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We tested the hypothesis that the amplitude of the additional slow component of O2 uptake (VO2) during heavy exercise is correlated with the percentage of type II (fast-twitch) fibers in the contracting muscles. Ten subjects performed transitions to a work rate calculated to require a VO2 equal to 50% between the estimated lactate (Lac) threshold and maximal VO2 (50% delta). Nine subjects consented to a muscle biopsy of the vastus lateralis. To enhance the influence of differences in fiber type among subjects, transitions were made while subjects were pedaling at 45, 60, 75, and 90 rpm in different trials. Baseline VO2 was designed to be similar at the different pedal rates by adjusting baseline work rate while the absolute increase in work rate above the baseline was the same. The VO2 response after the onset of exercise was described by a three-exponential model. The relative magnitude of the slow component at the end of 8-min exercise was significantly negatively correlated with % type I fibers at every pedal rate (r = 0.64 to 0.83, P < 0.05-0.01). Furthermore, the gain of the fast component for VO2 (as ml.min-1.W-1) was positively correlated with the % type I fibers across pedal rates (r = 0.69-0.83). Increase in pedal rate was associated with decreased relative stress of the exercise but did not affect the relationships between % fiber type and VO2 parameters. The relative contribution of the slow component was also significantly negatively correlated with maximal VO2 (r = -0.65), whereas the gain for the fast component was positively associated (r = 0.68-0.71 across rpm). The amplitude of the slow component was significantly correlated with net end-exercise Lac at all four pedal rates (r = 0.64-0.84), but Lac was not correlated with % type I (P > 0.05). We conclude that fiber type distribution significantly affects both the fast and slow components of VO2 during heavy exercise and that fiber type and fitness may have both codependent and independent influences on the metabolic and gas-exchange responses to heavy exercise.

Near infrared spectroscopy (NIRS) is a powerful noninvasive tool with which to study the matching of oxygen delivery to oxygen utilization and the number of new publications utilizing this technique has increased exponentially in the last 20 yr. By measuring the state of oxygenation of the primary heme compounds in skeletal muscle (hemoglobin and myoglobin), greater understanding of the underlying control mechanisms that couple perfusive and diffusive oxygen delivery to oxidative metabolism can be gained from the laboratory to the athletic field to the intensive care unit or emergency room. However, the field of NIRS has been complicated by the diversity of instrumentation, the inherent limitations of some of these technologies, the associated diversity of terminology, and a general lack of standardization of protocols. This Cores of Reproducibility in Physiology (CORP) will describe in basic but important detail the most common methodologies of NIRS, their strengths and limitations, and discuss some of the potential confounding factors that can affect the quality and reproducibility of NIRS data. Recommendations are provided to reduce the variability and errors in data collection, analysis, and interpretation. The goal of this CORP is to provide readers with a greater understanding of the methodology, limitations, and best practices so as to improve the reproducibility of NIRS research in skeletal muscle.

It is unclear whether hypoxia alters the kinetics of O2 uptake (VO2) during heavy exercise [above the lactic acidosis threshold (LAT)] and how these alterations might be linked to the rise in blood lactate. Eight healthy volunteers performed transitions from unloaded cycling to the same absolute heavy work rate for 8 min while breathing one of three inspired O2 concentrations: 21% (room air), 15% (mild hypoxia), and 12% (moderate hypoxia). Breathing 12% O2 slowed the time constant but did not affect the amplitude of the primary rise in VO2 (period of first 2-3 min of exercise) and had no significant effect on either the time constant or the amplitude of the slow VO2 component (beginning 2-3 min into exercise). Baseline heart rate was elevated in proportion to the severity of the hypoxia, but the amplitude and kinetics of increase during exercise and in recovery were unaffected by level of inspired O2. We conclude that the predominant effect of hypoxia during heavy exercise is on the early energetics as a slowed time constant for VO2 and an additional anaerobic contribution. However, the sum total of the processes representing the slow component of VO2 is unaffected.

The effect of cardiovascular adjustments on the coupling of cellular to pulmonary gas exchange during unsteady states of exercise remains controversial. Computer simulations were performed to assess these influences on O2 delivery and pulmonary O2 uptake (pVO2). Algorithms were developed representing muscle and "rest-of-body" compartments, connected in parallel by arterial and venous circulations to a pump-and-lungs compartment. Exercise-induced increases in VO2 and cardiac output went to the muscle compartment. Model parameters [e.g., time constants for blood flow and muscle O2 uptake (mVO2)] could be varied independently. Simulation results demonstrated that 1) the rise in pVO2 during exercise contains three phases; 2) the contribution of changes in venous O2 stores to pVO2 kinetics and the O2 deficit occur almost entirely in phase 1; 3) under a wide variety of manipulations, the kinetics of pVO2 in phase 2 were within a couple of seconds of that assigned to mVO2 (i.e., there is not an obligatory slowing of VO2 kinetics at the lungs relative to those at the muscles; 4) by use of available estimates of blood flow adjustment, O2 delivery would not limit mVO2 after exercise onset; and 5) blood flow could limit O2 delivery in recovery, if blood flow returned to base-line levels at rates similar to those during the on-transient phase.

. Muscle capillary blood flow kinetics estimated from pulmonary O2 uptake and near-infrared spectroscopy. J Appl Physiol 98: 1820 -1828, 2005. First published January 7, 2005 doi:10.1152/japplphysiol.00907.2004.-The near-infrared spectroscopy (NIRS) signal (deoxyhemoglobin concentration; [HHb]) reflects the dynamic balance between muscle capillary blood flow (Q cap) and muscle O2 uptake (V O2m) in the microcirculation. The purposes of the present study were to estimate the time course of Q cap from the kinetics of the primary component of pulmonary O2 uptake (V O2p) and [HHb] . However, there was no significant difference between MRT of Q cap and P-V O2 for both intensities (P ϭ 0.99), and these parameters were significantly correlated (M and H; r ϭ 0.99; P Ͻ 0.001). In conclusion, we have proposed a new method to noninvasively approximate Q cap kinetics in humans during exercise. The resulting overall Q cap kinetics appeared to be tightly coupled to the temporal profile of V O2m. exercise; skeletal muscle; oxygenation INSIGHTS ON THE CONTROL OF exercising muscle blood flow (Q m ) can be gained from the investigation of its response in the transitional phase (i.e., kinetics) (21, 27), but because of methodological constraints the kinetics of Q m in humans have been studied primarily in larger vessels (1,16,22,31,37,42,44).The difficulty in obtaining measurements with a time resolution that allows reliable kinetic analysis during large muscle mass exercise (e.g., cycling or running) has led to a predominant use of knee extensor or forearm exercise with measurements of blood flow made by Doppler ultrasound (11,22,31,37,42,44). These investigations have shown that the Q m response is biphasic with an initial fast phase determined by the combined effects of muscle contraction (muscle pump) (41) and possibly rapid vasodilation (48) followed by a second slower phase that appears to match O 2 delivery and utilization (43).Several studies have addressed the relationship between Q m and muscle O 2 uptake (V O 2m ) kinetic response after the onset of exercise (5,12,14,16,22,31 (27). To date, for technical and ethical reasons, assessing the kinetics of muscle capillary blood flow (Q cap ) in humans has been problematic. Resolution of this discrepancy in Q m kinetics relative to those of V O 2m is crucial to advancing our understanding of the mechanisms that govern the control of both Q m and V O 2m in health and disease.Near-infrared spectroscopy (NIRS) provides a noninvasive measure of muscle oxygenation (or O 2 extraction) in the microcirculation. Although distinction between hemoglobin (Hb) and myoglobin (Mb) with regard to absorption of the near-infrared light cannot be made, the deoxygenated Hb/Mb (deoxy-Hb/Mb) signal obtained by NIRS has been used as an index of local O 2 extraction reflecting the V O 2m -to-Q m ratio in the capillaries (9, 15). The time course of deoxy-Hb/Mb after the onset of exercise resembles qualitatively and quantitatively the arteriovenous O 2 difference [(a-v)O 2 ] observed in separate...

For exercise intensities that engender a sustained lactic acidosis (i.e. above the lactate threshold, LT), an additional increase in pulmonary O 2 uptake (V O 2 ) of delayed onset leads to a V O 2 which is higher than predicted from the V O 2 -work rate relationship for exercise performed in the sub-LT domain (Whipp & Mahler, 1980;Roston et al. 1987;Henson et al. 1989;Paterson & Whipp, 1991;Barstow et al. 1993). The physiological mechanism(s) underlying the V O 2 slow component (V O 2 SC) have yet to be clearly established. However, identifying the process(es) that increase the O 2 cost of performing heavy work would contribute significantly to our understanding of muscle energetics and the limitations to exercise tolerance in the heavy intensity exercise domain.Since Poole et al. (1994) demonstrated that the excess increase in pulmonary V O 2 observed during the slow component could, for the most part, be accounted for by an increase in leg V O 2 , considerable interest has been given to a mechanistic link between muscle fibre type and the V O 2 SC. Studies using isolated muscle preparations have shown that fast-twitch (i.e. type II) fibres are less efficient than slow-twitch (i.e. type I) fibres (Crow & Kushmerick, 1982;Kushmerick et al. 1992) and, therefore, would utilize more O 2 in order to regenerate the same amount of high-energy phosphates. Indeed, Barstow et al. (1996) 1. We hypothesized that either the recruitment of additional muscle motor units and/or the progressive recruitment of less efficient fast-twitch muscle fibres was the predominant contributor to the additional oxygen uptake (V O 2 ) observed during heavy exercise. Using surface electromyographic (EMG) techniques, we compared the V O 2 response with the integrated EMG (iEMG) and mean power frequency (MPF) response of the vastus lateralis with the V O 2 response during repeated bouts of moderate (below the lactate threshold, LT) intensity cycle ergometer exercise.2. Seven male subjects (age 29 ± 7 years, mean ± S.D.) performed three transitions to a work rate (WR) corresponding to 90 % LT and two transitions to a work rate that would elicit a V O 2 corresponding to 50 % of the difference between peak V O 2 and the LT (i.e. ∆50 %, >LT 1 and >LT 2 ). 4. Integrated EMG and MPF remained relatively constant and at the same level throughout both >LT 1 and >LT 2 exercise and therefore were not associated with the V O 2 slow component.5. These data are consistent with the view that the increased O 2 cost (i.e. V O 2 slow component) associated with performing heavy exercise is coupled with a progressive increase in ATP requirements of the already recruited motor units rather than to changes in the recruitment pattern of slow versus fast-twitch motor units. Further, the lack of speeding of the kinetics of the primary V O 2 component with prior heavy exercise, thought to represent the initial muscle V O 2 response, are inconsistent with O 2 delivery being the limiting factor in V O 2 kinetics during heavy ...

Patients with stable chronic heart failure can achieve significant improvement in functional capacity from a low intensity exercise training regimen. The mechanism responsible for this favorable effect involves an increase in mitochondrial density, which reflects an improvement in oxidative capacity of trained skeletal muscles.