Aerobically trained individuals have greater increases in rectal temperature than untrained ones during exercise in the heat at similar relative intensities

To determine if the increases in rectal temperature (T _REC) during exercise in the heat at a given percent of [(V)\dot]O_2 \textpeak \dot{V}\hbox{O}_{{2\,{\text{peak}}}} depend on a subject’s aerobic fitness level. On three occasions, 10 endurance-trained (Tr) and 10 untrained (UTr) subjects ([(V)\dot]O_2 peak \dot{V}\hbox{O}_{2\,{\rm peak}} : 60 ± 6 vs. 44 ± 3 mL kg⁻¹ min⁻¹, P < 0.05) cycled in a hot-dry environment (36 ± 1°C; 25 ± 2% humidity, airflow 2.5 m s⁻¹) at three workloads (40, 60, and 80% [(V)\dot]O_2 peak \dot{V}\hbox{O}_{2\,{\rm peak}} ). At the same percent of [(V)\dot]O_2 peak \dot{V}\hbox{O}_{2\,{\rm peak}} , on average, Tr had 28 ± 5% higher heat production but also higher skin blood flow (29 ± 3%) and sweat rate (20 ± 7%; P = 0.07) and lower skin temperature (0.5°C; P < 0.05). Pre-exercise T _REC was lower in the Tr subjects (37.4 ± 0.2 vs. 37.6 ± 0.2; P < 0.05) but similar to the UTr at the end of 40 and 60% [(V)\dot]O_2 peak \dot{V}\hbox{O}_{2\,{\rm peak}} trials. Thus, exercise T _REC increased more in the Tr group than in the UTr group (0.6 ± 0.1 vs. 0.3 ± 0.1°C at 40% [(V)\dot]O_2 peak \dot{V}\hbox{O}_{2\,{\rm peak}} and 1.0 ± 0.1 vs. 0.6 ± 0.3°C at 60% [(V)\dot]O_2 peak \dot{V}\hbox{O}_{2\,{\rm peak}} ; P < 0.05). At 80% [(V)\dot]O_2 peak \dot{V}\hbox{O}_{2\,{\rm peak}} not only the increase in T _REC (1.7 ± 0.1 vs. 1.3 ± 0.3°C) but also the final T _REC was larger in Tr than in UTr subjects (39.15 ± 0.1 vs. 38.85 ± 0.1°C; P < 0.05). During exercise in the heat at the same relative intensity, aerobically trained individuals have a larger rise in T _REC than do the untrained ones which renders them more hyperthermic after high-intensity exercise.     

Attenuated relationship between cardiac output and oxygen uptake during high-intensity exercise

Aim: Recent findings have challenged the belief that the cardiac output (CO) and oxygen consumption (VO₂) relationship is linear from rest to maximal exercise. The purpose of this study was to determine the CO and stroke volume (SV) response to a range of exercise intensities, 40–100% of VO_2max, during cycling. Methods: Ten well‐trained cyclists performed a series of discontinuous exercise bouts to determine the CO and SV vs. VO₂ responses. Results: The rate of increase in CO, relative to VO₂, during exercise from 40 to 70% of VO_2max was 4.4 ± 1.4 L L^?1. During exercise at 70–100% of VO_2max, the rate of increase in CO was reduced to 2.1 ± 0.9 L L^?1 (P = 0.01). Stroke volume during exercise at 80–100% of VO_2max was reduced by 7% when compared to exercise at 50–70% of VO_2max (134 ± 5 vs. 143 ± 5 mL per beat, P = 0.02). Whole body arterial‐venous O₂ difference increased significantly as intensity increased. Conclusion: The observation that the rate of increase in CO is reduced as exercise intensity increases suggests that cardiovascular performance displays signs of compromised function before maximal VO₂ is reached.     

Oxygen uptake kinetics during exercise in adults with Down syndrome

Persons with Down syndrome (DS) have diminished submaximal and peak work capacity. This study evaluated the dynamic response of oxygen uptake at onset and recovery (VO₂ kinetics) of constant-load exercise (moderate intensity 45% VO_2peak) in adults with DS. A total of 27 healthy participants aged 18–50 years performed graded treadmill exercise to assess peak VO₂: 14 with DS (9 males and 5 females) and 13 controls without disabilities (9 males and 4 females). Subjects also performed constant-load exercise tests at 45% VO_2peak to determine VO₂ on-transient and VO₂ off-transient responses. Peak VO₂ was lower in participants with DS as compared to controls (DS 30.2 ± 7.1; controls 46.1 ± 9.6 mL kg⁻¹ min⁻¹, P < 0.05). In contrast, at 45% VO_2peak, the time constants for the VO₂ on-transients (DS 34.6 ± 9.1; controls 37.6 ± 9.0 s) and VO₂ off-transients (DS 36.5 ± 12.3; controls 37.7 ± 7.0 s) were not significantly different between the groups. Additionally, there were no differences between on-transient and off-transient time constants in participants with DS or controls. These data demonstrate that the VO₂ kinetics at onset and recovery of moderate intensity exercise is similar between adults with DS and controls. Therefore, the submaximal exercise performance of these individuals is not affected by slowed VO₂ kinetics.     

Enhanced cerebral CO2 reactivity during strenuous exercise in man

Light and moderate exercise elevates the regional cerebral blood flow by ~20% as determined by ultrasound Doppler sonography (middle cerebral artery mean flow velocity; MCA V _mean). However, strenuous exercise, especially in the heat, appears to reduce MCA V _mean more than can be accounted for by the reduction in the arterial CO₂ tension (P _aCO₂). This study evaluated whether the apparently large reduction in MCA V _mean at the end of exhaustive exercise relates to an enhanced cerebrovascular CO₂ reactivity. The CO₂ reactivity was evaluated in six young healthy male subjects by the administration of CO₂ as well as by voluntary hypo- and hyperventilation at rest and during exercise with and without hyperthermia. At rest, P _aCO₂ was 5.1±0.2 kPa (mean ± SEM) and MCA V _mean 50.7±3.8 cm s⁻¹ and the relationship between MCA V _mean and P _aCO₂ was linear (double-log slope 1.1±0.1). However, the relationship became curvilinear during exercise (slope 1.8±0.1; P<0.01 vs. rest) and during exercise with hyperthermia (slope 2.3±0.3; P<0.05 vs. control exercise). Accordingly, the cerebral CO₂ reactivity increased from 30.5±2.7% kPa⁻¹ at rest to 61.4±10.1% kPa⁻¹ during exercise with hyperthermia (P<0.05). At exhaustion P _aCO₂ decreased 1.1±0.2 kPa during exercise with hyperthermia, which, with the determined cerebral CO₂ reactivity, accounted for the 28±10% decrease in MCA V _mean. The results suggest that during exercise changes in cerebral blood flow are dominated by the arterial carbon dioxide tension.     

Influence of sildenafil on lung diffusion during exposure to acute hypoxia at rest and during exercise in healthy humans

We sought to determine the influence of sildenafil on the diffusing capacity of the lungs for carbon monoxide (DL_CO) and the components of DL_CO (pulmonary capillary blood volume V _c, and alveolar–capillary membrane conductance D _M) at rest and following exercise with normoxia and hypoxia. This double-blind placebo-controlled, cross-over study included 14 healthy subjects (age = 33 ± 11 years, ht = 181 ± 8 cm, weight = 85 ± 14 kg, BMI = 26 ± 3 kg/m², peak normoxic VO₂ = 36 ± 6 ml/kg, mean ± SD). Subjects were randomized to placebo or 100 mg sildenafil 1 h prior to entering a hypoxic tent with an FiO₂ of 12.5% for 90 min. DLCO, V _c, and D _M were assessed at rest, every 3 min during exercise, at peak exercise, and 10 and 30 min post exercise. Sildenafil attenuated the elevation in PAP at rest and during recovery with exposure to hypoxia, but pulmonary arterial pressure immediately post exercise was not different between sildenafil and placebo. Systemic O₂ saturation and VO_2peak did not differ between the two conditions. DL_CO was not different between groups at any time point. V _C was higher with exercise in the placebo group, and the difference in D _M between sildenafil and placebo was significant only when corrected for changes in V _c (D _M/V _c = 0.57 ± 0.29 vs. 0.41 ± 0.16, P = 0.04). These results suggest no effect of sildenafil on DLCO, but an improvement in D _M when corrected for changes in V _c during short-term hypoxic exposure with exercise.     

Effects of anaemia and stepwise-induced polycythaemia on maximal aerobic power in individuals with high and low haemoglobin concentrations

Increasing the haemoglobin concentration ([Hb]) improves the oxygen transport capacity but it also increases the viscosity of the blood. The influence of changes in [Hb] and viscosity on submaximal exercise capacity and maximal aerobic power was investigated in eight healthy males in varying states of training and with a normal resting [Hb] ([Hb]_r), ranging from 123 to 178 g]^-1. The subjects were venesected five times (450 ml per unit) and exercise tests were performed in the anaemic state. After 5–7 weeks, when [Hb] had returned to the ‘normal’ value, a stepwise re-transfusion of three to five units of blood was performed with exercise tests after each transfusion. The [Hb]_r was 137 ± 15 g l^-1 in the anaemic state (A) and 170 ± 16 g l^-1 after the last re-transfusion (LT). The V_o2max rose from 3.94 ± 0.35 in A to 4.68 ± 0.30 1 min^-1 after LT. Individual regression lines for [Hb] and V_o2max revealed a mean increase in V_o2max of 19 ± 6 ml min^-1 per g l^-1 change in [Hb]. This value did not differ between individuals with high and low normal [Hb]. Furthermore, in intra-individual comparisons the relationship between [Hb] and V_o2max in high and low individual [Hb] ranges was not found to be statistically different despite a 40% increase in the in vitro viscosity from the anaemic to the polycythaemic state. The average individual correlation (based on five to seven measurements) between [Hb] at rest and after exercise and V_o2max was r= 0.89 (P > 0.01) in the former case and r= 0.92 (P > 0.01) in the latter. The running velocity corresponding to a blood lactate concentration of 4 mM (V_Hla4.0) increased from 15.3 ± 2.3 in the control state to 15.6±2.3 km h¹ after the last transfusion (P > 0.01). A leftward shift of the blood lactate curve, expressed as a percentage of V_o2max, was found. In conclusion, the results obtained indicate a close relationship between V_o2max and [Hb] up to at least 170 g l^-1. Furthermore, both inter-and intra-individual comparisons suggest that the influence of viscosity as such on V_o2max does not differ at high and low [Hb] levels.     

Middle cerebral artery blood velocity during exercise with β‐1 adrenergic and unilateral stellate ganglion blockade in humans

A reduced ability to increase cardiac output (CO) during exercise limits blood flow by vasoconstriction even in active skeletal muscle. Such a flow limitation may also take place in the brain as an increase in the transcranial Doppler determined middle cerebral artery blood velocity (MCA V_mean) is attenuated during cycling with β‐1 adrenergic blockade and in patients with heart insufficiency. We studied whether sympathetic blockade at the level of the neck (0.1% lidocain; 8 mL; n=8) affects the attenuated exercise – MCA V_mean following cardio‐selective β‐1 adrenergic blockade (0.15 mg kg^?1 metoprolol i.v.) during cycling. Cardiac output determined by indocyanine green dye dilution, heart rate (HR), mean arterial pressure (MAP) and MCA V_mean were obtained during moderate intensity cycling before and after pharmacological intervention. During control cycling the right and left MCA V_mean increased to the same extent (11.4 ± 1.9 vs. 11.1 ± 1.9 cm s^?1). With the pharmacological intervention the exercise CO (10 ± 1 vs. 12 ± 1 L min^?1; n=5), HR (115 ± 4 vs. 134 ± 4 beats min^?1) and ΔMCA V_mean (8.7 ± 2.2 vs. 11.4 ± 1.9 cm s^?1) were reduced, and MAP was increased (100 ± 5 vs. 86 ± 2 mmHg; P < 0.05). However, sympathetic blockade at the level of the neck eliminated the β‐1 blockade induced attenuation in ΔMCA V_mean (10.2 ± 2.5 cm s^?1). These results indicate that a reduced ability to increase CO during exercise limits blood flow to a vital organ like the brain and that this flow limitation is likely to be by way of the sympathetic nervous system.     

Middle cerebral artery blood velocity and plasma catecholamines during exercise

During dynamic exercise, mean blood velocity (V_mean) in the middle cerebral artery (MCA) demonstrates a graded increase to work rate and reflects regional cerebral blood flow. At a high work rate, however, vasoactive levels of plasma catecholamines could mediate vasoconstriction of the MCA and thereby elevate V_mean at a given volume flow. To evaluate transcranial Doppler-determined V_mean at high plasma catecholamine levels, seven elite cyclists performed a maximal performance test on a bicycle ergometer. Results were compared with those elicited during five incremental exercise bouts and during rhythmic handgrip when plasma catecholamines are low. During rhythmic handgrip the V_mean was elevated by 21±3% (mean±SE), which was not statistically different from that established during moderate cycling. However, at the highest submaximal and maximal work intensities on the bicycle ergometer, V_mean increased by 31±3% and 48±4%, respectively, and this was significantly higher compared to handgrip (P<0.05). During maximal cycling, plasma adrenaline increased from 0.21±0.04 nmol L^-1 at rest to 4.18±1.46 nmol L^-1, and noradrenaline increased from 0.79±0.08 to 12.70±1.79 nmol L^-1. These levels were 12- to 16-fold higher than those during rhythmic handgrip (adrenaline: 0.34±0.03 nmol L^-1; noradrenaline: 0.78±0.05 nmol L^-1). The increase in V_mean during intense ergometer cycling conforms to some middle cerebral artery constriction elicited by plasma catecholamines. Such an influence is unlikely during rhythmic handgrip compared with low intensity cycling.     

Exercise-induced decreases in sarcoplasmic reticulum Ca2+–ATPase activity attenuated by high-resistance training

Muscle biopsies were performed on the vastus lateralis muscle prior to and during a high-resistance training (HRT) programme in order to examine the effects of hypertrophy on sarcoplasmic reticulum Ca²⁺ ATPase activity at rest and during exercise. In six male untrained volunteers (peak aerobic power, V˙O ₂ peak = 3.39 ± 0.13 L min^?1, mean ± SE), the resting Ca²⁺ ATPase activity (μmol min^?1 g wet wt^?1) at 0 (4.89 ± 0.20), 4 (5.62 ± 0.56), 7 (5.15 ± 0.41) and 12 (4.82 ± 0.11) weeks was unchanged by HRT. During cycle ergometer exercise, prior to training, Ca²⁺-ATPase was reduced (P < 0.05) by 14% during the initial 30 min at 58% VO ₂ peak and (P < 0.05) a further 19% during 30 min at 72% VO ₂ peak. Following 7 and 12 weeks of training, the decreases in SR Ca²⁺-ATPase were less pronounced (P < 0.05). These results indicate that muscle hypertrophy, although incapable of altering Ca²⁺-ATPase pump activity at rest, can attenuate the decrease observed in exercise by mechanism(s) as yet unknown.     

Acute and adaptive responses in humans to exercise in a warm, humid environment

 Acute and repeated exposure for 8–13 consecutive days to exercise in humid heat was studied. Twelve fit subjects exercised at 150 W [45% of maximum O₂ uptake (V.O₂,_max)] in ambient conditions of 35°C and 87% relative humidity which resulted in exhaustion after 45 min. Average core temperature reached 39.9 ± 0.1°C, mean skin temperature (T– _sk) was 37.9 ± 0.1°C and heart rate (HR) 152 ± 6 beats min^–1 at this stage. No effect of the increasing core temperature was seen on cardiac output and leg blood flow (LBF) during acute heat stress. LBF was 5.2 ± 0.3 l min^–1 at 10 min and 5.3 ± 0.4 l min^–1 at exhaustion (n = 6). After acclimation the subjects reached exhaustion after 52 min with a core temperature of 39.9 ± 0.1°C, T– _sk 37.7 ± 0.2°C, HR 146 ± 4 beats min^–1. Acclimation induced physiological adaptations, as shown by an increased resting plasma volume (3918 ± 168 to 4256 ± 270 ml), the lower exercise heart rate at exhaustion, a 26% increase in sweating rate, lower sweat sodium concentration and a 6% reduction in exercise V.O₂. Neither in acute exposure nor after acclimation did the rise of core temperature to near 40°C affect metabolism and substrate utilization. The physiological adaptations were similar to those induced by dry heat acclimation. However, in humid heat the effect of acclimation on performance was small due to physical limitations for evaporative heat loss. Received: 3 July 1996 / Received after revision: 26 September 1996 / Accepted: 7 January 1997     

Myocardial function and aerobic fitness in adolescent females

A recent report indicated that variations in myocardial functional (systolic and diastolic) responses to exercise do not contribute to inter-individual differences in aerobic fitness (peak VO₂) among young males. This study was designed to investigate the same question among adolescent females. Thirteen highly fit adolescent football (soccer) players (peak VO₂ 43.5 ± 3.4 ml kg⁻¹ min⁻¹) and nine untrained girls (peak VO₂ 36.0 ± 5.1 ml kg⁻¹ min⁻¹) matched for age underwent a progressive cycle exercise test to exhaustion. Cardiac variables were measured by standard echocardiographic techniques. Maximal stroke index was greater in the high-fit group (50 ± 5 vs. 41 ± 4 ml m⁻²), but no significant group differences were observed in maximal heart rate or arterial venous oxygen difference. Increases in markers of both systolic (ejection rate, tissue Doppler S′) and diastolic (tissue Doppler E′, mitral E velocity) myocardial functions at rest and during the acute bout of exercise were similar in the two groups. This study suggests that among healthy adolescent females, like young males, myocardial systolic and diastolic functional capacities do not contribute to inter-individual variability in physiologic aerobic fitness.     

<Emphasis Type="Italic">V</Emphasis>O<Subscript>2</Subscript>max during successive maximal efforts

The concept of VO₂max has been a defining paradigm in exercise physiology for >75 years. Within the last decade, this concept has been both challenged and defended. The purpose of this study was to test the concept of VO₂max by comparing VO₂ during a second exercise bout following a preliminary maximal effort exercise bout. The study had two parts. In Study #1, physically active non-athletes performed incremental cycle exercise. After 1-min recovery, a second bout was performed at a higher power output. In Study #2, competitive runners performed incremental treadmill exercise and, after 3-min recovery, a second bout at a higher speed. In Study #1 the highest VO₂ (bout 1 vs. bout 2) was not significantly different (3.95 ± 0.75 vs. 4.06 ± 0.75 l min⁻¹). Maximal heart rate was not different (179 ± 14 vs. 180 ± 13 bpm) although maximal V _E was higher in the second bout (141 ± 36 vs. 151 ± 34 l min⁻¹). In Study #2 the highest VO₂ (bout 1 vs. bout 2) was not significantly different (4.09 ± 0.97 vs. 4.03 ± 1.16 l min⁻¹), nor was maximal heart rate (184 + 6 vs. 181 ± 10 bpm) or maximal V _E (126 ± 29 vs. 126 ± 34 l min⁻¹). The results support the concept that the highest VO₂ during a maximal incremental exercise bout is unlikely to change during a subsequent exercise bout, despite higher muscular power output. As such, the results support the “classical” view of VO₂max.     

Cardiac response to exercise in normal-weight and obese, Hispanic men and women: implications for exercise prescription

Aim: The effects of obesity on cardiac function during incremental exercise to peak oxygen consumption (VO_2peak) have not been previously described. The purpose of this study was to compare submaximal and maximal cardiac function during exercise in normal‐weight and obese adults. Methods: Normal‐weight (n = 20; means ± SE: age = 21.9 ± 0.5 years; BMI = 21.8 ± 0.4 kg m^?2) and obese (n = 15; means ± SE: age = 25.1 ± 5.2 years; BMI = 34.1 ± 01.0 kg m^?2) participants were assessed for body composition, VO_2peak and cardiac variables (thoracic bioimpedance analysis) at rest and at heart rates (HR) of 110, 130, 150 and 170 beats min^?1 and maximal HR during incremental cycling exercise to exhaustion. Differences between groups were assessed with mixed‐model ancova with repeated measures. Cardiac variables were statistically indexed for body surface area and resting HR. VO₂ and arteriovenous oxygen difference (a‐vO₂) were statistically indexed for fat‐free mass and resting HR. Results: Significant main effects for group indicated obese participants had higher cardiac output (Q) index and stroke volume (SV) index but lower ejection fraction (EF) and a‐vO₂ index during incremental exercise to exhaustion compared with their normal‐weight peers, despite similar submaximal and maximal VO₂ and absolute power outputs (P < 0.05). Conclusions: Our findings suggest that although Q index and SV index were higher in obese, young adults, EF and a‐vO₂ index were significantly lower when compared to matched, normal‐weight adults.     

Cerebral oxygenation is reduced during hyperthermic exercise in humans

Aim: Cerebral mitochondrial oxygen tension (P_mitoO₂) is elevated during moderate exercise, while it is reduced when exercise becomes strenuous, reflecting an elevated cerebral metabolic rate for oxygen (CMRO₂) combined with hyperventilation-induced attenuation of cerebral blood flow (CBF). Heat stress challenges exercise capacity as expressed by increased rating of perceived exertion (RPE). Methods: This study evaluated the effect of heat stress during exercise on P_mitoO₂ calculated based on a Kety-Schmidt-determined CBF and the arterial-to-jugular venous oxygen differences in eight males [27 ± 6 years (mean ± SD) and maximal oxygen uptake (VO_2max) 63 ± 6 mL kg⁻¹ min⁻¹]. Results: The CBF, CMRO₂ and P_mitoO₂ remained stable during 1 h of moderate cycling (170 ± 11 W, ∼50% of VO_2max, RPE 9–12) in normothermia (core temperature of 37.8 ± 0.4 °C). In contrast, when hyperthermia was provoked by dressing the subjects in watertight clothing during exercise (core temperature 39.5 ± 0.2 °C), P_mitoO₂ declined by 4.8 ± 3.8 mmHg (P < 0.05 compared to normothermia) because CMRO₂ increased by 8 ± 7% at the same time as CBF was reduced by 15 ± 13% (P < 0.05). During exercise with heat stress, RPE increased to 19 (19–20; P < 0.05); the RPE correlated inversely with P_mitoO₂ (r² = 0.42, P < 0.05). Conclusion: These data indicate that strenuous exercise in the heat lowers cerebral P_mitoO₂, and that exercise capacity in this condition may be dependent on maintained cerebral oxygenation.     

Exercise intensity and oxygen uptake kinetics in African-American and Caucasian women

The effect of exercise intensity on the on- and off-transient kinetics of oxygen uptake (VO₂) was investigated in African American (AA) and Caucasian (C) women. African American (n = 7) and Caucasian (n = 6) women of similar age, body mass index and weight, performed an incremental test and bouts of square-wave exercise at moderate, heavy and very heavy intensities on a cycle ergometer. Gas exchange threshold (LT_GE) was lower in AA (13.6 ± 2.3 mL kg⁻¹ min⁻¹) than C (18.6 ± 5.6 mL kg⁻¹ min⁻¹). The dynamic exercise and recovery VO₂ responses were characterized by mathematical models. There were no significant differences in (1) peak oxygen uptake (VO_2peak) between AA (28.5 ± 5 mL kg⁻¹ min⁻¹) and C (31.1 ± 6.6 mL kg⁻¹ min⁻¹) and (2) VO₂ kinetics at any exercise intensity. At moderate exercise, the on- and off- VO₂ kinetics was described by a monoexponential function with similar time constants τ _1,on (39.4 ± 12.5; 38.8 ± 15 s) and τ _1,off (52.7 ± 10.1; 40.7 ± 4.4 s) for AA and C, respectively. At heavy and very heavy exercise, the VO₂ kinetics was described by a double-exponential function. The parameter values for heavy and very heavy exercise in the AA group were, respectively: τ _1,on (47.0 ± 10.8; 44.3 ± 10 s), τ _2,on (289 ± 63; 219 ± 90 s), τ _1,off (45.9 ± 6.2; 50.7 ± 10 s), τ _2,off (259 ± 120; 243 ± 93 s) while in the C group were, respectively: τ _1,on (41 ± 12; 43.2 ± 15 s); τ _{2, on} (277 ± 81; 215 ± 36 s), τ _1,off (40.2 ± 3.4; 42.3 ± 7.2 s), τ _2,off (215 ± 133; 228 ± 64 s). The on- and off-transients were symmetrical with respect to model order and dependent on exercise intensity regardless of race. Despite similar VO₂ kinetics, LT_GE and gain of the VO₂ on-kinetics at moderate intensity were lower in AA than C. However, generalization to the African American and Caucasian populations is constrained by the small subject numbers.     

Impact of the exercise mode on heart rate recovery after maximal exercise

Heart rate recovery 1 min after exercise termination (HRR-1) is a prognostic predictor. However, the influence of the exercise mode on HRR-1 is incompletely characterised. Twenty-nine young and healthy subjects and 16 elderly patients with chronic heart failure underwent cardiopulmonary exercise testing using cycle ergometer and treadmill ramp protocols in random order. HRR-1 and heart rate recovery 2 and 3 min after exercise (HRR-2, HRR-3) during active recovery and peak oxygen consumption (peak VO₂) were measured. In both healthy subjects (32 ± 14 vs. 27 ± 10 bpm) and HF patients (19 ± 8 vs. 14 ± 9 bpm), HRR-1 was faster after cycle exercise (p = 0.029; p for between group difference 0.94). In contrast, HRR-2 and HRR-3 were similar after both tests in both groups. Peak VO₂ was lower during cycle as compared to treadmill exercise in both groups. In conclusion, in both healthy subjects and HF patients, HRR-1 depends on the mode of exercise as peak VO₂ does.     

Oral tyrosine supplementation improves exercise capacity in the heat

Increased brain dopamine availability improves prolonged exercise tolerance in the heat. It is unclear whether supplementing the amino-acid precursor of dopamine increases exercise capacity in the heat. Eight healthy male volunteers [mean age 32 ± 11 (SD) years; body mass 75.3 ± 8.1 kg; peak oxygen uptake ([(V)\dot]O_2peak \dot{V}O_{{2peak}} ) 3.5 ± 0.3 L min⁻¹] performed two exercise trials separated by at least 7 days in a randomised, crossover design. Subjects consumed 500 mL of a flavoured sugar-free drink (PLA), or the same drink with 150 mg kg body mass⁻¹ tyrosine (TYR) in a double-blind manner 1 h before cycling to exhaustion at a constant exercise intensity equivalent to 68 ± 5% [(V)\dot]O_2peak \dot{V}O_{{2peak}} in 30°C and 60% relative humidity. Pre-exercise plasma tyrosine:large neutral amino acids increased 2.9-fold in TYR (P < 0.01), while there was no change in PLA (P > 0.05). Subjects cycled longer in TYR compared to PLA (80.3 ± 19.7 min vs. 69.2 ± 14.0 min; P < 0.01). Core temperature, mean weighted skin temperature, heart rate, ratings of perceived exertion and thermal sensation were similar in TYR and PLA during exercise and at exhaustion (P > 0.05) despite longer exercise time in TYR. The results show that acute tyrosine supplementation is associated with increased endurance capacity in the heat in moderately trained subjects. The results also suggest for the first time that the availability of tyrosine, a nutritional dopamine precursor, can influence the ability to subjectively tolerate prolonged submaximal constant-load exercise in the heat.     

Effects of dietary nitrate on oxygen cost during exercise

Aim: Nitric oxide (NO), synthesized from l ‐arginine by NO synthases, plays a role in adaptation to physical exercise by modulating blood flow, muscular contraction and glucose uptake and in the control of cellular respiration. Recent studies show that NO can be formed in vivo also from the reduction of inorganic nitrate (NO₃^?) and nitrite (NO₂^?). The diet constitutes a major source of nitrate, and vegetables are particularly rich in this anion. The aim of this study was to investigate if dietary nitrate had any effect on metabolic and circulatory parameters during exercise. Method: In a randomized double‐blind placebo‐controlled crossover study, we tested the effect of dietary nitrate on physiological and metabolic parameters during exercise. Nine healthy young well‐trained men performed submaximal and maximal work tests on a cycle ergometer after two separate 3‐day periods of dietary supplementation with sodium nitrate (0.1 mmol kg^?1 day?1) or an equal amount of sodium chloride (placebo). Results: The oxygen cost at submaximal exercise was reduced after nitrate supplementation compared with placebo. On an average Vo ₂ decreased from 2.98 ± 0.57 during CON to 2.82 ± 0.58 L min^?1 during NIT (P < 0.02) over the four lowest submaximal work rates. Gross efficiency increased from 19.7 ± 1.6 during CON to 21.1 ± 1.3% during NIT (P < 0.01) over the four lowest work rates. There was no difference in heart rate, lactate [Hla], ventilation (VE), VE/Vo ₂ or respiratory exchange ratio between nitrate and placebo during any of the submaximal work rates. Conclusion: We conclude that dietary nitrate supplementation, in an amount achievable through a diet rich in vegetables, results in a lower oxygen demand during submaximal work. This highly surprising effect occurred without an accompanying increase in lactate concentration, indicating that the energy production had become more efficient. The mechanism of action needs to be clarified but a likely first step is the in vivo reduction of dietary nitrate into bioactive nitrogen oxides including nitrite and NO.     

Pathophysiological adaptations to walking and cycling in primary pulmonary hypertension

Exercise tolerance inversely correlates with the severity of the disease in patients with idiopathic pulmonary arterial hypertension (IPAH). Cycling and walking protocols are commonly utilized in the evaluation of exercise intolerance in IPAH, but little information exists on possible differences in ventilatory and gas exchange adaptations to these exercise modalities. In a group of patients with moderate to severe IPAH (n = 13), we studied the ventilatory, cardiovascular and gas exchange adaptations to maximal incremental walking (W) and maximal incremental cycling (C). During W, compared to C, the ventilatory equivalents for CO₂ output (V′_E/V′CO₂) were significantly higher either expressed as the rate of increment (56 ± 5 vs. 45 ± 3; P < 0.0001) or as the absolute values at anaerobic threshold (AT) and at peak exercise. At AT, the increase in V′_E/V′CO₂ during W was associated with a significant lower value of end-tidal carbon dioxide. At peak W, compared to peak C, dyspnea sensation was higher and arterial oxygen saturation (SpO₂) was lower (87 ± 2 vs. 91 ± 2, P < 0.001). In patients with IPAH the physiologic information obtained with W are different from those obtained with C. Tolerance to W exercise is limited by high ventilatory response and dyspnea sensation. W should be used to assess the degree of lung gas exchange inefficiency and arterial O₂ desaturation during exercise.     

Non-invasive haemodynamic assessments using Innocor™ during standard graded exercise tests

Cardiac output (Q) and stroke volume (V _S) represent primary determinants of cardiovascular performance and should therefore be determined for performance diagnostics purposes. Since it is unknown, whether measurements of Q and V _S can be performed by means of Innocor™ during standard graded exercise tests (GXTs), and whether current GXT stages are sufficiently long for the measurements to take place, we determined Q and V _S at an early and late point in time on submaximal 2 min GXT stages. 16 male cyclists (age 25.4 ± 2.9 years, body mass 71.2 ± 5.0 kg) performed three GXTs and we determined Q and V _S after 46 and 103 s at 69, 77, and 85% peak power. We found that the rebreathings could easily be incorporated into the GXTs and that Q and V _S remained unchanged between the two points in time on the same GXT stage (69% peak power, Q: 18.1 ± 2.1 vs. 18.2 ± 2.3 l min⁻¹, V _S: 126 ± 18 vs. 123 ± 21 ml; 77% peak power, Q: 20.7 ± 2.6 vs. 21.0 ± 2.3 l min⁻¹, V _S: 132 ± 18 vs. 131 ± 18 ml; 85% peak power, Q: 21.6 ± 2.4 vs. 21.8 ± 2.7 l min⁻¹, V _S: 131 ± 17 vs. 131 ± 22 ml). We conclude that Innocor™ may be a useful device for assessing Q and V _S during GXTs, and that the adaptation of Q and V _S to exercise-to-exercise transitions at moderate to high submaximal power outputs is fast enough for 1 and 2 min GXT stage durations.