +/- 0.49 l/min and Sa(O(2)) = 75.5 +/- 4.5) conditions. On a third occasion, subjects performed four 5-min cycle tests, each separated by 1 h at their respective VO(2 max), under randomly assigned conditions: normoxia (N), normoxia + NO (N/NO), hypoxia (H), and hypoxia + NO (H/NO). Gas exchange, heart rate, and metabolic parameters were determined during each condition. Arterial blood was drawn at rest and at each minute of the 5-min test. Arterial PO(2) (Pa(O(2))), arterial PCO(2), and Sa(O(2)) were determined, and the alveolar-arterial difference for PO(2) (A-aDO(2)) was calculated. Measurements of Pa(O(2)) and Sa(O(2)) were significantly lower and A-aDO(2) was widened during exercise compared with rest for all conditions (P < 0.05). No significant differences were detected between N and N/NO or between H and H/NO for Pa(O(2)), Sa(O(2)) and A-aDO(2) (P > 0.05). We conclude that inhalation of 20 ppm NO during normoxic and hypoxic exercise has no effect on gas exchange in highly trained cyclists.

Administration, Inhalation↗

PubMed2000

Relationship between decreased oxyhaemoglobin saturation and exhaled nitric oxide during exercise.

Decreases in oxyhaemoglobin saturation (SaO2) are frequently observed in highly trained male endurance athletes during heavy work and has been termed exercise-induced hypoxaemia (EIH). Ventilation perfusion (VA/Q) mismatching and diffusion limitations are thought to be responsible. Nitric oxide (NO), a potent vasodilator, is present in the exhaled air of resting and exercising humans. Endogenously produced NO is thought to play a role in VA/Q matching and maintenance of low pulmonary vascular resistance. The purpose of this study was to determine the relationship between exhaled NO and EIH. It was hypothesized that athletes with EIH would have lower NO levels compared with non-EIH athletes. Eighteen highly trained male cyclists (VO2max=67.7 +/- 5.2 mL kg-1 min-1, mean +/- SD) were divided into normal (NORM, n=12, SaO2= 93.9 +/- 0.8) or low (LOW, n=6, SaO2=90.3 +/- 1.0) group, based on significantly different peak exercise SaO2 values (P < 0.05). All other descriptive and physiological characteristics were similar between the groups. Subjects performed a ramped cycle test to exhaustion breathing NO-free gas. The concentration (CNO) and production rate (VNO) of NO were determined from mixed gas samples at rest and during exercise at 100, 200, 250, 300, 350, 400 and 450 W using a chemiluminescent analyser. CNO remained unchanged from resting values in all subjects. VNO increased significantly during exercise in all subjects but was not different between LOW and NORM groups. The correlation between change in SaO2 and VNO from rest to maximal exercise was not significant (r=-0.12, P > 0.05). Collectively, these data suggest that exhaled NO is not related to decreased SaO2 during heavy exercise in highly trained male cyclists.

Adult↗

PubMed2000

Alveolar epithelial integrity in athletes with exercise-induced hypoxemia.

The effect of incremental exercise to exhaustion on the change in pulmonary clearance rate (k) of aerosolized (99m)Tc-labeled diethylenetriaminepentaacetic acid ((99m)Tc-DTPA) and the relationship between k and arterial PO(2) (Pa(O(2))) during heavy work were investigated. Ten male cyclists (age = 25 +/- 2 yr, height = 180.9 +/- 4.0 cm, mass = 80.1 +/- 9.5 kg, maximal O(2) uptake = 5. 25 +/- 0.35 l/min, mean +/- SD) completed a pulmonary clearance test shortly (39 +/- 8 min) after a maximal O(2) uptake test. Resting pulmonary clearance was completed >/=24 h before or after the exercise test. Arterial blood was sampled at rest and at 1-min intervals during exercise. Minimum Pa(O(2)) values and maximum alveolar-arterial PO(2) difference ranged from 73 to 92 Torr and from 30 to 55 Torr, respectively. No significant difference between resting k and postexercise k for the total lung (0.55 +/- 0.20 vs. 0. 57 +/- 0.17 %/min, P > 0.05) was observed. Pearson product-moment correlation indicated no significant linear relationship between change in k for the total lung and minimum Pa(O(2)) (r = -0.26, P > 0.05). These results indicate that, averaged over subjects, pulmonary clearance of (99m)Tc-DTPA after incremental maximal exercise to exhaustion in highly trained male cyclists is unchanged, although the sampling time may have eliminated a transient effect. Lack of a linear relationship between k and minimum Pa(O(2)) during exercise suggests that exercise-induced hypoxemia occurs despite maintenance of alveolar epithelial integrity.

Adult↗

PubMed1999

The effect of repeat exercise on pulmonary diffusing capacity and EIH in trained athletes.

PURPOSE: The purpose of this study was to determine the effects of repeated heavy exercise on postexercise pulmonary diffusing capacity (DL) and the development of exercise induced arterial hypoxemia (EIH). METHODS: 13 endurance-trained, male athletes (age = 27+/-3 yr, height = 179.6+/-5.0 cm, weight = 71.8+/-6.9 kg, VO2max = 67.0+/-3.6 mL x kg(-1) x min(-1) performed two consecutive, continuous exercise tests on a cycle ergometer to VO2max, separated by 60 min of recovery. Arterial oxygen saturation (%SaO2) was measured via ear oximetry, and resting DL was measured and partitioned by the single-breath method, before exercise and 60 min after each exercise bout. RESULTS: No significant differences resulted in VO2max, VE, peak heart rate (HR), or breathing frequency between exercise bouts (P > 0.05). There was a small but significant decrease (454-446 W; P < 0.05) in peak power output in the second test. %SaO2 decreased from resting values during both exercise tasks, but there was no difference between the minimum saturation achieved in test 1 (91.4) or test 2 (91.6; P > 0.05). After the initial exercise bout, significant decreases (P < 0.05) occurred in DL (11%), membrane diffusing capacity (DM) (11%) and pulmonary capillary volume (VC) (10%). Further decreases occurred in DL (6%; P < 0.05), DM (2%; P > 0.05), and VC (10%; P < 0.05) after the second exercise bout. CONCLUSIONS: These observations question the meaning of post exercise measurements of pulmonary diffusion capacity, and its components, relative to pulmonary gas exchange and pulmonary fluid accumulation during exercise. The fact that there was no further change in %SaO2 after the second test suggests that if any interstitial edema developed, it was of no clinical significance; alternatively, the changes in DL(CO) may be related more to redistribution of blood than the development of pulmonary edema.

Adult↗

PubMed1999

Exhaled nitric oxide during exercise.

Endogenously produced nitric oxide (NO) is detectable in the exhaled air of resting humans, and the amount of exhaled NO increases during exercise. It is believed that NO is likely to have an important role in the normal physiological response to exercise. Despite accumulating evidence of exhaled NO during exercise, the effects and relevance of NO to exercise are not yet completely understood. Scientific debate surrounds the site of NO production and the stimuli for production. Resolution of these controversial issues will explain the significance of exhaled NO during exercise.

Animals↗

PubMed1998

The time course of pulmonary diffusing capacity for carbon monoxide following short duration high intensity exercise.

We investigated the time course of changes in post-exercise pulmonary diffusing capacity for carbon monoxide (DLCO), membrane diffusing capacity (DM), and pulmonary capillary blood volume (VC) in highly trained (HT), moderately trained (MT) and untrained (UT) male subjects (n = 8/group). Subjects were assigned to groups based on their aerobic capacity from a preliminary VO2max test (HT > or = 65, MT = 50-60, UT < or = 50 ml x kg(-1) x min(-1)). Resting (BASE) DLCO, DM and VC were obtained, then subjects cycled to fatigue at the highest workrate attained during the preliminary tests. Diffusion measurements were then made at 1, 2, 4, 6 and 24 h. DLCO was depressed at 1 h, lowest at 6 h and approached BASE values at 24 h in all groups. The DLCO change was paralleled by a change in VC. Alterations to VC were similar between groups except at 24 h where MT and HT subjects had returned to BASE while UT did not. DM was significantly lower than BASE at 1, 2, 4, and 6 h, and was similar between groups. The changes in DLCO post-exercise appear to be primarily due to a decrease in VC. Comparable diffusion decrements were observed in all subjects. The results of this study suggest that post-exercise alterations in DLCO, DM and VC are not related to aerobic capacity.

Bicycling↗

PubMed1996

Comparison of aero-bars versus traditional cycling postures on physiological parameters during submaximal cycling.

The purpose of this investigation was to quantify the difference in energy expenditure between traditional cycling handlebars and aero-bars during outdoor submaximal cycling. Eleven trained cyclists (age = 29.3 +/- 1.9 years, weight = 69.4 +/- 3.8 kg, VO2max = 58.1 +/- 2.0 ml.kg-1.min-1) were randomly assigned a sequence of three hand positions: brake hoods (BH), drop-bars (DB), and aero-bars (AB). Subjects cycled at 30 km.h-1 in one position for 5 minutes, then recovered until HR fell below 120 bpm. This was then repeated for the other hand positions. All cycling was completed on a standard racing bike fitted with aero-bars. Tire pressure was held constant for all trials. A portable telemetric system (Cosmed K-2) was used to measure VO2, VE and heart rate (HR) during the trials. No statistical differences were observed between AB and DB. Significant differences (p < .05) were found between BH (VE = 66.1 +/- 2.7 L.min-1; HR = 152 +/- 4 bpm; VO2 = 1.56 +/- .15 L.min-1) and AB (VE = 61.3 +/- 2.8 L.min-1; HR = 146 +/- 4 bpm; VO2 = 1.31 +/- .10 L.min-1). AB provides an energy savings over the traditional BH cycling posture.

Adolescent↗