The interactions between exercise, vascular and metabolic plasticity, and aging have provided insight into the prevention and restoration of declining whole body and small muscle mass exercise performance known to occur with age. Metabolic and vascular adaptations to normoxic knee-extensor exercise training (1 h 3 times a week for 8 wk) were compared between six sedentary young (20 ± 1 yr) and six sedentary old (67 ± 2 yr) subjects. Arterial and venous blood samples, in conjunction with a thermodilution technique facilitated the measurement of quadriceps muscle blood flow and hematologic variables during incremental knee-extensor exercise. Pretraining, young and old subjects attained a similar maximal work rate (WRmax) (young = 27 ± 3, old = 24 ± 4 W) and similar maximal quadriceps O2 consumption (muscle V̇o2 max) (young = 0.52 ± 0.03, old = 0.42 ± 0.05 l/min), which increased equally in both groups posttraining (WRmax, young = 38 ± 1, old = 36 ± 4 W, Muscle V̇o2 max, young = 0.71 ± 0.1, old = 0.63 ± 0.1 l/min). Before training, muscle blood flow was ∼500 ml lower in the old compared with the young throughout incremental knee-extensor exercise. After 8 wk of knee-extensor exercise training, the young reduced muscle blood flow ∼700 ml/min, elevated arteriovenous O2 difference ∼1.3 ml/dl, and increased leg vascular resistance ∼17 mmHg·ml–1·min–1, whereas the old subjects revealed no training-induced changes in these variables. Together, these findings indicate that after 8 wk of small muscle mass exercise training, young and old subjects of equal initial metabolic capacity have a similar ability to increase quadriceps muscle WRmax and muscle V̇o2 max, despite an attenuated vascular and/or metabolic adaptation to submaximal exercise in the old.
- vascular resistance
- pulse pressures
- O2 diffusional conductance
- exercise training
maximal quadriceps O2 consumption (V̇o2 max) in healthy subjects has been reported to decline at a rate of ∼10% per decade beyond 30 yr of age (4, 18). Although it has been suggested that there are simultaneous age-related declines in central and peripheral components of the cardiovascular system as well as in skeletal muscle metabolism, it is not clearly understood to what degree each contributes to the overall reduction in exercise capacity (5, 39). Central factors, such as reduced cardiac output reserve, decreased peak heart rate, attenuated peak stroke volume (22, 35), and a maldistribution of cardiac output (5, 37) appear to limit blood flow to active skeletal muscle. In addition, peripheral factors, such as declining vascular function and reduced metabolic demand may reduce exercise capacity in aging persons. For example, several studies (3, 27) have suggested that age-related declines in vascular function increase peripheral vascular resistance, thereby limiting the delivery of blood to active skeletal muscle. However, others argue that the decline in markers of metabolic function, such as mitochondrial density, oxidative capacity (11), and citrate synthase activity (8) are responsible for the age-related decline in exercise capacity. Thus the findings of declining central cardiovascular, peripheral vascular, and peripheral metabolic systems make it difficult to discern to what degree each component contributes to the attenuated blood flow to active skeletal muscle associated with diminished exercise capacity in aging persons.
Although persons >50 yr of age remain the most sedentary segment of the adult population (53), mounting evidence supports the role of regular aerobic exercise in the prevention and restoration of the muscle metabolic and vascular losses usually incurred with the aging process (5, 7, 14). However, during bicycle exercise, maximal work rate (WRmax) (39), V̇o2 max (10, 39), leg blood flow to active skeletal muscle (39), and leg vascular conductance (39) appear to remain reduced in endurance trained older subjects compared with their younger counterparts. In addition, although citrate synthase levels and cytochrome c oxidase levels appear to increase equally regardless of age (50), other improvements that result from endurance training in young subjects, such as increased mitochondrial volume (30), mitochondrial content (36), insulin sensitivity (50), and muscle fiber type alterations (9) are attenuated or absent in the training response of aging subjects. Together, these findings suggest that independent of fitness level, differences in skeletal muscle metabolism and skeletal muscle blood flow regulation persist in aging subjects. The interactions between exercise, vascular plasticity, and metabolic plasticity are worthy of further investigation, as they provide further insight into the prevention and restoration of declining whole body and small muscle mass exercise performance known to occur with age (33, 37, 51).
To our knowledge, few studies have directly examined the age-related differences in skeletal muscle metabolism and blood flow during incremental small muscle mass exercise (33). In addition, none have applied these methods in conjunction with longitudinal knee-extensor exercise training to quantify the relationship between age and muscle plasticity when the contributions of potentially limiting central factors are minimized. Therefore, the purpose of the current study was to determine the age-related metabolic and vascular adaptive responses to 8 wk of knee-extensor exercise training. Our specific hypotheses were the following: 1) on completion of 8 wk of small muscle mass knee-extensor exercise training, young and old sedentary subjects of equal initial ability will achieve similar increases in WRmax and muscle V̇o2 max; 2) as a result of the knee-extensor exercise training, both young and old subjects will reduce muscle blood flow and increase arteriovenous (a-v) O2 difference (a-vO2), resulting in an unchanged metabolic efficiency (muscle V̇o2/watt).
Subjects. Six young and six old healthy nonsmoking sedentary male volunteers participated in this study (Table 1). All subjects were determined to be sedentary by an interview questionnaire based on the work of Jacobs et al. (26) and were excluded from participation if they reported any exercise on a work-related, recreational, or competitive basis. The subjects' sedentary lifestyle was confirmed by a preliminary incremental cycle exercise test revealing a low pulmonary V̇o2 max in both groups (Table 1). Health histories and physical examinations were completed on all subjects. Subjects were not taking any medications that would alter vascular responsiveness. Informed consent was obtained according to the University of California San Diego Human Research Protection Program requirements. The baseline data for these subjects have previously been published (33).
Exercise modality, protocol, and training. Single leg knee-extensor exercise was performed limiting work to the quadriceps muscle group, as originally described by Andersen et al. (1), and more recently documented by Richardson et al. (42). The ergometer was adjusted so that contraction of the quadriceps muscles turned a flywheel producing a 90°-170° arc of the lower leg. To provide progressive levels of resistance to the quadriceps muscle, tension was incremented by increasing friction on a belt surrounding the flywheel as a percentage of WRmax until the subject could no longer maintain a contraction frequency of 1 Hz. Subjects were allowed sufficient practice during preliminary testing to familiarize themselves with the exercise equipment, ensuring that maximal effort was achieved during the catheter study. At each WR, data collection proceeded as follows: 1) the subjects were allowed to attain an equilibrium at the given WR, 2) blood samples (3 ml each) were taken from the arterial and venous catheters, 3) blood flow measurements were made, 4) blood sampling and blood flow measurements were repeated, 5) blood pressure readings were taken, and 6) the subjects were challenged with the next work rate.
After the initial catheter-based studies, subjects returned to the laboratory three times each week to complete the knee-extensor exercise training portion of the study. Various 1-h protocols (1 Hz, 30%-90% of WRmax, totaling 60 min), which have previously documented to illicit a large change in V̇o2 max in young healthy subjects (45), were completed under normoxic conditions. The exercise regime consisted of a repeating 2-wk cycle of short (5–10 min), high-intensity (70–95% of WRmax) intervals, long (15–45 min) low-intensity (40–65% of WRmax) work bouts. Graded knee-extensor exercise tests were performed to reevaluate WRmax after weeks 2, 4, 6, and 8 of the 8-wk training protocol. Because the young and old subjects had similar initial work rates and developed similar absolute improvements in knee extensor WRmax over time, both groups trained at equal absolute and relative intensities. All six of the old subjects who began the knee extensor training study completed the 8 wk of exercise training (≥95% adherence) and the posttesting. In contrast, a total of 12 young subjects were recruited and completed the preliminary catheter-based testing, yet only 50% of the young subjects completed the entire training (≥95% adherence) and posttesting portions of the study.
Subject instrumentation. On the two main study days (pre- and posttraining), two catheters (model DSA 400L, Cook; Bloomington, IN) were placed: one in the femoral artery and the second in the femoral vein. In addition, a thermocouple (model IT-18, Physitemp Instruments; Clifton, NJ) was placed in the femoral vein ∼10 cm proximal to the tip of the venous catheter. Catheters were inserted using a sterile technique as previously described (44) to facilitate blood sampling and thermodilution blood flow measurements.
Leg blood flow, heart rate, and blood pressure. Muscle blood flow during knee-extensor exercise was measured by the thermodilution technique as previously described (2, 17). Measured blood flow during knee-extensor exercise is accepted as a close approximation of quadriceps muscle blood flow by reason that blood is directed toward working muscle, and the quadriceps are the sole working muscle group of the leg during knee-extensor exercise (40, 441). Heart rate was obtained from a three-lead electrocardiogram signal (Lifepak 9A, Lifeline; Santa Barbara, CA). Femoral arterial and venous blood pressures were continuously monitored at heart level by pressure transducers (model PX-MK099, Baxter). Mean arterial pressure (MAP) and mean venous blood pressures (MVP) were computed by the integration of each pressure curve. Leg vascular resistance was calculated as (MAP–MVP)/ muscle blood flow. Pulse pressures were calculated as the difference between arterial systolic and diastolic pressures.
Blood analyses. Total hemoglobin ([Hb]) and arterial O2 saturation (Sao2) were determined spectrophotometrically with a cooximeter (model IL-682, Clayton, NC). Po2, Pco2, and pH were determined with a blood gas analyzer (IL-Synthesis), and the data were temperature corrected to match the subject's body temperature at each work rate. Blood lactate concentration was measured with the use of a lactate analyzer (YSI 2300 Stat Plus, Yellow Springs Instruments). Oxygen content (ml/dl) (CO2) was calculated as (1.39 × [Hb] × O2 saturation/100 + 0.003 × Po2). The a-v O2 difference was calculated as the O2 difference between the femoral artery (Cao2) and femoral vein (Cvo2). Muscle V̇o2 was calculated as the product of muscle blood flow and a-vO2 difference. Quadriceps muscle O2 delivery was calculated as the product of muscle blood flow and Cao2. All blood samples were pooled for each subject, and the P50 was calculated by a least-squares method, based on the O2 saturation and corresponding Po2 values for each subject. Net venous lactate outflow from the exercising quadriceps muscle was calculated as the product of muscle blood flow and venous-arterial lactate concentration.
Mean capillary Po2 and O2 diffusional conductance. A Bohr integration technique was used to calculate an estimate of mean capillary Po2 (PcapO2) and O2 diffusional conductance (DmO2) at WRmax. PcapO2 was calculated as the numerical average of all Po2 values computed equally spaced in time along the capillary as it traverses the muscle bed from arterial to venous end, as previously described (55). This technique has been discussed in detail elsewhere (23, 47) based on a proposal by Wagner (56) with the assumption of a homogeneously perfused muscle. Briefly, the drop in Po2 along a capillary is calculated using Fick's law of diffusion: V̇o2 = DmO2 (PcapO2 – PmitoO2), where PmitoO2 is mitochondrial Po2, which is set at 0 mmHg, only slightly less than that measured in the cytoplasm of canine muscle fibers (16) and in vivo measurements in human muscle (43). DmO2 is an expression of all phenomena that facilitate O2 unloading at the muscle and is useful as a comparison among conditions and subject populations for gas-exchange analyses (24, 25).
Thigh-volume measurement. With the use of thigh length, circumference, and skinfold measurements, thigh volume was calculated to allow an estimate of quadriceps femoris muscle mass as suggested by Jones and Pearson (28) and as previously utilized by Andersen and Saltin (2).
Statistical analysis. Data were analyzed with the use of post hoc regression analysis, paired and unpaired t-tests. Statistics were performed using commercially available software (GraphPad, San Diego, CA; and SPSS software version 10.1). The invasive nature of the current study limited the sample size, thereby increasing the likelihood of a type II error. However, the data were subjected to a power analysis resulting in a β-value ≥0.8 for the majority of variables (e.g., comparison of muscle V̇o2 max between young and old, β = 0.78). All data are expressed as mean values ± SE. Significance was established at an α-level of P ≤ 0.05.
Subjects. Six sedentary young (18–27 yr) and six sedentary old (61–77 yr) subjects participated in the study. Height, weight, body mass index, and quadriceps muscle mass were not different between young and old (Table 1). Preliminary cycle ergometry testing revealed a significantly higher cycle WRmax (young = 181 ± 4, old = 131 ± 12 W) and pulmonary V̇o2 max in the young subjects (Table 1).
Power output and muscle V̇o2 max. Before training, young and old sedentary subjects were equally matched in terms of knee extensor WRmax (Table 2) and muscle V̇o2 max (Fig. 1B and Table 2). In response to the knee-extensor exercise training, similar increases in WRmax were achieved by both young and old (young = 40%, 10 W; old = 48%, 10 W; Table 2). As a result of the training, neither the young nor old subjects altered their submaximal V̇o2 per watt, but both groups similarly increased muscle V̇o2 max (Fig. 1B and Table 2). After training, muscle V̇o2 max was again not different between young and old subjects (Table 2).
O2 transport. Before training, [Hb], Sao2, Pao2, and Cao2 were not different between young and old throughout graded knee-extensor exercise (Table 2). At maximal effort pretraining, young and old had similarly high Pao2 and Sao2 values, which are expected considering the hyperventilatory response typically associated with knee-extensor exercise. After 8 wk of knee-extensor exercise training, the old subjects revealed a reduced Pao2 and Sao2 throughout graded knee-extensor exercise and at WRmax compared with the respective pretraining values. However, Cao2 was not altered in the old due to variations in the [Hb] (Table 2).
Before training, muscle blood flow was ∼500 ml/min lower in the old subjects throughout graded knee-extensor exercise (Fig. 1A), accounting for the ∼30% lower pretraining O2 delivery in the old (Fig. 1D). Before training, the a-vO2 difference tended to be higher (∼20%, P = 0.08) in the old (Fig. 1C) resulting in the tendency toward a lower SvO2 in the old throughout submaximal knee-extensor exercise (Fig. 1C and Table 2). As a result of the knee-extensor exercise training, the young subjects revealed a significant fall in submaximal muscle blood flow, a proportional decline in O2 delivery, and a proportional elevation in a-vO2 difference (at 50% work rate, ∼700 ml/min, 0.14 l/min, and 0.9 ml/dl, respectively). In contrast, the old did not alter submaximal muscle blood flow, O2 delivery, and a-vO2 difference in response to the 8-wk training protocol (Fig. 1, A–D).
Net venous lactate outflow. Before training, submaximal net venous lactate outflow was not different between young and old subjects. However, at the pretraining WRmax net venous lactate outflow in the old subjects was significantly higher than in the young subjects (Fig. 1E and Table 2). After knee-extensor exercise training, neither group revealed a difference in submaximal net venous lactate outflow compared with the respective pretraining values. Maximal net venous lactate outflow was increased in both young and old subjects after the knee-extensor exercise training, and the magnitude of this increase was similar in the young and old subjects.
DmO2. Pre- and posttraining, DmO2 during maximal knee-extensor exercise was not different between young and old. As a result of the training, both young and old significantly increased DmO2 (Fig. 3).
Vascular pressures and vasodilation. The driving force on blood across the muscle bed (MAP-MVP) was not different between young and old pretraining throughout graded knee-extensor exercise. As a result of knee-extensor exercise training, neither young nor old altered MAP-MVP throughout graded knee-extensor exercise. Pulse pressures before knee-extensor exercise training were ∼36% higher in the old subjects compared with the young, whereas the rate of increase in pulse pressure throughout incremental knee-extensor exercise was similar in both groups (Fig. 2B). After training, the young revealed a significant fall in submaximal pulse pressures (Fig. 2B). The old, however, revealed no difference in pulse pressures from pre- to post-knee-extensor exercise training. Pretraining, the vasodilatory response to incremental knee-extensor exercise in the old subjects, measured as the change in leg vascular resistance (LVR)/watt, was ∼142% greater than that of the young subjects' pretraining and was not altered by 8 wk of knee-extensor exercise training (Fig. 2A). Both the LVR and the vasodilatory response to incremental knee-extensor exercise (change in LVR/watt) increased posttraining in the young to match the values attained by the old subjects (Fig. 2A).
There were several major findings of this study. First, after 8 wk of small muscle mass endurance training, young and old subjects of equal initial ability achieved similar improvements in single leg knee-extensor exercise WRmax (∼10 W, ∼44%) and muscle V̇o2 max (0.2 l/min, ∼43%). Second, after training, young subjects revealed an elevated submaximal LVR, which was responsible for the posttraining reductions in submaximal muscle blood flow and O2 delivery. An elevated a-vO2 difference in the young subjects after training resulted in an unchanged muscle V̇o2/watt. Third, although the improvement in maximal exercise capacity was similar in young and old subjects, the old subjects failed to alter the relationship between WR and muscle blood flow, O2 delivery, pulse pressures, a-vO2 difference, and LVR with knee-extensor exercise training. Thus the training-induced alterations in the submaximal exercise response reveal a plasticity in the young subjects, which contrasted with the somewhat inflexible nature of the aging system. However, the reduced submaximal plasticity of these O2 transport variables in the old appears unrelated to their ability to increase maximal knee-extensor exercise capacity.
Sedentary aging and response to exercise. The baseline findings for sedentary young and old subjects have previously been described (33). First, briefly, muscle blood flow measurements during knee-extensor exercise revealed a consistent attenuation (∼500 ml/min) in the old sedentary subjects when compared with the young sedentary subjects with a similar quadriceps muscle mass. Second, LVR was elevated in the old throughout knee-extensor exercise and was responsible for the reduction in muscle blood flow. Finally, old and young sedentary subjects of equal quadriceps muscle mass achieved similar WRmax and muscle V̇o2 max during small muscle mass knee-extensor exercise, whereas during whole body cycle exercise, the old revealed a lower WRmax and muscle V̇o2 max than the young. This suggests a more prominent age-related central limitation to maximal whole body exercise (Table 1). In summary, the baseline findings suggest that even when central limitations are minimized as they are during small muscle mass knee-extensor exercise, elevated LVR, elevated pulse pressures, and reduced muscle blood flow persist in the sedentary old subjects. Although these findings support the current understanding of age-associated declines in peripheral vascular function, they clearly do not compromise knee-extensor WRmax or muscle V̇o2 max in the old.
Age, training, and maximal exercise capacity. Age-related declines in maximal exercise capacity are considered a hallmark of the aging process (4, 18). Initial differences in WRmax of older subjects have frequently resulted in the comparison of young and old training responses in terms of percent change in WRmax (5, 7, 14) and V̇o2 max (4, 18). In addition, reduced muscle mass in old subjects can further confound results, as the loss of mass should be corrected for as it leads to a reduction in muscle function (31). In the current study, the findings of similar pretraining WRmax, similar absolute improvements in WRmax and muscle V̇o2 max, and similar quadriceps muscle mass between young and old subjects permit the direct comparison of the effect of knee-extensor exercise training on both young and old subjects without the potentially confounding normalization for power output or muscle mass.
Although an early exercise training study on aging subjects showed no improvements in V̇o2 max (32), more recent age-related studies have consistently documented results such as ∼20% to 30% increases in WRmax and V̇o2 max after endurance training programs (5, 9, 19, 49) and 174 ± 31% increases in strength (15) after resistance training programs. In the current study, the similar training-induced elevations in WRmax and muscle V̇o2 max in young and old subjects are in agreement with the vast majority of the recent literature that supports the training-induced improvements in aging skeletal muscle. Although this study is the first to compare the effects of knee-extensor exercise training on healthy young and old subjects, training-induced increases in WRmax (young ∼40%, old ∼48%) were similar to the 43% increases previously documented in congestive heart failure (CHF) patients after knee-extensor exercise training (34). The similar relative increase in WRmax between the centrally limited CHF patients and the healthy young and old subjects of the current study was likely achieved by the maintenance of adequate quadriceps muscle perfusion during knee-extensor exercise in the CHF patients, despite their declining cardiac function (34). These findings add credence to knee-extensor ergometry as a means to minimize the role of the central circulatory system in limiting acute exercise, and the peripheral adaptations promoted by exercise training. Under these conditions, young and old subjects with a similar initial WRmax are able to achieve a similar absolute increase in WRmax and muscle V̇o2 max.
The reduction in maximal LVR posttraining was similar between young and old subjects and resulted in similarly elevated maximal muscle blood flow and maximal convective O2 delivery. Regarding the diffusive component of O2 transport at maximal exercise, the young and old subjects revealed a similar elevation in DmO2 and muscle V̇o2 max as a result of the training. Although young and old subjects are approaching the previously reported muscle V̇o2 max and DmO2 of the endurance-trained athletes, neither has exceeded ∼50% of the absolute muscle V̇o2 max and DmO2 of the athletes (Fig. 3). However, it should be noted that in such a cross-sectional comparison of athletes versus the young and old subjects of the current study, there may be many important uncontrolled variables, such as length and type of training and genetics. The findings from the current study provide evidence that a low DmO2 and muscle V̇o2 max are associated with a sedentary lifestyle rather than age, and that age does not hinder the ability to increase DmO2.
Age training and submaximal exercise. Both young and old subjects had no training-induced changes in the muscle V̇o2 to work rate relationship throughout incremental knee-extensor exercise, which indicates that the quadriceps muscle efficiency (muscle V̇o2/watt) was unchanged by the knee-extensor exercise training in both groups. On the basis of the current literature, the effects of exercise training on submaximal efficiency are unclear. The results of several longitudinal cycle exercise studies have produced varying results including increased V̇o2/watt in old subjects (5), and both decreased V̇o2/watt (38), and unchanged V̇o2/watt in young subjects (5, 6). The findings from the study conducted by Beere et al. (5) of an elevated V̇o2/watt in old subjects after cycle exercise training suggest a training-induced decrease in efficiency, and are not supported by the current study. The current findings of an unaltered muscle V̇o2 for a given WR or even a reduction in V̇o2, as reported by Proctor et al. (38) are certainly the most intuitive, if exercise is presumed to result in beneficial adaptations.
The current finding of a reduced submaximal muscle blood flow due to a posttraining increase in LVR in the young subjects suggests that the total peripheral vasodilator to vasoconstrictor ratio is decreased after knee-extensor exercise training in the young subjects but is unchanged in the old subjects. The elevated a-vO2 difference and increased LVR revealed after training in the young is supported by the recent link between metabolic stress and vasodilator efflux (52). Although further mechanistic speculation is beyond the scope of the current study, the recognized multifaceted control of muscle blood flow implies potential angiogenic, sympathetic, and metabolic adaptations. Regardless of the mechanism, it is important to note that small muscle mass training adaptations in LVR occurred in the young subjects, whereas the old subjects who completed the same training protocol failed to modify LVR.
The current finding of reduced submaximal muscle blood flow posttraining in the young subjects is similar to findings of reduced submaximal leg blood flow in young subjects after high-intensity aerobic cycle exercise training (38). In the aforementioned study, however, the reduction in blood flow unfortunately cannot be divorced from the proportional posttraining decline in V̇o2 (38). Although the current work and the study by Proctor et al. (38) measured blood flow in the femoral vein with the same methodology, the differing exercise modality (bicycle vs. knee extensor) may explain the differences in the apparent training responses. It is possible, as Proctor et al. (38) suggested, that the bicycle exercise training resulted in the additional recruitment of accessory muscles such as gluteals, hip flexors, and/or hip extensors, which are not drained by the femoral vein and therefore are invisible to blood flow measurements made distal to the inguinal ligament, but may contribute to the work performed. The knee-extensor modality, however, minimizes the potential for experimental error of this type by limiting work performed to the quadriceps muscle group.
It is important to note that we cannot discern whether an increased metabolic capacity has permitted a reduction in muscle blood flow or whether a reduction in muscle blood flow has dictated that a-vO2 difference must be elevated to maintain a similar muscle V̇o2/watt. However, other local adaptations to exercise training such as an increased capillarity (12, 48), or increased mitochondrial density, size, number, and enzymatic activity (20, 21) may account for the increased O2 extraction in the young.
Findings of unchanged mitochondrial volume after 6 mo of endurance training (30), and reduced angiogenic factors (29, 46) in aging populations, may explain the somewhat unresponsive nature of the current a-vO2 difference and muscle blood flow during submaximal exercise in the old. Although the inability of the old to elevate a-vO2 difference may at first carry a negative connotation, it was the young subjects who reduced muscle blood flow and increased the a-vO2 difference after exercise training, thereby appearing more like the aging subjects. Perhaps the baseline findings of low muscle blood flow and elevated a-vO2 difference in the old sedentary subjects is actually a positive adaptation to compensate for the declining central system (5, 22, 35, 37). The young sedentary subjects may not have previously been exposed to a stimulus that requires a tighter control of muscle blood flow or a widened a-vO2 difference.
Age, training, and vascular compliance. The elevated LVR and decreased pulse pressures in the young posttraining may seem contradictory, given that increased vascular resistance implies decreased arteriolar radii, and pulse pressures are inversely proportional to vessel size (13). However, the elevated LVR resulted in a significantly reduced muscle blood flow in the young subjects and most likely plays a role in reducing pulse pressures (13) after training. However, we cannot disregard the possibility that knee-extensor exercise training has resulted in both reduced muscle blood flow and increased vascular compliance in the young, both of which contribute to the reduction in pulse pressures. Because perfusion/100 g muscle mass is higher during small muscle mass exercise than whole body exercise (44), and whole body aerobic training has been shown to decrease pulse pressures (13), it seems reasonable that small muscle mass training may also influence vessel compliance. If the latter theory is correct, the failure of the old subjects to alter their initially elevated pulse pressures is again an indicator of attenuated vascular plasticity.
In summary, the similar absolute elevations in WRmax and muscle V̇o2 max resulting from 8 wk of knee-extensor exercise training demonstrate that young and old sedentary subjects of similar initial ability are equally responsive to isolated skeletal muscle mass training. In addition, neither young nor old increased their muscle V̇o2/watt after knee-extensor exercise training. However, submaximally, the increased LVR, decreased muscle blood flow, decreased pulse pressures, and elevated a-vO2 difference achieved by the young was absent in the old. Together, this study reveals an attenuated vascular and metabolic plasticity associated with the aging process, even when an isolated small muscle mass model is employed.
We are grateful for the technical support provided by Dr. Jeannie Kim, Jeremy Barden, and Jennifer Poole. Also, we thank our subjects for volunteering to participate in this research.
This study was supported by National Heart, Lung, and Blood Institute Grant HL-17731, the Sam and Rose Stein Institute for Research on Aging, and the University of California San Diego Academic Senate.
The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked “advertisement” in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
- Copyright © 2004 by the American Physiological Society