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00005768-200610000-0001500005768_2006_38_1797_secher_competition_10report< 99_0_11_5 >Medicine & Science in Sports & Exercise©2006The American College of Sports MedicineVolume 38(10)October 2006pp 1797-1803Are the Arms and Legs in Competition for Cardiac Output?[SYMPOSIUM: Skeletal Muscle Blood Flow and Metabolism: Are There Inherent Limb Differences?]SECHER, NIELS H.1; VOLIANITIS, STEFANOS1,21The Copenhagen Muscle Research Center, Department of Anesthesia, Rigshospitalet, University of Copenhagen, DENMARK; and 2School of Sport and Education, Brunel University, UNITED KINGDOMAddress for correspondence: Stefanos Volianitis, Ph.D., School of Sport and Education, Brunel University, Uxbridge, Middlesex UB8 3PH United Kingdom; E-mail: Stefanos.Volianitis@brunel.ac.uk.Submitted for publication December 2005.Accepted for publication February 2006.AbstractABSTRACT: Oxygen transport to working skeletal muscles is challenged during whole-body exercise. In general, arm-cranking exercise elicits a maximal oxygen uptake (V˙O2max) corresponding to approximately 70% of the value reached during leg exercise. However, in arm-trained subjects such as rowers, cross-country skiers, and swimmers, the arm V˙O2max approaches or surpasses the leg value. Despite this similarity between arm and leg V˙O2max, when arm exercise is added to leg exercise, V˙O2max is not markedly elevated, which suggests a central or cardiac limitation. In fact, when intense arm exercise is added to leg exercise, leg blood flow at a given work rate is approximately 10% less than during leg exercise alone. Similarly, when intense leg exercise is added to arm exercise, arm blood flow and muscle oxygenation are reduced by approximately 10%. Such reductions in regional blood flow are mainly attributed to peripheral vasoconstriction induced by the arterial baroreflex to support the prevailing blood pressure. This putative mechanism is also demonstrated when the ability to increase cardiac output is compromised; during exercise, the prevailing blood pressure is established primarily by an increase in cardiac output, but if the contribution of the cardiac output is not sufficient to maintain the preset blood pressure, the arterial baroreflex increases peripheral resistance by augmenting sympathetic activity and restricting blood flow to working skeletal muscles.Oxygen transport to active muscles is challenged during whole-body exercise. The vasculature supplying skeletal muscles is described as "a sleeping giant" that can challenge blood pressure during exercise when extensive vasodilatation occurs, as illustrated in tetraplegic patients exposed to electrically evoked exercise (9). However, when electrically evoked exercise is conducted in paraplegic patients (9) or in subjects under epidural anesthesia (44), mean arterial pressure (MAP) is maintained at resting level. This observation is explained by the fact that, in contrast to tetraplegic patients, neural control of the splanchnic circulation in paraplegic patients and subjects under lumbar epidural anesthesia is not affected by the lesion or the neural blockade, respectively. Therefore, it appears that the vasculature of the splanchnic organs is the key to maintaining blood pressure control during exercise where the splanchnic organs act as "blood donors" of the circulation (21). During exercise with intact inervation of the internal organs, splanchnic vasoconstriction (32) "collapses" the hepatic sinousoids (28), and the recruited blood compensates for the approximately 10% increase in muscle blood volume (31). In most cases, during exercise in subjects with intact afferents from the working muscles, blood pressure rises. This is because the blood returning to the heart via the muscle pump enhances cardiac output (CO) more than the corresponding vasodilatation in the working skeletal muscles that remain under sympathetic nervous system control (2). Hence, even though vasodilatation in skeletal muscle challenges arterial pressure during exercise, the system seems to adequately handle the challenge.Historically, cardiovascular control during whole-body exercise has been associated with the determination of limitations to maximal oxygen uptake (V˙O2max) (23). Early studies evaluated systemic oxygen uptake (V˙O2) during arm, leg, and various modalities of combined arm plus leg exercise, and recent studies have evaluated regional blood flow for the arms and the legs, both while working separately and during combined exercise.These experimental models, in which the active muscle mass is increased by additional recruitment of exercising limbs, can also be compared using any type of exercise involving both legs; in theory, the two legs could compete for flow because each leg possesses a separate vasculature. Furthermore, this consideration is relevant to exercise physiology in general because most activities involve more than a single limb.To address cardiovascular control during exercise, the simplification of applying Ohm's law to the circulation (MAP = flow × peripheral vascular resistance) is useful. Considering the circulation from this three-element model, blood pressure and flow can not be regulated equally rigorously, although they may mutually influence each other. Vascular resistance or conductance is under the control of sympathetic nerve activity, which regulates blood pressure at the expense of flow. Thus, a prevailing tight coupling between CO (or limb blood flow) and the work rate does not mean that the circulation is geared to provide flow at the expense of pressure. An exercise-induced increase in MAP is established by an increase in CO. However, if there is a restriction on the level to which CO can be elevated, the prevailing MAP is achieved by reducing vascular conductance, even in working skeletal muscles. Similar observations are available for the control of cerebral blood flow during exercise (17) besides the well-established differentiated vasoconstriction in the splanchnic organs (32). Therefore, it is suggested that MAP is the primary regulated circulatory variable during exercise and that regional flow is the result of a balance between local vasodilatation and general sympathetic activity elevated from activation of all engaged muscles.V˙O2maxWhen people with untrained arms perform arm-cranking exercise, their V˙O2max corresponds to approximately 70% of the value reached during leg exercise (40) (Fig 1). However, with arm training, the ratio between arm and leg V˙O2max increases so that in rowers it is approximately 0.9, and in swimmers the arm-cranking V˙O2max may be larger than the leg value (40). Despite the similarity between arm-cranking and leg-exercise V˙O2max, during combined arm and leg exercise, V˙O2maxis not much different from the value obtained during leg exercise. In the non-arm-trained person, there may be no significant increase, whereas in an arm-trained person, the increase is approximately 10% (40). This similarity between V˙O2maxduring combined arm and leg exercise and leg exercise alone suggests a central or cardiac limitation to V˙O2max because the oxygen consumption of vascular beds that are common to all exercise activities (i.e., brain, heart, splanchnic organs, skin, and respiratory muscles) is only approximately 0.7 L·min−1, or 25% during cycling (31,39), increasing to approximately 0.9 L·min−1 during whole-body exercise (4), of which approximately 15% may serve the ventilatory muscles. However, the implication of a comparison of V˙O2max during different types of exercise for flow distribution remains uncertain without a determination of the regional values. It is also uncertain what is meant by a central limitation to V˙O2max, with part of the limitation to oxygen-transport capacity resting within the pulmonary system.FIGURE 1-Maximal oxygen uptake (V˙O2max) during arm and leg (combined) exercise related to the value reached during leg exercise. (Reprinted from Secher, N. H., N. Ruberg-Larsen, R. A. Binkhorst, and F. Bonde-Petersen. Maximal oxygen uptake during arm cranking and combined arm plus leg exercise. J. Appl. Physiol. 36:515-518, 1974. Used with permission).A PULMONARY LIMITATION TO V˙O2maxDuring exercise of increasing intensity, there is a curvilinear elevation in ventilation that can approach 270 L·min−1 in large well-trained rowers during (ergometer) rowing. The large ventilation during maximal exercise results in an elevated alveolar oxygen tension. This is needed because there is a pulmonary limitation to oxygen transport during whole-body exercise, especially in trained individuals, as the arterial oxygen tension (PaO2) decreases (26). In combination with the decrease in the arterial pH (lowest reported value 6.7 (25)) brought about by lactate production, particularly during maximal whole-body exercise, the lower PaO2 affects arterial oxygen saturation (SaO2), reducing it to about 90% (a Bohr effect (15)). Together with the associated hyperventilation, a lowering of the arterial carbon dioxide tension and, in turn, cerebral blood flow, results in a decrease in SaO2 large enough to affect oxygenation of the brain (26). Also, in accordance with the Bohr effect on the oxyhemoglobin dissociation curve, SaO2 is restored both when PaO2 is increased by breathing oxygen enriched air (~30% O2) (26) and, equally, when the exercise-induced drop in the arterial pH is prevented by bicarbonate administration (27). With an enhanced SaO2, V˙O2max also increases, suggesting that during whole-body exercise, there is an approximately 5-10% pulmonary limitation to V˙O2max. Because lung function can only be improved marginally with training, it follows that athletes who depend on their aerobic capacity but develop a marked decrease in their arterial pH during whole-body exercise, need to have large lung capacities. For rowers, performance is repetitively found to correlate with lung vital capacity; successful rowers present values close to 7 L, with a largest reported vital capacity of 9.1 L (38).LEG BLOOD FLOW AND COConditions in which CO is limited either by disease, aging, or experimental manipulation provide useful models for evaluating the role of CO in blood pressure control during exercise. With aging, the slope of the relationship between leg blood flow (LBF) and work intensity may become less steep (50). In patients with cardiac insufficiency, there is only a small increase in LBF with increasing workload (37). However, when CO in these patients is enhanced during exercise by approximately 1 L, by administration of digitalis, combined LBF also increases by approximately 0.8 L (37). Similarly, in healthy subjects, when the ability to increase CO during exercise is attenuated by administration of a β1-adrenergic blocker (metroprolol), LBF is also attenuated. This effect is attributed to sympathetic activation, as indicated by the increase in leg norepinephrine "spillover", despite the lower LBF (31). Accordingly, there is little difference in the MAP established during exercise with and without adrenergic beta blockade, whereas in cardiac patients treated with digitalis, the enhanced LBF is associated with an approximately 5-mm Hg (25%) lowering of the exercise-induced elevation of MAP (37). As suggested by Alam and Smirk, the increase in MAP may be considered the response mechanism aimed to overcome the desaturation (ischemia) of working skeletal muscles (26,46).BLOOD PRESSURE DURING EXERCISEThe understanding of blood pressure regulation during exercise has been elusive. On the one hand, blood pressure is enhanced not only by the influence of the insular area (29) of the central nervous system ("central command") but also by the "exercise pressor reflex" (22) from the contraction of skeletal muscles. On the other hand, because heart rate and blood pressure rise simultaneously during exercise, it has been difficult to justify the function of the arterial baroreceptors, which elicit a reverse relationship between heart rate and blood pressure. An explanation for the concomitant increase in heart rate and blood pressure during exercise is that the arterial baroreflex, influenced both from the muscle pressor reflex (12) and central command (11), is reset to control the elevated MAP, allowing heart rate to increase.During exercise, as at rest, the predominant mechanism by which the arterial baroreflex influences the circulation is by modulation of vascular conductance including working skeletal muscles (8) rather than stroke volume and, thereby, CO (30). Although during exercise the muscle vasculature is dilatated (31) in response to increasing levels of metabolites and a rising muscle temperature, this is not unconditional because the arterial baroreceptors control the actual blood pressure on a beat-to-beat basis. However, with vasodilatation in a large part of the circulation during exercise, the arterial baroreceptors may not be fully successful in establishing the pressure that they aim for. Despite the elevated MAP during exercise, the arterial baroreceptors may detect hypotension and therefore limit vascular conductance; the established carotid sinus pressure is, quite often, slightly lower than what corresponds to the maximum gain of the reflex.EXERCISE WITH TWO MUSCLE GROUPSKagaya et al. (18) have thoroughly evaluated the effect of exercise with different muscle groups on regional circulation and demonstrated a decrease in calf blood flow during plantar flexion when combined with intense handgrip exercise. In a study by Saito et al. (35) in which muscle sympathetic activity was measured, low intensities of forearm exercise had no influence on calf blood flow. On the other hand, when intense forearm exercise activated the sympathetic nervous system, calf blood flow was restricted, confirming the work carried out by Standell and Shepherd (43). Standell and Shepherd measured forearm blood flow while sympathoexcitation was provoked by application of lower-body negative pressure, and they found that during repeated handgrip exercise, forearm blood flow was restricted during low- but not high-intensity exercise. Equally, Sinoway and Prophet (41) found the peak postischemic forearm conductance to be attenuated during leg exercise, and Harms et al. (16) found that LBF was reduced during exercise when the work of breathing was intensified by an external obstruction. In a comparison of LBF during one- and two-legged exercise, Klausen et al. (20) demonstrated similar values during submaximal and maximal exercise. However, after one-legged training, there was a higher LBF during one- than during two-legged exercise. Evaluation of LBF during one-legged kicking, which allows estimation of the muscle mass involved in the exercise (1), provided a value of 270 mL·min−1·100 g−1, or, likely, three times the value typically seen during (ergometer) cycling (24). Furthermore, as stroke volume and CO decreased at exhaustion, systemic and leg vascular conductance were also reduced (13,24). These data are in support of O2 delivery to skeletal muscles being influenced by a variable central circulation.COMBINED ARM AND LEG EXERCISEThe evaluation of LBF during leg and combined arm and leg exercise provided similar results to the comparison of calf blood flow at different intensities of forearm exercise (18,35). During light arm exercise, there was no effect on LBF; when the load on the arms was increased, LBF was reduced by approximately 10% (Fig. 3), as calculated in a meta-analysis including 32 subjects (33,34,36,39) and confirmed during roller skiing on a treadmill (4). Similarly, when leg exercise is performed at the same time as arm exercise, arm blood flow (ABF) is reduced both in arm-trained and non-arm-trained subjects (46-48) (Fig. 4). The reduction in ABF has been attributed to two mechanisms. First, similar to the effect of arm exercise on LBF, ABF is reduced because of a lower-arm vascular conductance that affects not only flow but also arm muscle and venous oxygenation (39,46-48). Secondly, arm exercise is associated with a large MAP response that is attenuated by approximately 5 mm Hg when leg exercise is added to arm-cranking exercise, as demonstrated by a less marked resetting of the arterial baroreflex (Fig 2). Hence, about half of the reduction in ABF when leg exercise is added to arm-cranking exercise can be attributed to the reduction in the perfusion pressure to the arms.FIGURE 2-The carotid baroreflex during arm (A), leg (L), and combined arm and leg exercise (A+L). At rest, the actual pressure (arrow) corresponds to the maximum gain of the reflex (o), whereas during exercise, it may be positioned at a slightly lower estimated carotid sinus pressure (ECSP), suggesting that the baroreflex detects hypotension although blood pressure is elevated. HR, heart rate; MAP, mean arterial pressure. (Reprinted from Volianitis, S., C. C. Yoshiga, T. Vogelsang, and N. H. Secher. Arterial blood pressure and carotid baroreflex function during arm and combined arm and leg exercise in humans. Acta Physiol. Scand. 181:289-295, 2004. Used with permission) (49).FIGURE 3-Effect of adding arm exercise to leg exercise on leg oxygen uptake (V˙O2), leg blood flow (LBF), the leg arterial to venous oxygen difference [(a-v)O2 diff], and mean arterial pressure (MBP). (Reprinted from N. H. Secher, J. P. Clausen, K. Klausen, I. Noer, J. and Trap-Jensen. Central and regional circulatory effects of adding arm exercise to leg exercise. Acta Physiol. Scand. 100:288-297, 1977. Used with permission).FIGURE 4-Arm blood flow during arm cranking and after the addition of leg cycling. The temporal characteristics of the blood-flow reduction were obtained by the constant-thermodilution method. The projected value is from arm-cranking bouts of the same workload and duration. [Adapted from Volianitis, S., P. Krustrup, E. Dawson, and N. H. Secher. Arm blood flow and oxygenation on the transition from arm to combined arm and leg exercise in humans. J. Physiol. 547:641-648, 2003].The reduction in limb blood flow during intense exercise has implications for the energy production and the development of fatigue. First, there is an increased contribution from anaerobic metabolism, as indicated by the increased lactate release for a given arm workload (39,46-48). In contrast, the legs take up lactate during combined arm-cranking and leg exercise (39), supporting the notion that the arms' metabolism during exercise differs from that of the legs (3), but the lactate uptake in the legs is not large enough to make the arterial value stable. It is likely that lactate elimination is attenuated by the further reduction in splanchnic blood flow (28) as sympathetic activity increases with progressive increase of active muscle mass during exercise (36). Furthermore, the lactate uptake in the legs (and the brain) suggests that lactate is a fuel source during intense exercise. Finally, the reduced limb blood flow accelerates extracellular K+ accumulation, as indicated by the reduced K+release when muscle mass is increased (39,46-48), precipitating fatigue via an impaired membrane excitability.WHY DOES REGIONAL FLOW DECREASE?During whole-body exercise, the increased vascular conductance is the key to the elevation in V˙O2max (42). In a review of studies including a determination of CO and MAP during maximal exercise in subjects of different endurance-fitness levels, Clausen (5) found a tight reverse curvilinear relationship between total vascular resistance and V˙O2max, which becomes a direct linear relationship when the reverse relationship (1/resistance or conductance) is used (4) (Fig. 5). Equally, the large arm-exercise capacity found in rowers, even though the arms maintain a lower oxygen extraction compared with the legs (135 vs 175 mL·L−1 (3,39), is related to their twofold increase in arm vascular conductance and diffusion capacity for oxygen. In contrast, the load on the heart, expressed as HR × MAP, is comparable with untrained subjects (48), supporting an enlarged regional vascular capacitance for the trained subjects (42). Interestingly, Clausen and Trap-Jensen (6) found that endurance training and the associated attenuated MAP response to exercise increased the work capacity in cardiac patients with angina pectoris, with no apparent improvement in cardiac function, as exercise tolerance was reached at a similar rate-pressure product.FIGURE 5-Arm oxygen uptake and arm vascular conductance for 25 subjects. With increasing work intensity, arm oxygen uptake and vascular conductance increase. In trained subjects, there is a twofold enhanced arm vascular capacity. Also, the effect of adding leg exercise to arm exercise on arm vascular conductance is shown (insert). Data are Volianitis and Secher (47) and Volianitis, Yoshiga, Nissen, and Secher (48).If the elevation of CO limits vascular conductance during maximal exercise, it is worth asking what causes such a limitation. During maximal exercise, it is more likely the diastolic function of the heart, or its preload, that sets the limitation to CO, rather than its pumping capacity. That consideration is supported by the fact that healthy people during maximal and/or whole-body exercise may develop muscle pain-especially in the arms, reflecting local ischemia-but they do not present with angina.The balance between the importance of the systolic and diastolic function of the heart during exercise manifests in the morphological adaptation of the heart to training. Endurance-trained athletes are characterized by hearts with extraordinary large internal diameters rather than with a large wall thickness. Only when exercise is associated with large fluctuations in blood pressure, as during rowing (7), is the wall thickness of the heart also enlarged. Thus, V˙O2max relates to the ability of the heart to provide a large stroke volume rather than the ability to provide for a large external load by improving contractility.A limited preload to the heart may be inferred by a decrease in central venous pressure, resulting in an attenuation of stroke volume at the end of exhaustive cycling exercise (13). Experimentally, the consideration that preload to the heart limits oxygen transport is supported by the increase in V˙O2max in response to "blood doping" (10) and by the increase in stroke volume induced by the administration of fluid or plasma expanders during exercise (19). An alternative hypothesis is that the diastolic function of the heart is limited by pericardial restraint (45), but for humans that does not manifest during upright exercise. The central blood volume, as indicated by central venous pressure and plasma atrial natriuretic peptide as an indicator of atrial filling, are maintained at a lower level than during (seated) rowing (CC Yoshiga, personal communication, 2005), and the highest stroke volume is reached during supine exercise.CONCLUSIONComparison of exercise with the arms and the legs reveals that, although flow to working skeletal muscles is regulated to attenuate hemoglobin desaturation (14), the increase is limited, and muscle blood flow and oxygenation decrease when both the arms and the legs are engaged at a high intensity. Such muscle ischemia activates the muscle pressor reflex and resets the arterial baroceptors to control an elevated MAP. However, if the ability to increase CO is enhanced by an elevated blood volume (i.e., in response to endurance training), the ability to increase muscle flow is enhanced. 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