Biomedical subjects

Stefanos Volianitis

Publications and source records attributed to Stefanos Volianitis.

7 recordsLinked to original sources

PubMed2006

Are the arms and legs in competition for cardiac output?

Oxygen transport to working skeletal muscles is challenged during whole-body exercise. In general, arm-cranking exercise elicits a maximal oxygen uptake (VO2max) corresponding to approximately 70% of the value reached during leg exercise. However, in arm-trained subjects such as rowers, cross-country skiers, and swimmers, the arm VO2max approaches or surpasses the leg value. Despite this similarity between arm and leg VO2max, when arm exercise is added to leg exercise, VO2max is not markedly elevated, which suggests a central or cardiac limitation. In fact, when intense arm exercise is added to leg exercise, leg blood flow at a given work rate is approximately 10% less than during leg exercise alone. Similarly, when intense leg exercise is added to arm exercise, arm blood flow and muscle oxygenation are reduced by approximately 10%. Such reductions in regional blood flow are mainly attributed to peripheral vasoconstriction induced by the arterial baroreflex to support the prevailing blood pressure. This putative mechanism is also demonstrated when the ability to increase cardiac output is compromised; during exercise, the prevailing blood pressure is established primarily by an increase in cardiac output, but if the contribution of the cardiac output is not sufficient to maintain the preset blood pressure, the arterial baroreflex increases peripheral resistance by augmenting sympathetic activity and restricting blood flow to working skeletal muscles.

Arm↗

PubMed2004

Cerebral metabolism during upper and lower body exercise.

When continuation of exercise calls for a "will," the cerebral metabolic ratio of O2 to (glucose + lactate) decreases, with the largest reduction (30-50%) at exhaustion. Because a larger effort is required to exercise with the arms than with the legs, we tested the hypothesis that the reduction in the cerebral metabolic ratio would become more pronounced during arm cranking than during leg exercise. The cerebral arterial-venous differences for blood-gas variables, glucose, and lactate were evaluated in two groups of eight subjects during exhaustive arm cranking and leg exercise. During leg exercise, exhaustion was elicited after 25 +/- 6 (SE) min, and the cerebral metabolic ratio was reduced from 5.6 +/- 0.2 to 3.5 +/- 0.2 after 10 min and to 3.3 +/- 0.3 at exhaustion (P < 0.05). Arm cranking lasted for 35 +/- 4 min and likewise decreased the cerebral metabolic ratio after 10 min (from 6.7 +/- 0.4 to 5.0 +/- 0.3), but the nadir at exhaustion was only 4.7 +/- 0.4, i.e., higher than during leg exercise (P < 0.05). The results demonstrate that exercise decreases the cerebral metabolic ratio when a conscious effort is required, irrespective of the muscle groups engaged. However, the comparatively small reduction in the cerebral metabolic ratio during arm cranking suggests that it is influenced by the exercise paradigm.

Adult↗

PubMed2004

Brain and central haemodynamics and oxygenation during maximal exercise in humans.

During maximal exercise in humans, fatigue is preceded by reductions in systemic and skeletal muscle blood flow, O(2) delivery and uptake. Here, we examined whether the uptake of O(2) and substrates by the human brain is compromised and whether the fall in stroke volume of the heart underlying the decline in systemic O(2) delivery is related to declining venous return. We measured brain and central haemodynamics and oxygenation in healthy males (n= 13 in 2 studies) performing intense cycling exercise (360 +/- 10 W; mean +/-s.e.m.) to exhaustion starting with either high (H) or normal (control, C) body temperature. Time to exhaustion was shorter in H than in C (5.8 +/- 0.2 versus 7.5 +/- 0.4 min, P < 0.05), despite heart rate reaching similar maximal values. During the first 90 s of both trials, frontal cortex tissue oxygenation and the arterial-internal jugular venous differences (a-v diff) for O(2) and glucose did not change, whereas middle cerebral artery mean flow velocity (MCA V(mean)) and cardiac output increased by approximately 22 and approximately 115%, respectively. Thereafter, brain extraction of O(2), glucose and lactate increased by approximately 45, approximately 55 and approximately 95%, respectively, while frontal cortex tissue oxygenation, MCA V(mean) and cardiac output declined approximately 40, approximately 15 and approximately 10%, respectively. At exhaustion in both trials, systemic VO(2) declined in parallel with a similar fall in stroke volume and central venous pressure; yet the brain uptake of O(2), glucose and lactate increased. In conclusion, the reduction in stroke volume, which underlies the fall in systemic O(2) delivery and uptake before exhaustion, is partly related to reductions in venous return to the heart. Furthermore, fatigue during maximal exercise, with or without heat stress, in healthy humans is associated with an enhanced rather than impaired brain uptake of O(2) and substrates.

Adenosine Triphosphate↗

PubMed2004

Carotid baroreflex function ceases during vasovagal syncope.

Despite the arterial baroreflex control of heart rate and blood pressure, vasovagal syncope is a common cause of loss of consciousness in people exposed to stimuli that reduce the central blood volume, such as head-up tilt. Carotid baroreflex function was evaluated using a rapid pulse train of neck pressure and neck suction in three conscious volunteers who developed a vasovagal episode during head-up tilt. The maximal gain of the carotid-heart rate and carotid-blood pressure baroreflex function curves were identified as measures of carotid baroreceptor responsiveness. When presyncopal symptoms developed, one further baroreflex assessment was obtained before the subjects were returned to the supine position. The bradycardia and hypotension exhibited during pre-syncope and syncope reflected a leftward and downward relocation of both the cardiac and vasomotor stimulus response curves. In addition, during the vasovagal syncope, baroreflex control was suppressed as blood pressure remained low during neck pressure stimuli. In conclusion, arterial baroreflex function ceases during vasovagal syncope.

Adult↗

PubMed2003

Carotid baroreflex responsiveness to head-up tilt-induced central hypovolaemia: effect of aerobic fitness.

This investigation examined the interaction between carotid baroreflex (CBR) responsiveness during head-up tilt (HUT)-induced central hypovolaemia and aerobic fitness. Seven average fit (AF) individuals, with a mean maximal oxygen uptake (VO2max) of 49 +/- 1 (ml O2) kg-1 min-1, and seven high fit (HF) individuals, with a VO2max of 61 +/- 1 (ml O2) kg-1 min-1, voluntarily participated in the investigation. After 10-15 min supine, each subject was exposed to nine levels of progressively increasing HUT by 10 deg increments from -20 deg to +60 deg. During the final 3 min of each stage of HUT, the CBR responsiveness was measured using a rapid pulse (500 ms) train of neck pressure (NP) and neck suction (NS) ranging from +40 to -80 Torr. The maximal gain of the carotid-HR (Gmax-HR) and carotid-MAP (Gmax-MAP) baroreflex function curves was identified as measures of CBR responsiveness. During HUT-induced decreases in thoracic admittance, an index of central blood volume (CBV), the Gmax-HR and Gmax-MAP of the AF subjects increased more than the Gmax-HR and Gmax-MAP of the HF subjects (P < 0.05). The data demonstrate that the increase in the CBR responsiveness during a tilt-induced progressive unloading of the cardiopulmonary baroreceptors was attenuated in endurance-trained subjects. These findings provide an explanation for the predisposition to orthostatic hypotension and intolerance in well-trained athletes.

Adult↗

PubMed2002

Effects of hyperthermia on cerebral blood flow and metabolism during prolonged exercise in humans.

The development of hyperthermia during prolonged exercise in humans is associated with various changes in the brain, but it is not known whether the cerebral metabolism or the global cerebral blood flow (gCBF) is affected. Eight endurance-trained subjects completed two exercise bouts on a cycle ergometer. The gCBF and cerebral metabolic rates of oxygen, glucose, and lactate were determined with the Kety-Schmidt technique after 15 min of exercise when core temperature was similar across trials, and at the end of exercise, either when subjects remained normothermic (core temperature = 37.9 degrees C; control) or when severe hyperthermia had developed (core temperature = 39.5 degrees C; hyperthermia). The gCBF was similar after 15 min in the two trials, and it remained stable throughout control. In contrast, during hyperthermia gCBF decreased by 18% and was therefore lower in hyperthermia compared with control at the end of exercise (43 +/- 4 vs. 51 +/- 4 ml. 100 g(-1). min(-1); P < 0.05). Concomitant with the reduction in gCBF, there was a proportionally larger increase in the arteriovenous differences for oxygen and glucose, and the cerebral metabolic rate was therefore higher at the end of the hyperthermic trial compared with control. The hyperthermia-induced lowering of gCBF did not alter cerebral lactate release. The hyperthermia-induced reduction in exercise cerebral blood flow seems to relate to a concomitant 18% lowering of arterial carbon dioxide tension, whereas the higher cerebral metabolic rate of oxygen may be ascribed to a Q(10) (temperature) effect and/or the level of cerebral neuronal activity associated with increased exertion.

Adult↗

PubMed2002

Bicarbonate attenuates arterial desaturation during maximal exercise in humans.

The contribution of pH to exercise-induced arterial O2 desaturation was evaluated by intravenous infusion of sodium bicarbonate (Bic, 1 M; 200-350 ml) or an equal volume of saline (Sal; 1 M) at a constant infusion rate during a "2,000-m" maximal ergometer row in five male oarsmen. Blood-gas variables were corrected to the increase in blood temperature from 36.5 +/- 0.3 to 38.9 +/- 0.1 degrees C (P < 0.05; means +/- SE), which was established in a pilot study. During Sal exercise, pH decreased from 7.42 +/- 0.01 at rest to 7.07 +/- 0.02 but only to 7.34 +/- 0.02 (P < 0.05) during the Bic trial. Arterial PO2 was reduced from 103.1 +/- 0.7 to 88.2 +/- 1.3 Torr during exercise with Sal, and this reduction was not significantly affected by Bic. Arterial O2 saturation was 97.5 +/- 0.2% at rest and decreased to 89.0 +/- 0.7% during Sal exercise but only to 94.1 +/- 1% with Bic (P < 0.05). Arterial PCO2 was not significantly changed from resting values in the last minute of Sal exercise, but in the Bic trial it increased from 40.5 +/- 0.5 to 45.9 +/- 2.0 Torr (P < 0.05). Pulmonary ventilation was lowered during exercise with Bic (155 +/- 14 vs. 142 +/- 13 l/min; P < 0.05), but the exercise-induced increase in the difference between the end-tidal O2 pressure and arterial PO2 was similar in the two trials. Also, pulmonary O2 uptake and changes in muscle oxygenation as determined by near-infrared spectrophotometry during exercise were similar. The enlarged blood-buffering capacity after infusion of Bic attenuated acidosis and in turn arterial desaturation during maximal exercise.

Acidosis↗