INTRODUCTION

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A STRONG LINEAR RELATIONSHIP between peak vascular conductance of the calf and maximal aerobic power (O_{2 max}) has been described previously by our laboratory (19) and by others (25), suggesting a matching between whole body maximal aerobic function and peripheral vascular reserve in skeletal muscle. Conversely, prolonged physical training of specific routine by high-caliber athletes may cause an alteration of this relationship because specific adaptations occur in response to the unique demands of different types of training. For example, traditional resistance training programs promote increases in both muscle strength and muscle size (i.e., hypertrophy), with little or no change in skeletal muscle capillary supply or muscle fiber oxidative capacity in young adults (29), and may reduce the reactive hyperemic blood flow response (5). In contrast, the type of resistance training used by bodybuilders is qualitatively different, promoting modest increases in both capillary supply and oxidative capacity (4, 27, 28), in addition to increasing muscle strength and size. These muscle adaptations arise because of the high metabolic and blood flow demands of the multiple-set, high-repetition, and high-intensity muscle contractions that are characteristic of the resistance training used by bodybuilders (BB) (28). Because these muscle contractions represent activation of only a small percentage of total body muscle mass at any one time, the stress placed on the central circulation to provide blood flow (i.e., cardiac output) would be much less than that required by endurance types of activity, such as running. We hypothesized that the modality of training used by BB leads to structural and/or functional changes in the peripheral vasculature that are independent of changes in maximal central circulatory function, resulting in a lower O_{2 max} for a given peak vascular conductance compared with that normally seen. In contrast, we reasoned that the training employed by track and field jumpers and decathletes [power athletes (PA)], which includes traditional resistance training to maximize power relative to body mass in those muscles used in running and jumping, in addition to running training, would result in higher O_{2 max} and peak vascular conductance but an unchanged relationship between these variables compared with healthy sedentary subjects (HS). Similarly, the nature of training employed by highly trained endurance runners (ER; e.g., racing distances of 800-10,000 m), which includes a significant proportion of interval running at intensities greater than or equal to O_{2 max}, was expected to result in an even greater peripheral vascular reserve and systemic O_{2 max} but a maintained relationship between these variables compared with HS. To evaluate this, we determined peak vascular conductance in the calf after maximal ischemic plantar flexion exercise and whole body O_{2 max} on the treadmill in BB, subjects representing a wide scope of aerobic power (HS and ER), and practitioners of traditional resistance training (PA).

	METHODS

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Subjects. Thirty-six male subjects, including 7 BB, 10 ER, 11 PA, and 8 age-matched HS, were studied at the University of Toronto Cardiovascular Regulation Laboratory. The PA were included to compare the effect of traditional resistance training vs. the resistance training used by BB (see below). Details of the experimental protocol were explained, and informed consent was obtained from all subjects. Screening included completion of a physical activity readiness questionnaire, and an interview to obtain details of training history, before the study began.

O_{2 max} . O_{2 max} was determined by using open-circuit spirometry during an incremental exercise test to exhaustion on a motor-driven treadmill (model 1864, Collins). Subjects warmed up for 2 min at a self-selected speed, after which speed was held constant while the slope was increased by 2% every 2 min for the next 8 min, and by 1% for each additional minute thereafter until voluntary exhaustion. Heart rate was monitored by using a Polar heart rate monitor. Expired gases were sampled at 15-s intervals, passed through a mixing chamber, and analyzed via an infrared CO₂ monitor (Jaeger CO₂-test) and an O₂ analyzer (Ametek S3-A). Ventilation was measured with a ventilation monitor (Morgan Ventilometer Mark 2) connected to a pneumotachograph on the inspiratory arm of the mouthpiece. All cardiorespiratory data were collected and analyzed with the aid of a semiautomated metabolic cart (Morgan) on-line with a microcomputer. Criteria for acceptance of O_{2 max} included attainment of three or more of the following: 1) minute ventilation >115 l/min; 2) respiratory exchange ratio >1.15; 3) heart rate ±10 beats/min of age predicted; and 4) a plateau in O₂ uptake (increase of <2 ml · kg¹ · min¹ with an increase in workload) (18).

Strain-gauge venous occlusion plethysmography. Blood flow to the calf was measured by using venous occlusion strain-gauge plethysmography at rest and immediately after submaximal (data not presented) and maximal ischemic plantar flexion exercise on the dominant leg, as described previously (19). Briefly, a blood pressure cuff, placed around the ankle, was inflated to a pressure of 220 Torr to occlude blood flow from the foot. A second cuff, placed around the thigh just above the knee, was rapidly inflated (~1 s) to 60 Torr, and the change in volume of the leg was measured over a 14-s cycle via an indium-gallium strain gauge (model SPG16, Mediasonics) placed around the calf at the position of widest girth. Beat-to-beat systemic blood pressure and heart rate were recorded during the blood flow measurement via a finger cuff placed on the left index finger (with the hand at the level of the heart) by using a Finapress 2300 automated blood pressure monitor (Ohmeda). The data-collection period was 42 s (3 × 14-s cycles), and data were processed (at a sampling frequency of 100 Hz) on-line with a microcomputer by using a WATSMART data-acquisition unit and software customized to our system, allowing simultaneous collection of blood pressure, heart rate, and blood flow measurements. Blood flows were calculated from the slope of the line made by three manually selected points on the ascending portion of the blood flow vs. time tracing. The corresponding vascular conductance for each blood flow measurement was calculated as the quotient of blood flow and mean arterial pressure (MAP = systolic blood pressure +  pulse pressure). Muscle and adipose mass in the calf were estimated by using the equations of Clarys and Marfell-Jones (8), as described previously (19).

Statistical analysis. Data were analyzed by using one-way ANOVA and Student-Newman-Keuls post hoc test to identify differences between groups. Linear regression analysis was used to examine the relationship between O_{2 max} and peak vascular conductance and to interpolate O_{2 max} at a common peak vascular conductance (70 ml · min¹ · 10 l tissue¹ · Torr¹) in each subject. Values are presented as means ± SE.

	RESULTS

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Body mass was significantly greater in BB than all other groups, whereas body mass in ER was lower than in all other groups (Table 1). As expected, O_{2 max} (ml · min¹ · kg¹) was higher in ER (71.0 ± 1.2 ml · min¹ · kg¹) than in the other groups (Table 1). In addition, PA (50.7 ± 1.6 ml · min¹ · kg ¹) had a higher O_{2 max} than did HS (45.1 ± 1.9 ml · min¹ · kg¹) but not BB (44.7 ± 3.2 ml · min¹ · kg¹). The blood flow and blood pressure responses at rest and after the maximal ischemic plantar flexion exercise are presented in Table 2. The BB had a lower resting MAP (83 ± 2 Torr) than did HS (99 ± 5 Torr) and a greater resting blood flow and vascular conductance than did the other groups. The peak blood flow and vascular conductance in both ER and BB were higher than in PA and HS. Although BB demonstrated a greater estimated calf muscle mass (2.11 ± 0.11 kg) than did ER (1.74 ± 0.05 kg), there were no differences between groups in the ratio of estimated adipose mass to muscle mass of the calf (Table 2).

The relationship between peak calf vascular conductance and O_{2 max} obtained for healthy subjects in previous studies representing a broad scope of aerobic power (19, 25) along with the values for each group in the present study are shown in Fig. 1. For a given vascular conductance, the O_{2 max} in PA and HS was not different from that shown previously (19, 25). Addition of these results to the previous data (19, 25) yields the following regression equation: O_{2 max} = 21.12 + (0.488 × peak vascular conductance) (r = 0.79, P < 0.001). By using this regression equation to predict O_{2 max} at a vascular conductance of 70 ml · min¹ · 10 l tissue¹ · Torr¹ in each subject, a higher O_{2 max} in ER (70.0 ± 1.7 ml · min¹ · kg¹) and a lower O_{2 max} in BB (39.5 ± 4.2 ml · min¹ · kg¹) than in both HS (57.0 ± 1.9 ml · min¹ · kg¹) and PA (57.1 ± 2.4 ml · min¹ · kg¹; P < 0.05) was revealed.

View larger version (20K): [in this window] [in a new window]   Fig. 1.   Relationship between maximal aerobic power (O2 max) and peak vascular conductance in the calf muscle in healthy subjects across a broad scope of aerobic power and training backgrounds. Regression line includes previous data from healthy subjects (19, 25) and the healthy sedentary and power athletes of the present investigation [O2 max = 21.12 + (0.488 × peak vascular conductance); r = 0.79, P < 0.001].

	DISCUSSION

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We found that compared with healthy subjects who demonstrate a wide range of aerobic power (19, 25) (HS and PA of present study), both highly competitive ER and BB deviate from the previously described linear relationship between maximal aerobic power and calf muscle peak vascular conductance. Specifically, we observed that ER have a higher O_{2 max} than would be predicted from their peak vascular conductance, whereas BB have a lower O_{2 max} than would be predicted from their peak vascular conductance. It is suggested that this result is a consequence of the different training regimens and their effect on the balance between central vs. peripheral cardiovascular adaptation to muscle metabolic demand.

Venous occlusion plethysmography was used to noninvasively determine peak vascular conductance in calf muscle after exhaustive ischemic exercise. This approach provides peak blood flows that are markedly lower than those reported for the quadriceps during knee extensor exercise by direct methods (2, 20), which may reflect the difference in site of measurement (quadriceps vs. calf; for review see Ref. 16) and/or methodological issues [see Reading et al. (19) and Hiatt et al. (11) for a discussion of these issues]. Differences in peak vascular conductance between individuals have been interpreted as reflecting differences in the anatomic structure for conducting blood flow [e.g., arteriolar number and/or dimensions (3, 5, 26)], and/or an altered vasomotor response to exercise due to the balance between myogenic control (e.g., sympathetic drive) and local regulatory (e.g., nitric oxide release) factors (9, 19).

Differential effects of resistance training and endurance training on vascular conductance. Endurance training and traditional forms of resistance training have been shown to affect the muscle blood flow response in different ways. For example, an augmented muscle peak vascular conductance has been found after both whole body endurance training (17) and small- muscle-group endurance training (10, 24). In contrast, a reduction in reactive hyperemic blood flow has been shown after 4 wk of high-intensity resistance training of the calf, perhaps the result of muscle hypertrophy without concomitant vascular growth (5). Unfortunately, the impact of these adaptations on the relationship between O_{2 max} and peak vascular conductance was not considered in these studies. In this respect, the results for HS and PA in the present study are consistent with previous studies showing a strong relationship between O_{2 max} and peak vascular conductance (19, 25) (Fig. 1), and show that the type and/or volume of resistance training used by PA does not alter this relationship. The relationship between peak vascular conductance and O_{2 max} shows that, as O_{2 max} increases, peripheral vasodilatory reserve also increases. In other words, rather than increasing the proportion of vasodilatory capacity utilized as O_{2 max} is increased, vasodilatory capacity is increased in proportion to O_{2 max} such that the scope of the vasodilatory reserve is maintained. Nevertheless, it is also noteworthy that long-term physical training may cause a dissociation of the relationship between peak vascular conductance and O_{2 max} as illustrated by the responses of the ER and BB. In this respect, the response of ER in the present investigation is quite different from that demonstrated by the study of Snell et al. (25), in which the runners demonstrated the same response as other healthy individuals. The training history (an average of 9.1 ± 1.6 yr of training) and small variability in the O_{2 max} seen in the ER subjects of the present investigation suggest that they were more highly trained than were those of the study of Snell et al., which may in part account for the deviation of our ER subjects' response.

Physiological basis of peak vascular conductance. The high peak vascular conductance response in BB could reflect anatomic and/or functional differences in the peripheral vasculature induced by their training behavior. It is worth noting that the literature of animal studies supports the possibility that an increased size of the arteriolar bed may result from a chronically elevated blood flow (i.e., as occurs with BB training) (for review see Ref. 12). In addition, it has been suggested that the greater peak vascular conductance after training of small muscle groups (10, 24) and in athletes compared with sedentary subjects (25) is secondary to an increased diameter and/or number of the resistance vessels (23) rather than changes in sympathetic vascular control (24) or nitric oxide mediated vasodilation (10). In this respect, the only modestly greater muscle capillarization and oxidative capacity found previously in BB compared with practitioners of more traditional resistance training paradigms (27) do not preclude more significant growth in the arteriolar resistance vessels with BB training because elevated blood flow per se (as occurs during BB training) is not thought to be a major cause of angiogenesis (14, 21) but is thought to induce both arteriolar proliferation and increased vessel diameter (15). This explanation may also account for the response observed in ER in whom O_{2 max} was significantly greater for a given peak vascular conductance. Specifically, whereas we would expect the chronically elevated blood flows during running training to induce arteriolar proliferation and/or enlargement (as is suggested by their greater peak vascular conductance compared with HS and PA), adaptations in capillary growth and mitochondrial structure may be relatively greater consequent to the intramuscular environment [e.g., intracellular hypoxia (6, 14)] created when running at intensities greater than or equal to O_{2 max}. Indeed, a greater capillarization in endurance-trained subjects is well described (e.g., Refs. 1, 7) and is thought to play an important role in the greater O_{2 max} in this population (13).

Conclusions. In summary, we observed that both competitive BB and ER demonstrate an altered relationship between peak vascular conductance in the calf muscle and whole body O_{2 max}, compared with HS representing a broad scope of aerobic power. Specifically, ER have a higher O_{2 max} and BB a lower O_{2 max} compared with both HS and PA at a similar vascular conductance. It is suggested that this result is a consequence of the unique cardiovascular demands of long-term running training and the type of resistance training routinely used by BB and the subsequent adaptations in central vs. peripheral cardiovascular structure and/or function.