Effect of temperature on skeletal muscle energy turnover during dynamic knee-extensor exercise in humans.

The present study examined the effect of elevated temperature on muscle energy turnover during dynamic exercise. Nine male subjects performed 10 min of dynamic knee-extensor exercise at an intensity of 43 W (SD 10) and a frequency of 60 contractions per minute. Exercise was performed under normal (C) and elevated muscle temperature (HT) through passive heating. Thigh oxygen uptake (V(O2)) was determined from measurements of thigh blood flow and femoral arterial-venous differences for oxygen content. Anaerobic energy turnover was estimated from measurements of lactate release as well as muscle lactate accumulation and phosphocreatine utilization based on analysis of muscle biopsies obtained before and after each exercise. At the start of exercise, muscle temperature was 34.5 degrees C (SD 1.7) in C compared with 37.2 degrees C (SD 0.5) during HT (P < 0.05). Thigh V(O2) after 3 min was 0.52 l/min (SD 0.11) in C and 0.63 l/min (SD 0.13) in HT, and at the end of exercise it was 0.60 l/min (SD 0.14) and 0.61 l/min (SD 0.10) in C and HT, respectively (not significant). Total lactate release was the same between the two temperature conditions, as was muscle lactate accumulation and PCr utilization. Total ATP production (aerobic + anaerobic) was the same between each temperature condition [505.0 mmol/kg (SD 107.2) vs. 527.1 mmol/kg (SD 117.6); C and HT, respectively]. In conclusion, within the range of temperatures studied, passively increasing muscle temperature before exercise has no effect on muscle energy turnover during dynamic exercise.     

Plateau in muscle blood flow during prolonged exercise in miniature swine

Cardiovascular, metabolic, and thermoregulatory responses were studied in eight male miniature swine during a prolonged treadmill run. Each animal underwent 8-10 wk of exercise training, thoracic surgery, and 3 wk of retraining before the experimental run. This regimen enabled the animals to run at 65% of the heart rate range (210-220 beats/min) for approximately 100 min. Skin wetting and a fan were used to cool the pigs during the run. Regional blood flow was significantly altered with the onset of exercise; however, hindlimb muscle and total gastrointestinal blood flow were unchanged throughout the exercise period. Compared with 5-min values, heart rate and cardiac output were significantly elevated by 17 beats/min and 31 ml.min-1.kg-1 at 60 min and by 20 beats/min and 33 ml.min-1.kg-1 at end exercise, respectively. Core temperatures increased between 5 and 30 min of exercise (39.4 vs. 39.9 degrees C) but then remained unchanged to the end of exercise. Mean arterial pressure, O2 consumption, and blood lactate did not change during the exercise bout. These data indicate that limiting increases in core temperature during prolonged exercise was associated with a plateau in active muscle blood flow.     

The effects of hyperthermia and hypoxia on ventilation during low-intensity steady-state exercise

This study assessed whether the elevated sensitivity of ventilation to hypoxia during exercise is accounted for by an elevation of esophageal temperature (T(es)). Eleven males volunteered for two exercise sessions on an underwater, head-out cycle ergometer at a steady-state rate of oxygen consumption (V(.)(O(2))) of approximately 0.87 l/min (SD 0.07). In one exercise session, 31.5 degrees C (SD 1.4) water held T(es) at a normothermic level of approximately 37.1 degrees C, and in the other exercise session, water at 38.2 degrees C (SD 0.1) maintained a hyperthermic T(es) of approximately 38.5 degrees C. After a 30-min rest and 20-min warm-up, exercising participants inhaled air for 10 min [Euoxia 1 (E1)], an isocapnic hypoxic gas mixture with 12% O(2) in N(2) (H1) for the next 10 min and air again [Euoxia 2 (E2)] for the last 10 min. A significant increase in V(.)(E) during all hyperthermia conditions (0.01< P < 0.048) was evident; however, during hyperthermic hypoxia, there was a disproportionate and significant (P = 0.017) increase in V(.)(E) relative to normothermic hypoxia. This was the main explanation for a significant esophageal temperature and gas type interaction (P = 0.012) for V(.)(E). Significant effects of hyperthermia, isocapnic hypoxia, and their positive interaction remained evident after removing the influence of (V(.)(O(2))) on V(.)(E). Serum lactate and potassium concentrations, as well as hemoglobin oxygen saturation, were each not significantly different between normothermic and hyperthermic-hypoxic conditions. In conclusion, the elevated sensitivity of exercise ventilation to hypoxia during exertion appears to be modulated by elevations in esophageal temperature, potentially because of a temperature-mediated stimulation of the peripheral chemoreceptors.     

Skeletal muscle metabolism during exercise is influenced by heat acclimation

The influence of heat acclimation on skeletal muscle metabolism during submaximal exercise was studied in 13 healthy men. The subjects performed 30 min of cycle exercise (70% of individual maximal O2 uptake) in a cool [21 degrees C, 30% relative humidity (rh)] and a hot (49 degrees C, 20% rh) environment before and again after they were heat acclimated. Aerobic metabolic rate was lower (0.1 l X min-1; P less than 0.01) during exercise in the heat compared with the cool both before and after heat acclimation. Muscle and plasma lactate accumulation with exercise was greater (P less than 0.01) in the hot relative to the cool environment both before and after acclimation. Acclimation lowered (P less than 0.01) aerobic metabolic rate as well as muscle and plasma lactate accumulation in both environments. The amount of muscle glycogen utilized during exercise in the hot environment did not differ from that in the cool either before or after acclimation. These findings indicate that accumulation of muscle lactate is increased and aerobic metabolic rate is decreased during exercise in the heat before and after heat acclimation; increased muscle glycogen utilization does not account for the increased muscle lactate accumulation during exercise under extreme heat stress; and heat acclimation lowers the aerobic metabolic rate and muscle and blood lactate accumulation during exercise in a cool as well as a hot environment.     

Influence of menstrual cycle on thermoregulatory, metabolic, and heart rate responses to exercise at night

Ten women [mean maximal O2 uptake (VO2max), 2.81 l X min-1] exercised for 15 min on a cycle ergometer in the middle of the luteal phase (L) and in the early follicular phase (F) of the menstrual cycle at the same constant work rates (mean 122 W) and an ambient temperature of 18 degrees C. Serum progesterone averaged 44.7 nmol X l-1 in L and 0.7 nmol X l-1 in F. After a 4-h resting period, exercise was performed between 3 and 4 A.M., when the L-F core temperature difference is maximal. Preexercise esophageal (Tes), tympanic (Tty), and rectal (Tre) temperatures averaged 0.6 degrees C higher in L. During exercise Tes, Tty, and Tre averaged 0.5 degrees C higher. The thresholds for chest sweating and cutaneous vasodilation (heat clearance technique) at the thumb and forearm were elevated in L by an average of 0.47 degrees C, related to mean body temperature (Tb(es) = 0.87Tes + 0.13Tskin), Tes, Tty, or Tre. The above-threshold chest sweat rate and cutaneous heat clearances were also increased in L. The mean exercise heart rate was 170.0 beats X min-1 in L and 163.8 beats X min-1 in F. The mean exercise VO2 in L (2.21 l X min-1) was 5.2% higher than in F (2.10 l X min-1), the metabolic rate was increased in L by 5.6%, but the net efficiency was 5.3% lower. No significant L-F differences in the respiratory exchange ratio and postexercise plasma lactate were demonstrated.(ABSTRACT TRUNCATED AT 250 WORDS)     

The effects of blood loss on the performance of physical exercise

Seven male subjects were studied before and up to 53 days after the loss of 11 of blood. The resting hematocrit fell from 44.0 to 38.7% and returned to control level after 3 weeks. Maximal oxygen uptake decreased from 4.00 1/min to 3.54 1/min and returned to the initial level within 2 weeks. Submaximal oxygen uptake, pulmonary ventilation, maximal heart rate and blood lactate were not found to change significantly. Submaximal heart rate was increased from 125 beats . min-1 to about 135 beats . min-1 and remained elevated for 3 weeks, whereas blood lactate was increased only in the first week. Maximal work time decreased from 5.1 min to 3.8 min and remained low for the first 2 weeks, but rose thereafter above the starting level. Comparison with a control study suggested that there is some training effect, which, when allowed for, indicates that maximal work time returns to starting values at the same time as does the maximal oxygen uptake. It is concluded that the drop in Hct, maximal oxygen uptake and work capacity, found after the loss of 11 of blood, are related to each other both in magnitude and duration.     

Metabolic effects of exposure to hypoxia plus cold at rest and during exercise in humans

To determine effects on metabolic responses, subjects were exposed to four environmental conditions for 90 min at rest followed by 30 min of exercise: breathing room air with an ambient temperature of 25 degrees C (NN); breathing room air with an ambient temperature of 8 degrees C (NC); hypoxia (induced by breathing 12% O2 in N2) with a neutral temperature (HN); and hypoxia in the cold (HC). Hypoxia increased heart rate (HR), systolic blood pressure (SBP), pulmonary ventilation (VE), respiratory exchange ratio (R), blood lactate, and perceived exertion during exercise while depressing rectal temperature (Tre) and O2 uptake (VO2). Cold exposure elevated SBP, diastolic blood pressure (DBP), VE, VO2, blood glucose, and blood glycerol but decreased HR, Tre, and R. Shivering and DBP were higher and Tre was lower in HC compared with NC. HR, SBP, VE, R, and lactate tended to be higher in HC compared with NC, whereas VO2 and blood glycerol tended to be depressed. These results suggest that cold exposure during hypoxia results in an increased reliance on shivering for thermogenesis at rest whereas, during exercise, heat loss is accelerated.     

Effect of pyridostigmine on the exercise-heat response of man

The effect of pyridostigmine on thermoregulatory responses was evaluated during exercise and heat stress. Eight heat acclimated, young adult male subjects received four doses of pyridostigmine (30 mg) or identical placebo tablets every 8 h, in a double blind, randomized, cross-over trial. A 30.3%, SD 4.6% inhibition of the circulating cholinesterase (ChE) activity was induced in the pyridostigmine-treated group. The subjects were exposed to 170-min exercise and heat-stress (dry bulb temperature, 33 degrees C; relative humidity 60%) consisting of 60 min in a sitting position and two bouts of 50-min walking (1.39 m.s-1, 5% gradient) which were separated by 10-min rest periods. No differences were found between treatments in the physiological responses and heat balance parameters at the end of exposure: heart rate (fc) was 141 beats.min-1, SD 16 and 150 beats.min-1, SD 12, rectal temperature (Tre) was 38.5 degrees C, SD 0.4 degrees and 38.6 degrees C, SD 0.3 degrees, heat storage was 60 W.m-2, SD 16 and 59 W.m-2, SD 15 and sweat rate was 678 g.h-1, SD 184 and 661 g.h-1, SD 133, in the pyridostigmine and placebo treatments, respectively. The changes in Tre and fc over the heat-exercise period were parallel in both study and control groups. Pyridostigmine caused a slight slowing of fc (5 beats.min-1) which was consistent throughout the entire exposure (P less than 0.001) but was of no clinical significance. The overall change in fc was similar for both groups.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of feeding on muscle blood flow during prolonged exercise in miniature swine

Eight exercise-trained miniature swine were studied during prolonged treadmill runs (100 min) under fasting and preexercise feeding conditions. Each animal ran at identical external work loads that corresponded to 65% of the heart rate reserve (210-220 beats/min) for the two exercise bouts. Cardiac outputs and stroke volumes were higher and heart rates lower for fed than for fasting runs (P less than 0.05). Preexercise feeding did not alter oxygen consumption, core temperature, mean arterial pressure, and arterial-mixed venous oxygen difference during prolonged exercise; however, mixed venous lactate concentration was lower at end exercise than during fasting conditions (1.2 vs. 2.6 mM, P less than 0.05). Microsphere measurements of regional blood flow revealed significantly higher total gastrointestinal flow (23%) for fed than for fasting conditions. Throughout the exercise bout, blood flow to the biceps femoris, semitendinosus, and tibialis anterior muscles was lower in fed than in fasted animals (P less than 0.05). Combined hindlimb muscle blood flow averaged 15 ml.min-1.100 g-1 (18%, P less than 0.05) lower under feeding than fasting run conditions. These findings provide further evidence that cardiovascular reflexes originate in the gut after feeding to increase cardiac output and redistribute a portion of the blood flow away from active muscle to the gastrointestinal tract during prolonged exercise.     

Oxygen consumption following exercise of moderate intensity and duration.

To study the effects of exercise intensity and duration on excess postexercise oxygen consumption (EPOC), 8 men [age = 27.6 (SD 3.8) years, VO2max = 46.1 (SD 8.5) ml min-1 kg-1] performed four randomly assigned cycle-ergometer tests (20 min at 60% VO2max, 40 min at 60% VO2max, 20 min at 70% VO2max, and 40 min at 70% VO2max). O2 uptake, heart rate and rectal temperature were measured before, during, and for 1 h following the exercise tests. Blood for plasma lactate measurements was obtained via cannulae before, and at selected times, during and following exercise. VO2 rapidly declined to preexercise levels following each of the four testing sessions, and there were no differences in EPOC between the sessions. Blood lactate and rectal temperature increased (P < 0.05) with exercise, but had returned to preexercise levels by 40 min of recovery. The results indicate that VO2 returned to resting levels within 40 min after the end of exercise, regardless of the intensity (60% and 70% VO2max) or duration (20 min and 40 min) of the exercise, in men with a moderate aerobic fitness level.     

Effect of muscle temperature on leg extension force and short-term power output in humans

The effect of changing muscle temperature on performance of short term dynamic exercise in man was studied. Four subjects performed 20 s maximal sprint efforts at a constant pedalling rate of 95 crank rev.min-1 on an isokinetic cycle ergometer under four temperature conditions: from rest at room temperature; and following 45 min of leg immersion in water baths at 44; 18; and 12 degrees C. Muscle temperature (Tm) at 3 cm depth was respectively 36.6, 39.3, 31.9 and 29.0 degrees C. After warming the legs in a 44 degrees C water bath there was an increase of approximately 11% in maximal peak force and power (PPmax) compared with normal rest while cooling the legs in 18 and 12 degrees C water baths resulted in reductions of approximately 12% and 21% respectively. Associated with an increased maximal peak power at higher Tm was an increased rate of fatigue. Two subjects performed isokinetic cycling at three different pedalling rates (54, 95 and 140 rev.min-1) demonstrating that the magnitude of the temperature effect was velocity dependent: At the slowest pedalling rate the effect of warming the muscle was to increase PPmax by approximately 2% per degree C but at the highest speed this increased to approximately 10% per degree C.     

Leg muscle metabolism during exercise in the heat and cold.

In an effort to assess the effects of environmental heat stress on muscle metabolism during exercise, 6 men performed work in the heat (Tdb = 44 degrees C, RH = 15%) and cold (Tdb = 9 degrees C, RH = 55%). Exercise consisted of three 15-min cycling bouts at 70 to 85% VO2max, with 10-min rest between each. Muscle biopsies obtained from the vastus lateralis before and after each work bout were analyzed for glycogen and triglyceride content. Venous blood samples drawn before and after exercise were assayed for lactate, glucose, free fatty acids, hemoglobin, and hematocrit. Oxygen uptake, heart rates and rectal temperatures were all significantly higher during exercise in the heat. Blood lactate concentration was roughly twice as great during the heat experiments as that measured in the 9 degrees C environment. Muscle glycogen utilization per 60 min was significantly greater in the heat ( - 74 m moles/kg-wet muscle) as compared to the cold exercise (- 42 m moles/kg-wet muscle). On the average, muscle triglyceride declined 23% during exercise in the cold and 11% in the heat. The findings of an enhanced glycolysis during exercise in the heat is compatible with earlier studies which demonstrate a decreased availability of oxygen due to a reduction in muscle blood flow.     

Altered sarcoplasmic reticulum function after high-intensity exercise

This study examined the effects of acute high-intensity exercise on the rate and capacity of Ca2+ uptake and Ca2+-stimulated adenosinetriphosphatase (ATPase) activity of the sarcoplasmic reticulum and the reversibility of these effects. Thoroughbred horses were run at maximal O2 uptake on a high-speed treadmill until fatigued. Muscle temperatures and biopsy samples were collected at rest, immediately after exercise, and 30 and 60 min after exercise. Blood samples were collected at rest and 5 min after exercise. Muscle and blood (lactate concentration) were three- and fivefold greater than pre-exercise values. Muscle temperature and pH immediately after post-exercise were 43 degrees C and 6.55, respectively, but approached rest values by 60 min after exercise. The initial rate and maximal capacity of Ca2+ uptake of muscle homogenates and isolated sarcoplasmic reticulum were significantly depressed immediately after exercise. This depression was paralleled by decreased activity of the Ca2+-stimulated ATPase. However, both Ca2+ uptake (rate and capacity) and Ca2+4-ATPase activity had returned to normal by 60 min after exercise. These findings demonstrate that changes in sarcoplasmic reticulum function after high-intensity exercise may be induced but not sustained by local changes in muscle pH and/or temperature.     

Effect of previous supramaximal work on lacticaemia during supra-anaerobic threshold exercise

Twelve male and female subjects (eight trained, four untrained) exercised for 30 min on a treadmill at an intensity of maximal O2 consumption (% VO2max) 90.0%, SD 4.7 greater than the anaerobic threshold of 4 mmol.l-1 (Than = 83.6% VO2max, SD 8.9). Time-dependent changes in blood lactate concentration [( lab]) during exercise occurred in two phases: the oxygen uptake (VO2) transient phase (from 0 to 4 min) and the VO2 steady-state phase (4-30 min). During the transient phase, [lab] increased markedly (1.30 mmol.l-1.min-1, SD (0.13). During the steady-state phase, [lab] increased slightly (0.02 mmol.l-1.min-1, SD 0.06) and when individual values were considered, it was seen that there were no time-dependent increases in [lab] in half of the subjects. Following hyperlacticaemia (8.8 mmol.l-1, SD 2.0) induced by a previous 2 min of supramaximal exercise (120% VO2max), [lab] decreased during the VO2 transient (-0.118 mmol.l-1.min-1, SD 0.209) and steady-state (-0.088 mmol.l-1.min-1, SD 0.103) phases of 30 min exercise (91.4% VO2max, SD 4.8). In conclusion, it was not possible from the Than to determine the maximal [lab] steady state for each subject. In addition, lactate accumulated during previous supramaximal exercise was eliminated during the VO2 transient phase of exercise performed at an intensity above the Than. This effect is probably largely explained by the reduction in oxygen deficit during the transient phase. Under these conditions, the time-course of changes in [lab] during the VO2 steady state was also affected.     

Effect of saline infusion on body temperature and endurance during heavy exercise

We tested the hypothesis that volume infusion during strenuous exercise, by expanding blood volume, would allow better skin blood flow and better temperature homeostasis and thereby improve endurance time. Nine males exercised to exhaustion at 84.0 +/- 3.14% (SE) of maximum O2 consumption on a cycle ergometer in a double-blind randomized protocol with either no infusion (control) or an infusion of 0.9% NaCl (mean vol 1,280.3 +/- 107.3 ml). Blood samples and expired gases (breath-by-breath), as well as core and skin temperatures, were analyzed. Plasma volume decreased less during exercise with the infusion at 15 min (-13.7 +/- 1.4% control vs. -5.3 +/- 1.7% infusion, P less than 0.05) and at exhaustion (-13.6 +/- 1.2% vs. -1.3 +/- 2.2%, P less than 0.01). The improved fluid homeostasis was associated with a lower core temperature during exercise (39.0 +/- 0.2 degrees C for control and 38.5 +/- 0.2 degrees C for infusion at exhaustion, P less than 0.01) and lower heart rate (194.1 +/- 3.9 beats/min for control and 186.0 +/- 5.1 beats/min for infusion at exhaustion, P less than 0.05). However, endurance time did not differ between control and infusion (21.96 +/- 3.56 and 20.82 +/- 2.63 min, respectively), and neither did [H+], peak O2 uptake, and CO2 production, end-tidal partial pressure of CO2, blood lactate, or blood pressure. In conclusion, saline infusion increases heat dissipation and lowers core temperature during strenuous exercise but does not influence endurance time.     

Effect of heat stress on muscle blood flow during dynamic handgrip exercise

During exercise in a hot environment, blood flow in the exercising muscles may be reduced in favour of the cutaneous circulation. The aim of our study was to examine whether an acute heat exposure (65-70 degrees C) in sauna conditions reduces the blood flow in forearm muscles during handgrip exercise in comparison to tests at thermoneutrality (25 degrees C). Nine healthy men performed dynamic handgrip exercise of the right hand by rhythmically squeezing a water-filled rubber tube at 13% (light), and at 34% (moderate) of maximal voluntary contraction. The left arm served as a control. The muscle blood flow was estimated as the difference in plethysmographic blood flow between the exercising and the control forearm. Skin blood flow was estimated by laser Doppler flowmetry in both forearms. Oesophageal temperature averaged 36.92 (SEM 0.08) degrees C at thermoneutrality, and 37.74 (SEM 0.07) degrees C (P less than 0.01) at the end of the heat stress. The corresponding values for heart rate were 58 (SEM 2) and 99 (SEM 5) beats.min-1 (P less than 0.01), respectively. At 25 degrees C, handgrip exercise increased blood flow in the exercising forearm above the control forearm by 6.0 (SEM 0.8) ml.100 ml-1.min-1 during light exercise, and by 17.9 (SEM 2.5) ml.100 ml-1.min-1 during moderate exercise. In the heat, the increases were significantly higher: 12.5 (SEM 2.2) ml.100 ml-1.min-1 at the light exercise level (P less than 0.01), and 32.2 (SEM 5.9) ml.100 ml-1.min-1 (P less than 0.05) at the moderate exercise level.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of PDH activation by dichloroacetate in human skeletal muscle during exercise in hypoxia

During the onset of exercise in hypoxia, the increased lactate accumulation is associated with a delayed activation of pyruvate dehydrogenase (PDH; Parolin ML, Spreit LL, Hultman E, Hollidge-Horvat MG, Jones NL, and Heigenhauser GJF. Am J Physiol Endocrinol Metab 278: E522-E534, 2000). The present study investigated whether activation of PDH with dichloroacetate (DCA) before exercise would reduce lactate accumulation during exercise in acute hypoxia by increasing oxidative phosphorylation. Six subjects cycled on two occasions for 15 min at 55% of their normoxic maximal oxygen uptake after a saline (control) or DCA infusion while breathing 11% O(2). Muscle biopsies of the vastus lateralis were taken at rest and after 1 and 15 min of exercise. DCA increased PDH activity at rest and at 1 min of exercise, resulting in increased acetyl-CoA concentration and acetylcarnitine concentration at rest and at 1 min. In the first minute of exercise, there was a trend toward a lower phosphocreatine (PCr) breakdown with DCA compared with control. Glycogenolysis was lower with DCA, resulting in reduced lactate concentration ([lactate]), despite similar phosphorylase a mole fractions and posttransformational regulators. During the subsequent 14 min of exercise, PDH activity was similar, whereas PCr breakdown and muscle [lactate] were reduced with DCA. Glycogenolysis was lower with DCA, despite similar mole fractions of phosphorylase a, and was due to reduced posttransformational regulators. The results from the present study support the hypothesis that lactate production is due in part to metabolic inertia and cannot solely be explained by an oxygen limitation, even under conditions of acute hypoxia.     

Water immersion delays the oxygen uptake response to sitting arm-cranking in humans

We investigated the effect of central hypervolaemia during water immersion up to the xiphoid process on the oxygen uptake (VO2) and heart rate (HR) response to arm cranking. Seven men performed a 6-min arm-cranking exercise at an intensity requiring a VO2 at 80% ventilatory threshold both in air [C trial, 29 (SD 9) W] and immersed in water [WI trial, 29 (SD 11) W] after 6 min of sitting. The VO2 (phase 2) and HR responses to exercise were obtained from a mono-exponential fit [f(t) = baseline + gain x (1 - e(-(t-TD)/tau))]. The response was evaluated by the mean response time [MRT; sum of time constant (tau) and time delay (TD)]. No significant difference in VO2 and HR gains between the C and WI trials was observed [VO2 0.78 (SD 0.1) vs 0.80 (SD 0.2) l x min(-1), HR 36 (SD 7) vs 37 (SD 8) beats x min(-1), respectively]. Although the HR MRT was not significantly different between the C and WI trials [17 (SD 3), 19 (SD 8) s, respectively), VO2 MRT was greater in the WI trial than in the C trial [40 (SD 6), 45 (SD 6) s, respectively; P < 0.05]. Assuming no difference in VO2 in active muscle between the two trials, these results would indicate that an increased oxygen store and/or an altered response in muscle blood distribution delayed the VO2 response to exercise.     

Effects of prolonged exercise in highly trained traumatic paraplegic men

This study investigated the cardiovascular and metabolic responses to prolonged wheelchair exercise in a group of highly trained, traumatic paraplegic men. Six endurance-trained subjects with spinal cord lesions from T10 to T12/L3 underwent a maximal incremental exercise test in which they propelled their own track wheelchairs on a motor-driven treadmill to exhaustion to determine maximal O2 uptake (VO2max) and related variables. One week later each subject exercised in the same wheelchair on a motorized treadmill at 60-65% of VO2max for 80 min in a thermoneutral environment (dry bulb 22 degrees C, wet bulb 17 degrees C). Approximately 10 ml of venous blood were withdrawn both 20 min and immediately before exercise (0 min), after 40 and 80 min of exercise, and 20 min postexercise. Venous blood was analyzed for hematocrit (Hct), hemoglobin (Hb), and lactate, and the separated plasma was analyzed for glucose, K+, Na+, Cl-, free fatty acid (FFA), and osmolality. VO2, CO2 production (VCO2), minute ventilation (VE), respiratory exchange ratio (R), net efficiency, and wheelchair strike rate were determined at four intervals throughout the exercise period. Data were analyzed with an analysis of variance repeated-measures design and a Scheffé post hoc test. VO2max was 47.5 +/- 1.8 (SE) ml.min-1.kg-1 with maximal VE BTPS and maximal heart rate (HR) being 100.1 +/- 3.8 l/min and 190 +/- 1 beats/min, respectively. During prolonged exercise there were no significant changes in VO2, VCO2, VE, R, net efficiency, wheelchair strike rate, and lactate, glucose, and Na+ concentrations. Significant increases occurred in HR, FFA, K+, Cl-, osmolality, Hb, and Hct throughout exercise.(ABSTRACT TRUNCATED AT 250 WORDS)     

Endurance training slows down the kinetics of heart rate increase in the transition from moderate to heavier submaximal exercise intensities

To find out whether endurance training influences the kinetics of the increases in heart rate (fc) during exercise driven by the sympathetic nervous system, the changes in the rate of fc adjustment to step increments in exercise intensities from 100 to 150 W were followed in seven healthy, previously sedentary men, subjected to 10-week training. The training programme consisted of 30-min cycle exercise at 50%-70% of maximal oxygen uptake (VO2max) three times a week. Every week during the first 5 weeks of training, and then after the 10th week the subjects underwent the submaximal three-stage exercise test (50, 100 and 150 W) with continuous fc recording. At the completion of the training programme, the subjects' VO2max had increased significantly (39.2 ml.min-1.kg-1, SD 4.7 vs 46 ml.min-1.kg-1, SD 5.6) and the steady-state fc at rest and at all submaximal intensities were significantly reduced. The greatest decrease in steady-state fc was found at 150 W (146 beats.min-1, SD 10 vs 169 beats.min-1, SD 9) but the difference between the steady-state fc at 150 W and that at 100 W (delta fc) did not decrease significantly (26 beats.min-1, SD 7 vs 32 beats.min-1, SD 6). The time constant (tau) of the fc increase from the steady-state at 100 W to steady-state at 150 W increased during training from 99.4 s, SD 6.6 to 123.7 s, SD 22.7 (P less than 0.01) and the acceleration index (A = 0.63.delta fc.tau-1) decreased from 0.20 beats.min-1.s-1, SD 0.05 to 0.14 beats.min-1.s-1, SD 0.04 (P less than 0.02). The major part of the changes in tau and A occurred during the first 4 weeks of training. It was concluded that heart acceleration following incremental exercise intensities slowed down in the early phase of endurance training, most probably due to diminished sympathetic activation.