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Review: Application of near infrared pectroscopy in evaluating cerebral and muscle haemodynamics during exercise and sport

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Abstract

Near infrared (NIR) spectroscopy is a non-invasive optical technique that has been used to evaluate cerebral and muscle haemodynamic responses during exercise in situ. Its ease of use, portability, relatively low cost, along with the capability of evaluating cardiorespiratory responses simultaneously, has made it a useful technique to study exercise performance in a more holistic manner. The evidence indicates that there are systematic changes in the muscle and cerebral haemodynamic responses which are coincident with the respiratory gas exchange alterations occurring at the lactate and respiratory compensation thresholds during incremental exercise. During the Wingate (anaerobic) test, the peak oxygen uptake and degree of muscle deoxygenation is comparable to that attained during maximal incremental exercise, implying that there is a large aerobic component during a short duration of intense anaerobic exercise. Studies that have measured cerebral and muscle NIR spectroscopy simultaneously during dynamic whole body exercise support the hypotheses that at exercise intensities above the respiratory compensation threshold: (i) the accessory respiratory muscles compromise oxygen availability to the muscles directly involved in exercise, thereby contributing to fatigue and (ii) there is a systematic decline in cerebral oxygenation until exercise is terminated, thereby supporting the possibility of a supraspinal component to fatigue. Research pertaining to the application of NIR spectroscopy on cerebral and muscle haemodynamics under hypoxic conditions has indicated that the reductions in maximal exercise and aerobic capacity cannot be explained solely on the basis of these acute changes. Additionally, the improvements in maximal and submaximal exercise performance subsequent to endurance, interval and simulated hypoxic training programmes can occur independently of any alterations in cerebral and muscle haemodynamics. Wireless NIR spectroscopy is a useful technique to evaluate sport performance in the field setting and will evolve as an important method for designing and implementing training methods for this purpose.

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... There are comprehensive reviews of the applicable science related to NIRS, the principles underlying monitoring and measurement of quantifiable parameters, and the limitations of the technology for clinical monitoring [13,16,27,[41][42][43][44]53,142]. The unique properties of NIR light have been central to urological studies. ...
... Reference to the broader literature has greatly assisted our learning how to interpret bladder NIRS data, and understand how this information reflects and contributes to knowledge of normal bladder physiology and the etiology of lower urinary tract pathology. The relevant literature is broad coming from studies of muscle, brain, and other tissues where reproducible effects on NIRS parameters are seen in response to physiologic effects generated in experimental studies, or observed to occur in the microcirculation due to specific systemic and organ pathology [12,13,16,24,34,42,53,59,100,130,132,133,142]. Reproducibility of data in asymptomatic adults and children has been illustrated [77], and also between NIRS devices [83]. ...
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... Such data, plus as yet unpublished data from other studies, includes evidence supporting our hypothesis that OAB in particular has different causal physiology -including central nervous system mediated symptoms [32,36] and dysfunctional or absent detrusor contraction associated with oxygen debt developing in the detrusor [29,[31][32][33]47]. The original rationale for PET studies was that abnormal brain responses could cause urge incontinence [7], and fMRI derived responses in OAB subjects imply an abnormality in either the nature of afferent signals to the brain or how they are handled [22]; and NIRS data of fatigue onset in voluntary muscle [6,25,42,54], are comparable to the changes observed in forms of dysfunctional voiding [29,33,47]. ...
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... Near-infrared spectroscopy (NIRS) provides continuous, on-line estimation and display of concentration changes in oxy-( [O 2 Hb]), deoxy-( [HHb]), and total hemoglobin ( [Hb tot ]) and myoglobin ([Mb]) within the region of interrogation during dynamic exercise (Bhambhani, 2012). While ensuring an accurate quantitation of the oxygenation changes, NIRS reflects the dynamic balance between O 2 supply and O 2 consumption in the investigated tissue volume (Boushel et al., 2001;Ferrari et al., 2011;Mancini et al., 1994). ...
... Men had greater C(a-v)O 2 than women throughout exercise, analogous to previous studies (Mitchell et al., 1992;Ogawa et al., 1992), and at peak exercise men's value was on average 9% greater than women's. This difference is likely due to men's greater arterial O 2 content as there is no sex difference in the calculated mixed venous O 2 content during maximal exercise (Mitchell et al., 1992), although local blood flow and capillary density, as well as mitochondrial density and oxidative capacity do affect arteriovenous O 2 difference (Bhambhani, 2012). Our results confirmed the previous finding (Bhambhani et al., 1999), that tissue deoxygenation, as analyzed by TSI and ...
... The change of brain oxygenation reflects the regulation of brain function activation and the degree of athlete's mental fatigue (Bhambhani, 2012). Although the PFC may not be as directly involved in the neural control of movement as the motor area, it is located "upstream" of the motor cortex and indirectly participates in the motor control. ...
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Chapter
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The time course and mechanisms of adjustment of pulmonary oxygen uptake (V(O(2))) kinetics (time constant tauV(O(2p))) were examined during step transitions from 20 W to moderate-intensity cycling in eight older men (O; 68 +/- 7 yr) and eight young men (Y; 23 +/- 5 yr) before training and at 3, 6, 9, and 12 wk of endurance training. V(O(2p)) was measured breath by breath with a volume turbine and a mass spectrometer. Changes in deoxygenated hemoglobin concentration (Delta[HHb]) were measured by near-infrared spectroscopy. V(O(2p)) and Delta[HHb] were modeled with a monoexponential model. Training was performed on a cycle ergometer three times per week for 45 min at approximately 70% of peak V(O(2)). Pretraining tauV(O(2p)) was greater (P < 0.05) in O (43 +/- 10 s) than Y (34 +/- 8 s). tauV(O(2p)) decreased (P < 0.05) by 3 wk of training in both O (35 +/- 9 s) and Y (22 +/- 8 s), with no further changes thereafter. The pretraining overall adjustment of Delta[HHb] was faster than tauV(O(2p)) in both O and Y, resulting in Delta[HHb]/V(O(2p)) displaying an "overshoot" during the transient relative to the subsequent steady-state level. After 3 wk of training the Delta[HHb]/V(O(2p)) overshoot was attenuated in both O and Y. With further training, this overshoot persisted in O but was eliminated after 6 wk in Y. The training-induced speeding of V(O(2p)) kinetics in O and Y at 3 wk of training was associated with an improved matching of local O(2) delivery to muscle V(O(2)) (as represented by a lower Delta[HHb]/V(O(2p))). The continued overshoot in Delta[HHb]/V(O(2p)) in O may reflect a reduced vasodilatory responsiveness that may limit muscle blood flow distribution during the on-transient of exercise.
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The purpose of this study was to investigate the role of training and power output on muscle oxygen desaturation during and resaturation after an arm Wingate test (WAnT). Two groups of subjects were studied; the first group consisted of nine athletes participating in upper arm anaerobic sports and the second group of 11 university students. As a consequence, the group of athletes (HP) produced higher peak and mean power output (p < 0.01) than the group of university students (LP). Muscle oxygenation status was evaluated by using near infrared spectroscopy at the triceps brachii. The HP group exhibited 17.6 +/- 8.0% less muscle oxygen desaturation than the LP group (p < 0.05) but similar muscle total hemoglobin during exercise and faster (p < 0.05) muscle oxygen resaturation during recovery (tau = 12.4 +/- 5.2 sec in HP vs. tau = 24.2 +/- 11.0 sec in LP). These results indicate that the HP group exhibits less muscle desaturation during an arm WAnT and has a faster resaturation rate, probably attributed to differences in muscle mass, muscle fiber recruitment capability, and ATP production through anaerobic pathways.
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Cerebral blood flow (CBF) and its distribution are highly sensitive to changes in the partial pressure of arterial CO(2) (Pa(CO(2))). This physiological response, termed cerebrovascular CO(2) reactivity, is a vital homeostatic function that helps regulate and maintain central pH and, therefore, affects the respiratory central chemoreceptor stimulus. CBF increases with hypercapnia to wash out CO(2) from brain tissue, thereby attenuating the rise in central Pco(2), whereas hypocapnia causes cerebral vasoconstriction, which reduces CBF and attenuates the fall of brain tissue Pco(2). Cerebrovascular reactivity and ventilatory response to Pa(CO(2)) are therefore tightly linked, so that the regulation of CBF has an important role in stabilizing breathing during fluctuating levels of chemical stimuli. Indeed, recent reports indicate that cerebrovascular responsiveness to CO(2), primarily via its effects at the level of the central chemoreceptors, is an important determinant of eupneic and hypercapnic ventilatory responsiveness in otherwise healthy humans during wakefulness, sleep, and exercise and at high altitude. In particular, reductions in cerebrovascular responsiveness to CO(2) that provoke an increase in the gain of the chemoreflex control of breathing may underpin breathing instability during central sleep apnea in patients with congestive heart failure and on ascent to high altitude. In this review, we summarize the major factors that regulate CBF to emphasize the integrated mechanisms, in addition to Pa(CO(2)), that control CBF. We discuss in detail the assessment and interpretation of cerebrovascular reactivity to CO(2). Next, we provide a detailed update on the integration of the role of cerebrovascular CO(2) reactivity and CBF in regulation of chemoreflex control of breathing in health and disease. Finally, we describe the use of a newly developed steady-state modeling approach to examine the effects of changes in CBF on the chemoreflex control of breathing and suggest avenues for future research.
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Reductions in prefrontal oxygenation near maximal exertion may limit exercise performance by impairing executive functions that influence the decision to stop exercising; however, whether deoxygenation also occurs in motor regions that more directly affect central motor drive is unknown. Multichannel near-infrared spectroscopy was used to compare changes in prefrontal, premotor, and motor cortices during exhaustive exercise. Twenty-three subjects performed two sequential, incremental cycle tests (25 W/min ramp) during acute hypoxia [79 Torr inspired Po(2) (Pi(O(2)))] and normoxia (117 Torr Pi(O(2))) in an environmental chamber. Test order was balanced, and subjects were blinded to chamber pressure. In normoxia, bilateral prefrontal oxygenation was maintained during low- and moderate-intensity exercise but dropped 9.0 +/- 10.7% (mean +/- SD, P < 0.05) before exhaustion (maximal power = 305 +/- 52 W). The pattern and magnitude of deoxygenation were similar in prefrontal, premotor, and motor regions (R(2) > 0.94). In hypoxia, prefrontal oxygenation was reduced 11.1 +/- 14.3% at rest (P < 0.01) and fell another 26.5 +/- 19.5% (P < 0.01) at exhaustion (maximal power = 256 +/- 38 W, P < 0.01). Correlations between regions were high (R(2) > 0.61), but deoxygenation was greater in prefrontal than premotor and motor regions (P < 0.05). Prefrontal, premotor, and motor cortex deoxygenation during high-intensity exercise may contribute to an integrative decision to stop exercise. The accelerated rate of cortical deoxygenation in hypoxia may hasten this effect.
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This review addresses three types of causes of respiratory system limitations to O(2) transport and exercise performance that are experienced by significant numbers of active, highly fit younger and older adults. First, flow limitation in intrathoracic airways may occur during exercise because of narrowed, hyperactive airways or secondary to excessive ventilatory demands superimposed on a normal maximum flow-volume envelope. Narrowing of the extrathoracic, upper airway also occurs in some athletes at very high flow rates during heavy exercise. Examination of the breath-by-breath tidal flow-volume loop during exercise is key to a noninvasive diagnosis of flow limitation and to differentiation between intrathoracic and extrathoracic airway narrowing. Second exercise-induced arterial hypoxemia occurs secondary to an excessively widened alveolar-arterial oxygen pressure difference. This inefficient gas exchange may be attributable in part to small intracardiac or intrapulmonary shunts of deoxygenated mixed venous blood during exercise. The existence of these shunts at rest and during exercise may be determined by using saline solution contrast echocardiography. Finally, fatigue of the respiratory muscles resulting from sustained, high-intensity exercise and the resultant vasoconstrictor effects on limb muscle vasculature will also compromise O(2) transport and performance. Exercise in the hypoxic environments of even moderately high altitudes will greatly exacerbate the negative influences of these respiratory system limitations to exercise performance, especially in highly fit individuals.
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Using near-infrared spectroscopy (NIRS) and the tracer indocyanine green (ICG), we quantified blood flow in calf muscle and around the Achilles tendon during plantar flexion (1-9 W). For comparison, blood flow in calf muscle was determined by dye dilution in combination with magnetic resonance imaging measures of muscle volume, and, for the peritendon region, blood flow was measured by (133)Xe washout. From rest to a peak load of 9 W, NIRS-ICG blood flow in calf muscle increased from 2.4+/-0.2 to 74+/-5 ml x 100 ml tissue(-1) x min(-1), similar to that measured by reverse dye (77+/-6 ml x 100 ml tissue(-1) x min(-1)). Achilles peritendon blood flow measured by NIRS-ICG rose with exercise from 2.2+/-0.5 to 15.1+/-0.2 ml x 100 ml(-1) x min(-1), which was similar to that determined by (133)Xe washout (2.0+/-0.6 to 14.6+/-0.3 ml x 100 ml tissue(-1) x min(-1)). This is the first study using NIRS and ICG to quantify regional tissue blood flow during exercise in humans. Due to its high spatial and temporal resolution, the technique may be useful for determining regional blood flow distribution and regulation during exercise in humans.
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Near infrared spectroscopy can be used in non-invasive monitoring of changes in skeletal muscle oxygenation in exercising subjects. To evaluate whether this method can be used to assess metabolic capacity of muscles. Two distinctive variables abstracted from a curve of changes in muscle oxygenation were assessed. Exercise on a cycle ergometer was performed by 18 elite male athletes and eight healthy young men. A measuring probe was placed on the skin of the quadriceps muscle to measure reflected light at two wavelengths (760 and 850 nm), so that the relative index of muscle oxygenation could be calculated. Exercise intensity was increased from 50 W in 50 W increments until the subject was exhausted. During exercise, changes in muscle oxygenation and blood lactate concentration were recorded. The following two variables for assessment of muscle oxygenation were then abstracted and analysed by plotting curves of changes in muscle oxygenation: the rate of recovery of muscle oxygen saturation (R(R)) and the relative value of the effective decrease in muscle oxygenation (D(eff)). Data analysis showed a correlation between muscle oxygenation and blood lactate concentration at the various exercise intensities and verified the feasibility of the experiment. Data for the athletes were compared with those for the controls using the Aspin-Welch test of significance; t = 2.3 and 2.86 for R(R) and D(eff) respectively. There were significant differences (p = 0.05) between the athletes and the control group with respect to these two variables. R(R) and D(eff) may be distinctive variables that can be used to characterise muscle oxidative metabolism during human body movement.
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In the early 1960s, Norris introduced near infrared (NIR) spectroscopy (700-2500 nm) as an analytical technique for agricultural products. In 1977, Jobsis founded in vivo medical NIR spectroscopy, reporting that the relatively high degree of transparency of brain tissue in the NIR spectral window (700-1000 nm) enables safe real-time non-invasive detection of regional haemoglobin oxygenation using trans-illumination spectroscopy. In order to place current medical NIR spectroscopy in its proper perspective, this review provides a snapshot of the roots of the discovery and the early years of medical NIR spectroscopy research and development. Starting in 1992, the opportunity of measuring quantitatively, by different NIR spectroscopy techniques, regional oxy-haemoglobin saturation by NIR oximetry, it is possible to monitor brain/muscle reserve capacity following tissue oxygen extraction in different pathophysiological conditions. This review reports the status of the current commercial oximeters (including wireless instrumentation) and their main clinical and physiological applications. In the last decade, NIR spectroscopy brain oximetry has obtained significant clinical relevance as suggested by the more than 10,000 instruments sold and the high number of related scientific publications. The most relevant clinical application is represented by the evaluation of cerebral oxy-haemoglobin saturation during adult cardiac surgery and cardiopulmonary bypass. Many commercial oximeters are presently available. However, their relatively poor precision and the lack of standardisation amongst the different instruments suggest that further technological advances are required before NIR spectroscopy oximetry can be adopted more widely under the "guidelines" of regulatory authorities.
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To examine if cerebral (frontal cortex) and skeletal muscle (m. vastus lateralis) deoxygenation and cerebral blood flow velocity (Vmean) in the middle cerebral artery differentiated between normoxic and hypoxic (end-tidal PO2 71 mmHg) conditions, and if they were associated with hypoxic ventilatory chemosensitivity and cerebrovascular responsiveness, 8 men performed incremental cycling trials (30 W/min ramp) under normoxic (T1-N) and hypoxic (T1-H) conditions until volitional fatigue, or until arterial O2 saturation decreased below 80%. The tests were repeated (T2-N; T2-H) on another day with supplemental O2 (Sup-O2) at the end of exercise. The Vmean response was similar in normoxia and hypoxia. In hypoxia compared to normoxia, cerebral deoxygenation (↑ deoxyhemoglobin concentration (Δ[HHb]) and ↓ tissue oxygenation index (TOI)) was greater at a given work rate. A strong hypoxic ventilatory chemosensitivity was associated with a rapid reduction of cerebral TOI (r = 0.94, P < 0.001). Muscle deoxygenation was similar in normoxia and hypoxia suggesting greater muscle blood flow in hypoxia compared to normoxia and thus the existence of control features that match muscle perfusion and O2 delivery tightly with O2 demand during exercise. Sup-O2 reduced both cerebral and muscle deoxygenation, at least transiently.
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It has been suggested that, because of the low sitting position in short-track speed skating, muscle blood flow is restricted, leading to decreases in tissue oxygenation. Therefore, wearable wireless-enabled near-infrared spectroscopy (NIRS) technology was used to monitor changes in quadriceps muscle blood volume and oxygenation during a 500-m race simulation in short-track speed skaters. Six elite skaters, all of Olympic standard (age = 23 ± 1.8 yr, height = 1.8 ± 0.1 m, mass = 80.1 ± 5.7 kg, midthigh skinfold thickness = 7 ± 2 mm), were studied. Subjects completed a 500-m race simulation time trial (TT). Whole-body oxygen consumption was simultaneously measured with muscle oxygenation in right and left vastus lateralis as measured by NIRS. Mean time for race completion was 44.8 ± 0.4 s. VO2 peaked 20 s into the race. In contrast, muscle tissue oxygen saturation (TSI%) decreased and plateaued after 8 s. Linear regression analysis showed that right leg TSI% remained constant throughout the rest of the TT (slope value = 0.01), whereas left leg TSI% increased steadily (slope value = 0.16), leading to a significant asymmetry (P < 0.05) in the final lap. Total muscle blood volume decreased equally in both legs at the start of the simulation. However, during subsequent laps, there was a strong asymmetry during cornering; when skaters traveled solely on the right leg, there was a decrease in its muscle blood volume, whereas an increase was seen in the left leg. NIRS was shown to be a viable tool for wireless monitoring of muscle oxygenation. The asymmetry in muscle desaturation observed on the two legs in short-track speed skating has implications for training and performance.
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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.
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In 1923, Nobel Laureate A.V. Hill proposed that maximal exercise performance is limited by the development of anaerobiosis in the exercising skeletal muscles. Variants of this theory have dominated teaching in the exercise sciences ever since, but 90 years later there is little biological evidence to support Hill's belief, and much that disproves it. The cardinal weakness of the Hill model is that it allows no role for the brain in the regulation of exercise performance. As a result, it is unable to explain at least 6 common phenomena, including (i) differential pacing strategies for different exercise durations; (ii) the end spurt; (iii) the presence of fatigue even though homeostasis is maintained; (iv) fewer than 100% of the muscle fibers have been recruited in the exercising limbs; (v) the evidence that a range of interventions that act exclusively on the brain can modify exercise performance; and (vi) the finding that the rating of perceived exertion is a function of the relative exercise duration rather than the exercise intensity. Here I argue that the central governor model (CGM) is better able to explain these phenomena. In the CGM, exercise is seen as a behaviour that is regulated by complex systems in the central nervous system specifically to ensure that exercise terminates before there is a catastrophic biological failure. The complexity of this regulation cannot be appreciated if the body is studied as a collection of disconnected components, as is the usual approach in the modern exercise sciences.
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The aim of this study was to investigate the relationship between the attenuation point of muscle deoxygenation (APMD) and the EMG threshold (EMGT) during incremental cycling exercise under different fractions of inspired O2 (FIO2). Nine male subjects performed ramp cycling exercise tests (20 W·min(-1)) to exhaustion under normoxic and hypoxic conditions (FIO2 = 0.12). Pulmonary O2 uptake (VO2), muscle deoxygenation, and EMG activity in the vastus lateralis muscle were simultaneously measured during the tests, and both APMD and EMGT were calculated. Hypoxia significantly reduced peak VO2 (VO2peak). At the same absolute exercise intensity and at VO2peak, muscle deoxygenation, but not EMG activity, was significantly greater in hypoxia. VO2 at APMD was significantly decreased in hypoxia (P < 0.01). Similarly, VO2 at EMGT was significantly lower in hypoxia than in normoxia (P < 0.01). In addition, VO2 was lower at APMD than at EMGT under both conditions (P < 0.01). However, the relationships between APMD and EMGT were significant under both normoxic (r = 0.95, P < 0.01) and hypoxic (r = 0.89, P < 0.01) conditions. These results suggest that the attenuation of muscle deoxygenation near VO2peak is related to and precedes changes in neuromuscular activity under normoxic and hypoxic conditions.
Article
The purpose of the study was to investigate the effect of 30-min voluntary hyperpnoea on cerebral, respiratory and leg muscle balance between O(2) delivery and utilization during a subsequent constant-power test. Eight males performed a V˙O(2max) test, and two exercise tests at 85% of peak power output: (a) a control constant-power test (CPT), and (b) a constant-power test after a respiratory maneuver (CPT(RM)). Oxygenated (Δ[O(2)Hb]), deoxygenated (Δ[HHb]) and total (Δ[tHb]) hemoglobin in cerebral, intercostal and vastus lateralis were monitored with near-infrared spectroscopy. The performance time dropped ∼15% in CPT(RM) (6:55±2:52min) compared to CPT (8:03±2:33min), but the difference was not statistically significant. The vastus lateralis and intercostal Δ[tHb] and Δ[HHb] were lower in CPT(RM) than in CPT (P≤0.05). There were no differences in cerebral oxygenation between the trials. Thus, respiratory work prior to an exercise test influences the oxygenation during exercise in the leg and respiratory muscles, but not in the frontal cortex.
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During exercise, as end-tidal carbon dioxide (P(ET)(CO₂)) drops after the respiratory compensation point (RCP), so does cerebral blood flow velocity (CBFv) and cerebral oxygenation. This low-flow, low-oxygenation state may limit work capacity. We hypothesized that by preventing the fall in P(ET)(CO₂) at peak work capacity (W(max)) with a newly designed high-flow, low-resistance rebreathing circuit, we would improve CBFv, cerebral oxygenation, and W(max). Ten cyclists performed two incremental exercise tests, one as control and one with P(ET)(CO₂) constant (clamped) after the RCP. We analyzed , middle cerebral artery CBFv, cerebral oxygenation, and cardiopulmonary measures. At W(max), when we clamped P(ET)(CO₂) (39.7 ± 5.2 mmHg vs. 29.6 ± 4.7 mmHg, P < 0.001), CBFv increased (92.6 ± 15.9 cm/s vs. 73.6 ± 12.5 cm/s, P < 0.001). However, cerebral oxygenation was unchanged (ΔTSI -21.3 ± 13.1% vs. -24.3 ± 8.1%, P = 0.33), and W(max) decreased (380.9 ± 20.4W vs. 405.7 ± 26.8 W, P < 0.001). At W(max), clamping P(ET)(CO₂) increases CBFv, but this does not appear to improve W(max).
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The effects of intermittent hypoxic exposure (IHE) on cerebral and muscle oxygenation, arterial oxygen saturation (SaO2), and respiratory gas exchange during a 20-km cycle time trial (20TT) were examined (n=9) in a placebo-controlled randomized design. IHE (7:3 min hypoxia to normoxia) involved 90-min sessions for 10 days, with SaO2 clamped at ~80%. Prior to, and 2 days after the intervention, a 20TT was performed. During the final minute of the 20TT, in the IHE group only, muscle oxyhemoglobin (oxy-Hb) was elevated (mean+/-95% confidence interval 1.3+/-1.2 ΔmicroM, p=0.04), whereas cerebral oxy-Hb was reduced (-1.9%+/-1.0%, p<0.01) post intervention compared with baseline. The 20TT performance was unchanged between groups (p=0.7). In the IHE group, SaO2 was higher (1.0+/-0.7Δ%, p=0.006) and end-tidal PCO2 was lower (-1.2+/-0.1 mm Hg, p=0.01) during the final stage of the 20TT post intervention compared with baseline. In summary, reductions in muscle oxy-Hb and systemic SaO2 occurring at exercise intensities close to maximal at the end of a 20TT were offset by IHE, although this was not translated into improved performance.
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We conducted a systematic review and meta-regression analysis to quantify effects of exercise on brain hemodynamics measured by near-infrared spectroscopy (NIRS). The results indicate that acute incremental exercise (categorized relative to aerobic capacity (VO(2)peak) as low - <30% VO(2)peak; moderate - ≥30% VO(2)peak to <60% VO(2)peak; hard - ≥60% VO(2)peak to <VO(2)peak; and very hard - ≥VO(2)peak intensities) performed by 291 healthy people in 21 studies is accompanied by moderate-to-large increases (mean effect, dz±95% CI) in the prefrontal cortex of oxygenated hemoglobin (O(2)Hb) or other measures of oxygen level (O(2)Hbdiff) or saturation (SCO(2)) (0.92±0.67, 1.17), deoxygenated hemoglobin (dHb) (0.87±0.56, 1.19), and blood volume estimated by total hemoglobin (tHb) (1.21±0.84, 1.59). After peaking at hard intensities, cerebral oxygen levels dropped during very hard intensities. People who were aerobically trained attained higher levels of cortical oxygen, dHb, and tHb than untrained people during very hard intensities. Among untrained people, a marked drop in oxygen levels and a small increase in dHb at very hard intensities accompanied declines in tHb, implying reduced blood flow. In 6 studies of 222 patients with heart or lung conditions, oxygenation and dHb were lowered or unchanged during exercise compared to baseline. In conclusion, prefrontal oxygenation measured with NIRS in healthy people showed a quadratic response to incremental exercise, rising between moderate and hard intensities, then falling at very hard intensities. Training status influenced the responses. While methodological improvements in measures of brain oxygen are forthcoming, these results extend the evidence relevant to existing models of central limitations to maximal exercise.
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This review covers the control of blood pressure, cardiac output and muscle blood flow by the muscle metaboreflex which involves chemically sensitive nerves located in muscle parenchyma activated by metabolites accumulating in the muscle during contraction. The efferent response to metaboreflex activation is an increase in sympathetic nerve activity that constricts the systemic vasculature and also evokes parallel inotropic and chronotropic effects on the heart to increase cardiac output. The metaboreflex elicits a significant blood pressure elevating response during exercise and functions to redistribute blood flow and blood volume. Regional specificity in the efferent response to the metaboreflex activated from either the leg or the arm is seen in the balance between signals for vasoconstriction to curtail blood flow and signals to increase cardiac output. The metaboreflex has dual functions. It can both elevate and decrease muscle blood flow depending on (1) the intensity and mode of contraction, (2) the limb in which the reflex is evoked, (3) the strength of the signal defined by the muscle mass, (4) the extent to which blood flow is redistributed from inactive vascular beds to increase central blood volume and (5) the extent to which cardiac output can be increased.
Article
The reduction in cerebral oxygenation (Cox) is associated with the cessation of exercise during constant work rate and incremental tests to exhaustion. Yet in exercises of this nature, ecological validity is limited due to work rate being either fully or partly dictated by the protocol, and it is unknown whether cerebral deoxygenation also occurs during self-paced exercise. Here, we investigated the cerebral haemodynamics during a 5-km running time trial in trained runners. Rating of perceived exertion (RPE) and surface electromyogram (EMG) of lower limb muscles were recorded every 0.5 km. Changes in Cox (prefrontal lobe) were monitored via near-infrared spectroscopy through concentration changes in oxy- and deoxyhaemoglobin (Delta[O(2)Hb], Delta[HHb]). Changes in total Hb were calculated (Delta[THb] = Delta[O(2)Hb] + Delta[HHb]) and used as an index of change in regional blood volume. During the trial, RPE increased from 6.6 +/- 0.6 to 19.1 +/- 0.7 indicating maximal exertion. Cox rose from baseline to 2.5 km ( upward arrowDelta[O(2)Hb], upward arrowDelta[HHb], upward arrowDelta[THb]), remained constant between 2.5 and 4.5 km, and fell from 4.5 to 5 km ( downward arrowDelta[O(2)Hb], upward arrowDelta[HHb], <-->Delta[THb]). Interestingly, the drop in Cox at the end of the trial coincided with a final end spurt in treadmill speed and concomitant increase in skeletal muscle recruitment (as revealed by higher lower limb EMG). Results confirm the large tolerance for change in Cox during exercise at sea level, yet further indicate that, in conditions of self-selected work rate, cerebral deoxygenation remains within a range that does not hinder strenuous exercise performance.
Article
The response of cerebral vasculature to exercise is different from other peripheral vasculature; it has a small vascular bed and is strongly regulated by cerebral autoregulation and the partial pressure of arterial carbon dioxide (Pa(CO(2))). In contrast to other organs, the traditional thinking is that total cerebral blood flow (CBF) remains relatively constant and is largely unaffected by a variety of conditions, including those imposed during exercise. Recent research, however, indicates that cerebral neuronal activity and metabolism drive an increase in CBF during exercise. Increases in exercise intensity up to approximately 60% of maximal oxygen uptake produce elevations in CBF, after which CBF decreases toward baseline values because of lower Pa(CO(2)) via hyperventilation-induced cerebral vasoconstriction. This finding indicates that, during heavy exercise, CBF decreases despite the cerebral metabolic demand. In contrast, this reduced CBF during heavy exercise lowers cerebral oxygenation and therefore may act as an independent influence on central fatigue. In this review, we highlight methodological considerations relevant for the assessment of CBF and then summarize the integrative mechanisms underlying the regulation of CBF at rest and during exercise. In addition, we examine how CBF regulation during exercise is altered by exercise training, hypoxia, and aging and suggest avenues for future research.
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Acute exposure to hypoxia provokes a decrease in peak oxygen consumption ( V(O)(2peak)). At and above 4000 m, the decrease in V(O)(2peak) is greater than expected from the decrease in arterial oxygen content (C(a)O(2)) suggesting the participation of other factors. We hypothesized that O(2) transfer within the active muscle may play a role. Therefore we used Near Infra Red Spectroscopy (NIRS) to assess oxy (O2Hb) and deoxyhemoglobin (HHb) concentration in the vastus lateralis of trained athletes (TA) and untrained subjects (US) exercising at various inspired oxygen pressure (PI(O)(2), 131.4, 107.3 and 87.0 mmHg). A mathematical model has been developed to compute: (i) the pulmonary (K(p)) and muscular (K(tm)) O(2) diffusion coefficients and (ii) the proportion of arteriolar:capillary:venous blood participating in the NIRS signal at every exercise intensity from rest to peak exercise in the normoxic and various hypoxic conditions. In TA, O2Hb decreased near maximal exercise at 2500 and 4000 m, while in US, altitude had no effect. In normoxia O2Hb was higher in TA than in US, the difference disappearing in hypoxia. K(tm) increased linearly with workload and altitude and was higher in TA than US while K(p) plateaued near maximal exercise, which was consistent with athletes' greater decrease in C(a)O(2). The greater participation of arterial blood in the NIRS signal in TA at altitudes account for their higher O2Hb values as well as the greater decrease they underwent in hypoxia. At 4000m, athletes loose their advantages of adaptation to training due to a reduced arterial content, and both from NIRS variables and model output, characteristics of O(2) transfer of TA converge toward those of US.
Article
We hypothesized that a short-term training program involving repeated all-out sprint training (RST) would be more effective than work-matched, low-intensity endurance training (ET) in enhancing the kinetics of oxygen uptake (Vo(2)) and muscle deoxygenation {deoxyhemoglobin concentration ([HHb])} following the onset of exercise. Twenty-four recreationally active subjects (15 men, mean +/- SD: age 21 +/- 4 yr, height 173 +/- 9 cm, body mass 71 +/- 11 kg) were allocated to one of three groups: RST, which completed six sessions of four to seven 30-s RSTs; ET, which completed six sessions of work-matched, moderate-intensity cycling; and a control group (CON). All subjects completed moderate-intensity and severe-intensity "step" exercise transitions before (Pre) and after the 2-wk intervention period (Post). Following RST, [HHb] kinetics were speeded, and the amplitude of the [HHb] response was increased during both moderate and severe exercise (P < 0.05); the phase II Vo(2) kinetics were accelerated for both moderate (Pre: 28 +/- 8, Post: 21 +/- 8 s; P < 0.01) and severe (Pre: 29 +/- 5, Post: 23 +/- 5 s; P < 0.05) exercise; the amplitude of the Vo(2) slow component was reduced (Pre: 0.52 +/- 0.19, Post: 0.40 +/- 0.17 l/min; P < 0.01); and exercise tolerance during severe exercise was improved by 53% (Pre: 700 +/- 234, Post: 1,074 +/- 431 s; P < 0.01). None of these parameters was significantly altered in the ET and CON groups. Six sessions of RST, but not ET, resulted in changes in [HHb] kinetics consistent with enhanced fractional muscle O(2) extraction, faster Vo(2) kinetics, and an increased tolerance to high-intensity exercise.
Article
A simple muscle tissue spectrophotometer is adapted to measure the recovery time (TR) for hemoglobin/myoglobin (Hb/Mb) desaturation in the capillary bed of exercising muscle, termed a deoxygenation meter. The use of the instrument for measuring the extent of deoxygenation is presented, but the use of TR avoids difficulties of quantifying Hb/Mb saturation changes. The TR reflects the balance of oxygen delivery and oxygen demand in the localized muscles of the quadriceps following work near maximum voluntary contraction (MVC) in elite male and female rowers (a total of 22) on two occasions, 1 yr apart. TR ranged from 10 to 80 s and was interpreted as a measure of the time for repayment of oxygen and energy deficits accumulated during intense exercise by tissue respiration under ADP control. The Hb/Mb resaturation times provide a noninvasive localized indication of the degree of O2 delivery stress as evoked by rowing ergometry and may provide directions for localized muscle power output improvement for particular individuals in rowing competitions.
Article
Near-infrared (NIR) spectroscopy is a noninvasive technique that uses the differential absorption properties of hemoglobin to evaluate skeletal muscle oxygenation. Oxygenated and deoxygenated hemoglobin absorb light equally at 800 nm, whereas at 760 nm absorption is primarily from deoxygenated hemoglobin. Therefore, monitoring these two wavelengths provides an index of deoxygenation. To investigate whether venous oxygen saturation and absorption between 760 and 800 nm (760-800 nm absorption) are correlated, both were measured during forearm exercise. Significant correlations were observed in all subjects (r = 0.92 +/- 0.07; P < 0.05). The contribution of skin flow to the changes in 760-800 nm absorption was investigated by simultaneous measurement of skin flow by laser flow Doppler and NIR recordings during hot water immersion. Changes in skin flow but not 760-800 nm absorption were noted. Intra-arterial infusions of nitroprusside and norepinephrine were performed to study the effect of alteration of muscle perfusion on 760-800 nm absorption. Limb flow was measured with venous plethysmography. Percent oxygenation increased with nitroprusside and decreased with norepinephrine. Finally, the contribution of myoglobin to the 760-800 nm absorption was assessed by using 1H-magnetic resonance spectroscopy. At peak exercise, percent NIR deoxygenation during exercise was 80 +/- 7%, but only one subject exhibited a small deoxygenated myoglobin signal. In conclusion, 760-800 nm absorption is 1) closely correlated with venous oxygen saturation, 2) minimally affected by skin blood flow, 3) altered by changes in limb perfusion, and 4) primarily derived from deoxygenated hemoglobin and not myoglobin.
Article
We studied cerebral hemodynamic response to a sequential motor task in 56 subjects to investigate the time course and distribution of blood oxygenation changes as monitored by near-infrared spectroscopy (NIRS). To address whether response is modulated by different performance velocities, a group of subjects (n = 12) was examined while performing the motor task at 1, 2, and 3 Hz. The results demonstrate that 1) the NIRS response reflects localized changes in cerebral hemodynamics, 2) the response, consisting of an increase in oxygenated hemoglobin concentration [oxy-Hb] and a decrease in deoxygenated hemoglobin concentration ([deoxy-Hb]), is lateralized and increases in amplitude with higher performance rates, and 3) changes in [oxy-Hb] and [deoxy-Hb] differ in time course. Changes in [oxy-Hb] are biphasic, with a fast initial increase and a pronounced poststimulus undershoot. The stimulus-associated decrease in [deoxy-Hb] is monophasic, and response latency is greater. We conclude that NIRS is able to detect even small changes in cerebral hemodynamic response to functional stimulation.
Article
The characteristic low "sitting" position of competitive speed skating has been shown to result in a right shifted heart rate-VO2 curve and elevated submaximal blood lactate values compared with running or cycling. This is thought to be a consequence of reduced blood flow and subsequent oxygen delivery to the exercising muscle while speed skating. Duel wavelength spectrophotometry was used to measure oxygenated and deoxygenated hemoglobin/myoglobin (OD) in the capillary bed of five muscle groups during in-line skating in upright (US) and low (LS) positions. Eight U.S. speed skaters (4 category 1) performed US and LS at 2.68 and 3.13 m.s-1 (4% grade) on a wide (2.44 m) treadmill (4 trials, 5 min each, 20 min recovery between trials). Expired gas parameters and blood lactate (LA) concentrations were determined for each trial. Hip and knee angles were measured (PEAK Motion Analysis) and were significantly different in US and LS. For similar oxygen uptake during US and LS (44.9 +/- 2.79, 45.6 +/- 3.52), heart rate and LA were significantly higher during LS (172 +/- 11 vs 179 +/- 10, 4.35 +/- 2.19 vs 8.70 +/- 3.60). Deoxygenation was significantly greater during LS than during US at both speeds and was greater at 3.13 m.s-1 (P < 0.05). OD was highly related to LA (r > 0.95) but not to whole body VO2. Blood volume change was less for LS than for US (P < 0.05). Increased deoxygenation in the capillary bed of the exercising quadriceps during LS versus US is consistent with the hypothesis that blood flow and subsequent O2 delivery is compromised in the low speed skating position.
Article
The onset of anaerobic (lactate) metabolism during incremental exercise, which may be a result of an imbalance between tissue oxygen supply and demand, has been associated with the gas exchange ventilatory threshold (VT). This study was designed to examine whether near infrared spectroscopy (NIRS) could be used to detect the VT in healthy subjects. Twenty-one men and 19 women completed incremental cycle ergometry during which NIRS measurements were obtained from the right vastus lateralis and gas exchange measurements were monitored simultaneously using a metabolic cart. The VT was identified from the metabolic data by the V-slope method and from NIRS data as the intensity at which tissue absorbency crossed the resting baseline value observed immediately prior to the initiation of exercise. Pearson correlations for the relative oxygen uptake and power output observed for the two methods of detecting VT were 0.90 and 0.88, respectively, in men and 0.89 and 0.86, respectively, in women (P < 0.01). No significant differences were observed between the two methods of detecting VT for any of the physiological responses (P > 0.05). No significant (P > 0.05) gender differences were observed in muscle oxygenation values at the VT, 32% in men and 38% in women. These results validate the use of NIRS as an alternate noninvasive method for detecting VT during cycle exercise in healthy subjects.
The purpose of this study was to compare the rates of muscle deoxygenation in the exercising muscles during incremental arm cranking and leg cycling exercise in healthy men and women. Fifteen men and 10 women completed arm cranking and leg cycling tests to exhaustion in separate sessions in a counterbalanced order. Cardiorespiratory measurements were monitored using an automated metabolic cart interfaced with an electrocardiogram. Tissue absorbency was recorded continuously at 760 nm and 850 nm during incremental exercise and 6 min of recovery, with a near infrared spectrometer interfaced with a computer. Muscle oxygenation was calculated from the tissue absorbency measurements at 30%, 45%, 60%, 75% and 90% of peak oxygen uptake (VO2) during each exercise mode and is expressed as a percentage of the maximal range observed during exercise and recovery (%Mox). Exponential regression analysis indicated significant inverse relationships (P < 0.01) between %Mox and absolute VO2 during arm cranking and leg cycling in men (multiple R = -0.96 and -0.99, respectively) and women (R = -0.94 and -0.99, respectively). No significant interaction was observed for the %Mox between the two exercise modes and between the two genders. The rate of muscle deoxygenation per litre of VO2 was 31.1% and 26.4% during arm cranking and leg cycling, respectively, in men, and 26.3% and 37.4% respectively, in women. It was concluded that the rate of decline in %Mox for a given increase in VO2 between 30% and 90% of the peak VO2 was independent of exercise mode and gender.
Article
Near-infrared spectroscopy (NIRS) could allow insights into controversial issues related to blood lactate concentration ([La](b)) increases at submaximal workloads (). We combined, on five well-trained subjects [mountain climbers; peak O(2) consumption (VO(2peak)), 51.0 +/- 4.2 (SD) ml. kg(-1). min(-1)] performing incremental exercise on a cycle ergometer (30 W added every 4 min up to voluntary exhaustion), measurements of pulmonary gas exchange and earlobe [La](b) with determinations of concentration changes of oxygenated Hb (Delta[O(2)Hb]) and deoxygenated Hb (Delta[HHb]) in the vastus lateralis muscle, by continuous-wave NIRS. A "point of inflection" of [La](b) vs. was arbitrarily identified at the lowest [La](b) value which was >0.5 mM lower than that obtained at the following. Total Hb volume (Delta[O(2)Hb + HHb]) in the muscle region of interest increased as a function of up to 60-65% of VO(2 peak), after which it remained unchanged. The oxygenation index (Delta[O(2)Hb - HHb]) showed an accelerated decrease from 60- 65% of VO(2 peak). In the presence of a constant total Hb volume, the observed Delta[O(2)Hb - HHb] decrease indicates muscle deoxygenation (i.e., mainly capillary-venular Hb desaturation). The onset of muscle deoxygenation was significantly correlated (r(2) = 0.95; P < 0.01) with the point of inflection of [La](b) vs., i.e., with the onset of blood lactate accumulation. Previous studies showed relatively constant femoral venous PO(2) levels at higher than approximately 60% of maximal O(2) consumption. Thus muscle deoxygenation observed in the present study from 60-65% of VO(2 peak) could be attributed to capillary-venular Hb desaturation in the presence of relatively constant capillary-venular PO(2) levels, as a consequence of a rightward shift of the O(2)Hb dissociation curve determined by the onset of lactic acidosis.
Article
The combined effects of hyperventilation and arterial desaturation on cerebral oxygenation (ScO2) were determined using near-infrared spectroscopy. Eleven competitive oarsmen were evaluated during a 6-min maximal ergometer row. The study was randomized in a double-blind fashion with an inspired O2 fraction of 0.21 or 0.30 in a crossover design. During exercise with an inspired O2 fraction of 0.21, the arterial CO2 pressure (35 +/- 1 mmHg; mean +/- SE) and O2 pressure (77 +/- 2 mmHg) as well as the hemoglobin saturation (91.9 +/- 0.7%) were reduced (P < 0.05). ScO2 was reduced from 80 +/- 2 to 63 +/- 2% (P < 0.05), and the near-infrared spectroscopy-determined concentration changes in deoxy- (DeltaHb) and oxyhemoglobin (DeltaHbO2) of the vastus lateralis muscle increased 22 +/- 3 microM and decreased 14 +/- 3 microM, respectively (P < 0.05). Increasing the inspired O2 fraction to 0.30 did not affect ventilation (174 +/- 4 l/min), but arterial CO2 pressure (37 +/- 2 mmHg), O2 pressure (165 +/- 5 mmHg), and hemoglobin O2 saturation (99 +/- 0.1%) increased (P < 0. 05). ScO2 remained close to the resting level during exercise (79 +/- 2 vs. 81 +/- 2%), and although the muscle DeltaHb (18 +/- 2 microM) and DeltaHbO2 (-12 +/- 3 microM) were similar to those established without O2 supplementation, work capacity increased from 389 +/- 11 to 413 +/- 10 W (P < 0.05). These results indicate that an elevated inspiratory O2 fraction increases exercise performance related to maintained cerebral oxygenation rather than to an effect on the working muscles.
Article
We have previously hypothesized restricted muscle blood flow during speed skating, secondary to the high intramuscular forces intrinsic to the unique posture assumed by speed skaters and to the prolonged duty cycle of the skating stroke. To test this hypothesis, we studied speed skaters (N = 10) during submaximal and maximal cycling and in-line skating, in both low (knee angle = 107 degrees) and high (knee angle = 112 degrees) skating positions (CE vs SkL vs SkH). Supportive experiments evaluated muscle desaturation and lactate accumulation during on-ice speed skating and muscle desaturation during static exercise at different joint positions. Consistent with the hypothesis were reductions during skating in VO2peak (4.28 vs 3.83 vs 4.26 L x min(-1)), the VO2 at 4 mmol x L(-1) blood lactate (3.38 vs 1.93 vs 3.31 L x min(-1)), and cardiac output during maximal exercise (33.2 vs 25.3 vs 25.6 L x min(-1)). The reduction in maximal cardiac output was not attributable to differences in HRmax (197 vs 192 vs 193 b x min(-1)) but to a reduction in SVmax (172 vs 135 vs 134 mL x beat(-1)). The reduction in SV appeared to be related to an increased calculated systemic vascular resistance (354 vs 483 vs 453 dynes x s(-1) x cm(-1)). During maximal skating there was also a greater % O2 desaturation of the vastus lateralis based on near infrared spectrophotometry (50.3 vs 74.9 vs 60.4% of maximal desaturation during cuff ischemia). The results were supported by greater desaturation with smaller knee angles during static exercise and by greater desaturation and accelerated blood lactate accumulation during on-ice speed skating in the low vs high position. The results of this study support the hypothesis that physiological responses during speed skating are dominated by restriction of blood flow, attributable either to high intramuscular forces, the long duty cycle of the skating stroke, or both.
Article
Near-infrared spectroscopy (NIRS) measures hemoglobin saturation in small vessels. A number of interesting studies have used this method. However, difficulties with signal quantification and studies in which NIRS oxygen saturation did not behave as expected raise concerns. NIRS remains promising for studies of skeletal muscle, but a better understanding of the method is needed.
Article
The purpose of this study was to examine the validity of the quantitative measurement of muscle oxidative metabolism in exercise by near-infrared continuous-wave spectroscopy (NIRcws). Twelve male subjects performed two bouts of dynamic handgrip exercise, once for the NIRcws measurement and once for the (31)P-magnetic resonance spectroscopy (MRS) measurement as a standard measure. The resting muscle metabolic rate (RMRmus) was independently measured by (31)P-MRS during 15 min of arterial occlusion at rest. During the first exercise bout, the quantitative value of muscle oxidative metabolic rate at 30 s postexercise was evaluated from the ratio of the rate of oxyhemoglobin/myoglobin decline measured by NIRcws during arterial occlusion 30 s after exercise and the rate at rest. Therefore, the absolute values of muscle oxidative metabolic rate at 30 s after exercise [VO(2NIR(30))] was calculated from this ratio multiplied by RMRmus. During the second exercise bout, creatine phosphate (PCr) resynthesis rate was measured by (31)P-MRS at 30 s postexercise [Q((30))] under the same conditions but without arterial occlusion postexercise. To determine the validity of NIRcws, VO(2NIR(30)) was compared with Q((30)). There was a significant correlation between VO(2NIR(30)), which ranged between 0.018 and 0. 187 mM ATP/s, and Q((30)), which ranged between 0.041 and 0.209 mM ATP/s (r = 0.965, P < 0.001). This result supports the application of NIRcws to quantitatively evaluate muscle oxidative metabolic rate in exercise.
Article
To investigate muscle blood volume (BV) change and hemoglobin/myoglobin oxygen desaturation (OD) during simulated giant slalom (GS) and slalom (SL) Alpine ski racing. Joint angle, BV, OD, and heart rate (HR) were evaluated during GS and SL events in 30 junior elite skiers ages 9--17 yr (13.5 +/- 2.3). Subjects were stratified by ski class and age: group I, J1 and J2, ages 15--18 yr (16.8 +/- 0.8); group II, J3, 13--14 yr (13.6 +/- 0.7); and group III, J4 and J5, 9--12 yr (11.5 +/- 1.2). Near-infrared spectrophotometry (NIRS) was used to measure BV and OD in the capillary bed of the vastus lateralis during trials. Maximal OD was determined during thigh cuff ischemia (CI). Quadriceps cross-sectional area (CSA) was estimated by skin-fold and thigh circumference. Joint angles were smaller (P < 0.05) during GS than SL for ankle (83.8 +/- 11.9 degrees; 98.6 +/- 15.7 degrees ), knee (107.4 +/- 14.9 degrees; 118.3 +/- 18.0 degrees ), and hip (98.8 +/- 14.3 degrees; 107.5 +/- 16.2 degrees ). BV reduction from rest to peak exercise (Delta BV) was 30% greater (P < 0.05) during the GS than SL, whereas Delta OD was 33% greater (P < 0.05) during GS. Delta OD, relative to CI OD, was greater for all subjects during GS (79.2 +/- 3.7%) than SL (65.7 +/- 4.4%). This pattern continued within groups; group II displayed the greatest relative desaturation (82.9 +/- 7.6%). CSA was larger in older skiers (92.5 +/- 21.6; 72.5 +/- 12.3; 65.3 +/- 21.2 cm(2)) and correlated with Delta OD (P < 0.05). The larger reduction in BV (Delta BV change) and greater OD when skiers assumed lower posture during GS than SL may be related to greater effective static load secondary to higher percent of maximal voluntary contraction and is consistent with compromised blood flow to working muscle.
Article
To elevate effects of carbon dioxide (CO2) retention by way of an increased respiratory load during submaximal exercise (150 W), the concentration changes of oxy- (DeltaHbO2) and deoxy-haemoglobin (DeltaHb) of active muscles and the brain were determined by near-infrared spectroscopy (NIRS) in eight healthy males. During exercise, pulmonary ventilation increased to 33 (28-40) L min-1 (median with range) with no effect of a moderate breathing resistance (reduction of the pneumotach diameter from 30 to 14 and 10 mm). The end-tidal CO2 pressure (PETCO2) increased from 45 (42-48) to 48 (46-58) mmHg with a reduction of only 1% in the arterial haemoglobin O2 saturation (SaO2). During control exercise (normal breathing resistance), muscle and brain DeltaHbO2 were not different from the resting levels, and only the leg muscle DeltaHb increased (4 (-2-10) microM, P < 0.05). Moderate resistive breathing increased DeltaHbO2 of the intercostal and vastus lateralis muscles to 6 +/- (-5-14) and 1 (-7-9) microM(P < 0.05), respectively, while muscle DeltaHb was not affected. Cerebral DeltaHbO2 and DeltaHb became elevated to 6 (1-15) and 1 (-1-6) microM by resistive breathing (P < 0.05). Resistive breathing caused an increased concentration of oxygenated haemoglobin in active muscles and in the brain. The results indicate that CO2 influences blood flow to active skeletal muscle although its effect appears to be smaller than for the brain.
Article
Near infrared spectroscopy (NIRS) is becoming a widely used research instrument to measure tissue oxygen (O2) status non-invasively. Continuous-wave spectrometers are the most commonly used devices, which provide semi-quantitative changes in oxygenated and deoxygenated hemoglobin in small blood vessels (arterioles, capillaries and venules). Refinement of NIRS hardware and the algorithms used to deconvolute the light absorption signal have improved the resolution and validity of cytochrome oxidase measurements. NIRS has been applied to measure oxygenation in a variety of tissues including muscle, brain and connective tissue, and more recently it has been used in the clinical setting to assess circulatory and metabolic abnormalities. Quantitative measures of blood flow are also possible using NIRS and a light-absorbing tracer, which can be applied to evaluate circulatory responses to exercise along with the assessment of tissue O2 saturation. The venular O2 saturation can be estimated with NIRS by applying venous occlusion and measuring changes in oxygenated vs. total hemoglobin. These various measurements provide the opportunity to evaluate several important metabolic and circulatory patterns in very localized regions of tissue and may be fruitful in the study of occupational syndromes and a variety of diseases.
Article
The purposes of this study were to compare the acute cardiorespiratory responses and muscle oxygenation trends during incremental cycle exercise to exhaustion with those observed during 30 s and 45 s Wingate tests in healthy men and women, and to examine the relationships between selected variables among these tests. Seventeen healthy junior badminton players, nine men [mean age, height, body mass and maximal oxygen uptake (VO2max) were 15.8 (SD 0.8) years, 1.73 (SD 0.08) m, 65.6 (SD 6.3) kg and 50.6 (SD 6.9) ml x kg(-1) x min(-1) respectively] and eight women [mean age, height, body mass and VO2max were 16.6 (SD 1.0) years, 1.65 (SD 0.03) m, 62.7 (SD 4.5) kg and 42.0 (SD 5.0) ml x kg(-1) x min(-1) respectively] completed a stepwise incremental exercise test to voluntary exhaustion and two Wingate tests lasting 30 s and 45 s in three separate sessions in random order. Cardiorespiratory responses were monitored breath-by-breath using a metabolic cart interfaced with an electrocardiogram. Tissue absorbancy trends were continuously recorded from the right vastus lateralis muscle using dual wavelength near infrared spectroscopy. Oxygen uptake and heart rate were significantly higher during the incremental test when compared to the two Wingate tests in the men and women. However, the oxygen pulse (oxygen utilization per heart beat, i.e., the product of stroke volume and arterio-venous oxygen difference) was not significantly different among the three tests in both sexes. The minimal tissue absorbancy, an index of muscle deoxygenation, was also not significantly different among the three tests in both sexes. Significant relationships were observed for the oxygen uptake (r2=0.72) and oxygen pulse (r2=0.60) between the incremental and 45 s Wingate tests in the sample for both sexes combined. The minimal tissue absorbancy, however, was not significantly related between the two tests. It was concluded that the significantly higher oxygen uptake during the incremental test was due to the higher heart rate because: firstly, oxygen pulse was not significantly different among the three tests, and secondly, peripheral factors, as indicated by the changes in muscle oxygenation, were not significantly different among the three test conditions. Although the peak values of the oxygen pulse during the incremental and 45 s Wingate tests were significantly correlated, the common variance of the minimal tissue absorbancy measurements between these two tests was quite low, suggesting considerable variation in the peripheral contribution during these two tests.
Article
Previous research has demonstrated that blood flow and subsequent O2 desaturation (OD) in exercising muscle is related to the static component during exercise. In speed skating, increased OD is dissociated from whole body VO2 and heart rate (HR) when the skater increases the static component by 'sitting low'. This phenomenon was evaluated in cross-country skiers by manipulating speed and incline during treadmill roller skiing. Eight male cross-country skiers (22.4 +/- 3.2 yrs old) randomly performed constant incline- and constant speed-based protocols in which increased load was manipulated in five 4min stages by treadmill incline or speed change, respectively. A strong relationship (r = 0.83) was observed between VO2 and % OD while blood volume change (deltaBV) was minimal. Unexpectedly, no HR/ VO2 or HR/OD shifts were observed between protocols. The % OD response, in relation to blood lactate values, during submaximal exercise was very similar to that of VO2. The lack of an observed greater desaturation at higher inclines suggests that the expected static load may be attenuated by an increased contribution of poling. The strong relationship of % OD to whole body VO2 may be attributed to O2 dissociation in the capillary bed of the muscle to meet aerobic energy demand and is independent of blood flow dynamics during cross-country ski skating.
Article
Endurance training improves the oxygen delivery and muscle metabolism. Muscle oxygen saturation measured by near infrared spectroscopy (IR-SO(2)), which is primarily influenced by the local delivery/demand balance, should thus be modified by training. We examined this effect by determining the influence of change in blood lactate and muscle capillary density with training on IR-SO(2) in seven healthy young subjects. Two submaximal exercise tests at 50% (Ex1) and 80% pretraining VO(2max) (Ex2) were performed before and after a 4-wk endurance-training program. VO(2max) increased only slightly (+8%, NS) with training but the training effect was confirmed by the increased capillary density (+31%, P < 0.01) and citrate synthase activity (50%, P < 0.01), determined from muscle biopsy samples. Before training, blood lactate increased during the first 5 min of Ex1 and then remained constant (3.8 +/- 0.5 mmol x L(-1), P < 0.01), whereas it increased continuously during Ex2 (8.9 +/- 1.8 mmol x L(-1), P < 0.001). After training, lactate decreased significantly and remained constant during the two bouts of exercise (2.0 +/- 0.4 and 3.7 +/- 1.2 at the end of Ex1 and Ex2, respectively, both P < 0.001). During Ex1, IR-SO(2) dropped initially at the onset of exercise and recovered progressively without reaching the resting level. Training did not change this pattern of IR-SO(2). During Ex2, IR-SO(2) decreased progressively during the 15 min of exercise (P < 0.05); IR-SO2 kept constant after the initial drop after training. We found a significant relationship (r = 0.42, P = 0.03) between blood lactate and IR-SO(2) at the end of both bouts of exercise; this relationship was closer before training. By contrast, IR-SO(2) or IR-BV was not related to the capillary density. The training-induced adaptation in blood lactate influences IR-SO(2) during mild- to hard-intensity exercise. Thus, NIRS could be used as a noninvasive monitoring of training-induced adaptations.
Article
In this study we examined the oxygenation trend of the vastus medialis muscle during sustained high-intensity exercise. Ten cyclists performed an incremental cycle ergometer test to voluntary exhaustion [mean (SD) maximum oxygen uptake 4.29 (0.63) l x min(-1); relative to body mass 60.8 (2.4) ml x kg(-1)min(-1)] and a simulated 20-km time trial (20TT) on a wind-loaded roller system using their own bicycle (group time = 23-31 min) in two separate sessions. Cardiorespiratory responses were monitored using an automated metabolic cart and a wireless heart rate monitor. Tissue absorbency, which was used as an index of muscle oxygenation, was recorded simultaneously from the vastus medialis using near-infrared spectroscopy. Group mean values for oxygen uptake, ventilation, heart rate, respiratory exchange ratio, power output, and rating of perceived exhaustion were significantly (P < or = 0.05) higher during the incremental test compared to the 20TT [4.29 (0.63) l x min(-1) vs 4.01 (0.55) l x min(-1), 120.4 (26) l x min(-1) vs 97.6 (16.1) l x min(-1), 195 (8) beats x min(-1) vs 177 (9) beats min(-1), 1.15 (0.06) vs 0.93 (0.06), 330.1 (31) W vs 307.2 (24.5) W, and 19 (1.5) vs 16 (1.7), respectively]. Oxygen uptake and heart rate during the 20TT corresponded to 93.5% and 90.7%, respectively, of the maximal values observed during the incremental test. Comparison of the muscle oxygenation trends between the two tests indicated a significantly greater degree of deoxygenation during the 20TT [-699 (250) mV vs 439 (273) mV; P < or = 0.05] and a significant delay in the recovery oxygenation from the 20TT. The mismatching of whole-body oxygen uptake and localised tissue oxygenation between the two tests could be due to differences in muscle temperature, pH, localised blood flow and motor unit recruitment patterns between the two tests.