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ENVIRONMENTAL, EXERCISE AND RESPIRATORY PHYSIOLOGY
Department of Human Biology and Nutritional Science, University of Guelph, Guelph, Ontario, Canada
Submitted 20 August 2004 ; accepted in final form 13 April 2005
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ABSTRACT |
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contraction frequency; stimulus frequency; train duration; muscle contraction; hyperemia
Skeletal muscle metabolism has been hypothesized to be the source of dilators responsible for the vasodilation and resulting changes in blood flow in response to muscle contraction (for a review, see Refs. 11, 14, 22). On the basis of this hypothesis, changes in blood flow or indexes of blood flow have been investigated as to their relation to the metabolic demand of active skeletal muscle. Indexes of metabolism such as oxygen consumption (8), contraction strength, (2, 12, 19, 39), running speed (23), power (30), and muscular work (1, 20) have been shown to be linearly related to blood flow. Changing metabolic demand by altering basic stimulation parameters such as stimulus frequency was first shown to be related directly to the magnitude of blood flow by Anrep and von Saalfed (2). More recently, the magnitude of blood flow (4, 16) and microvascular dilations that are responsible for these changes in blood flow (17, 24, 27, 28) have also been related to stimulus frequency. Metabolism of a skeletal muscle fiber can be altered by changing the muscle's basic stimulation characteristics; stimulus frequency, duration of the train of stimuli, and contraction frequency. Each index of metabolism used to relate metabolism to hyperemia is determined by these basic stimulation parameters. For example, work is derived from tension (derived from the number of fibers recruited and stimulus frequency) and train duration, and these parameters that derive work have been shown to be more directly related to changes in blood flow to contracting muscle than work itself (2, 19). Therefore, the basic stimulation characteristics of skeletal muscle may be the primary determinants of the dilatory responses to skeletal muscle activity. However, there is a distinct lack of information regarding how basic stimulation parameters affect the vasculature.
In the present study, I sought to determine which stimulation characteristics of skeletal muscle were most influential in determining vasodilation in the microvasculature. To investigate this issue, a small bundle of skeletal muscle fibers in hamster cremaster muscle in situ was repetitively contracted with the chosen stimulation pattern for 2 min. The stimulation pattern was changed by systematically changing the parameters that comprise a tetanic contraction (contraction frequency, train duration and stimulus frequency). Stimulation parameters that are physiologically relevant to movement and locomotion were used where possible; this encompassed a range of stimulus frequencies within a train and short-train durations, under 1,000 ms depending on the nature of the activity (18, 31, 35, 40).
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METHODS |
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Preparations
Blood-perfused cremaster muscle in situ.
Adult male Golden hamsters (100–130 g) were anesthetized with pentobarbital sodium (70 mg/kg ip) and tracheotomized. Catheters were placed in the right femoral artery and right femoral vein to monitor mean arterial pressure and for supplemental pentobarbital administration, respectively. Supplemental pentobarbital was given as needed during surgery and constantly infused throughout the experimental protocol (10 mg/ml saline, 0.56 ml/h). Hamster esophageal temperature was maintained at 37°C via convective heat from a coiled water-filled glass tube (42.0°C) secured under the hamster. The right cremaster was prepared for in situ microscopy as previously described (3, 26). Briefly, the cremaster was isolated, cut longitudinally, separated from the testis and epididymis, and gently spread over a semicircular lucite platform. The edges of the tissue were secured with insect pins to maintain tension but not stretch the muscle. Once exposed, the cremaster muscle was constantly superfused with a bicarbonate-buffered salt solution containing (in mMol/l) 131.9 NaCl, 4.7 KCl, 2.0 CaCl2, 1.2 MgSO4, 30 NaHCO3, and 0.3 mg/l tubarine (curare) equilibrated with gas containing 5% CO2-95% N2 (pH 7.35–7.45). Cremaster muscle temperature was maintained at 34.0°C. After the surgery, all preparations were allowed to equilibrate for 45–60 min before data collection. The cremaster microvasculature was visualized by transillumination with a tungsten lamp and with an Olympus BX51WI microscope using a 20x long working distance water immersion objective [numerical aperture (na) 0.50] and a x1.6 magnification changer. The microscope image was displayed via a video camera (Hitachi VK-C370) on a monitor and recorded on a videotape recorder (Sony, SVO-9600MD). Final magnification of the site was x2000. Diameter measurements were reproducible to ±0.3 µm, which is 
1–2% of the expected diameter.
Transverse arterioles of 40 µm maximum diameter were observed. Transverse arterioles were identified as previously described (24). Briefly, capillaries were initially identified, and traced back to their inflow arteriole. The inflow arteriole was traced back to its vessel of origin, and this branch arteriole was, in turn, traced back to its arteriole of origin. If more than 2 branches arose from that vessel, it was considered a transverse arteriole (which typically has 3–8 branches) (38). Our only selection criterion required that muscle fibers associated with the transverse arteriole run approximately perpendicular to the vessel. This architecture is common and can be found in all areas of the tissue preparation.
Muscle fiber bundles (3–5 fibers) were stimulated directly using a platinum wire microelectrode (tip diameter 25 µm), which was placed in close proximity to, but not touching, muscle fibers running approximately perpendicular to the arteriole. The microelectrode was positioned at least 1000 µm away from the chosen site of the arteriole/stimulated muscle fiber intersection. Curare was added to the superfusate to ensure direct electrode stimulation of the skeletal muscle cells and not nervous stimulation of the muscle fibers. Blocking nicotinic cholinergic membrane receptors on the skeletal muscle ensured that if a motor nerve were stimulated by the electrode, then the resulting acetylcholine release would not stimulate skeletal muscle cell contraction. Therefore the addition of curare isolated any muscle contraction to the control of the electrode only. The ground electrode was placed in the superfusate around the outer rim of the tissue support pedestal. Each stimulus was a square wave pulse of 0.4-ms duration and 4–10 V (Grass S48 stimulator, Quincy, MA).
The overall state of vascular responsiveness in each preparation was assessed. Only the data collected on preparations that clearly displayed arteriolar constriction to 10% oxygen and dilation to 10–4 M sodium nitroprusside were kept for further analysis (4% of all preparations were discarded). After each experiment, arteriolar diameters were recorded after 2 min of superfusion of the preparation with 10–4 M sodium nitroprusside (considered to be maximal diameter).
Hamster cremaster muscle in vitro. To establish the force-frequency relationship for the hamster cremaster muscle, hamsters were overdosed with pentobarbitol sodium, and the left cremaster was isolated, cut longitudinally, separated from the testis and epididymus, and cut into strips. The muscle strips were tied at each end with 4.0 surgical silk and arranged in the stimulating apparatus. The distal tie was attached to a fixed anchor and the proximal tie to a hollow, stainless steel rod. The stainless steel rod was attached to a force transducer [either model FT03, Grass Medical Instruments (Quincy, MA) or model 60–2995, Harvard Apparatus (Southmatic, MA)]. The force transducer was supported by a ratchet system, which allowed the transducer to be raised and lowered for the adjustment of the length of the muscle. The stimulating apparatus was placed in an organ chamber filled with Krebs-Henseleit solution, heated to 27°C, and aerated continuously with 95% O2-5% CO2. The Krebs-Henseleit solution contained in mMol/l: 118 NaCl, 4.69 KCl, 1.18 KH2PO4, 2.52 CaCl2, 1.18 MgSO4·7H2O, 24.76 NaHCO3, 11.1 glucose, and 10 U/l insulin with tubarine (curare) added to 0.3 mg/l. The pH of the solution ranged from 7.35 to 7.45.
Muscle strips were stimulated through stainless steel electrodes using a Model S80 stimulator (Grass Instruments, Quincy, MA). Each square wave pulse was 5 ms long and of supermaximal stimulation voltage (100 V). All contractions were isometric, and the length of each muscle was set for maximal tetanic force development at 40 Hz. Data were collected and analyzed using the MP100WSW data acquisition system and AcqKnowledge III software (Biopac Systems, Goleta, CA) on an IBM computer. Experiments were conducted after a 45–60 min equilibration period. At the end of each experiment, muscle length and wet mass were measured.
Experimental Protocols
Blood-perfused cremaster muscle in situ. Arteriolar diameter at the observation site was continuously recorded for 1 min prior to muscle stimulation, for 2 min during muscle stimulation and for 2 min after muscle stimulation. Muscles were stimulated using a stimulation pattern consisting of a contraction frequency, a train duration and a stimulus frequency (Table 1). Within any given experiment, a train duration and a contraction frequency were selected and the stimulus frequencies were varied randomly. A 5-min rest period was allowed between subsequent stimulus frequencies. Stimulation patterns were chosen to avoid producing a maximal arteriolar dilation (dilation equal to the sodium nitroprusside-induced dilation); therefore, the same combination of stimulation patterns are not tested at each contraction frequency (Table 1).
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Data Analysis and Statistics
All data are reported as means ± SE. Arteriolar diameters are expressed as change in diameter (diameter-baseline diameter) in micrometers. Baseline diameter was defined as the diameter just before muscle stimulation. Only one arteriole per preparation was used to collect data and n indicates the number of arterioles observed. All in situ experiments were videotaped and analyzed off line. Images were digitized and arteriolar diameters were measured via Image-Pro Plus software. Diameter was measured before stimulation, every 10 s during the 2 min of stimulation and every 30 s for 2 min after stimulation.
In hamster cremaster muscle strip experiments in vitro, force developed by each contraction was normalized to mN/mm2. Normalization of force to mN/mm2 involves dividing the force developed in grams by the weight of the muscle to calculate a force per cross-sectional area [mN/mm2 = grams x (muscle length/muscle weight) x gravity x muscle density]. The cremaster muscle is a sheet muscle 5 to 6 muscle cell layers thick with fibers oriented in many different directions; thus, when muscle strips are removed, their ends tied, and are then stimulated to contract, not every layer contributes to the generation of force, but all the muscle layers contribute to the muscle weight. The mass of the active, force-generating fibers is therefore being overestimated, and normalized force is being underestimated. If only one or two muscle cell layers are correctly oriented to contribute to measured force, normalized force may be be underestimated by 4–5 times. Given the error in estimating the force generated by these muscles, the rate of decrease in developed force in the control contraction period was used as a marker of the viability of the preparation rather than the absolute amount of force developed.
Group means were compared with a repeated measures ANOVA. If significance were found at the P < 0.05 level, a protected least squares difference test was used post hoc to analyze the data further. Linear and nonlinear (using classical equations to describe a hyperbola) regression analysis was used to determine the nature of the relationships between stimulation parameters and changes in diameter (36).
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RESULTS |
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The dilation that occurred over the 2-min stimulation period for each stimulus frequency for each stimulation parameter set is shown in Fig. 2. It is interesting to note that at least 40% of the total dilation occurred within the first 10 s in 43% of the arterioles and in 83% of the vessels 25% or more of the total dilation occurred within the first 10 s. Therefore, in most cases, there is a fast dilatory component early in the stimulation bout followed by a slower phase of dilation, secondary to this initial fast phase.
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A more direct indication that train duration had little effect on the magnitude of the dilation is shown in Fig. 3C. Figure 3C shows the relationship between frequency and the change in dilation at different train durations when the contraction frequency is constant at 6 cpm. Although some of the stimulus frequencies at 500 ms differ significantly from both 250 and 750 ms, the pattern and magnitude of the dilation between 250 and 750 ms do not differ. Thus the amount of dilation did not systematically differ when train duration was altered.
Figure 3D shows the effects of changing contraction frequency, with train duration constant (500 ms). The change in diameter across all stimulus frequencies at 6 cpm were significantly different than 24 cpm, and both showed an initial component from 4 to 20 Hz (500 ms, 6 cpm: 0.33 ± 0.03 µm/Hz; 500 ms, 24 cpm: 0.64 ± 0.09 µm/Hz) and a slower secondary component from 20 to 40 Hz (500 ms, 6 cpm: 0.02 ± 0.14 µm/Hz; 500 ms, 24 cpm: 0.01 ± 0.0001 µm/Hz). This differed from the dilatory pattern at 12 cpm, which was linear across all stimulus frequencies (slope = 0.38 ± 0.03 µm/Hz).
Figure 4 shows the relationship between stimuli per minute and change in diameter. This presentation allows for the comparison of the dilatory response across a wide range of possible stimulation patterns. The number of stimuli per minute was calculated as the product of the duration, stimulus frequency, and the contraction frequency. A direct comparison of the magnitude of the dilation associated with twitch unfused tetanic and fused tetanic contractions is highlighted in this figure. The type of contraction was determined by the in vitro force-frequency relationship. Five stimulation patterns, 250 ms at 4 Hz at 6 and 12 cpm and 500 ms at 4 Hz at 6, 12, and 24 cpm resulted in a series of single, individual twitch contractions, while the rest of the points represent unfused (below 30 Hz) or fused (30 Hz and above) tetanic contractions.
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Hamster cremaster muscle strips in vitro. In vitro cremaster muscle strip initial developed force averaged 94 ± 11.4 mN/mm2, and the rate of decrease in force during the 20-min control contraction protocol was 0.22 ± 0.07 mN·mm–2·min–1. This rate of decrease in force was similar to that of other isolated muscles contracting in vitro under similar stimulation conditions (25).
The in vitro relationship between force and frequency for the cremaster muscle showed that this muscle produced maximal force (a fused tetanic contraction) at 30 Hz. There was no significant difference of the force developed between different train durations at similar frequencies (data not shown).
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DISCUSSION |
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Microvascular response to muscle contraction. In this bioassay system, the initiation of the arteriolar dilations observed represent the production and release of dilatory signals by active skeletal muscle fibers. Because so few muscle fibers are stimulated to contract and because of the distance between the arteriole and the contracting muscle fibers (arteriole is either above or below the contracting muscle fibers), there are no vascular compressive forces exerted on the arteriolar or the venous vasculature; thus the muscle pump does not influence flow or dilation in this preparation. There may be a small role for flow-induced dilatory modulation of the vessel diameter over time, but only once the whole arteriole has dilated. If flow-induced dilation made a significant contribution to the dilations observed in this study, then there should be a time period at which the relationships between contraction parameters and vascular diameter should have a step increase, as new dilators are introduced, but this did not occur. Therefore, any contribution of flow-induced dilation was considered small and the majority of the dilatory response observed was attributed to products released from active skeletal muscle cells.
The nonlinearity of the dilations over time (2-min stimulation period) was expected. The changes in dilation over time are the result of the rate of production of dilators and their rate of removal either by degradation or removal by blood flow. Thus over time an equilibrium or steady state dilation would be reached. What was not expected, given this scenario, was the large percentage of the total dilation that occurred within the first 10 s. This large, early dilation may indicate that dilation is determined by certain factors early in the contraction bout but by different factors, as the muscle continues to contract over time. A variety of patterns of changes in blood flow have been observed (5), and these patterns were dependent on the contractile activity of the skeletal muscle. Large changes in flow were observed at the onset of contraction followed by either an increase, a decrease, or no change in flow depending on the contractile activity of the muscle. Similar patterns to each of these flow patterns were mimicked in the current experiments by the arteriolar dilatory response depending on the stimulation pattern of the muscle. Further studies will be required to better understand how blood vessels respond to muscle contraction within the first 10 s and what determines the pattern of dilation over time.
The relationship between vasodilation and stimulus frequency was not a simple linear relationship but a more complex curvilinear one. Vasodilation was dependent more on submaximal stimulus frequencies(below 30 Hz) than maximal stimulus frequencies. Given the metabolic hypothesis, whereby vasodilators are hypothesized to be by-products of skeletal muscle metabolism, it would be expected that if metabolism increased (i.e., an increase in ATP utilization) with an increase in stimulation frequency, then the amount of dilator produced should increase. Therefore, if a constant amount of vasodilator or vasodilators are released per stimuli or per action potential, then a positive, linear relationship between stimulus frequency and vessel diameter would be expected. The present data show that this occurred at stimulus frequencies up to 30 Hz but at higher stimulation frequencies (above 30 Hz) the slope of the relation decreased dramatically. The change in the relationship between vasodilation and stimulus frequency coincides with the stimulus frequency at which this muscle produces a fused tetanic contraction and maximal force.
The nonlinearity of the relationship between vasodilation and a wide range of stimulus frequencies could indicate that 1) there is not a constant release of dilator per stimulus (per action potential), 2) the type of dilator changes once the skeletal muscle tetanic contraction becomes fused and generates maximal force, and 3) changes in reactivity of the vascular smooth muscle occur. The change in vascular smooth muscle reactivity could be due to changes in the smooth muscle's ability to dilate as the smooth muscle cell changes length (the length-tension relation) (13, 34). Figure 1A shows a lack of relationship between the change in diameter to skeletal muscle contracting at 40 Hz and the baseline diameter of the vessels (from 5 to 30 µm). This figure demonstrates that a 25 µm difference in microvascular diameter (larger than the dilations induced in this study) does not significantly alter the vessels reactivity to skeletal muscle contractile activity. Thus it would appear that the length-tension relation of smooth muscle does not significantly impact the dilatory response to skeletal muscle contractile activity or the shape of the relationship between vasodilation and stimulation parameters. Changes in reactivity of the smooth muscle could also result from the saturation of processes such as receptor-mediated responses. Understanding the impact of this on the relationship between vasodilation and stimulus parameters would first require the identity of the vasodilators themselves. Further studies will be required to determine the cause of the nonlinearity of the relationship between stimulus frequency and vasodilation.
Contraction frequency was also a large contributor in determining the magnitude of the dilation. Given the metabolic hypothesis, if metabolism increased due to an increase in contraction frequency, then the amount of dilator produced should increase. There is evidence that the rate of ATP hydrolysis increases with a step increase in contraction frequency (15, 37), but how ATP hydrolysis changes over a range of contraction frequencies is unknown; thus, on the basis of metabolism, how contraction frequency effects dilator production is unknown. The relation between contraction frequency and vasodilation may be influenced by the time between contractions. At lower contraction frequencies, there is more time between contractions, therefore, more time for removal of the dilatory signal produced from the first contraction before the next contraction. At higher contraction frequencies the subsequent production of dilatory signal will be arriving at the blood vessel before the diameter has returned to precontraction values. Thus the relationship between contraction frequency and dilation is a complex function of multiple variables.
Train duration had very little impact on the magnitude of the microvascular dilation. If vasodilators are produced on the basis of the number of stimuli delivered, then at any given stimulus frequency, the longer the train of stimuli (train duration), the more stimuli would be delivered, thus longer train durations should produce larger dilations. This did not occur. Train duration had an inconsistent effect on the magnitude of the dilation, but the dilation in response to contractions of 250- and 750-ms-train duration were not significantly different. Thus train duration is not a large contributing factor in determining dilator production. There are reports to suggest that the duration of a contraction is not linearly related to metabolic cost of the contraction. Studies have repeatedly shown that brief, intermittent contractions produced a greater ATP turnover than longer sustained contractions (7, 9, 21, 29, 32, 33). It has been demonstrated that the rate of ATP hydrolysis decreased as the train duration increased (33). If metabolism is not directly related to train duration, then the amount of dilator produced via metabolism may not be directly related to train duration, and therefore, we would not expect to see dilation increase with increases in train duration.
In the present experiments, twitch (250 ms, 4 Hz), unfused tetanic contractions (4–20 Hz at most train durations), and fused tetanic contractions (30 Hz and above at any train duration) were used to stimulate the microvasculature. This range incorporated stimulation patterns that are physiologically relevant; however, a difficulty lies in comparing these different contraction types. For example, when comparing the amount of dilation at 20 Hz for 250, 500, and 750 ms, the result is 4, 10, and 15 stimuli per contraction which produce 40, 55, and 70% of maximal developed force, thus comparing points where the force generated, and possibly the metabolic state of the muscles, were very different. One approach to compare the different stimulation patterns is to plot the dilation as a function of the stimuli delivered per minute regardless of how they were delivered (6). The overall relationship between stimuli per minute and dilation was curvilinear whereby the slope of the relationship changes as stimuli per minute increases. Thus lower stimuli per minute were more instrumental in determining the magnitude of the change in dilation than high stimuli per minute; greater changes in dilation occurred with unfused tetanic contractions, but once the contraction was fused no further dilation occurred. This pattern is similar to the relationship between dilation over a range of stimulus frequencies, indicating, again, a difference in the vasodilatory response from unfused and fused tetanic contractions (or between submaximal and maximal force production). Vasodilatory responses have been shown to be determined by the total tension developed by muscle cells (39), tension being altered by changing stimulus frequencies from submaximal up to maximal, but the dilatory response to frequencies above maximal were not tested. Data presented here would predict that using frequencies above those necessary to produce maximal force would not produce a further increase in vasodilation. Whether force generation is a primary determinant driving vasodilation could not be tested with the current model but certainly requires further investigation.
Implications for dilator production.
If skeletal muscle metabolism is responsible for producing the vasodilators during hyperemia, then by altering the stimulus and contractile parameters of skeletal muscle, metabolism will also be altered, thereby potentially altering the vasodilators produced. Different metabolic byproducts may be produced as a result of the changes in metabolism that occur with different stimulation parameters. Possibly the most powerful parameter to change metabolism would be the duration of the contraction period. At the onset of contraction, the production and maintenance of ATP come from creatine phosphate; after 30 s of contraction, the primary source of ATP generation is from glycolysis and the longer the contraction bout continues, the greater the reliance on aerobic metabolism. Thus the potential for metabolic byproducts to change over time is dramatic. Other stimulation parameters such as contraction frequency (7, 9, 15, 29, 37) and train duration (9, 21, 29, 33) have been shown to have a significant impact on ATP hydrolysis and metabolism. It has even been suggested that metabolism fluctuates within the duration of a single contraction (10). In the present study, the nonlinearity of the relationships between contraction frequency and dilation and stimulus frequency and dilation may indicate that under specific stimulation conditions, and, therefore, metabolic conditions, the type of dilator is different. Therefore, depending on the metabolic profile produced within the muscle (determined by the stimulation pattern), it is possible for one metabolic vasodilator to be predominantly produced, but there may be other stimulation conditions in which it is not. Thus, to identify the dilators produced by active muscle fibers, careful consideration must be given to the stimulation and contraction parameters that determine metabolism.
In conclusion, this study has identified that the stimulation variables that have the greatest influence on vasodilation are the contraction frequency, submaximal stimulus frequencies, and the total contraction period duration, while train duration has little impact. These results suggest that magnitude of the dilation produced by skeletal muscle contraction cannot simply be described by a constant release of dilator per stimulus or per contraction and cannot be predicted by the number of stimuli (action potentials) or the contraction frequency alone. Evidence does support the idea that the type of contraction, unfused vs. fused tetanic contractions, is also a potential determinant of the magnitude of the vasodilation induced by muscle contraction. This may imply that force is also a determinant of the amount of vasodilation, as unfused tetanic contractions produce less force than tetanic contractions, but further studies are required to better understand this relationship.
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ACKNOWLEDGMENTS |
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FOOTNOTES |
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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.
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), 250 ms, 12 cpm (
), 500 ms, 6 cpm (
), 500 ms, 12 cpm (
), 500 ms, 24 cpm (
) and 750 ms, 6 cpm (
) and (A) baseline diameter, (B) the dilatory potential (maximum diameter-baseline diameter). B: The line indicates the maximum dilatory potential for each experiment.
), 20 Hz(
), 30 Hz(
), 40 Hz (
