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Biomedical subjects

J González-Alonso

Publications and source records attributed to J González-Alonso.

At least 19 recordsLinked to original sources
PubMed2005

Skeletal muscle mitochondrial DNA content in exercising humans.

Several weeks of intense endurance training enhances mitochondrial biogenesis in humans. Whether a single bout of exercise alters skeletal muscle mitochondrial DNA (mtDNA) content remains unexplored. Double-stranded mtDNA, estimated by slot-blot hybridization and real time PCR and expressed as mtDNA-to-nuclear DNA ratio (mtDNA/nDNA) was obtained from the vastus lateralis muscle of healthy human subjects to investigate whether skeletal muscle mtDNA changes during fatiguing and nonfatiguing prolonged moderate intensity [2.0-2.5 h; approximately 60% maximal oxygen consumption (Vo(2 max))] and short repeated high-intensity exercise (5-8 min; approximately 110% Vo(2 max)). In control resting and light exercise (2 h; approximately 25% Vo(2 max)) studies, mtDNA/nDNA did not change. Conversely, mtDNA/nDNA declined after prolonged fatiguing exercise (0.863 +/- 0.061 vs. 1.101 +/- 0.067 at baseline; n = 14; P = 0.005), remained lower after 24 h of recovery, and was restored after 1 wk. After nonfatiguing prolonged exercise, mtDNA/nDNA tended to decline (n = 10; P = 0.083) but was reduced after three repeated high-intensity exercise bouts (0.900 +/- 0.049 vs. 1.067 +/- 0.071 at baseline; n = 7; P = 0.013). Our findings indicate that prolonged and short repeated intense exercise can lead to significant reductions in human skeletal muscle mtDNA content, which might function as a signal stimulating mitochondrial biogenesis with exercise training.

Adult↗
PubMed2004

Hemodynamics and O2 uptake during maximal knee extensor exercise in untrained and trained human quadriceps muscle: effects of hyperoxia.

To elucidate the potential limitations on maximal human quadriceps O2 capacity, six subjects trained (T) one quadriceps on the single-legged knee extensor ergometer (1 h/day at 70% maximum workload for 5 days/wk), while their contralateral quadriceps remained untrained (UT). Following 5 wk of training, subjects underwent incremental knee extensor tests under normoxic (inspired O2 fraction = 21%) and hyperoxic (inspired O2 fraction = 60%) conditions with the T and UT quadriceps. Training increased quadriceps muscle mass (2.9 +/- 0.2 to 3.1 +/- 0.2 kg), but did not change fiber-type composition or capillary density. The T quadriceps performed at a greater peak power output than UT, under both normoxia (101 +/- 10 vs. 80 +/- 7 W; P < 0.05) and hyperoxia (97 +/- 11 vs. 81 +/- 7 W; P < 0.05) without further increases with hyperoxia. Similarly, thigh peak O2 consumption, blood flow, vascular conductance, and O2 delivery were greater in the T vs. the UT thigh (1.4 +/- 0.2 vs. 1.1 +/- 0.1 l/min, 8.4 +/- 0.8 vs. 7.2 +/- 0.8 l/min, 42 +/- 6 vs. 35 +/- 4 ml x min(-1) x mmHg(-1), 1.71 +/- 0.18 vs. 1.51 +/- 0.15 l/min, respectively) but were not enhanced with hyperoxia. Oxygen extraction was elevated in the T vs. the UT thigh, whereas arteriovenous O2 difference tended to be higher (78 +/- 2 vs. 72 +/- 4%, P < 0.05; 160 +/- 8 vs. 154 +/- 11 ml/l, respectively; P = 0.098) but again were unaltered with hyperoxia. In conclusion, the present results demonstrate that the increase in quadriceps muscle O2 uptake with training is largely associated with increases in blood flow and O2 delivery, with smaller contribution from increases in O2 extraction. Furthermore, the elevation in peak muscle blood flow and vascular conductance with endurance training seems to be related to an enhanced vasodilatory capacity of the vasculature perfusing the quadriceps muscle that is unaltered by moderate hyperoxia.

Adult↗
PubMed2004

Standing up to the challenge of standing: a siphon does not support cerebral blood flow in humans.

Model studies have been advanced to suggest both that a siphon does and does not support cerebral blood flow in an upright position. If a siphon is established with the head raised, it would mean that internal jugular pressure reflects right atrium pressure minus the hydrostatic difference from the brain. This study measured spinal fluid pressure in the upright position, the pressure and the ultrasound-determined size of the internal jugular vein in the supine and sitting positions, and the internal jugular venous pressure during seated exercise. When the head was elevated approximately 25 cm above the level of the heart, internal jugular venous pressure decreased from 9.5 (SD 2.8) to 0.2 (SD 1.0) mmHg [n = 15; values are means (SD); P < 0.01]. Similarly, central venous pressure decreased from 6.2 (SD 1.8) to 0.6 (SD 2.6) mmHg (P < 0.05). No apparent lumen was detected in any of the 31 left or right internal veins imaged at 40 degrees head-up tilt, and submaximal (n = 7) and maximal exercise (n = 4) did not significantly affect internal jugular venous pressure. While seven subjects were sitting up, spinal fluid pressure at the lumbar level was 26 (SD 4) mmHg corresponding to 0.1 (SD 4.1) mmHg at the base of the brain. These results demonstrate that both for venous outflow from the brain and for spinal fluid, the prevailing pressure approaches zero at the base of the brain when humans are upright, which negates that a siphon supports cerebral blood flow.

Adult↗
PubMed2002

Effect of mild carboxy-hemoglobin on exercising skeletal muscle: intravascular and intracellular evidence.

We studied muscle blood flow, muscle oxygen uptake (VO(2)), net muscle CO uptake, Mb saturation, and intracellular bioenergetics during incremental single leg knee-extensor exercise in five healthy young subjects in conditions of normoxia, hypoxia (H; 11% O(2)), normoxia + CO (CO(norm)), and 100% O(2) + CO (CO(hyper)). Maximum work rates and maximal oxygen uptake (VO(2 max)) were equally reduced by approximately 14% in H, CO(norm), and CO(hyper). The reduction in arterial oxygen content (Ca(O(2))) (approximately 20%) resulted in an elevated blood flow (Q) in the CO and H trials. Net muscle CO uptake was attenuated in the CO trials. Suprasystolic cuff measurements of the deoxy-Mb signal were not different in terms of the rate of signal rise or maximum signal attained with and without CO. At maximal exercise, calculated mean capillary PO(2) was most reduced in H and resulted in the lowest Mb-associated PO(2). Reductions in ATP, PCr, and pH during H, CO(norm), and CO(hyper) occurred earlier during progressive exercise than in normoxia. Thus the effects of reduced Ca(O(2)) due to mild CO poisoning are similar to H.

Adenosine Triphosphate↗
PubMed2001

Muscle heat production and anaerobic energy turnover during repeated intense dynamic exercise in humans.

1. The aim of the present study was to examine muscle heat production, oxygen uptake and anaerobic energy turnover throughout repeated intense exercise to test the hypotheses that (i) energy turnover is reduced when intense exercise is repeated and (ii) anaerobic energy production is diminished throughout repeated intense exercise. 2. Five subjects performed three 3 min intense one-legged knee-extensor exercise bouts (EX1, EX2 and EX3) at a power output of 65 +/- 5 W (mean +/- S.E.M.), separated by 6 min rest periods. Muscle, femoral arterial and venous temperatures were measured continuously during exercise for the determination of muscle heat production. In addition, thigh blood flow was measured and femoral arterial and venous blood were sampled frequently during exercise for the determination of muscle oxygen uptake. Anaerobic energy turnover was estimated as the difference between total energy turnover and aerobic energy turnover. 3. Prior to exercise, the temperature of the quadriceps muscle was passively elevated to 37.02 +/- 0.12 degrees C and it increased 0.97 +/- 0.08 degrees C during EX1, which was higher (P < 0.05) than during EX2 (0.79 +/- 0.05 degrees C) and EX3 (0.77 +/- 0.06 degrees C). In EX1 the rate of muscle heat accumulation was higher (P < 0.05) during the first 120 s compared to EX2 and EX3, whereas the rate of heat release to the blood was greater (P < 0.05) throughout EX2 and EX3 compared to EX1. The rate of heat production, determined as the sum of heat accumulation and release, was the same in EX1, EX2 and EX3, and it increased (P < 0.05) from 86 +/- 8 during the first 15 s to 157 +/- 7 J s(-1) during the last 15 s of EX1. 4. Oxygen extraction was higher during the first 60 s of EX2 and EX3 than in EX 1 and thigh oxygen uptake was elevated (P < 0.05) during the first 120 s of EX2 and throughout EX3 compared to EX1. The anaerobic energy production during the first 105 s of EX2 and 150 s of EX3 was lower (P < 0.05) than in EX1. 5. The present study demonstrates that when intense exercise is repeated muscle heat production is not changed, but muscle aerobic energy turnover is elevated and anaerobic energy production is reduced during the first minutes of exercise.

Adult↗
PubMed2001

Brain activity and fatigue during prolonged exercise in the heat.

We hypothesized that fatigue due to hyperthermia during prolonged exercise in the heat is in part related to alterations in frontal cortical brain activity. The electroencephalographic activity (EEG) of the frontal cortex of the brain was measured in seven cyclists [maximal O2 uptake (VO2max) 4.8 +/- 0.1 (SE) 1 min-1] cycling at 60% VO2max in a hot (H, 42 degrees C) and a cool (C, 19 degrees C) environment. Fast Fourier transformation of the EEG was used to obtain power spectrum areas in the alpha (8-13 Hz) and beta (13-30 Hz) frequencies. The ratio alpha/beta was calculated as an index of arousal level; an elevated alpha/beta index reflects suppressed arousal. In H, subjects fatigued after 34.4 +/- 1.4 min coinciding with an oesophageal temperature (Toes) of 39.8 +/- 0.1 degrees C, an almost maximal heart rate (HR 192 +/- 3 beats.min-1), a rating of perceived exertion (RPE) of 19.0 +/- 0.8 and significantly elevated alpha/beta index (188 +/- 71% of the value after 2 min of exercise; P < 0.05). In C, subjects cycled for a similar period while Toes was below 38 degrees C, HR and RPE were low, and the alpha/beta index was not significantly elevated (59 +/- 27% of 2 min value; P = NS). Increases in the alpha/beta index were strongly correlated to increases in Toes (r2 = 0.98; P = 0.0001).

Adult↗
PubMed2001

ATP production and efficiency of human skeletal muscle during intense exercise: effect of previous exercise.

The aim of the present study was to examine whether ATP production increases and mechanical efficiency decreases during intense exercise and to evaluate how previous exercise affects ATP turnover during intense exercise. Six subjects performed two (EX1 and EX2) 3-min one-legged knee-extensor exercise bouts [66.2 +/- 3.9 and 66.1 +/- 3.9 (+/-SE) W] separated by a 6-min rest period. Anaerobic ATP production, estimated from net changes in and release of metabolites from the active muscle, was 3.5 +/- 1.2, 2.4 +/- 0.6, and 1.4 +/- 0.2 mmol ATP x kg dry wt(-1) x s(-1) during the first 5, next 10, and remaining 165 s of EX1, respectively. The corresponding aerobic ATP production, determined from muscle oxygen uptake, was 0.7 +/- 0.1, 1.4 +/- 0.2, and 4.7 +/- 0.4 mmol ATP x kg dry wt(-1) x s(-1), respectively. The mean rate of ATP production during the first 5 s and next 10 s was lower (P < 0.05) than during the rest of the exercise (4.2 +/- 1.2 and 3.8 +/- 0.7 vs. 6.1 +/- 0.3 mmol ATP x kg dry wt(-1) x s(-1)). Thus mechanical efficiency, expressed as work per ATP produced, was lowered (P < 0.05) in the last phase of exercise (39.6 +/- 6.1 and 40.7 +/- 5.8 vs. 25.0 +/- 1.3 J/mmol ATP). The anaerobic ATP production was lower (P < 0.05) in EX2 than in EX1, but the aerobic ATP turnover was higher (P < 0.05) in EX2 than in EX1, resulting in the same muscle ATP production in EX1 and EX2. The present data suggest that the rate of ATP turnover increases during intense exercise at a constant work rate. Thus mechanical efficiency declines as intense exercise is continued. Furthermore, when intense exercise is repeated, there is a shift toward greater aerobic energy contribution, but the total ATP turnover is not significantly altered.

Adenosine Triphosphate↗
PubMed2001

Effects of marked hyperthermia with and without dehydration on VO(2) kinetics during intense exercise.

This study determined whether marked hyperthermia alone or in combination with dehydration reduces the initial rate of rise in O(2) consumption (VO(2) on-kinetics) and the maximal rate of O(2) uptake (VO(2 max)) during intense cycling exercise. Six endurance-trained male cyclists completed four maximal cycle ergometer exercise tests (402 +/- 4 W) when euhydrated or dehydrated (4% body wt) with normal (starting esophageal temperature, 37.5 +/- 0.2 degrees C; mean skin temperature, approximately 31 degrees C) or elevated (+1 and +6 degrees C, respectively) thermal strain. In the euhydrated and normal condition, subjects reached VO(2 max) (4.7 +/- 0.2 l/min) in 228 +/- 34 s, with a mean response time of 42 +/- 2 s, and fatigued after 353 +/- 39 s. Hyperthermia alone or in combination with dehydration reduced mean response time (17-23%), VO(2 max) (16%), and performance time (51-53%) (all P < 0.01) but did not alter the absolute response time (i.e., the time to reach 63% response in the control trial, 3.2 +/- 0.1 l/min, 42 s). Reduction in VO(2 max) was accompanied by proportional decline in O(2) pulse and significantly elevated maximal heart rate (195 vs. 190 beats/min for hyperthermia vs. normal). Preventing hyperthermia in dehydrated subjects restored VO(2 max) and performance time by 65 and 50%, respectively. These results demonstrate that impaired high-intensity exercise performance with marked skin and internal body hyperthermia alone or in combination with dehydration is not associated with a diminished rate of rise in VO(2) but decreased VO(2 max).

Adult↗
PubMed2000

Heat production in human skeletal muscle at the onset of intense dynamic exercise.

1. We hypothesised that heat production of human skeletal muscle at a given high power output would gradually increase as heat liberation per mole of ATP produced rises when energy is derived from oxidation compared to phosphocreatine (PCr) breakdown and glycogenolysis. 2. Five young volunteers performed 180 s of intense dynamic knee-extensor exercise ( approximately 80 W) while estimates of muscle heat production, power output, oxygen uptake, lactate release, lactate accumulation and ATP and PCr hydrolysis were made. Heat production was determined continuously by (i) measuring heat storage in the contracting muscles, (ii) measuring heat removal to the body core by the circulation, and (iii) estimating heat transfer to the skin by convection and conductance as well as to the body core by lymph drainage. 3. The rate of heat storage in knee-extensor muscles was highest during the first 45 s of exercise (70-80 J s-1) and declined gradually to 14 +/- 10 J s-1 at 180 s. 4. The rate of heat removal by blood was negligible during the first 10 s of exercise, rising gradually to 112 +/- 14 J s-1 at 180 s. The estimated rate of heat release to skin and heat removal via lymph flow was < 2 J s-1 during the first 5 s and increased progressively to 24 +/- 1 J s-1 at 180 s. The rate of heat production increased significantly throughout exercise, being 107 % higher at 180 s compared to the initial 5 s, with half of the increase occurring during the first 38 s, while power output remained essentially constant. 5. The contribution of muscle oxygen uptake and net lactate release to total energy turnover increased curvilinearly from 32 % and 2 %, respectively, during the first 30 s to 86 % and 8 %, respectively, during the last 30 s of exercise. The combined energy contribution from net ATP hydrolysis, net PCr hydrolysis and muscle lactate accumulation is estimated to decline from 37 % to 3 % comparing the same time intervals. 6. The magnitude and rate of elevation in heat production by human skeletal muscle during exercise in vivo could be the result of the enhanced heat liberation during ATP production when aerobic metabolism gradually becomes dominant after PCr and glycogenolysis have initially provided most of the energy.

Adenosine Triphosphate↗
PubMed2000

Stroke volume during exercise: interaction of environment and hydration.

Euhydrated and dehydrated subjects exercised in a hot and a cold environment with our aim to identify factors that relate to reductions in stroke volume (SV). We hypothesized that reductions in SV with heat stress are related to the interaction of several factors rather than the effect of elevated skin blood flow. Eight male endurance-trained cyclists [maximal O(2) consumption (VO(2 max)) 4.5 +/- 0.1 l/min; means +/- SE] cycled for 30 min (72% VO(2 max)) in the heat (H; 35 degrees C) or the cold (C; 8 degrees C) when euhydrated or dehydrated by 1.5, 3.0, or 4.2% of their body weight. When euhydrated, SV and esophageal temperature (T(es) 38. 2-38.3 degrees C) were similar in H and C, whereas skin blood flow was much higher in H vs. C (365 +/- 64% higher; P < 0.05). With each 1% body weight loss, SV declined 6.4 +/- 1.3 ml (4.8%) in H and 3.4 +/- 0.4 ml (2.5%) in C, whereas T(es) increased 0.21 +/- 0.02 and 0. 10 +/- 0.02 degrees C in H and C, respectively (P < 0.05). However, reductions in SV were not associated with increases in skin blood flow. The reduced SV was highly associated with increased heart rate and reduced blood volume in both H (R = 0.96; P < 0.01) and C (R = 0. 85; P < 0.01). In conclusion, these results suggest that SV is maintained in trained subjects during exercise in euhydrated conditions despite large differences in skin blood flow. Furthermore, the lowering of SV with dehydration appears largely related to increases in heart rate and reductions in blood volume.

Adult↗
PubMed2000

Muscle oxygen kinetics at onset of intense dynamic exercise in humans.

The present study examined the onset and the rate of rise of muscle oxidation during intense exercise in humans and whether oxygen availability limits muscle oxygen uptake in the initial phase of intense exercise. Six subjects performed 3 min of intense one-legged knee-extensor exercise [65.3 +/- 3.7 (means +/- SE) W]. The femoral arteriovenous blood mean transit time (MTT) and time from femoral artery to muscle microcirculation was determined to allow for an examination of the oxygen uptake at capillary level. MTT was 15.3 +/- 1.8 s immediately before exercise, 10.4 +/- 0.7 s after 6 s of exercise, and 4.7 +/- 0.5 s at the end of exercise. Arterial venous O(2) difference (a-v(diff) O(2)) of 18 +/- 5 ml/l before the exercise was unchanged after 2 s, but it increased (P < 0.05) after 6 s of exercise to 43 +/- 10 ml/l and reached 146 +/- 4 ml/l at the end of exercise. Thigh oxygen uptake increased (P < 0.05) from 32 +/- 8 to 102 +/- 28 ml/min after 6 s of exercise and to 789 +/- 88 ml/min at the end of exercise. The time to reach half-peak a-v(diff) O(2) and thigh oxygen uptake was 13 +/- 2 and 25 +/- 3 s, respectively. The difference between thigh oxygen delivery (blood flow x arterial oxygen content) and thigh oxygen uptake increased (P < 0.05) after 6 s and returned to preexercise level after 14 s. The present data suggest that, at the onset of exercise, oxygen uptake of the exercising muscles increases after a delay of only a few seconds, and oxygen extraction peaks after approximately 50 s of exercise. The limited oxygen utilization in the initial phase of intense exercise is not caused by insufficient oxygen availability.

Adult↗
PubMed1999

Metabolic and thermodynamic responses to dehydration-induced reductions in muscle blood flow in exercising humans.

1. The present study examined whether reductions in muscle blood flow with exercise-induced dehydration would reduce substrate delivery and metabolite and heat removal to and from active skeletal muscles during prolonged exercise in the heat. A second aim was to examine the effects of dehydration on fuel utilisation across the exercising leg and identify factors related to fatigue. 2. Seven cyclists performed two cycle ergometer exercise trials in the heat (35 C; 61 +/- 2 % of maximal oxygen consumption rate, VO2,max), separated by 1 week. During the first trial (dehydration, DE), they cycled until volitional exhaustion (135 +/- 4 min, mean +/- s.e.m.), while developing progressive DE and hyperthermia (3.9 +/- 0.3 % body weight loss and 39.7 +/- 0.2 C oesophageal temperature, Toes). On the second trial (control), they cycled for the same period of time maintaining euhydration by ingesting fluids and stabilising Toes at 38.2 +/- 0.1 degrees C. 3. After 20 min of exercise in both trials, leg blood flow (LBF) and leg exchange of lactate, glucose, free fatty acids (FFA) and glycerol were similar. During the 20 to 135 +/- 4 min period of exercise, LBF declined significantly in DE but tended to increase in control. Therefore, after 120 and 135 +/- 4 min of DE, LBF was 0.6 +/- 0.2 and 1.0 +/- 0.3 l min-1 lower (P < 0.05), respectively, compared with control. 4. The lower LBF after 2 h in DE did not alter glucose or FFA delivery compared with control. However, DE resulted in lower (P < 0.05) net FFA uptake and higher (P < 0.05) muscle glycogen utilisation (45 %), muscle lactate accumulation (4.6-fold) and net lactate release (52 %), without altering net glycerol release or net glucose uptake. 5. In both trials, the mean convective heat transfer from the exercising legs to the body core ranged from 6.3 +/- 1.7 to 7.2 +/- 1.3 kJ min-1, thereby accounting for 35-40 % of the estimated rate of heat production ( approximately 18 kJ min-1). 6. At exhaustion in DE, blood lactate values were low whereas blood glucose and muscle glycogen levels were still high. Exhaustion coincided with high body temperature ( approximately 40 C). 7. In conclusion, the present results demonstrate that reductions in exercising muscle blood flow with dehydration do not impair either the delivery of glucose and FFA or the removal of lactate during moderately intense prolonged exercise in the heat. However, dehydration during exercise in the heat elevates carbohydrate oxidation and lactate production. A major finding is that more than one-half of the metabolic heat liberated in the contracting leg muscles is dissipated directly to the surrounding environment. The present results indicate that hyperthermia, rather than altered metabolism, is the main factor underlying the early fatigue with dehydration during prolonged exercise in the heat.

Adult↗
PubMed1999

Skeletal muscle substrate metabolism during exercise: methodological considerations.

The aim of the present article is to evaluate critically the various methods employed in studies designed to quantify precisely skeletal muscle substrate utilization during exercise. In general, the pattern of substrate utilization during exercise can be described well from O2 uptake measurements and the respiratory exchange ratio. However, if the aim is to quantify limb or muscle metabolism, invasive measurements have to be carried out, such as the determination of blood flow, arterio-venous (a-v) difference measurements for O2 and relevant substrates, and biopsies of the active muscle. As many substrates and metabolites may be both taken up and released by muscle at rest and during exercise, isotopes can be used to determine uptake and/or release and also fractional uptake can be accounted for. Furthermore, the use of isotopes opens up further possibilities for the estimation of oxidation rates of various substrates. There are several methodological concerns to be aware of when studying the metabolic response to exercise in human subjects. These concerns include: (1) the muscle mass involved in the exercise is largely unknown (bicycle or treadmill). Moreover, whether the muscle sample obtained from a limb muscle and the substrate and metabolite concentrations are representative can be a problem; (2) the placement of the venous catheter can be critical, and it should be secured so that the blood sample represents blood from the active muscle with a minimum of contamination from other muscles and tissues; (3) the use of net limb glycerol release to estimate lipolysis is probably not valid (triacylglycerol utilization by muscle), since glycerol can be metabolized in skeletal muscle; (4) the precision of blood-borne substrate concentrations during exercise measured by a-v difference is hampered since they become very small due to the high blood flow. Recommendations are given in order to obtain more quantitative and conclusive data in studies investigating the regulatory mechanisms for substrate choice by muscle.

Arteries↗
PubMed1999

Supine exercise restores arterial blood pressure and skin blood flow despite dehydration and hyperthermia.

We determined whether the deleterious effects of dehydration and hyperthermia on cardiovascular function during upright exercise were attenuated by elevating central blood volume with supine exercise. Seven trained men [maximal oxygen consumption (VO(2 max)) 4.7 +/- 0. 4 l/min (mean +/- SE)] cycled for 30 min in the heat (35 degrees C) in the upright and in the supine positions (VO(2) 2.93 +/- 0.27 l/min) while maintaining euhydration by fluid ingestion or while being dehydrated by 5% of body weight after 2 h of upright exercise. When subjects were euhydrated, esophageal temperature (T(es)) was 37. 8-38.0 degrees C in both body postures. Dehydration caused equal hyperthermia during both upright and supine exercise (T(es) = 38. 7-38.8 degrees C). During upright exercise, dehydration lowered stroke volume (SV), cardiac output, mean arterial pressure (MAP), and cutaneous vascular conductance and increased heart rate and plasma catecholamines [30 +/- 6 ml, 3.0 +/- 0.7 l/min, 6 +/- 2 mmHg, 22 +/- 8%, 14 +/- 2 beats/min, and 50-96%, respectively; all P < 0. 05]. In contrast, during supine exercise, dehydration did not cause significant alterations in MAP, cutaneous vascular conductance, or plasma catecholamines. Furthermore, supine versus upright exercise attenuated the increases in heart rate (7 +/- 2 vs. 9 +/- 1%) and the reductions in SV (13 +/- 4 vs. 21 +/- 3%) and cardiac output (8 +/- 3 vs. 14 +/- 3%) (all P < 0.05). These results suggest that the decline in cutaneous vascular conductance and the increase in plasma norepinephrine concentration, independent of hyperthermia, are associated with a reduction in central blood volume and a lower arterial blood pressure.

Adult↗
PubMed1999

Influence of body temperature on the development of fatigue during prolonged exercise in the heat.

We investigated whether fatigue during prolonged exercise in uncompensable hot environments occurred at the same critical level of hyperthermia when the initial value and the rate of increase in body temperature are altered. To examine the effect of initial body temperature [esophageal temperature (Tes) = 35.9 +/- 0.2, 37.4 +/- 0. 1, or 38.2 +/- 0.1 (SE) degrees C induced by 30 min of water immersion], seven cyclists (maximal O2 uptake = 5.1 +/- 0.1 l/min) performed three randomly assigned bouts of cycle ergometer exercise (60% maximal O2 uptake) in the heat (40 degrees C) until volitional exhaustion. To determine the influence of rate of heat storage (0.10 vs. 0.05 degrees C/min induced by a water-perfused jacket), four cyclists performed two additional exercise bouts, starting with Tes of 37.0 degrees C. Despite different initial temperatures, all subjects fatigued at an identical level of hyperthermia (Tes = 40. 1-40.2 degrees C, muscle temperature = 40.7-40.9 degrees C, skin temperature = 37.0-37.2 degrees C) and cardiovascular strain (heart rate = 196-198 beats/min, cardiac output = 19.9-20.8 l/min). Time to exhaustion was inversely related to the initial body temperature: 63 +/- 3, 46 +/- 3, and 28 +/- 2 min with initial Tes of approximately 36, 37, and 38 degrees C, respectively (all P < 0.05). Similarly, with different rates of heat storage, all subjects reached exhaustion at similar Tes and muscle temperature (40.1-40.3 and 40. 7-40.9 degrees C, respectively), but with significantly different skin temperature (38.4 +/- 0.4 vs. 35.6 +/- 0.2 degrees C during high vs. low rate of heat storage, respectively, P < 0.05). Time to exhaustion was significantly shorter at the high than at the lower rate of heat storage (31 +/- 4 vs. 56 +/- 11 min, respectively, P < 0.05). Increases in heart rate and reductions in stroke volume paralleled the rise in core temperature (36-40 degrees C), with skin blood flow plateauing at Tes of approximately 38 degrees C. These results demonstrate that high internal body temperature per se causes fatigue in trained subjects during prolonged exercise in uncompensable hot environments. Furthermore, time to exhaustion in hot environments is inversely related to the initial temperature and directly related to the rate of heat storage.

Adult↗
PubMed1998

Muscle blood flow is reduced with dehydration during prolonged exercise in humans.

1. The present study examined whether the blood flow to exercising muscles becomes reduced when cardiac output and systemic vascular conductance decline with dehydration during prolonged exercise in the heat. A secondary aim was to determine whether the upward drift in oxygen consumption (VO2) during prolonged exercise is confined to the active muscles. 2. Seven euhydrated, endurance-trained cyclists performed two bicycle exercise trials in the heat (35 C; 40-50 % relative humidity; 61 +/- 2 % of maximal VO2), separated by 1 week. During the first trial (dehydration trial, DE), they bicycled until volitional exhaustion (135 +/- 4 min, mean +/- s.e.m.), while developing progressive dehydration and hyperthermia (3.9 +/- 0.3 % body weight loss; 39.7 +/- 0.2 C oesophageal temperature, Toes). In the second trial (control trial), they bicycled for the same period of time while maintaining euhydration by ingesting fluids and stabilizing Toes at 38.2 +/- 0.1 C after 30 min exercise. 3. In both trials, cardiac output, leg blood flow (LBF), vascular conductance and VO2 were similar after 20 min exercise. During the 20 min-exhaustion period of DE, cardiac output, LBF and systemic vascular conductance declined significantly (8-14 %; P < 0.05) yet muscle vascular conductance was unaltered. In contrast, during the same period of control, all these cardiovascular variables tended to increase. After 135 +/- 4 min of DE, the 2.0 +/- 0.6 l min-1 lower blood flow to the exercising legs accounted for approximately two-thirds of the reduction in cardiac output. Blood flow to the skin also declined markedly as forearm blood flow was 39 +/- 8 % (P < 0.05) lower in DE vs. control after 135 +/- 4 min. 4. In both trials, whole body VO2 and leg VO2 increased in parallel and were similar throughout exercise. The reduced leg blood flow in DE was accompanied by an even greater increase in femoral arterial-venous O2 (a-vO2) difference. 5. It is concluded that blood flow to the exercising muscles declines significantly with dehydration, due to a lowering in perfusion pressure and systemic blood flow rather than increased vasoconstriction. Furthermore, the progressive increase in oxygen consumption during exercise is confined to the exercising skeletal muscles.

Adult↗
PubMed1998

Separate and combined influences of dehydration and hyperthermia on cardiovascular responses to exercise.

During endurance exercise in the heat athletes lose 1-21/h of fluid due to thermoregulatory sweating. The ensuing dehydration is accompanied by higher and faster increases in core temperature, which per se can cause fatigue. The main cardiovascular consequences of combined dehydration and hyperthermia [1 degree C higher core temperature and 3-4 kg (4%) body weight loss] are the significant reductions in cardiac output (3 l/min), muscle blood flow, skin blood flow and blood pressure. Separately, however, hyperthermia (i.e., 39.3 C) and dehydration do not significantly reduce cardiac output or blood pressure. In conclusion, the superimposition of dehydration on hyperthermia during exercise in the heat causes greater alterations in cardiovascular function that make the dehydrated athlete much less able to cope with hyperthermia.

Blood Pressure↗