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Symposium Reports |
1 Department of Kinesiology and Department of Anatomy and Physiology, Kansas State University, Manhattan, KS 66506, USA
Abstract
Sustained performance of muscular exercise is contingent upon increasing muscle O2 delivery (
; the product of blood flow and arterial O2 content, i.e. 
) and utilization (
) rapidly at exercise onset and sustaining necessary conductive and diffusive O2 fluxes throughout exercise. A tight co-ordination of pulmonary, cardiovascular and muscle system responses is therefore required to prevent muscle microvascular O2 pressures (PmvO2) from falling to levels that impair blood–muscle O2 exchange and/or impact metabolic control and reduce exercise tolerance. Microvascular O2 pressures are determined by the balance between 
and 
, and emerging evidence indicates that this balance is regulated differently across muscle fibre types and also in aged muscle. Moreover, disease states such as diabetes (type I and II) and chronic heart failure (CHF) also impact PmvO2. This brief review primarily examines evidence obtained in animals that ageing: (1) redistributes exercising 
away from highly oxidative muscles and muscle fibres; (2) alters muscle capillary haemodynamics; and (3) reduces the O2 pressure head within the microcirculation (PmvO2) that serves to facilitate blood–muscle O2 transfer. In many respects, these alterations found in healthy ageing animals bear a striking resemblance to those present in some chronic diseases (e.g. diabetes, CHF) and may help explain the compromised exercise tolerance present in aged individuals. Putative mechanistic insights are explored within the context of current knowledge and future investigative approaches.
(Received 13 December 2006;
accepted after revision 14 December 2006; first published online 21 December 2006)
Corresponding author D. C. Poole: Department of Anatomy and Physiology, Kansas State University, Manhattan, KS 66506, USA. Email: poole{at}vet.ksu.edu
At present, the mechanistic bases of skeletal muscle fatigue are viewed as both complex and contentious. That different mediators of fatigue become deterministic within specific exercise intensity domains (i.e. moderate, heavy and severe) and for different types of exercise and muscle contraction profiles undoubtedly contributes to the difficulty in resolving ‘the cause of fatigue’ under a given circumstance. However, there is compelling evidence that exercise tolerance and thus the fatigue process(es) can be modulated by alterations in muscle O2 delivery (
; the product of blood flow and arterial O2 content, i.e. 
; Hogan et al. 1994; Hepple, 2002). Thus, conditions that reduce 
decrease exercise tolerance and those that elevate 
can increase exercise tolerance. This brief review will explore the ageing-related alterations in exercising muscle 
, capillary haemodynamics and microvascular oxygenation and, by inference, provide putative mechanistic insights into the reduced exercise tolerance characteristic of elderly individuals.
A popular and convenient window into human muscle energetics during exercise (e.g. cycling, knee-extension) has been provided by measurement of breath-to-breath pulmonary O2 uptake (
). Modelling (Barstow et al. 1990) and, subsequently, invasive measurements of muscle O2 uptake (
) in healthy humans (Poole et al. 1991; Grassi et al. 1996; Bangsbo et al. 2000) demonstrated that, beyond the immediate 10–20 s transient at exercise onset (phase I), the time course and magnitude of the primary (phase II) and slow component responses measured at the mouth closely reflect events occurring across the exercising muscles.
The conventional wisdom is that the kinetics of 
, by determining the size of the O2 deficit and reliance on finite energy sources [e.g. glycogen and phosphocreatine (PCr)], are mechanistically related to exercise tolerance, thereby emphasizing the practical relevance of understanding what factors control 
kinetics following the onset of exercise. For healthy young individuals performing moderate or even heavy exercise, the speed of increase of muscle 
either equals or exceeds that of 
(Grassi, 2001), suggesting that the rate of increase in 
is not limited by muscle bulk 
per se. Although heterogeneity of 
distribution is an important factor in this debate (see next section below), the contention presented above is consistent with the matching of PCr and 
kinetics (Rossiter et al. 1999) and with models of mitochondrial respiratory control (Meyer & Foley, 1996) and has survived rigorous testing that includes use of the nitric oxide (NO) synthase inhibitor L-NAME, which has been shown to cause profound mismatch between O2 delivery and uptake (Ferreira et al. 2006). Specifically, although L-NAME reduces cardiac output (Kindig et al. 2000) and muscle 
(Hirai et al. 1994), it simultaneously relieves the NO inhibition of mitochondrial function such that 
kinetics are speeded (Kindig et al. 2002a; Jones et al. 2003).
The dynamic matching of O2 delivery and uptake can be examined using phosphorescence quenching technology to measure muscle microvascular O2 pressures [PmvO2
(
)/
] in rat skeletal muscle. This technique uses a phosphorescent probe that is negatively charged and also binds to albumin, both properties that restrict it to the blood plasma. In the first investigation of its kind, Behnke et al. (2001) tested the hypothesis that, in the presence of an adequate or excess 
compared with 
as predicted from the work of Grassi et al. (1996) and others (Bangsbo et al. 2000), PmvO2 would not fall precipitously at the onset of contractions. Their data demonstrated a plateau (
70% of instances) or increase of spinotrapezius PmvO2 for up to 20 s of 1 Hz twitch contractions prior to a close-to-monoexponential fall to the steady state. There was no indication of PmvO2 plummeting to levels below the steady state, as has subsequently been demonstrated for this mixed-fibre type muscle in type I diabetes and chronic heart failure (CHF; Diederich et al. 2002; Behnke et al. 2002). Therefore, the PmvO2 data provided direct evidence that at the onset of contractions, muscle microvascular 
increased at either the same or a faster rate than 
(Behnke et al. 2001; Kindig et al. 2002b), suggesting adequate or excess 
in the transitional phase.
Despite the obvious utility and practical relevance of pulmonary 
measurements, investigation of the mechanistic determinants of blood–muscle O2 exchange in health and derangement of these processes in ageing, diabetes or CHF might be best accomplished within skeletal muscle, where feasible. In humans, technical limitations have precluded high-fidelity determination of: (1) blood flow distribution within and among exercising muscles; (2) microcirculatory dynamics within those muscles; and (3) muscle microvascular O2 pressures (PmvO2). However, such valuable measurements have recently been made in rat muscles, permitting determination of perfusive and diffusive O2 transport, and recent data indicate that derangements in blood–muscle O2 transfer are present in aged and also diseased muscle. Such derangements may play a deterministic role in the slowed 
kinetics and reduced maximal 
(decreased 
and fractional O2 extraction; McGuire et al. 2001) and also the increased fatigability present in aged individuals and/or those suffering from diabetes or CHF.
In recent years, the United States National Institutes of Health have promoted use of the Fisher 344 Brown Norway hybrid rat (F344 x BN) as a model for investigating the ageing process. One major advantage of the F344 x BN rat is that it is free from many of the age-related pathologies which plague their highly inbred counterparts (Lipman et al. 1996). In the following sections, we describe how the F344 x BN rat model has been employed extensively to resolve the mechanisms by which ageing impacts muscle O2 delivery and exchange. In that model, 6–12 months represents young adult, 24–30 months old, and 
35 months very old or senescent (Poole et al. 2006).
Distribution of blood flow (
) within and among muscles
Appropriate distribution of 
(and therefore O2 delivery) within and among exercising muscles and quiescent tissues during exercise depends on the effective integration of cardiovascular function at several levels. Exercise simultaneously evokes profound vasodilatation within contracting muscles and vasoconstriction in vascular beds of inactive organs (e.g. kidney, spleen and non-recruited muscles). However, blood flow (
) to active muscles is not homogeneous, being greater in highly oxidative muscles, and this apparently results, in part, from differences in endothelium-dependent vasodilatation (Laughlin et al. 1997; Muller-Delp, 2006). Dysregulation of these control processes provides an excess 
flow and therefore O2 delivery to less metabolically active tissues or muscles with diminished ability for O2 exchange (which reduces muscle and whole-body fractional O2 extraction), whilst muscles with a high ATP turnover may be forced to resort to substrate-level phosphorylation to meet their energy needs. In this context, exercise training improves endothelial function and fine-tunes 
distribution during exercise (reviewed by Laughlin et al. 1997). Musch et al. (2004) tested the hypothesis that ageing would have the opposite effect. Figure 1 demonstrates that during submaximal running, in the absence of any alteration in total hindlimb blood flow, aged animals redistribute 
preferentially towards low-oxidative muscles and muscle portions, in marked contrast to the response seen in young animals (Laughlin et al. 1997; Musch et al. 2004). These insightful macroscopic observations were complemented by assessment of muscle microcirculatory function (see next section) in order to explain the derangements found in convective and diffusive O2 transport in ageing (Lawrenson et al. 2003) and chronic diseases (e.g. chronic obstructive pulmonary disease; Wagner, 1996).
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In skeletal muscles, 80–90% of capillaries support continuous red blood cell (RBC) flux at rest, and at the onset of exercise (Fig. 2) RBC velocity and flux increase (elevated perfusive O2 conductance) substantially within the first contraction cycle and progress to reach a steady state within 60–90 s (Kindig et al. 2002b). There is also a significant increase in capillary haematocrit that serves to elevate the number of RBCs adjacent to the muscle fibres (increased diffusive O2 conductance; Kindig et al. 2002b). In resting muscle from aged rats, the lineal density of capillaries supporting continuous RBC flux (capillaries (mm muscle)–1) is decreased significantly from that seen in young adults, whilst capillary RBC flux and velocity are both elevated such that lineal RBC flux and thus O2 delivery are unaltered (Russell et al. 2003). In contrast, in response to electrical stimulation at a mild-to-moderate intensity, neither perfusive nor diffusive O2 conductance was increased in aged muscle compared to the extent seen in young rat muscle.
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and redistribution to low-oxidative muscles or muscle portions in elderly individuals (see Fig. 1) severely impairs the ability for O2 exchange during exercise, which probably plays a major role in the well-described decrease in maximal 
(Overend et al. 1992; Neder et al. 1999; McGuire et al. 2001) and slowed 
kinetics in elderly humans (Scheuermann et al. 2002).
Microvascular PO2 (PmvO2) in contracting muscle: 
-to-
matching
Microvascular PO2 provides the pressure head required to drive O2 diffusion from the microcirculation into the contracting muscle fibres. According to Fick's law of diffusion: 
=
DO2(PmvO2
–
PimO2), where DO2 is the diffusing capacity for O2, PimO2 is the intramyocyte PO2, and PmvO2 approximates the mean capillary O2 pressure. Experimental evidence from very different techniques, namely the rapid freezing of canine gracilis muscle (Honig et al. 1997) and proton magnetic resonance spectroscopy in human quadriceps (Richardson et al. 1995), indicates that during exercise of even moderate intensity, intramyocyte PO2 falls to approximately 3 mmHg at the steady state of contractions. If correct, this suggests that the overwhelming majority of the change in blood–muscle PO2 gradient, for example from moderate to heavy or severe intensity exercise or under conditions of impaired O2 delivery, must come from alterations of PmvO2 rather than PimO2. This logic does not mean that even disappearingly small changes in PimO2 are not important for metabolic regulation; they clearly are (Haseler et al. 2004); but it does indicate that under these circumstances Fick's law can be reduced to 
=
DO2(PmvO2) with little error on the calculation of apparent DO2 (Wagner, 1996). Thus, measurement of PmvO2 becomes a powerful variable, modulating oxidative phosphorylation, and a tool for resolving the mechanistic bases for impaired blood–myocyte O2 exchange under physiological or pathological conditions.
Following demonstration of the ageing-induced alteration of 
distribution among muscles (Musch et al. 2004) and impaired microcirculatory function in the resting spinotrapezius (Russell et al. 2003), Behnke et al. (2005) hypothesized that at the onset of contractions, PmvO2 would decrease below that seen in healthy young rats. Their data validated this hypothesis and demonstrated a pronounced fall in PmvO2 below that seen in the young rats (Fig. 4), reflecting a sluggish increase in 
relative to the dynamics of 
. Although PmvO2 in old rats returned to a steady-state contracting value that was not significantly different from that found in their young counterparts, from rest to 90 s, PmvO2 was 30–40% lower in the old rats. It is important to recognize that this lowered PmvO2 occurs at the time when 
is increasing most rapidly and is therefore likely to constrain the kinetics of 
. Aged individuals typically demonstrate slowed 
kinetics at exercise onset (Scheuermann et al. 2002), and it is quite possible that this results from a lowered O2 driving pressure (PmvO2) and DO2 (inferred from steady-state measurements) in the transitional phase of exercise. These slowed 
kinetics elevate the O2 deficit at exercise onset and exacerbate disturbances in the intramyocyte physicochemical milieu which probably contributes to the reduced exercise tolerance in this population (Overend et al. 1992; Neder et al. 2000).
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) and PmvO2
Following the onset of exercise, muscle 
is regulated by a complex interplay among mechanical (muscle pump), neural (sympatholysis), propagated (conducted vasodilatation) and vasoactive processes (i.e. metabolites, NO and prostanoids; all discussed in detail by Behnke et al. 2005; Ferreira et al. 2006). The net result is that in young individuals, muscle 
increases within the first contraction cycle consequent to muscle pumping activity and possibly to rapid-onset vasodilatation of uncertain origin (for details see Kindig et al. 2002b). The presence of an initial plateau or slowly changing region of PmvO2 (Fig. 4) in the old muscle suggests that if these initial 
-increasing processes are impaired then the degree of such impairment is matched relative to that of 
. The major effect appears subsequently, when PmvO2 in aged muscles falls substantially below that in young muscles. It is in this region that NO (and possibly prostacyclin) are thought to contribute to the exercise hyperaemia that maintains the elevated PmvO2 seen in healthy young muscles (Ferreira et al. 2006). It is pertinent that NO and prostacyclin production are both downregulated in aged individuals (Muller-Delp, 2006), and reduction of their contribution to vasodilatation at a time when 
is increasing at its fastest rate will decrease PmvO2 as observed (Behnke et al. 2005).
Unanswered questions
In spite of substantial progress in our understanding of how ageing impacts the convective and diffusive delivery of O2 to skeletal muscle, important gaps in our knowledge remain. For example, the kinetics of DO2 during exercise and the mechanistic bases for its manyfold increase have not been determined in either young or old individuals because of technical difficulties in measuring the dynamics of PimO2 following the onset of exercise. Thus, this variable cannot be dropped from the Fick's law of diffusion equation in the rest-to-exercise transition and the equation (see above) is left with two unknowns (DO2 and PimO2). Kinetics of DO2 may be determined in the near future, which will be an important step to further our understanding of the mechanistic bases for slowed 
kinetics in old individuals. Another aspect relevant in the context of ageing is the function of the endothelial glycocalyx, a dynamic structure that modulates capillary haematocrit and microvascular network resistance to flow (Desjardins & Duling, 1990). It is not clear whether ageing is associated with dysfunction of the glycocalyx, and resolution of this matter may help explain some of the microcirculatory alterations described herein.
Conclusions
Ageing-induced alterations in pulmonary gas exchange (slowed 
kinetics and decreased maximal 
) reflect, in part, profound derangements in the skeletal muscle 
distribution and capillary haemodynamics during contractions. These are consistent with downregulation of vasodilatory mediators such as NO and prostacyclins. One consequence of this phenomenon is that at the onset of muscle contractions, the temporal matching of O2 delivery to uptake is impaired such that the microcirculatory O2 driving pressure (PmvO2), which powers blood–muscle O2 movement, is reduced. It is quite possible that in aged individuals, restoration of the ability to redistribute 
effectively to and within skeletal muscle and to do so rapidly at exercise onset will improve microvascular oxygenation and 
kinetics and, hence, exercise tolerance.
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Acknowledgements
The studies developed in the author's laboratory were supported by grants from the American Heart Association, Heartland Affiliate (0455582Z) and the National Institutes of Health, HL-50306 and AG-19228. We thank Drs Timothy I. Musch and Brad. J. Behnke for insightful discussions and their major input in the studies reviewed herein.
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) in 6 of the more highly oxidative muscles (A) but increased (
) in 8 of the less oxidative muscles (B) when old rats (hatched bars) were compared with young rats (filled bars). Abbreviations: S, soleus; P, plantaris; GR, red portion of the gastrocnemius; TAR, red portion of the tibialis anterior; VI, vastus intermedius; VLR, red portion of the vastus lateralis; GW, white portion of the gastrocnemius; TP, tibialis posterior; VLW, white portion of the vastus lateralis; BFA, anterior portion of biceps femoris; AMB, adductor magnus and brevis; GR, gracilis; SMW, white portion of the semimembranosus; and SMR, red portion of the semimembranosus. Values are means +
S.E.M.
*P < 0.05 versus young rats. Reprinted from 
; 
) and uptake (
) within the microcirculation. Therefore, if 
kinetics were proportionally slower than those of 
, an initial rapid drop in PmvO2 of possibly greater magnitude would be expected, followed by a slow increase to the steady state, as seen in this figure. From 