[show abstract][hide abstract] ABSTRACT: During maximal hypoxic exercise, a reduction in cerebral oxygen delivery may constitute a signal to the central nervous system to terminate exercise. We investigated whether the rate of increase in frontal cerebral cortex oxygen delivery is limited in hypoxic compared to normoxic exercise. We assessed frontal cerebral cortex blood flow using near-infrared spectroscopy and the light-absorbing tracer indocyanine green dye, as well as frontal cortex oxygen saturation (S(tO2)%) in 11 trained cyclists during graded incremental exercise to the limit of tolerance (maximal work rate, WRmax) in normoxia and acute hypoxia (inspired O2 fraction (F(IO2)), 0.12). In normoxia, frontal cortex blood flow and oxygen delivery increased (P < 0.05) from baseline to sub-maximal exercise, reaching peak values at near-maximal exercise (80% WRmax: 287 ± 9 W; 81 ± 23% and 75 ± 22% increase relative to baseline, respectively), both leveling off thereafter up to WRmax (382 ± 10 W). Frontal cortex S(tO2)% did not change from baseline (66 ± 3%) throughout graded exercise. During hypoxic exercise, frontal cortex blood flow increased (P = 0.016) from baseline to sub-maximal exercise, peaking at 80% WRmax (213 ± 6 W; 60 ± 15% relative increase) before declining towards baseline at WRmax (289 ± 5 W). Despite this, frontal cortex oxygen delivery remained unchanged from baseline throughout graded exercise, being at WRmax lower than at comparable loads (287 ± 9 W) in normoxia (by 58 ± 12%; P = 0.01). Frontal cortex S(tO2)% fell from baseline (58 ± 2%) on light and moderate exercise in parallel with arterial oxygen saturation, but then remained unchanged to exhaustion (47 ± 1%). Thus, during maximal, but not light to moderate, exercise frontal cortex oxygen delivery is limited in hypoxia compared to normoxia. This limitation could potentially constitute the signal to limit maximal exercise capacity in hypoxia.
The Journal of Physiology 08/2011; 589(Pt 16):4027-39. · 4.38 Impact Factor
[show abstract][hide abstract] ABSTRACT: In most patients with COPD, rehabilitative exercise training partially reverses the morphologic and structural abnormalities of peripheral muscle fibers. However, whether the degree of improvement in muscle fiber morphology and typology with exercise training varies depending on disease severity remains unknown.
Forty-six clinically stable patients with COPD classified by GOLD (Global Initiative for Obstructive Lung Disease) as stage II (n = 14), III (n = 18), and IV (n = 14) completed a 10-week comprehensive pulmonary rehabilitation program consisting of high-intensity exercise three times weekly.
At baseline, muscle fiber mean cross-sectional area and capillary density did not significantly differ between patients with COPD and healthy control subjects, whereas muscle fiber type I and II proportion was respectively lower (P < .001) and higher (P < .002) in patients with GOLD stage IV compared with healthy subjects and patients with GOLD stages II and III. Exercise training improved, to a comparable degree, functional capacity and the St. George Respiratory Questionnaire health-related quality of life score across all three GOLD stages. Vastus lateralis muscle fiber mean cross-sectional area was increased (P < .001) in all patient groups (stage II: from 4,507 ± 280 μm² to 5,091 ± 271 μm² [14% ± 3%]; stage III: from 3,753 ± 258 μm² to 4,212 ± 268 μm² [14% ± 3%]; stage IV: from 3,961 ± 266 μm² to 4,551 ± 262 μm² [17% ± 5%]), whereas all groups exhibited a comparable reduction (P < .001) in type IIb fiber proportion (stage II: by 6% ± 2%; stage III: by 6% ± 1%; stage IV: by 7% ± 1%) and an increase (P < .001) in capillary to fiber ratio (stage II: from 1.48 ± 0.10 to 1.81 ± 0.10 [23% ± 5%]; stage III: from 1.29 ± 0.06 to 1.56 ± 0.09 [21% ± 5%]; stage IV: from 1.43 ± 0.10 to 1.71 ± 0.13 [18 ± 3%]). The magnitude of changes in the aforementioned variables did not differ across GOLD stages.
Functional capacity and morphologic and typologic adaptations to rehabilitation in peripheral muscle fibers were similar across GOLD stages II to IV. Pulmonary rehabilitation should be implemented in patients at all COPD stages.
[show abstract][hide abstract] ABSTRACT: Emerging evidence indicates that, besides dyspnea relief, an improvement in locomotor muscle oxygen delivery may also contribute to enhanced exercise tolerance following normoxic heliox (replacement of inspired nitrogen by helium) administration in patients with chronic obstructive pulmonary disease (COPD). Whether blood flow redistribution from intercostal to locomotor muscles contributes to this improvement currently remains unknown. Accordingly, the objective of this study was to investigate whether such redistribution plays a role in improving locomotor muscle oxygen delivery while breathing heliox at near-maximal [75% peak work rate (WR(peak))], maximal (100%WR(peak)), and supramaximal (115%WR(peak)) exercise in COPD. Intercostal and vastus lateralis muscle perfusion was measured in 10 COPD patients (FEV(1) = 50.5 ± 5.5% predicted) by near-infrared spectroscopy using indocyanine green dye. Patients undertook exercise tests at 75 and 100%WR(peak) breathing either air or heliox and at 115%WR(peak) breathing heliox only. Patients did not exhibit exercise-induced hyperinflation. Normoxic heliox reduced respiratory muscle work and relieved dyspnea across all exercise intensities. During near-maximal exercise, quadriceps and intercostal muscle blood flows were greater, while breathing normoxic heliox compared with air (35.8 ± 7.0 vs. 29.0 ± 6.5 and 6.0 ± 1.3 vs. 4.9 ± 1.2 ml·min(-1)·100 g(-1), respectively; P < 0.05; mean ± SE). In addition, compared with air, normoxic heliox administration increased arterial oxygen content, as well as oxygen delivery to quadriceps and intercostal muscles (from 47 ± 9 to 60 ± 12, and from 8 ± 1 to 13 ± 3 mlO(2)·min(-1)·100 g(-1), respectively; P < 0.05). In contrast, normoxic heliox had neither an effect on systemic nor an effect on quadriceps or intercostal muscle blood flow and oxygen delivery during maximal or supramaximal exercise. Since intercostal muscle blood flow did not decrease by normoxic heliox administration, blood flow redistribution from intercostal to locomotor muscles does not represent a likely mechanism of improvement in locomotor muscle oxygen delivery. Our findings might not be applicable to patients who hyperinflate during exercise.
[show abstract][hide abstract] ABSTRACT: It has been hypothesized that, because of the high work of breathing sustained by patients with chronic obstructive pulmonary disease (COPD) during exercise, blood flow may increase in favor of the respiratory muscles, thereby compromising locomotor muscle blood flow.
To test this hypothesis by investigating whether, at the same work of breathing, intercostal muscle blood flow during exercise is as high as during resting isocapnic hyperpnea when respiratory and locomotor muscles do not compete for the available blood flow.
Intercostal and vastus lateralis muscle perfusion was measured simultaneously in 10 patients with COPD (FEV₁ = 50.5 ± 5.5% predicted) by near-infrared spectroscopy using indocyanine green dye.
Measurements were made at several exercise intensities up to peak work rate (WRpeak) and subsequently during resting hyperpnea at minute ventilation levels up to those at WRpeak. During resting hyperpnea, intercostal muscle blood flow increased with the power of breathing to 11.4 ± 1.6 ml/min per 100 g at the same ventilation recorded at WRpeak. Conversely, during graded exercise, intercostal muscle blood flow remained unchanged from rest up to 50% WRpeak (6.8 ± 1.3 ml/min per 100 g) and then fell to 4.5 ± 0.8 ml/min per 100 g at WRpeak (P = 0.003). Cardiac output plateaued above 50% WRpeak (8.4 ± 0.1 l/min), whereas vastus lateralis muscle blood flow increased progressively, reaching 39.8 ± 7.1 ml/min per 100 g at WRpeak.
During intense exercise in COPD, restriction of intercostal muscle perfusion but preservation of quadriceps muscle blood flow along with attainment of a plateau in cardiac output represents the inability of the circulatory system to satisfy the energy demands of locomotor and respiratory muscles.
American Journal of Respiratory and Critical Care Medicine 11/2010; 182(9):1105-13. · 11.04 Impact Factor
[show abstract][hide abstract] ABSTRACT: We investigated whether expiratory muscle loading induced by the application of expiratory flow limitation (EFL) during exercise in healthy subjects causes a reduction in quadriceps muscle blood flow in favor of the blood flow to the intercostal muscles. We hypothesized that, during exercise with EFL quadriceps muscle blood flow would be reduced, whereas intercostal muscle blood flow would be increased compared with exercise without EFL. We initially performed an incremental exercise test on eight healthy male subjects with a Starling resistor in the expiratory line limiting expiratory flow to approximately 1 l/s to determine peak EFL exercise workload. On a different day, two constant-load exercise trials were performed in a balanced ordering sequence, during which subjects exercised with or without EFL at peak EFL exercise workload for 6 min. Intercostal (probe over the 7th intercostal space) and vastus lateralis muscle blood flow index (BFI) was calculated by near-infrared spectroscopy using indocyanine green, whereas cardiac output (CO) was measured by an impedance cardiography technique. At exercise termination, CO and stroke volume were not significantly different during exercise, with or without EFL (CO: 16.5 vs. 15.2 l/min, stroke volume: 104 vs. 107 ml/beat). Quadriceps muscle BFI during exercise with EFL (5.4 nM/s) was significantly (P = 0.043) lower compared with exercise without EFL (7.6 nM/s), whereas intercostal muscle BFI during exercise with EFL (3.5 nM/s) was significantly (P = 0.021) greater compared with that recorded during control exercise (0.4 nM/s). In conclusion, increased respiratory muscle loading during exercise in healthy humans causes an increase in blood flow to the intercostal muscles and a concomitant decrease in quadriceps muscle blood flow.
Journal of Applied Physiology 08/2010; 109(2):388-95. · 3.48 Impact Factor
[show abstract][hide abstract] ABSTRACT: It is known that non-cachectic patients with chronic obstructive pulmonary disease (COPD) respond well to pulmonary rehabilitation, but whether cachectic COPD patients are capable of adaptive responses is both important and unknown. 10 cachectic and 19 non-cachectic COPD patients undertook high-intensity cycling training, at the same relative intensity, for 45 min x day(-1), 3 days x week(-1) for 10 weeks. Before and after rehabilitation vastus lateralis muscle biopsies were analysed morphologically and for the expression of muscle remodelling factors (insulin-like growth factor (IGF)-I, myogenic differentiation factor D (MyoD), tumour necrosis factor (TNF)-alpha, nuclear factor (NF)-kappaB and myostatin) and key components of ubiquitin-mediated proteolytic systems (muscle ring finger protein (MURF)-1 and Atrogin-1). Rehabilitation improved peak work-rate and the 6-min walk distance similarly in non-cachectic (18+/-3% and 42+/-13 m, respectively) and cachectic (16+/-2% and 53+/-16 m, respectively) patients, but quality of life only improved in non-cachectic COPD. Mean muscle fibre cross-sectional area increased in both groups, but significantly less in cachectic (7+/-2%) than in non-cachectic (11+/-2%) patients. Both groups equally decreased the proportion of type IIb fibres and increased muscle capillary/fibre ratio. IGF-I mRNA expression increased in both groups, but IGF-I protein levels increased more in non-cachectic COPD. MyoD was upregulated, whereas myostatin was downregulated at the mRNA and protein level only in non-cachectic patients. Whilst rehabilitation had no effect on TNF-alpha expression, it decreased the activation of the transcription factor NF-kappaB in both groups by the same amount. Atrogin-1 and MURF-1 expression were increased in cachectic COPD, but it was decreased in non-cachectic patients. Cachectic COPD patients partially retain the capacity for peripheral muscle remodelling in response to rehabilitation and are able to increase exercise capacity as much as those without cachexia, even if they exhibit both quantitative and qualitative differences in the type of muscle fibre remodelling in response to exercise training.
European Respiratory Journal 08/2010; 36(2):301-10. · 6.36 Impact Factor
[show abstract][hide abstract] ABSTRACT: Near-infrared spectroscopy (NIRS) with the tracer indocyanine green (ICG) may be used for measuring muscle blood flow (MBF) during exercise, if arterial ICG concentration is measured simultaneously. Although pulse dye densitometry allows for noninvasive measurement of arterial dye concentration, this technique is sensitive to motion and may not be applicable during exercise. The aim of this study was to evaluate a noninvasive blood flow index (BFI), which is derived solely from the muscle ICG concentration curve. In 10 male cyclists 5 mg ICG were injected into an antecubital vein at rest and during cycling at 30, 60, 70, 80, 90, and 100% of previously determined maximal work load. Simultaneously blood was withdrawn through a photodensitometer at 20 ml/min from the radial artery to measure arterial ICG concentration. To measure muscle tissue ICG concentrations, two sets of NIRS optodes were positioned on the skin, one over the left seventh intercostal space and the other over the left vastus lateralis muscle. MBF was calculated from the arterial and muscle concentration data according to Fick's principle. BFI was calculated solely from the muscle concentration curve as ICG concentration difference divided by rise time between 10 and 90% of peak. During exercise mean BFI values changed similarly to MBF in both intercostal and quadriceps muscles and showed excellent correlations with MBF: r = 0.98 and 0.96, respectively. Individual data showed some scattering among BFI and MBF values but still reasonable correlations of BFI with MBF: r = 0.73 and 0.72 for intercostal and quadriceps muscles, respectively. Interobserver variability, as analyzed by Bland-Altman plots, was considerably less for BFI than MBF. These data suggest that BFI can be used for measuring changes in muscle perfusion from rest to maximal exercise. Although absolute blood flow cannot be determined, BFI has the advantages of being essentially noninvasive and having low interobserver variability.
Journal of Applied Physiology 04/2010; 108(4):962-7. · 3.48 Impact Factor
[show abstract][hide abstract] ABSTRACT: We investigated whether, during maximal exercise, intercostal muscle blood flow is as high as during resting hyperpnoea at the same work of breathing. We hypothesized that during exercise, intercostal muscle blood flow would be limited by competition from the locomotor muscles. Intercostal (probe over the 7th intercostal space) and vastus lateralis muscle perfusion were measured simultaneously in ten trained cyclists by near-infrared spectroscopy using indocyanine green dye. Measurements were made at several exercise intensities up to maximal (WRmax) and subsequently during resting isocapnic hyperpnoea at minute ventilation levels up to those at WRmax. During resting hyperpnoea, intercostal muscle blood flow increased linearly with the work of breathing (R2 = 0.94) to 73.0 +/- 8.8 ml min-1 (100 g)-1 at the ventilation seen at WRmax (work of breathing approximately 550-600 J min-1), but during exercise it peaked at 80% WRmax (53.4 +/- 10.3 ml min-1 (100 g)-1), significantly falling to 24.7 +/- 5.3 ml min-1 (100 g)-1 at WRmax. At maximal ventilation intercostal muscle vascular conductance was significantly lower during exercise (0.22 +/- 0.05 ml min-1 (100 g)-1 mmHg-1) compared to isocapnic hyperpnoea (0.77 +/- 0.13 ml min-1 (100 g)-1 mmHg-1). During exercise, both cardiac output and vastus lateralis muscle blood flow also plateaued at about 80% WRmax (the latter at 95.4 +/- 11.8 ml min-1 (100 g)-1). In conclusion, during exercise above 80% WRmax in trained subjects, intercostal muscle blood flow and vascular conductance are less than during resting hyperpnoea at the same minute ventilation. This suggests that the circulatory system is unable to meet the demands of both locomotor and intercostal muscles during heavy exercise, requiring greater O2 extraction and likely contributing to respiratory muscle fatigue.
The Journal of Physiology 06/2009; 587(Pt 14):3665-77. · 4.38 Impact Factor
[show abstract][hide abstract] ABSTRACT: The BODE index is frequently used to assess functional capacity in patients with COPD. The aim of this study was to investigate the effectiveness of interval-load training (ILT) to improve the BODE index in comparison to the commonly implemented constant-load training (CLT). Forty-two patients with COPD [FEV(1): (mean+/-SEM) 42+/-3% predicted] were randomly allocated to either ILT (n=21) or CLT (n=21). The training program consisted of cycling exercise 3 days/week for 10 weeks. Patients assigned to ILT exercised at a mean intensity of 126+/-4% of baseline peak work rate (Wpeak) with 30-s work periods alternated with 30-s rest periods for 45 min per day, whereas patients allocated to CLT exercised at a mean intensity of 76+/-5% of baseline Wpeak for 30 min per day. The BODE index and its components: body mass index, FEV(1), MMRC dyspnea score and the 6-min walk test (6-MWT) as well as cycling Wpeak were assessed before and after both exercise training regimes. Both ILT and CLT significantly (p<0.001) decreased the BODE index (from 4.8+/-0.5 to 4.0+/-0.5 units and from 4.4+/-0.5 to 3.8+/-0.5 units, respectively). In addition, both ILT and CLT significantly decreased the MMRC dyspnea score by 0.4+/-0.1 units and increased the 6-MWT (by 52+/-16 and 44+/-12 m, respectively) as well as cycling Wpeak (by 14+/-2 and 10+/-2W, respectively). The magnitude of these changes was not significantly different between ILT and CLT. Consequently, ILT is equally effective to CLT in terms of improving the BODE index in patients with COPD and as such it may constitute an alternative rehabilitative modality in COPD.
Respiratory medicine 04/2009; 103(9):1392-8. · 2.33 Impact Factor
[show abstract][hide abstract] ABSTRACT: We investigated whether the greater degree of exercise-induced diaphragmatic fatigue previously reported in highly trained athletes in hypoxia (compared with normoxia) could have a contribution from limited respiratory muscle blood flow. Seven trained cyclists completed three constant load 5 min exercise tests at inspired O(2) fractions (FIO2) of 0.13, 0.21 and 1.00 in balanced order. Work rates were selected to produce the same tidal volume, breathing frequency and respiratory muscle load at each FIO2 (63 +/- 1, 78 +/- 1 and 87 +/- 1% of normoxic maximal work rate, respectively). Intercostals and quadriceps muscle blood flow (IMBF and QMBF, respectively) were measured by near-infrared spectroscopy over the left 7th intercostal space and the left vastus lateralis muscle, respectively, using indocyanine green dye. The mean pressure time product of the diaphragm and the work of breathing did not differ across the three exercise tests. After hypoxic exercise, twitch transdiaphragmatic pressure fell by 33.3 +/- 4.8%, significantly (P < 0.05) more than after both normoxic (25.6 +/- 3.5% reduction) and hyperoxic (26.6 +/- 3.3% reduction) exercise, confirming greater fatigue in hypoxia. Despite lower leg power output in hypoxia, neither cardiac output nor QMBF (27.6 +/- 1.2 l min(-1) and 100.4 +/- 8.7 ml (100 ml)(-1) min(-1), respectively) were significantly different compared with normoxia (28.4 +/- 1.9 l min(-1) and 94.4 +/- 5.2 ml (100 ml)(-1) min(-1), respectively) and hyperoxia (27.8 +/- 1.6 l min(-1) and 95.1 +/- 7.8 ml (100 ml)(-1) min(-1), respectively). Neither IMBF was different across hypoxia, normoxia and hyperoxia (53.6 +/- 8.5, 49.9 +/- 5.9 and 52.9 +/- 5.9 ml (100 ml)(-1) min(-1), respectively). We conclude that when respiratory muscle energy requirement is not different between normoxia and hypoxia, diaphragmatic fatigue is greater in hypoxia as intercostal muscle blood flow is not increased (compared with normoxia) to compensate for the reduction in PaO2, thus further compromising O(2) supply to the respiratory muscles.
The Journal of Physiology 10/2008; 586(Pt 22):5575-87. · 4.38 Impact Factor
[show abstract][hide abstract] ABSTRACT: The present study investigated how end-expiratory ribcage and abdominal volume regulation during exercise is related to the degree of dynamic chest wall hyperinflation in patients with different spirometric severity of chronic obstructive pulmonary disease (COPD) based on the Global Initiative for Chronic Obstructive Lung Disease (GOLD) classification. In total, 42 COPD patients and 11 age-matched healthy subjects were studied during a ramp-incremental cycling test to the limit of tolerance (W(peak)). Volume variations of the chest wall (at end expiration (EEV(cw)) and end inspiration) and its compartments (ribcage (V(rc)) and abdominal (V(ab))) were computed by optoelectronic plethysmography. At W(peak), only patients in GOLD stages III and IV exhibited a significant increase in EEV(cw) (increase of 454+/-509 and 562+/-363 mL, respectively). These patients did not significantly reduce end-expiratory V(ab), whereas patients in GOLD stage II resembled healthy subjects with significantly reduced end-expiratory V(ab) (decrease of 287+/-350 mL). In patients, the greater the increase in EEV(cw) at W(peak), the smaller the reductions in end-expiratory V(ab) and the greater the increase in end-expiratory V(rc). In chronic obstructive pulmonary disease patients with different spirometric disease severity, greater degrees of exercise-induced dynamic chest wall hyperinflation were accompanied by lower degrees of end-expiratory abdominal volume displacement and larger increases in end-expiratory ribcage volume.
European Respiratory Journal 08/2008; 32(1):42-52. · 6.36 Impact Factor
[show abstract][hide abstract] ABSTRACT: Exercise is well known to cause arterial PO2 to fall and the alveolar-arterial PO2 difference(Aa PO2 ) to increase. Until recently, the physiological basis for this was considered to be mostly ventilation/perfusion ((.)VA/(.)Q) inequality and alveolar-capillary diffusion limitation. Recently, arterio-venous shunting through dilated pulmonary blood vessels has been proposed to explain a significant part of the Aa PO2 during exercise. To test this hypothesis we determined venous admixture during 5 min of near-maximal, constant-load, exercise in hypoxia (in inspired O2 fraction, FIO2 , 0.13), normoxia (FIO2 , 0.21) and hyperoxia (FIO2 , 1.0) undertaken in balanced order on the same day in seven fit cyclists ((.)VO2max, 61.3 +/- 2.4 ml kg(-1) min(-1); mean +/- S.E.M.). Venous admixture reflects three causes of hypoxaemia combined: true shunt, diffusion limitation and ((.)VA/(.)Q) inequality. In hypoxia, venous admixture was 22.8 +/- 2.5% of the cardiac output; in normoxia it was 3.5 +/- 0.5%; in hyperoxia it was 0.5 +/- 0.2%. Since only true shunt accounts for venous admixture while breathing 100% O2, the present study suggests that shunt accounts for only a very small portion of the observed venous admixture, Aa PO2 and hypoxaemia during heavy exercise.
The Journal of Physiology 06/2008; 586(9):2381-91. · 4.38 Impact Factor
[show abstract][hide abstract] ABSTRACT: This study was designed to assess quadriceps oxygenation during symptom-limited and constant-load exercise in patients with chronic obstructive pulmonary disease (COPD) and healthy age-matched controls. Thirteen male COPD patients [FEV(1): 43 +/- 5% predicted (mean +/- SEM)] and seven healthy male controls performed an incremental exercise test at peak work rate (WR) and a constant-load test at 75% peak WR on a cycle ergometer. Quadriceps hemoglobin saturation (StO2) was measured by continuous-wave near-infrared spectrophotometry throughout both exercise tests. StO2 is the ratio of oxygenated hemoglobin to total hemoglobin and reflects the relative contributions of tissue O2 delivery and tissue O2 utilization. Oxygen was supplemented to all patients in order to maintain arterial O2 saturation normal (> 95%). The StO2 decreased during symptom-limited exercise, reaching the nadir at peak WR. The decrease in StO2 was greater (P < 0.05) in healthy subjects (from 74 +/- 2% to 38 +/- 6%) compared with that in COPD patients (from 61 +/- 5% to 45 +/- 4%). However, when StO2 was normalized relative to the WR, the slope of change in StO2 during exercise was nearly identical between COPD patients and healthy subjects (0.47 +/- 0.10%/W and 0.51 +/- 0.04%/W, respectively). During constant-load exercise, the kinetic time constant of StO2 desaturation after the onset of exercise (i.e., equivalent to time to reach approximately 63% of StO2 decrease) was not different between COPD patients and healthy subjects (19.0 +/- 5.2 and 15.6 +/- 2.5 s, respectively). In O2-supplemented COPD patients, peripheral muscle oxygenation for a given work load is similar to that in healthy subjects, thus suggesting that skeletal muscle O2 consumption becomes normal for a given O2 delivery in COPD patients
Scandinavian Journal of Medicine and Science in Sports 05/2008; 19(3):364-72. · 3.21 Impact Factor
[show abstract][hide abstract] ABSTRACT: The aim of the present study was to investigate why blood lactate after prolonged quadriceps contraction during hiking is only marginally increased. Eight sailors performed five 3-min hiking bouts interspersed with 5-s recovery periods. Whole body oxygen uptake, heart rate and lactate were recorded, along with continuous-wave near-infrared spectroscopy measures of quadriceps oxygenation. The time for 50% re-oxygenation was also assessed as an indication of the degree of localized oxygen delivery stress. Hiking elicited a significant (p = 0.001) increase in mean (+/- SD) heart rate (124 +/- 10 beats . min (-1)) which was accompanied by a disproportionately low oxygen uptake (12 +/- 2 ml.kg(-1).min(-1)). Lactate was significantly (p = 0.001) increased throughout hiking manoeuvres, though post-exercise it remained low (3.2 +/- 0.9 mmol.l(-1)). During the hiking bouts mean quadriceps oxygenation was significantly (p = 0.001) reduced compared to baseline (by 33 +/- 5%), indicating an imbalance between muscle oxygen accessibility and oxygen demand. During rest intervals quadriceps oxygenation was partially restored. After the end of the final bout the time for 50 % re-oxygenation was only 8 +/- 2 s, whereas recovery of quadriceps oxygenation and oxygen uptake was completed within 3 min. We conclude that the observed low lactate could be attributed to the small oxygen and energy deficits during hiking as the muscles' oxygen accessibility is presumably partially restored during the brief rest intervals.
International Journal of Sports Medicine 02/2008; 29(1):11-5. · 2.27 Impact Factor