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Difference between reciprocal inhibition and regular muscle movement?

Difference between reciprocal inhibition and regular muscle movement?



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I was looking into a condition I have, anterior pelvic tilt, quite a bit. I ran into a website describing part of the issue as reciprocal inhibition. This was my confusion:

Reciprocal inhibition, defined by just about everyone, is the relaxation of muscles antagonistic to muscles currently contracting, and vice versa. How is this different from regular muscular flex? When we flex a muscle, don't the antagonistic muscles relax to compensate, same as in reciprocal inhibition? Thanks.


What is the difference between reciprocal inhibition and regular muscle movement?

Reciprocal inhibition is part of regular muscle movement. It is controlled by the stretch reflex controlled by the muscle spindle. It's an important part of a functioning muscle and spinal cord, and not pathologic at all. However, this same reflex, in an excessively tight muscle on one end of a joint, would cause an excessively loose muscle on another end of a joint.

Here is an image showing this reflex, from Brust Practice of Neural Science, Chapter 6.

I can't give you any medical advice on this site, so I can't put that in context, but I think that answers your biology question.


Sonographer's Perspective of Evaluating Diastolic Function

ANNITTA J. MOREHEAD BA, RDCS , in Diastology , 2008

Isometric Hand Exercise

Isometric exercise such as a sustained handgrip is used to increase afterload. The patient should be instructed to squeeze rolled towels or tennis balls simultaneously in a squeeze/release, squeeze/release pattern and continue performing it until the maneuver yields an adequate response. The patient should not hold his breath or perform Valsalva while doing isometric exercise.

Physiologically, the hemodynamic effects of an isometric handgrip are related to decreased vagal tone and increased sympathetic tone. In a patient with normal diastolic function, performing an isometric handgrip causes increased heart rate, blood pressure, cardiac output, and venous reversal. Individual response depends on the amount of exercise, baseline LV function, and baseline hemodynamic state. In patients with baseline LV dysfunction, isometric exercise will increase LV filling pressures.


Age reduces cortical reciprocal inhibition in humans

Age alters the control of voluntary movement. A widely observed age-related adaptation is the heightened activation of the antagonist muscles during voluntary movements. We examined the possibility that age also modifies cortical reciprocal inhibition. In young (age 27, n=6) and old (age 73, n=6) adults a mild conditioning electrical stimulus was delivered to the median nerve at the elbow. The test stimulus, delivered by transcranial magnetic stimulation (TMS) at 1-ms increments between 11 and 24 ms after the electrical conditioning stimulus, evoked motor potentials (MEP) in the extensor carpi radialis (ECR) and flexor carpi radialis (FCR). The absolute TMS intensity, expressed as the percent of stimulator output, used to produce 1-mV control MEPs in the ECR was similar in young (mean 58.5, standard deviation ±12.8%) and old adults (60.3±20.3%, P=0.855). The size of the control MEP in the ECR was also similar in young (0.98±0.10 mV) and old subjects (0.90±0.14 mV, P=0.686). The age by conditioning interval interaction (P=0.001) showed that the MEPs in the ECR were significantly depressed at 14, 15, 16, 17, 18, and 19 ms (range 55.5--65.9% of control, all P<0.05) compared with control value of 100% and with old adults who showed no depression. The MEPs remained at control level in the FCR and were also unaffected in the first dorsal interosseus. These data confirm the existence of cortical reciprocal inhibition reported previously in young humans and show that age reduces this inhibition similarly to the previously reported reduction of spinal reciprocal inhibition reported in old adults. Activation of agonist and antagonist muscle pairs are most likely organized around a dual system of cortically and spinally mediated reciprocal inhibition that is altered by age. The data also indicate the need to use age-matched control subjects when comparing individuals with abnormalities resulting from disorders that occur at an old age.

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The Truth About PNF Techniques


Vol. 15 •Issue 26 • Page 40

Proprioceptive neuromuscular rehabilitation is more than just stretching and functional movement

Mention proprioceptive neuromuscular facilitation (PNF), and most clinicians think of stretching or functional movement patterns. While it is true that PNF focuses on stretching and functional movement, it is also much more. PNF techniques help develop muscular strength and endurance, joint stability, mobility, neuromuscular control and coordination-all of which are aimed at improving the overall functional ability of patients.

Developed in the 1940s, PNF techniques are the result of work by Kabat, Knott and Voss. 1-3 They combined their analysis of functional movement with theories from motor development, motor control, motor learning and neurophysiology. 1

To that end, PNF techniques have broad applications in treating people with neurologic and musculoskeletal conditions, most frequently in rehabilitating the knee, shoulder, hip and ankle. 4

Stretching Techniques

Stretching is a main component of PNF. In fact, PNF stretching is superior to other stretching techniques. 5-7

Neuromuscular inhibition procedures reflexively relax the contractile components of shortened muscles so patients can gain range of movement. Various techniques are used, among them:

Hold-Relax. Familiar to most clinicians, this technique involves lengthening a tight muscle and asking the patient to isometrically contract it for several seconds.

As the patient relaxes, the clinician lengthens the involved muscle further and holds the stretch at the newfound end-range of motion. This technique relies on the firing of the Golgi-tendon organ (GTO) to cause reflexive muscle relaxation. It’s easily applied and can be incorporated in home exercise and preventive programs.

But while activating the GTO can increase flexibility, it also may predispose the patient to injury. Specifically, PNF stretching can decrease activity of selected hamstring muscles. A sudden stretch, which might occur during functional activity, may predispose patients to increased risk of musculotendinous injury, if PNF stretching is applied directly before activity. 8

Hold-Relax with Agonist Contraction. This technique follows the same procedure as the Hold-Relax technique. However, after the tight muscle is contracted isometrically against the clinician’s resistance, the patient concentrically contracts the muscle opposite the tight muscle to actively move the joint through the increased range. 1 The clinician then applies a static stretch at the end of this new range of motion and repeats the process several times.

Agonist Contraction. With this stretch, the clinician passively lengthens the tight muscle (the antagonist) to its end-range. The patient then concentrically contracts the muscle opposite the tight muscle (the agonist) to move the joint to a new position in the range of motion. 1 The clinician applies mild resistance during this contraction, being careful to allow for movement through the range of motion. This technique uses reciprocal inhibition to encourage the tight muscle to relax and lengthen during agonist muscle contraction.

Of the three techniques, the Hold-Relax is the most frequently used. 4 But over the last decade, the Hold-Relax with Agonist Contraction has gained popularity. 4 Research indicates that sub-maximal contractions that are progressive in intensity over the course of a rehab program increase flexibility. 9 For the best results, clinicians should use PNF stretching early in the rehabilitation program and gradually increase the intensity of the contractions throughout the rehab process.

While clinicians know the difference between the three techniques, they often intermix terminology. For example, many clinicians and authors refer to Hold-Relax stretching as Contract-Relax stretching. Some even incorporate a concentric contraction of the tight muscle against minimal resistance before applying a second stretch.

This procedure, however, is incorrect and doesn’t allow for maximum gains in flexibility any firing of the GTO is negated by the time the person moves the extremity back to the starting point of the concentric contraction.

Strengthening Techniques

Along with stretching, PNF strengthens the body through diagonal patterns, often referred to as D1 and D2 patterns. It also applies sensory cues, specifically proprioceptive, cutaneous, visual and auditory feedback, to improve muscular response. 1 The diagonal movements associated with PNF involve multiple joints through various planes of motion. These patterns incorporate rotational movements of the extremities, but also require core stability if patients are to successfully complete the motions.

Two pairs of diagonal patterns exist. 10 These patterns can be performed in flexion or extension and are often referred to as D1 flexion, D1 extension, D2 flexion or D2 extension techniques for the upper or lower extremity. 1 Although patients can perform these patterns with many forms of resistance, the interaction between patient and clinician is key to the early success of PNF strengthening. 1

This interaction requires manual resistance throughout the range of motion through carefully positioned hand placement and appropriately choreographed resistance. By placing the hands over the agonist muscles, the clinician applies resistance to the appropriate muscle group, while guiding the patient through the proper range of movement. 1

In using manual resistance, the clinician can make minor adjustments as the patient’s coordination improves or fatigue occurs during the rehab session. In general, the amount of resistance applied is the maximum amount that allows for smooth, controlled, pain-free movement throughout the range of motion. 10 In addition to manual resistance strengthening, PNF diagonal patterns enhance proper sequencing of muscular contraction, from distal to proximal. This promotes neuromuscular control and coordination. 1

To enhance coordination, movement and stability, clinicians use numerous techniques during PNF exercises, among them:

Rhythmic stabilization. This technique, which incorporates passive movement of the joint through the desired range of motion, is a teaching tool to re-educate the neuromuscular system to initiate the desired movement. The technique begins with the clinician passively moving the extremity through the desired movement pattern at the desired speed several times. It then progresses to promote active assistive or active movement, with resistance, through the same pattern to help the patient improve coordination and control.

Slow reversal. This technique involves a dynamic concentric contraction of the stronger agonist muscle group. A second dynamic concentric contraction immediately follows, this time involving the weaker antagonist muscle group. 1 Rest periods don’t occur between contractions. Therefore, this technique promotes the rapid, reciprocal activities the agonist and antagonist muscle groups need for many functional activities.

Slow reversal hold. This technique adds an isometric contraction (hold) at the end-range of each muscle group. It’s especially beneficial in enhancing dynamic stability of the larger proximal muscle groups.

Alternating isometrics. This technique encourages stability of postural trunk muscles and stabilizers of the hip and shoulder girdle. With alternating isometrics, the patient “holds” his position, while manual resistance is alternately applied in a single plane from one side of the body to the other. No motion should occur.

Instead, the patient should maintain the starting position of the involved limb. This technique can strengthen the trunk, a single extremity or bilateral extremities, and can be applied with the limbs in the open- or closed-kinetic chain.

Alternating rhythmic stabilization. This technique is simply an extension of alternating isometrics in which the involved muscle groups co-contract. Rhythmic stabilization is most commonly performed in a closed-chain position to further enhance muscular co-contraction and joint stability. 1

With this technique, the clinician applies manual isometric resistance in a multidirectional pattern. The clinician may apply simultaneous manual resistance in multiple directions, forcing the multiple muscle groups to contract simultaneously to support and stabilize the extremity. This technique is particularly beneficial in isometrically contracting the proximal joint rotators. 1

PNF exercises can be applied to patients of all ages. Klein et al. found that using PNF techniques for older adults improved range of motion, isometric strength and selected physical function tasks. 11

Additional studies have shown that PNF stretching is superior to static stretching in improving hamstring flexibility in people 45 to 75 years of age. 12

One study compared PNF stretching to static stretching in active seniors. While static stretching and PNF stretching yielded gains in hamstring flexibility, PNF stretching was most beneficial in participants younger than 65. 13

Still another study demonstrated the value of PNF stretching vs. static stretching when comparing the techniques in Special Olympic athletes. 14

Whether promoting flexibility, developing muscular strength and endurance, improving joint stability or increasing neuromuscular control and coordination, PNF is a valuable part of every rehabilitation program. Proprioceptive neuromuscular facilitation encompasses all aspects of the rehabilitation process-and can help patients with various dysfunctions achieve their goals.


Results

All subjects completed all experimental conditions. None of the subjects experienced any side effects from TMS during the experiments.

Motor representational map

The RMTs of the FCR and ECR muscles were 46.0±1.6% and 43.6±5.0% of the maximum stimulator output, respectively. Map areas for the FCR and ECR muscles are shown in Figure 2. The reciprocal muscle areas clearly overlapped, although they were not identical. The CoG of the FCR was more laterally located than that of the ECR in 5 of 8 subjects. The CoG of the FCR was located at x (anteroposterior) = 6.5±2.6 mm and y (mediolateral) = 56.5±2.3 mm, and that of the ECR was at x = 4.5±3.6 mm and y = 56.4±2.7 mm. The midpoint between the CoGs of the FCR and ECR muscles was located at x = 5.3±3.0 mm and y = 56.4±2.3 mm.

The color code of each map of FCR (A) and ECR (B) muscles ranges from gray (0 mV) to white (0.5 mV or over). The map areas of the FCR and ECR muscles clearly overlapped, although they were spread differently. The center of gravity (black circle) of the FCR muscle was located at x (anteroposterior) = 6.5±2.6 mm and y (mediolateral) = 56.5±2.3 mm and that of the ECR muscle was located at x = 4.5±3.6 mm and y = 56.4±2.7 mm. FCR: flexor carpi radialis ECR: extensor carpi radialis.

Cortical excitability

The EMG traces of the right FCR and ECR muscles in one representative subject during the probabilistic reward task are shown in Figure 3. Peak-to-peak MEP amplitude of the FCR muscle at 2 s after the red fixation cross was the highest for 10% reward probability, whereas that of the ECR muscle was the lowest for 10% reward probability (top 2 rows). However, peak-to-peak MEP amplitude of FCR muscle at 1 s after reward stimuli was the highest for 90% reward probability, whereas that of the ECR muscle was the lowest for 90% reward probability (bottom 2 rows).

MEP amplitude of the FCR muscle at 2 s before response was the highest for 10% reward probability during the task, whereas that of the ECR muscle was the lowest for 10% reward probability. However, MEP amplitude of the FCR muscle at 1 s before response was the highest for 90% reward probability during the task, whereas that of the ECR muscle was the lowest for 90% reward probability. MEP, motor-evoked potential FCR, flexor carpi radialis ECR, extensor carpi radialis.

Relative MEP amplitudes for the FCR to ECR muscles during probabilistic reward tasks are shown in Figure 4 (A, B) and Table 1. Use of repeated measures ANOVA revealed a significant difference of probabilities at 2 s after the red fixation cross (F = 4.153, p = 0.016) and at 1 s after reward/non-reward stimuli (F = 1.86, p<0.0001). Post hoc testing showed relative MEP amplitude at 2 s after the red fixation cross was significantly higher for 10% reward probability than for 90% reward probability (p = 0.008), whereas relative MEP amplitude at 1 s after reward/non-reward stimuli was significantly higher for 90% reward probability than for 10% (p = 0.001) and 50% (p = 0.001) reward probabilities. Relative MEP amplitudes for the FCR and ECR muscles at 1 s after only reward stimulus presentation are shown in Figure 4C and Table 2. Use of repeated measures ANOVA revealed a significant difference of probabilities at 1 s after reward stimuli (F = 12.98, p<0.0001). Post hoc testing showed relative MEP amplitude at 1 s after reward stimuli was significantly higher for 90% reward probability than for 10% (p<0.0001) and 50% (p = 0.006) reward probabilities. However, relative MEP amplitudes for FCR and ECR muscles at 1 s after only non-reward stimuli presentation were not significantly changed (p = 0.225) (Figure 4D and Table 2).

Relative MEP amplitude at 2(A) and at 1 s after reward/non-reward stimuli (B) during the task. Relative MEP amplitude at 2 s after the red fixation cross was significantly higher for 10% reward probability than for 90% reward probability (p = 0.008) during the task, whereas relative MEP amplitude at 1 s after reward/non-reward stimuli was significantly higher for 90% reward probability than for 10% (p = 0.001) and 50% (p = 0.001) reward probabilities. Bar graphs of relative MEP amplitudes for FCR and ECR muscles at 1 s after only reward stimuli presentation (C) and only non-reward stimuli presentation (D) during the task. Relative MEP amplitude at 1 s after only reward stimuli presentation was significantly higher for 90% reward probability than for 10% (p<0.0001) and 50% (p = 0.006) reward probabilities. However, relative MEP amplitudes for FCR and ECR muscles at 1 s after only non-reward stimuli presentation were not significantly changed. MEP, motor-evoked potential FCR, flexor carpi radialis ECR, extensor carpi radialis.

Differences in RMT, relative MEP, SICI, and SAI before and after probabilistic reward tasks are shown in Table 3 and Figure 5. The changes in RMT of the FCR and ECR, relative MEP, SICI of the FCR and ECR, and SAI of the FCR and ECR for 10%, 50%, and 90% reward probabilities were small and were not significantly different before and after probabilistic reward tasks. However, SICI of the FCR was significantly decreased after 10% probabilistic reward tasks (p = 0.0008).

RMT of FCR (A) and ECR (B) for 10% reward probability, RMT of FCR (C) and ECR (D) for 50% reward probability, RMT of FCR (E) and ECR (F) for 90% reward probability, SICI of FCR (G) and ECR (H) for 10% reward probability, SICI of FCR (I) and ECR (J) for 50% reward probability, SICI of FCR (K) and ECR (L) for 90% reward probability, SAI of FCR (M) and ECR (N) for 10% reward probability, SAI of FCR (O) and ECR (P) for 50% reward probability, and SAI of FCR (Q) and ECR (R) for 90% reward probability. Only the SICI of the FCR was significantly decreased after 10% probabilistic reward tasks (p = 0.0008). RMT, resting motor threshold SICI, short-interval intracortical inhibition SAI, short-latency afferent inhibition FCR, flexor carpi radialis ECR, extensor carpi radialis.

Behavioral results

The mean reaction time was 913.3±17.3 ms for 10% reward probability, 931.8±14.7 ms for 50% probability, and 874.1±14.3 ms for 90% reward probability. Repeated measures ANOVA revealed no significant difference in reaction time between reward probabilities (F = 0.810, p = 0.446). Each subject received a total of 750 Japanese yen (about $7.5) at the end of the experiment.


Difference between reciprocal inhibition and regular muscle movement? - Biology

Determinants of Flexibility
Andersen (2006) suggests that the foundational determinants of flexibility are a multi-factorial cluster of elements . Recognizing and understanding these determinants of flexibility will help the exercise professional better determine the adequate flexibility goals for each client. It is also acknowledged that flexibility is a characteristic that is specific to each joint or group of joints, and thus not an absolute characteristic of all of the joints of the body. Further inspection of the association of age, gender and physical activity to flexibility is relevant to exercise professionals.

Age and Flexibility
Flexibility has been shown to decrease up to 50% in some joint areas with chronological age. From a population base of 1000 elderly men and women, Bassey et al. (1989) showed that shoulder abduction was reduced gradually and consistently with age, and is about 25% less than norms from a younger population. Eingauf et al. (1987) examined the changes in spinal mobility for 109 women aged 20 to 84 years. The results of this study indicated that spinal mobility decreased by 20%, 33% and 50% for anterior flexion, lateral flexion and extension, respectively. Brown and Miller (1998) showed that sit-and-reach range of motion decrease approximately 30% for women 20 to 70 plus years of age. Buckwalter (1997) proposes that a gradual deterioration in cell function in the cartilage, ligaments, tendons and muscles with age is the mechanism for this loss of flexibility. Misner and colleagues (1992) add that collagen, a main constituent of connective tissue, becomes dense (and stiffer) with aging. However, Bassey and associates suggest that this loss of motion can be minimized with regular stretching and range of motion exercise.

Gender and Flexibility
It has been shown that due to minor differences in joint structures and connective tissue anatomy, women have slightly greater range of motion than men for most joint motions. With a sample of 190 male and female subjects ranging in age from 18 to 88 years, Bell and Hoshizaki (1981) measured 17 joint actions in 8 specific joints. It was found that women did have greater overall flexibility then males. In assessment of the upper body joints (shoulder, elbow, wrist, trunk and neck) of a group of 41 subjects (22 young male and female subjects aged 25 to 35 years and 19 mature male and female subjects aged 65 to 80 years), Doriot and Wang (2006) also found females to have significantly greater range of motion in several joint actions. However, Doriot and Wang note that the effect of gender on range of motion is much less than that of age.

Physical Activity and Flexibility
For the most part, physically active individuals have greater flexibility in the joints they regularly utilize as compared to their physically inactive counterparts. Voorrips et al. (2009) confirmed with a population of 50 mature women (mean age 71 years) that those subjects who regularly did more walking (and more physically activity) had greater flexibility in the hip and spine (as assessed by the sit-and-reach test) than their less active counterparts. Kerrigan et al. (2001) declare these data suggest a very meaningful application with fall prevention. The researchers showed that hip tightness is associated with more falls, when comparing 16 elderly (8 men and 8 women average age = 77 years) subjects with a history of falling to 23 healthy non-fallers (10 men and 13 women average age = 73 years). The authors specifically recommend hip extension stretching as a necessary intervention for fall prevention in this population. Misner and colleagues (1992), in a 5-year long-term study with 12 women aged 50-71 years showed that regular exercise (15-30 minutes of stretching and 30-60 minutes of walking or water aerobics) 3 times per week for 5 years increased shoulder and hip range of motion significantly (3% - 22% in various joint actions). The authors add that exercise also helped the subjects perform activities of daily living much more efficiently. Indeed, ACSM (2006) recommends that preventive and rehabilitative exercise programs should include activities that promote the maintenance of flexibility.

What are the stretching methods to increase flexibility?
There are several known methods (and variations within each method) to increase flexibility including passive stretching, static stretching, ballistic stretching, dynamic stretching, proprioceptive neuromuscular facilitation (PNF) techniques, contract-relax stretching and resistance stretching.

Passive stretching is usually performed with a partner who applies a sustained stretch to a relaxed joint. Partner stretching requires close communication between client and exercise professional, and a slow application of the stretch in order to prevent a forceful manipulation of the body segment and possible injury.
Ballistic stretching involves a bouncy approach to reach the target muscle's endpoint of motion. A concern with ballistic stretching usage is that it is often performed in a jerky, bobbing fashion that may produce undesirable tension or trauma to the stretched muscle and associated connective tissues. It may produce a potent stretch reflex (see Side Bar 1. Question #10 for detailed explanation) that will oppose the muscle lengthening.

Dynamic stretching incorporates active range of motion movements that tend to resemble sport-specific or movement-specific actions. For instance, a volleyball player might do some shoulder flexion/extension actions prior to playing in a volleyball game. Thus the rhythmic nature of a controlled dynamic stretch has a functional application due to its similarity to the primary movement task. Dynamic stretching is often incorporated in the 'active' phase of Group X class warm-ups.

Static, or hold stretching is probably the most commonly used flexibility techniques and is very safe and effective. With this technique, a muscle or muscle group is gradually stretched to the point of limitation (a mild even strain), and then typically held in that position for a period of 15 to 30 seconds.

PNF stretching techniques were developed by Dr. Herman Kabat in the 1950's as part of his therapeutic work with patients suffering from paralysis and muscular diseases (Sharman, Cresswell, and Rick, 2006). There are several variations of PNF stretching. The contract-relax method involves initially contracting the target muscle followed by relaxing and stretching the target muscle with an assist from a partner or applied force such as a towel or rope. A variation of the contract-relax method is to perform a contraction of the OPPOSING muscle (muscle on opposite side of joint) during the stretching phase of the target muscle to take it to a new endpoint of motion (further increase in stretch). This method is referred to as the contract-relax agonist-contract method (Sharman, Cresswell, and Rick, 2006). Importantly, traditional PNF techniques involve doing the stretches in diagonal or spiral motions to promote movement through various planes of motion. See Focus Box 1 to read about the proposed neurophysiological mechanisms of PNF stretching.

Contract-relax techniques follow the same 'contract-relax' methodology of PNF stretching, although the movement pattern tends to involve a single-joint motion through one plane.

Resistance stretching has gained much media attention and exercise professional interest. This is the stretching/strengthening technique that 4-time Olympic swimmer sensation Dara Torres endorses as an important component of her training success. Resistance stretching focuses on contracting the target muscles as they are lengthened. In the first phase of this technique, the target muscles are placed in the shortened position. In this position the client CONTRACTS the target muscle(s). While contracted, the muscle is taken through a full range of motion (lengthened). So, resistance stretching incorporates a strengthening component through the entire range of motion. In essence, it is a carefully performed ECCENTRIC contraction (with a skilled professional). The originators of resistance training incorporate some very detailed rotational patterns (to challenge the muscle in multiple planes) with this particular technique. For more information and resources on resistance stretching the IFJ reader is referred to this web site: http://www.innovativebodysolutions.com/

Controversial Issues of Flexibility
The most controversial issues with flexibility include injury avoidance, muscle soreness prevention, muscular strength training and performance improvement. Several hundred studies have been conducted on these topics from randomized, controlled studies (the most powerful form of evidence) to those from general observation (the least certain type of evidence). To specifically address these controversial questions, recent review articles published in influential peer-reviewed publications were selected for this article. The efficacy of this approach is that review articles rigorously evaluate and summarize findings across a number of scientific studies and provide the overall 'state of knowledge' on a specific topic.

The impact of pre-exercise stretching on injury risk
Perhaps one of the most exhaustive and comprehensive research reviews on the impact of stretching and sport injury risk was completed by Thacker et al. (2004). The authors conclude that pre-exercise stretching does not prevent injury among competitive or recreational athletes. Thacker and colleagues add that the theories explaining why pre-exercise stretching prior to exercise may not prevent injury propose there is an alteration in joint connective tissue compliance (ability of the tissue to extend appropriately in response to applied pressure). In some cases this alteration may lead to greater joint instability. Thacker and colleagues point out that studies incorporating a pre-exercise combination of resistance exercise, body conditioning and warm-up show promise for better injury prevention. Perhaps this will be a new direction for fitness professionals to pursue.

The impact of stretching on preventing or reducing muscle soreness
Herbert and de Noronha (2009) summarize that stretching before and after exercise has not been shown to impart any additional protection from muscle soreness. Therefore, stretching does not lesson some of the mechanisms of muscle soreness including damage to the ultra structure of muscle, accumulation of calcium ions, cell inflammation, swelling and activation of pain receptors.

The impact of stretching on muscular strength
Although stretching and strength training are recommended as part of any comprehensive training program, better ways to include them in a training session are now being realized. When viewing the acute (immediate) effects of stretching before strength training, Rubini, Costa and Gomes (2007) note that the research indicates that static and PNF stretching (which is what most of what studies have utilized) have shown decreases in MAXIMAL strength from 4.5% to 28%. Yet most of this research has used more than one stretching exercise for the same muscle group with total stretching times of 120 to 3600 seconds, which is much more than recommended for optimal flexibility increases (according to ACSM (2006), 4 stretches of 30 seconds totaling 120 seconds is optimal). Rubini, Costa and Gomes add that when the total flexibility session is shorter (from 30 seconds to 480 seconds) the research shows little or no compromise from stretching right before maximal force production. Importantly (and practically), exercise enthusiasts do not train daily to their maximal voluntary contraction, where compromises in strength are observed in the research. Interestingly, Rubini and colleagues highlight there is no scientific consensus in the research for the underlying mechanism explaining the force production loss in muscle after stretching.

The impact of stretching on performance
The studies investigating flexibility and sport performance center attention on the areas of jumping ability, torque (rotary force), running economy and maximal force production. Shrier (2004) reviewed 23 studies, which when combined have included static, PNF, and ballistic stretching techniques with both genders (from children through adults) of untrained individuals to highly competitive athletes. The findings of this research, which is supported by other reviews (Haff, 2006), reveals that regular stretching, when performed at times other than BEFORE performance, may elicit positive long-term performance outcomes. However, pre-performance stretching may educe insignificant or negative performance outcomes.

Final Thoughts
This article symbolizes an important triumph for applied research. For many decades, coaches, athletes and others have touted numerous benefits of flexibility. As seen in similar disciplines, the empirical beliefs of key pioneers often guide the field. However, as observed with flexibility, many of these beliefs have not been shown to be accurate when challenged through the benchmark of scientific investigation. This does not minimize the importance of flexibility as a component of fitness, yet it better directs the exercise professional how to incorporate it into program designs for clients.

Focus Box 1. Proposed mechanisms of PNF stretching: A controversy continues!
The proposed mechanism of PNF stretching involve two neurophysiological phenomenon referred to as autogenic inhibition and reciprocal inhibition (Sharman, Cresswell, and Rick, 2006). Autogenic inhibition, also called the 'reverse myotatic reflex,' refers to a reduction (or inhibition) in excitability of a contracting muscle. This inhibitory input comes from the sensory receptors in the tendons (of the target muscle) known as the Golgi tendon organs. Thus, in the contract phase of the contract-relax PNF stretch, the target muscle (to be stretched) is contracted, which elicits autogenic inhibition. This is followed by a stretch to the target muscle (thus having inhibited neural input and allowing for greater range of motion). Reciprocal inhibition involves the 'agonist-contract' phase of the contract-relax agonist-contract PNF method. When the opposing muscle contracts, it is felt that inhibitory messages are signaled to the target muscle to relax (thus allowing for a lengthened stretch). Therefore, the thought is the more the muscle can be relaxed through autogenic inhibition and reciprocal inhibition, the more the muscle can be lengthened, and the greater the gains in flexibility (Haff, 2006).
The controversial plot 'thickens'
In a contemporary review article, Gordon Chalmers (2004) argues that the historical explanation of autogenic and reciprocal inhibition are convenient explanations, but recent decades of research denote that a much more complex neuromuscular response is in play. He states that the research shows that possible viscoelastic properties of muscle (see Focus Box 2 for more on viscoelastic) and an unexplained phenomenon known as 'stretch tolerance' are possible mechanisms observed with acute changes in range of motion from PNF stretching. Shrier (1999) continues that stretching may elicit an 'analgesic effect', resulting in an increased pain threshold (or pain tolerance) without actual changes in muscle stiffness to stretch. This 'analgesic effect' hypothesis is referred to as 'stretch tolerance'. Clearly more sophisticated research is needed to identify and understand this new hypothesis with stretching.

Focus Box 2. What are the 'viscoelastic' properties of muscle?
Muscle is composed of viscous (sarcoplasm), elastic (muscle filaments) and nonelastic (connective tissue) fibers. The elastic properties of muscle are very similar to a spring (Chalmers, 2006). A spring will lengthen in direct proportion to an applied force, and return to its natural resting length upon release of the force. When a muscle is stretched, the passive resistance to the elongation of the stretch is referred to as 'stress relaxation.' With sustained holding of the stretch, the muscle will gradually elongate, a viscoelastic property known as 'creep.' Clalmers explains that when a stretch is sustained, there is a reduction (about 30%) in the 'stress relaxation' (thus a transitory relaxation in muscle tension). Woods, Bishop and Jones (2007) underscore that the greater increases in muscle length are within the first 15 minutes after completing three, 30-second static stretches. Viscoelastic properties of muscle show that a muscle will provide its greatest resistance to stretch when the stretch is applied rapidly thus the scientific rational for slow stretching of a muscle (Chalmers, 2006). With regular, long-term stretching there are proposed viscoelastic changes in the surrounding connective tissue and tendon (attached to the target muscle), which slightly increase the elasticity of the muscle-tendon unit (Kubo, et al. 2001). De Deyne (2001) concludes that other cellular and molecular biological changes occur in muscle including the addition more sarcomeres (structural unit of a muscle cell) to muscle.

Side Bar 1. Frequent Questions and Answers on Flexibility
1) How long should you hold a stretch for flexibility improvement? In review of the existing scientific literature, ACSM (2006) recommends holding a stretch from 15 to 30 seconds.
2) What are the optimal times to repeat a stretching? According to ACSM (2006), two to four repetitions is optimal as further repetitions do not elicit additional benefits.
3) How many days per week should someone stretch? The range of motion demands of each person differs, but ACSM (2006) suggests 2 to 3 days per week as a minimum. ACSM continues that 5 to 7 days per week of some type of stretching routine would be the ideal for most persons.
4) What is hypermobility syndrome? Hypermobility syndrome is a congenital (present at birth but not necessarily hereditary) laxity of some ligaments and joints. It occurs most frequently in the knees, elbows, wrists, hands and ankles (Adib et al., 2005).
5) What are proprioceptors? The specialized nerves that communicate information about the musculoskeletal system to the central nervous system are called proprioceptors. Proprioceptors (also called mechanoreceptors) are the source of all proprioception, which is the perception of one's own body position and movement. Proprioceptors are found in all nerve endings of the joints, muscles, and tendons. The proprioceptors related to stretching are located in the tendons (Golgi tendon organs) and in the muscle fibers (muscle spindles).
6) What is the best flexibility method? In a review of 27 peer-reviewed studies on these range of motion techniques, Thacker et al. (2004) noted that all methods have been shown to be very effective in improving range of motion with no clear best method. In fact, several studies show PNF to be superior to static and dynamic where as other studies have show equal effectiveness of several stretching methods (Haff, 2006). However, Sharman, Cresswell, and Rick (2006)
contend that since PNF stretching improves passive and active range of motion, it may provide additional functional benefits.
7) When doing PNF stretches, do you maximally contract the target muscle? Conventionally, maximal contractions have been recommended because it was felt that the Golgi tendon organs (receptors in the tendon of muscle-tendon units) only respond to high forces. In fact, the Golgi tendon organs are sensitive to very low forces, and a contraction of as little as 20% to 70% of maximal contraction will suffice (Sharman, Cresswell, and Rick, 2006). The lower intensity of contractions will help to reduce the risk of any type of injury from the PNF stretching.
8) Does the research suggest the best application of PNF stretching? Evidence-based research provides the following recommendations (Sharman, Cresswell, and Rick, 2006).
a. Static contraction duration of the target muscle 3 to 15 seconds
b. Contraction intensity of target muscle from 20%-70% (see #7 for explanation). Sharman, Cresswell, and Rick (2006) note that there is evidence that progressive increases of intensity (within the 20%-70% range) may provide greater gains in range of motion.
c. Opposing muscle contraction intensity: no studies have investigated this phase of PNF stretches
d. One complete repetition seems to be sufficient (i.e., ONE contract-relax or ONE contract-relax agonist-contract)
9) Will heat packs before stretching enhance the range of motion? Knight and colleagues (2001) compared active stretching, static stretching, hot packs (superficial heat before stretching), and ultra sound (deep heat before stretching) of the plantar-flexor muscles with ninety-seven (59 women, 38 men) subjects who had limited dorsiflexion range of motion. All groups increased active and passive range of motion with the deep heat intervention being the most effective.
10) Please explain the stretch reflex. As a muscle is stretched, so is the muscle spindle (which runs parallel to muscle fibers). The muscle spindle records the change in length (and speed of length change) and transmits this signal to the spinal cord. This triggers the stretch reflex (also called the myotatic stretch reflex), which initially attempts to oppose the change in muscle length by causing the stretched muscle to contract. The more sudden the change in muscle length, the stronger the muscle contraction. Thus the muscle spindle attempts to protect the muscle from injury. One of the reasons for holding a stretch for a sustained period of time (15-30 seconds) is that the muscle spindle gradually becomes accustomed to the new length, and reduces its opposing signaling, thus allowing for greater muscle lengthening.

Side Bar 2. Warm-up versus stretching: Let's clear up the confusion
The workout warm-up and flexibility (stretching) component of a workout should not be confused. Warming up before exercise is the essential preparation needed to augment the workout. Thacker and colleagues (2004) state that the warm-up is physical activity that increases blood flow (vasodilatation) to working tissues, velocity of nerve impulses to muscles, and delivery of oxygen and foodstuffs for energy liberation. This increase in blood flow also enhances the removal of waste products from muscle. Combined altogether, Thacker et al. submit that these changes prepare the body for vigorous exercise by enhancing the muscle's metabolic (reactions to make ATP) properties and enhancing the mechanical efficiency of muscle contraction and force production. Safran et al. (1988) demonstrated (from their research with an animal model) that warming up is an imperative pre-exercise injury prevention component because it increases the elasticity of the muscle-tendon unit. Contrariwise, the purpose of stretching, as described throughout this article, is to increase of range of motion about a joint and group of joints. Woods, Bishop and Jones (2007) state that the warm-up should be at a relative intensity of 40-60% of a person's VO2max, perhaps inducing some mild sweating without fatigue.

Side Bar 3. Flexibility Guidelines for the Exercise Professional
Here are some useful stretching guidelines for exercise professionals to consider with their clients' stretching programs. Note, some guidelines are NOT appropriate all methods. For example, the resistance stretching technique involves muscle contracting throughout the range of motion, which is quite different from traditional stretching methods.
1. Assess your client's flexibility in order to pinpoint strengths and weaknesses.
2. Design a stretching program that enables a client to boost her/his physical activity and/or sport participation.
3. Make sure the muscles are appropriately warmed up before taking them through any muscle stretching technique.
4. Perform stretching minimally 2 to 3 times per week, and ideally 5 to 7 days per week.
5. Stretch all the major muscle groups as well as opposing muscle groups.
6. Focus on the muscles involved in the stretch, minimizing the movement of other body parts.
7. Hold stretches between 15 and 30 seconds.
8. Stretch to the limit of movement, not to the point of pain. This is referred to as the "endpoint" of the stretch.
9. Keep the breathing slow and rhythmical while holding stretches. Instruct the client to EXHALE slowly as they extend to the endpoint of the stretch. Explain that as a person exhales the diaphragm muscle and thoracic cavity muscles are relaxing, thus promoting a more effective relaxation of the target muscles during the stretch.
10. Stretch the muscles in various positions, as stretching in different planes may improve the overall range of motion at the joint.
11. Incorporate some stretches that attempt to relax the target muscle before going into the stretch. This may be accomplished by taking the muscle out of a weight bearing and/or body stabilization position prior to the stretch.
12. Stretch after each vigorous workout to encourage mind and body relaxation.
13. If the stretch yields pain in the joint area, back off the movement and make sure the stretching technique is correct. It may be necessary to try another position or a different stretching exercise (or method) for the target muscles.

Bio:
Len Kravitz, Ph.D., is the Program Coordinator of Exercise Science and Researcher at the University of New Mexico where he recently won the "Outstanding Teacher of the Year" award. Len was honored with the 1999 Canadian Fitness Professional “International Presenter of the Year” and the 2006 Canadian Fitness Professional “Specialty Presenter of the Year” awards and chosen as the American Council on Exercise 2006 "Fitness Educator of the Year”.

References:
ACSM. (2006). ACSM's Guidelines for Exercise Testing and Prescription (7th ed.). Philadelphia: Lippincott Williams & Wilkins.

Adib, N., Davies, K., Grahame, R., Woo, P. Murray, K.J. 2005). Joint hypermobility syndrome in childhood. A not so benign multisystem disorder? Rheumatology, 44(6), 744-750.

Andersen, J.C. (2006). Flexibility in performance: Foundational concepts and practical issues. Athletic Therapy Today, 11(3), 9-12.

Bassey, E.J., Morgan, K., Dallosso, H.M., and Ebrahim, S.B. (1989). Flexibility of the shoulder joint measured as range of abduction in a large representative sample of men and women over 65 years of age. European Journal of Applied Physiological and Occupational Physiology, 58(4), 353-360.

Bell, R.D., and Hoshizaki, T.B. (1981). Relationships of age and sex with range of motion of seventeen joint actions in humans. Canadian Journal of Applied Sport Sciences, 6(4), 202-206.

Brown, D.A. and Miller, W.C. (1998). Normative data for strength and flexibility of women throughout life. European Journal of Applied Physiological and Occupational Physiology, 78(1), 77-82.

Buckwalter, J.A. (1997). Maintaining and restoring mobility in middle and old age: the importance of the soft tissues. Instructional Course Lectures, 46, 459-469.

Chalmers, G. (2004). Re-examination of the possible role of golgi tendon organ and muscle spindle reflexes in proprioceptive neuromuscular facilitation muscle stretching. Sports Biomechanics, 3(1), 159-183.

De Deyne, P.G. (2001). Applications of passive stretch and its implications for muscle fibers. Physical Therapy, 81(2), 819-827.

Doriot, N. and Wang, X. (2006). Effects of age and gender on maximum voluntary range of motion of the upper body joints. Ergonomics, 49(3), 269-281.

Einkauf, D.K, Gohdes, M.L., Jensen, G.M. and Jewel, M.J. (1987). Changes in spinal mobility with increasing age in women. Physical Therapy, 67(3), 370-375.

Haff, G.G. (2006). Roundtable discussion. Flexibility training. Strength and Conditioning Journal, 28(2), 64-85.

Herbert, R.D. and de Noronha, M. (2009). Stretching to prevent or reduce muscle soreness after exercise (Review). The Chochrane Collaboration, 1, 1-31.

Kerrigan, D.C., Lee, L.W., Collins, J.J., Riley, P.O., and Lipsitz, L.A. (2001). Reduced hip extension during walking: Healthy elderly and fallers versus young adults. Archives of Physical Medicine and Rehabilitation, 82, 26-30.

Knight, C.A., Rutledge, C.R., Cox, M.E., Acosta, M., and Hall, S.J. (2001). Effect of superficial heat, deep heat, and active exercise warm-up on the extensibility of the plantar flexors. Physical Therapy, 81(6), 1206-1214.

Kubo, K., Kaneshisa, H., Kawakami, Y., and Fukunaga, T. (2001). Influence of static stretching on viscoelastic properties of human tendon structures in vivo. Journal of Applied Physiology, 90, 520-527.

Misner, J.E., Massey, B.H., Bemben, M., Going. S., and Patrick, J. (1992). Long-term effects of exercise on range of motion of aging women. Journal of Orthopedic & Sports Physical Therapy, 16(1), 37-42. 213-224.

Rubini, E.C., Costa, A.L.L., and Gomes, P.S.C. (2007). The effects of stretching on strength performance. Sports Medicine, 37(3), 213-224.

Safran, M.R., Garrett, W.E., Seaber, A.V., Glisson, R.R., and Ribbeck, B.M. (1988). The role of wamup in muscular injury prevention. American Journal of Sports Medicine, 16(2), 123-129.

Sharman, M.J., Cresswell, A.G., and Riek, S. (2006). Proprioceptive neuromuscular facilitation stretching: Mechanisms and clinical implications. Sports Medicine, 36(11), 929-939.

Shrier, I. (2004). Does stretching improve performance? A systematic and critical review of the literature. Clinical Journal of Sports Medicine, 14(5), 267-273.

Shrier, I. (1999). Stretching before exercise does not reduce the risk of local injury. A critical review of the clinical and basic science literature. Clinical Journal of Sports Medicine, 9(4), 221-227.


Effective Stretching

To work with postural/phasic theory, it is essential to have good stretching techniques and teaching skills and to visualize the functional pathway of a muscle. In the above example, the rectus femoris is the only postural muscle of the quadriceps group. As a biarticular muscle, the stretch for it must take into account both the hip and the knee joints.

(The familiar heel-to-buttock stretch applies only to the short quads.) The long quads require a kneeling (Figure 1) or side-lying position (Figure 2) in which, in its ideal configuration, the hip joint is at least in neutral extension and the knee joint flexed to 90 degrees. The stretch should be held for at least 30 seconds, performed at least twice and be supervised in the learning stage. Trainers should coach their clients to gradually develop the full resting length in this intensive stretching exercise.


Range of Motion and Flexibility

Jeff G. Konin PT, PhD, ATC, FACSM, FNATA , Brittany Jessee PT, DPT , in Physical Rehabilitation of the Injured Athlete (Fourth Edition) , 2012

Proprioceptive Neuromuscular Facilitation Techniques

PNF can be defined as a method of promoting or hastening the response of neuromuscular mechanisms through stimulation of mechanoreceptors. 56, 87 PNF stretching techniques are based on a reduction in sensory activity through the spinal reflexes to cause relaxation of the muscle to be stretched. Sherrington's principle of reciprocal inhibition demonstrates relaxation of the muscle being stretched (agonist) through voluntary concentric contraction of its opposite (antagonist) muscle. 56, 64, 70 Many studies 58, 59-61, 64-68 , 70, 71, 88, 89 support the efficacy of PNF and show greater increases in flexibility when PNF is used rather than static or dynamic stretching techniques. Other investigations 57, 62, 63, 69, 72 have found PNF to be at least as effective as other types of stretching. Originally, PNF was described as a rehabilitation technique for those recovering from neurologic disorders, 56 but the technique has the capability of being used for various orthopedic conditions as well. 66, 68, 90-97

PNF patterns can be performed in a single plane, such as flexion-extension, or in rotational and diagonal patterns that incorporate multiple planes and synergistic patterns ( Table 6-1 ). PNF techniques generally consist of five 5-second trials of passive stretching followed by a 5- to 10-second maximal voluntary contraction, as indicated by the technique used. The work of Cornelius et al 59 has shown that significant increases in systolic blood pressure occur after three trials consisting of a protocol of 5 seconds of passive stretching, followed by a 6-second maximal voluntary antagonist contraction. Thus, caution is warranted when one works with populations who have a predisposition to cardiovascular conditions.

Contract-relax

The contract-relax technique 61, 65, 66, 87, 98 produces increased range of motion in the agonist pattern by using consecutive isotonic contractions of the antagonist. Box 6-3 outlines how this technique is performed.

The procedure is repeated several times, followed by the athlete moving actively through the obtained range ( Fig. 6-9 ). When performing the contract-relax technique, the clinician must maintain proper stabilization to ensure that an isometric contraction occurs.

Hold-relax

Hold-relax 56, 58, 59, 98 is a PNF technique used to increase joint range of motion that is based on an isometric contraction of the antagonist performed against maximal resistance. This technique is done in the same sequence as the contract-relax technique, but because no motion is allowed on isometric contraction, this is the method of choice when joint restriction is accompanied by muscle spasm and pain. The intensity of each contraction is gradually increased with each successive repetition ( Fig. 6-10 ).

Slow reversal hold-relax

The slow reversal hold-relax technique 56, 87 uses reciprocal inhibition, as does the hold-relax technique. Box 6-4 outlines how this technique is performed. The technique is good for increasing range of motion when the primary limiting factor is the antagonist muscle group ( Fig. 6-11 ).


Sir Charles Sherrington

That a muscle on irritation of its nerve contracts had already long been familiar to physiology when the 19th century found a nerve which when irritated prevented its muscle from contracting. This observation seemed for a time too strange to be believed. Its truth did not gain acceptance for ten years but at last in 1848 the Webers accepted the fact at its face value and proclaimed the vagus nerve to be inhibitory of the heart muscle. Two hundred years earlier Descartes, in writing the De Homine, had assumed that muscle was supplied with nerves which caused muscular relaxation. An analogous suggestion was put forward by Charles Bell in 1819. The inhibition suggested was in each case “peripheral”. “Peripheral” inhibition, despite its inherent probability, was however to prove void of the fact for skeletal muscle. As just said, it did in fact prove true for the heart it was found somewhat later to hold good likewise for visceral muscle and, somewhat later still, was found for the constrictor muscles of the blood vessels. Peripheral inhibition became thus by the sixties and seventies of the 19th century a recognized fact, save for the one important exception of the skeletal muscles.

The first experimental indication of inhibition as a process working within the nervous system itself appeared in 1863. Setschenov then noted in the frog that the local reflexes of the limb are depressed by stimulation of the exposed midbrain. Later (1881), somewhat similarly, stimulation of the foot (dog) was found to restrain movements of the foot excited from the brain (Bubnoff and Heidenhain). Matters had, broadly put, reached and remained at that stage, when in the century’s last decade experimental examination of mammalian reflexes detected (1892) examples of inhibition of surprising potency and machine-like regularity, readily obtainable from the mammalian spinal cord in its action on the extensors of the hind limb the inhibitory relaxation of the extension was linked with concomitant reflex contraction of their antagonistic muscles, the flexors. This “reciprocal innervation” was quickly found to be of wide occurrence in reflex actions operating the skeletal musculature. Its openness to examination in preparations with “tonic” background (decerebrate rigidity) made it a welcome and immediate opportunity for the more precise study of inhibition as a central nervous process.

The seat of this inhibition was soon shown to be central, e.g. for spinal reflexes, in the grey matter of the spinal cord. The resulting relaxation of the muscle was found to be both in range and nicety as amenable to grading as is reflex contraction itself. In other words the inhibitory process was found capable of no less delicate quantitative adjustment than is the excitatory process. In “reciprocal innervation” the two effects, excitation and inhibition, ran broadly pari passu a weak stimulus evoked weak inhibitory relaxation along with weak excitatory contraction in the antagonist muscle a strong stimulus evoked greater and quicker relaxation accompanying greater and speedier contraction of the antagonist. No evidence was forthcoming that the centripetal nervous impulses which on their central arrival give rise to inhibition differ in nature from nerve impulses giving rise centrally to “excitation”, or indeed differ from the impulses travelling nerve fibres elsewhere. An “inhibitory” afferent nerve emerged simply as an afferent nerve whose impulses at certain central loci cause, directly or indirectly, inhibition, while at other central loci the same nerve, probably even the same nerve fibre can produce excitation. There was no satisfactory evidence that an afferent nerve fibre whose end-effect is inhibitory ever for its end-effect at that same locus evokes excitation or indeed any other effect than inhibition. That is to say its inhibitory influence never changes to an excitatory influence, or vice versa. Fixity of central effect, inhibitory or excitatory respectively, has to be accepted for the individual afferent fibre acting in a specified direction, i.e. on a specified individual effector unit. That does not of course exclude the contingency that an inhibitory influence on a given unit may under some circumstances be unable to produce effective inhibition there owing to its being too weak to overcome concurrent excitation.

I will not dwell upon the features of reciprocal innervation they are well known. I would only remark that owing to the wide occurrence of reciprocal innervation it was not unnatural to suppose at first that the entire scope of reflex inhibition lay within the ambit of the taxis of antagonistic muscles and antagonistic movements. Further study of central nervous action, however, finds central inhibition too extensive and ubiquitous to make it likely that it is confined solely to the taxis of antagonistic muscles.

In instance let us take a reflex especially facile and regular to type, the well-known spinal flexion-reflex of the leg, evoked by stimulation of any afferent.280 1932 nerve of the leg itself Its experimental stimulus may be reduced to a single induction shock evoking a single volley of centripetal impulses in the bared afferent nerve. The reflex effect, observed in an isolated flexor muscle, e.g. of the ankle, is apart from exceptional circumstances, a single contraction wave indicating discharge of a single volley of motor impulses from the spinal centre. This “twitch-reflex”, recorded isometrically by the myograph, exhibits a tension proportional to the number of motor units engaged, in other words to the size of the single centrifugal impulse volley. The contraction of each motor unit is on the all-or-nothing principle. The maximal contraction-tension for the reflex twitch will be reached only when all of the motor units composing the muscle are activated. The contraction-tension developed by the reflex being proportional to the number of motor units engaged, an average contraction-tension value for the individual motor unit can be found. The contraction developed by the reflex twitch is less the weaker the induction shock exciting the afferent nerve, in other words the fewer the afferent fibres excited, in short, the smaller the size of the centripetal impulse volley. With a given single-shock stimulus the tension developed by the reflex twitch remains closely constant when sampled at not too frequent intervals. In the case of the spinal flexion-reflex therefore, though with many other reflexes it is not so, a standard reflex twitch of desired size (tension) can be obtained at repeated intervals.

The only index available at present for inhibition is its effect on excitation thus, a standard twitch-reflex, representing a standard-sized volley of centrifugal discharge, can serve as a quantitative test for reflex inhibition. It serves for this with less ambiguity than does a reflex tetanus. In the tetanus the tension developed will depend within limits on the repetitive-frequency of the contraction waves forming the tetanus. Maximal tetanic contraction is reached only when the frequency reaches a rate which, in many reflex tetani, some of the units do not attain. In reflexes the rate of tetanic discharge can differ from unit to unit in one and the same muscle at one and the same time. The rate will differ too at different stages of the same reflex and according as the reflex is weak or strong. Reflex inhibition acting against a reflex titanic contraction may diminish the contraction in one or other or all of several different ways. In some units it may suppress the motor discharge altogether, in some it may merely slow the motor discharge thus lessening the wave frequency of the contraction and so the tension. The same aggregate diminution of tension may thus be brought about variously and by various combinations of ways, a result too equivocal for analysis. The same gross result might accrue (a) from total suppression of activity in some units or (b) from mere slackening of discharge in a larger number of units. These difficulties of interpretation are avoided by using as gauge for inhibition a standard reflex twitch. The deficit of contraction-tension then observed shows unequivocally the number of motor units inhibited out of the total activated for the standard. Since the direct maximal motor twitch compared with the standard reflex twitch can reveal the proportion of the whole muscle which the standard reflex twitch activates, we can find further what proportion of the whole muscle is reflexly inhibited. Of course subliminal excitation and subliminal inhibition are not revealed by the test and require other means for detection.

A stable excitatory twitch-reflex as standard allows us to proceed further in our quantitative examination of inhibition. We then find that inhibition can be admixt in our simple-seeming flexion-reflex itself, and indeed usually is so. To detect it we have simply to add to the earlier excitation of the reflex a following one at not too long interval we then find the response to the second stimulus-volley partly cut down by an inhibition latent in the first.

This is usually evident with intervals between 300-1,200 sigma. The very shortest interval at which the inhibitory effect occurs is difficult to determine, for the reason that the excitatory effect has a subliminal fringe and the second stimulus repeats the subliminal effect of the first, and the two subliminal effects can sum to liminal. The second response is therefore enlarged by summation of subliminal fringe in some of the responsive motor units. This activation by the second stimulus of some motor units facilitated for it by the first though not activated by the first alone tends of course to obscure the inhibitory inactivation the shrinkage due to the latter is offset by the increment due to the former. The inhibition is traceable only by the net diminution of the second reflex twitch. How quickly the inhibitory element in the stimulus develops centrally is not fully ascertainable, because the sooner the second reflex follows on the first the more the facilitation from it that it gets. This increment will conceal at least in part the decrement due to inhibition. Similarly the beginning of the inhibition may be concealed from observation by concomitant excitatory facilitation. This uncertainty does not attach to the longer intervals between the two stimuli because the central inhibitory process considerably outlasts the central excitatory facilitation.

The reflex therefore, which at first sight seems a purely excitatory reaction, proves on closer examination to be in fact a commingled excitation and inhibition. Usually clearly demonstrable in the simple spinal condition of the reflex, this complexity of character is yet more evident in the decerebrate condition.

We may hesitate to generalize from this example, because a stimulus applied to a bared afferent nerve is of course “artificial” in as much as it is applied to an anatomical collection of nerve fibres not homogeneous in function and, we may suppose, not usually excited together. If cutaneous, its fibres will belong to such different species of sense as “touch” and “pain” which often provoke movements of opposite direction and are therefore in their effect on a given muscle opposed in effect. That a strong stimulus to such an afferent nerve, exciting most or all of its fibres, should in regard to a given muscle develop inhibition and excitation concurrently is not surprising.

With weak stimuli the case is somewhat different. Such stimuli excite only a few of the constituent fibres of the afferent nerve, and those of similar calibre, presumably an indication of some functional likeness. Nevertheless, as shown above, the reflex result even then exhibits admixed excitatory and inhibitory influence on one and the same given muscle. And this admixture of excitation and inhibition persists when the stimulus is reduced in strength still further so as to be merely liminal. It still is so when the afferent nerve chosen is homogeneous in the sense that it is a purely muscular afferent, e.g. the afferent from one head of the gastrocnemius muscle. But we must remember that the afferent nerve from an extensor muscle has been shown to contain fibres which exert opposite reflex influences upon their own muscle, some exciting and some inhibiting that muscle’s contraction. This brings with it the question whether admixture of exciting and inhibiting influence in the reflex effect obtains when instead of stimulation of a bared nerve some more “natural” stimulation is employed.

For this the reflex evoked by passive flexion of knee in the decerebrate preparation has been taken. The single-joint extensor (vasto-crureus) of each knee is isolated and nothing but that muscle pair thus retained is still innervated in the whole of the two limbs. The preparation thus obtained is a tonic preparation one of the two muscles is then stretched by passively flexing a knee. This passive flexion excites in the extensor muscle which it stretches a reflex relaxation, i.e. the lengthening reaction this relaxation at one knee is accompanied in the opposite fellow vasto-crureus by a reflex contraction enhancing the existing “tonic” contraction. The reflex contraction thus provoked is characteristically deliberate and smooth in performance and passes without overshoot into a maintained extension posture. Let however the manoeuvre be then repeated with the one difference of condition, that the muscle contralateral to that which is passively stretched has been deafferented. In the deafferented muscle contraction is still obtained, and more easily than before, but the deafferented condition of the muscle alters the course of its contraction in two respects. The course is no longer deliberate. The contraction is an abrupt rush, with overshoot of the succeeding postural contraction, and this latter is hardly maintained at all. The severance of the afferent nerve has removed a reflex self-restraint from the contracting muscle. Normally the proprioceptives of the contracting muscle put a brake on the speed of the contracting muscle (autogenous inhibition). The explosive rush and momentum of these deafferented extensor reflexes recall the ataxy of tabes. They recall also the abruptness and overshooting of the “willed” movements of a deafferented limb. In both cases a normal self-braking has been lost along with the deprivation of the muscle of its own proprioceptive afferents. These latter mediate both a self-braking and a self-exciting (autogenous excitation) reflex action of the muscle. Thus here again there is admixture of reflex inhibition and excitation, and in this case the admixture obtains in response to a “natural” stimulation. Here therefore the admixture of central inhibition with central excitation is a normal feature of a natural reflex.

This makes it clear that for the study of normal nervous coordinations we require to know how central inhibition and excitation interact. As said above, the centripetal impulses which evoke inhibition do not differ in nature from those which evoke excitation. Inhibition like excitation can be induced in a “resting” centre. The only test we have for the inhibition is excitation. Existence of an excited state is not a prerequisite for the production of inhibition inhibition can exist apart from excitation no less than, when called forth against an excitation already in progress, it can suppress or moderate it. The centripetal volley which excites a “centre” finds, if preceded by an inhibitory volley, the centre so treated is already irresponsive or partly so.

A first question is, are there degrees of “central inhibitory state” and are they, like central excitatory state, capable of summation. This can be examined in several ways. Thus: against the central inhibition caused by a given single volley of inhibitory impulses a standard single volley of excitatory impulses can be launched at an appropriate interval. The relatively long duration of the central inhibitory state allows a second inhibitory volley to be interpolated between the original inhibitory volley and the standard excitatory volley. The standard excitation is found to be then diminished (as shown by the twitch-contraction which it evokes) more than it is if subjected to either one inhibitory volley only. This holds even when the second inhibitory volley, launched from the same cathode as the first, is arranged to be clearly smaller than the first. Since the distribution of the effect of the smaller impulse volley (launched from the same cathode as the larger) among the motoneurones of the centre must lie completely included within that of the first, the added inhibition due to the second volley indicates that the combined influence of the two volleys prevents activation of some motoneurones which neither inhibitory volley acting alone was able to prevent from being activated. Evidently therefore central inhibition sums consequently it is capable of subliminal existence. Also, successive subliminal degrees of inhibition can by temporal overlap sum to supraliminal degree. In these ways central inhibition presents analogy with its converse “central excitations” both exhibit various degrees of intensity in respect to the individual motoneurone.

Summation of inhibition is well exhibited when a given twitch-reflex is evoked at various times during and after a tetanic inhibition. The cutting down of the reflex twitch is progressively greater, as within limits, the inhibitory tetanus proceeds. After cessation of the tetanus the inhibitory state, similarly tested, passes off gradually, more quickly at first than later.

The relatively long persistence of the central inhibitory state induced by a single centripetal impulse volley allows examination of the effect on it of two successive excitation volleys as compared with one of the two alone. An excitatory volley is interpolated between the inhibitory volley and a subsequent standard excitatory volley. The interpolated excitatory volley is found to lessen the inhibitory effect upon the final excitatory volley. The interpolated excitation volley neutralizes some of the inhibition which otherwise would have counteracted the final test excitation. Just as central inhibitory state (c.i.s.) counteracts central excitatory state (c.e.s.) so c.e.s. neutralizes c.i.s. The mutual inactivation is quantitative. There occurs at the individual neurone an algebraic summation of the values of the two opposed influences.

It is still early to venture any definite view of the intimate nature of “central inhibition”. It is commonly held that nerve excitation consists essentially in the local depolarization of a polarized membrane on the surface of the neurone. As to “central excitation”, it is difficult to suppose such depolarization of the cell surface can be graded any more than can that of the fibre. But its antecedent step (facilitation) might be graded, e.g. subliminal. Local depolarization having occurred the difference of potential thus arisen gives a current which disrupts the adjacent polarization membrane, and so the “excitation>. travels. As to inhibition the suggestion is made that it consists in the temporary stabilization of the surface membrane which excitation would break down. As tested against a standard excitation the inhibitory stabilization is found to present various degrees of stability. The inhibitory stabilization of the membrane might be pictured as a heightening of the “resting” polarization, somewhat on the lines of an electrotonus. Unlike the excitation-depolarization it would not travel and, in fact, the inhibitory state does not travel.

The quantitative character of the interaction between opposed inhibition and excitation is experimentally demonstrable. Thus: a given inhibitory tetanus exerted on a certain set of motoneurones fails to prevent their excitation in response to strong stimulation of a given afferent nerve but when the stimulation of the excitatory afferent is weaker the given standard inhibitory tetanus does prevent the response of the motor neurones to the excitatory stimulation. With the weaker stimulation of the afferent nerve there are fewer of its fibres acting, and therefore fewer converge for central effect on some of the units. On these the standard c.i.s. has therefore less c.e.s. to counteract.

Many features characteristic of reflex myographic records of various type become interpretable in light of the stimulus volley from a single afferent nerve trunk, even small, evoking an admixture of inhibition and excitation, with consequent central conflict and interaction between them. Features which find facile explanation in this way are the following. (A) The flexion-reflex (spinal) commonly has a d’emblée opening that is, a steep initial contraction passes abruptly into a plateau, giving an approximately rectangular beginning to the myogram. Here the initial reflex excitation is closely followed by an ensuing reflex inhibition commingled with and partially counter-acting the concurrent excitation. (B) Allied to this and of analogous explanation is the so-called “fountain”- form of flexion-reflex. After the first uprush of contraction a component of reflex inhibition grows relatively more potent and the contraction-tension drops low before continuing-level. Between these extreme forms there are intermediates. The key to the production of them all is admixture of central excitation with central inhibition the excitation is prepotent earlier, and later suffers from encroaching inhibition.

(C) Again, the typical opening of the crossed extensor reflex (decerebrate) “recruits”. A variably long latent period precedes a contraction which climbs slowly, taking perhaps seconds to reach its plateau. Here, struggling with excitation, inhibition has the upper hand at first. The action currents of the muscle marking the serial stimuli to the afferent nerve are not choked by secondary waves of after-discharge. The concurrent inhibition cuts them out. The inhibition is traceable partly to the proprioceptive reflex mechanism attached to the contracting muscle itself the progress of the reflex contraction is partly freed from inhibition by deafferenting the muscle, but still not wholly freed. A residuum of inhibition in the reflex is traceable to the crossed afferent nerve employed. This again illustrates the ubiquitous commingling of inhibition and excitation in the spinal and decerebrate reflexes evoked by direct stimulation of afferent nerves.

An instance of combination of excitation and inhibition for coordinative effect is the rhythmic reflex of stepping. In the “spinal” cat and dog there occurs “stepping” of the hind limbs it starts when the “spinal” hind limbs, lifted from the ground, hang freely, the animal being supported vertically from the shoulders. The extensor phase in one limb occurs with the flexor phase in the other. This “stepping” can also be evoked by a stigmatic electrode carrying a mild tetanic current to a point in the cross-face of the cut spinal-cord. The “stepping” then opens with Aexion in the ipsilateral hind limb accompanied by extension in the contralateral. To reproduce this stepping movement by appropriately timed repetitions of tetanization of, for instance, a flexion producing afferent of one limb or an extension-producing afferent of the other never succeeds even remotely in exciting the rhythmic stepping. In the true rhythmic movement itself, which has been examined particularly by Graham Brown, the contraction in each phase develops smoothly to a climax and then as smoothly declines, waxing and waning much as does the activity of the diaphragm in normal inspiration. But although this rhythmically intermittent tetanus affecting alternately the flexors and extensors of the limb and giving the reflex step cannot be copied reflexly by employing excitation alone, it can be easily and faithfully reproduced and with perfect alternation of phase and with its characteristic asymmetrical bilaterality, by employing a stimulation in which reflex excitation and reflex inhibition are admixt in approximately balanced intensity. The result is then a rhythmic sea-saw about a neutral point. The effect on the individual motor unit appears then to run its course thus: if we start to trace the cycle with the moment when c.e. and c.i. are so equal as to cancel out, the state of the motoneurone is a zero state, for which the term “rest”, although often applied to it, is perhaps better avoided. With supervention of preponderance of c.e. over c.i. the motor neurone’s discharge commences and under progressive increase of that preponderance the frequency of discharge increases in the individual motor neurone, and more motor neurones are “recruited” for action until in due course the preponderance of c.e. begins to fail and c.i. in its turn asserts itself more. The recruitment and frequency of discharge begin to wane, and then reach their lowest, and may cease, and an interval of zero state or quiescense may ensue. The quiescence may be inhibitory or merely lack of excitation. Which of these it were could be directly determined only by testing the threshold of excitation. However brought about, it is synchronous with the excitation-phase in the antagonistic muscle and with the excitation-phase in the symmetrical fellow muscles of the opposite limb. Since reciprocal innervation has been observed to obtain between these muscles, the phase of lapse of excitation is probably one of filer active inhibition. The rhythm induced by stimulation of the “stepping”-point in the cut face of the lateral column of the cord would seem to act therefore by evoking concurrently excitation and inhibition, and so playing them off one against the other as to induce alternate dominance of each. Intensifying the mild current applied to the point quickens the tempo of the rhythm, i.e. of the alternation.

Another class of events revealing inhibition as a factor wide and decisive in the working of the central nervous system is presented by the “release” phenomenon of Hughlings Jackson. The depression of activity called “shock” supervenes on injury of a distant but related part conversely there supervenes often an over-action due likewise to injury or destruction of some distant but related part. “Shock” is traceable to loss of excitatory influence, which, though perhaps commonly subliminal in itself, lowers the threshold for other excitation. The over-action conversely is traceable to loss of inhibitory influence, perhaps subliminal in itself and yet helping concurrent influences of like direction to maintain a normal restraint, the normal height of threshold against excitation. Where the relation between one group of muscles and another, e.g. between flexors and extensors, is reciprocal, the effect of removal (by trauma or disease) of some influence exerted by another part of the nervous system is commonly two-fold in direction. There is “shock”, i.e. depression of excitability in one field of the double mechanism and “release”, i.e. exaltation of excitability, in another. Thus spinal transection, cutting off the hind-limb spinal reflexes from prespinal centers inflicts “shocks” on the extensor half-centre and produces “release” of the flexor half-centre. In this case the direction both of the “shock” and of the “release” runs aborally but it can run the other way, as in the influence that the hind-limb centres have on the fore-limb. Which way it runs, of course, depends simply on the relative anatomical situation of the influencing and the influenced centres.

The role of inhibition in the working of the central nervous system has proved to be more and more extensive and more and more fundamental as experiment has advanced in examining it. Reflex inhibition can no longer be regarded merely as a factor specially developed for dealing with the antagonism of opponent muscles acting at various hinge-joints. Its role as a coordinative factor comprises that, and goes beyond that. In the working of the central nervous machinery inhibition seems as ubiquitous and as frequent as is excitation itself. The whole quantitative grading of the operations of the spinal cord and brain appears to rest upon mutual interaction between the two central processes “excitation” and “inhibition”, the one no less important than the other. For example, no operation can be more important as a basis of coordination for a motor act than adjustment of the quantity of contraction, e.g. of the number of motor units employed and the intensity of their individual tetanic activity. This now appears as the outcome of nice co-adjustment of excitation and inhibition upon each of all the individual units which cooperate in the act.

In reflexes, even under simple spinal or decerebrate conditions, interplay between excitation and inhibition is commonly induced even by the simplest stimulus. It need not surprise us therefore that variability of reflex result is met by the experimenter. Indeed, that it troubles him by being partly beyond his control, need not surprise him in view of the multiplicity and complicity of the sources of the inhibition and of the excitation. This variability seems underestimated by those who regard reflex action as too rigid to provide a prototype for cerebral behaviour. It is in virtue of their containing inhibition and excitation admixt that, in accord with central conditions prevailing for the time being, a limb-reflex provoked by a given stimulus in the decerebrate preparation can on one occasion be opposite in direction to what it is on another, e.g. extension instead of Aexion (“reversal”) Excitation and inhibition are both present from the very stimulus out-set and are pitted against one another. The central circumstances may favour one at one time, the other at another. Again, if the quantity of contraction needed normally for a given act be reached by algebraic summation of central excitation and inhibition, it can obviously be attained by variously compounded quantities of those two. Hence when disease or injury has caused a deficit of excitation, a readjustment of concurrent inhibition offers a means of arriving once more at the normal quantity required. The admixture of inhibition and excitation as a mechanism for coordination thus provides a means of understanding the remarkable “compensations” which restore in course of time, and even quickly, the muscular competence for execution of an act which has been damaged by central nervous lesions. More than one way for doing the same thing is provided by the natural constitution of the nervous system. This luxury of means of compassing a given combination seems to offer the means of restitution of an act after its impairment or loss in one of its several forms.

From Nobel Lectures, Physiology or Medicine 1922-1941, Elsevier Publishing Company, Amsterdam, 1965


DISCUSSION

Behavior entails a constant competition between the possible actions that the environment presents, according to our current goals. Although the decision-making literature has generally focused on choices between objects (e.g., orange juice or apple juice), there has been growing interest in action-based choices (Rangel & Hare, 2010). These choices are usually viewed as emerging from a competitive process involving interactions between potential responses (see Cisek & Kalaska, 2010). TMS has provided an important tool to probe the dynamics underlying action selection and preparation, with prior work having established the existence of two distinct inhibitory mechanisms (Duque et al., 2010 Duque & Ivry, 2009), one associated with determining which response to make and the other with regulating the initiation of the selected response. The current pair of experiments specifies important constraints on the operation of these two mechanisms.

Robustness of Inhibition Arising from IC

Our earlier work had revealed the seemingly counterintuitive inhibition of the selected response during a delay period. This inhibition is quite pronounced, with MEPs being attenuated by approximately 40–50% from baseline. This inhibition arises although the cortical representation of that response exhibits increased excitability (Duque & Ivry, 2009 Davranche et al., 2007), suggesting a downstream locus of operation. Consistent with this hypothesis, spinal reflexes in the selected response are attenuated (Duque et al., 2010). This pattern of results suggests that IC provides a mechanism to inhibit a response in the face of on-going preparation.

In the current pair of experiments, IC was unaffected by the task context. It was of similar magnitude when the response choices involved homologous muscles, nonhomologous muscles of the same effectors, or nonhomologous muscles of different effectors that were either both in the upper limbs or upper and lower limbs. It is important to note that this inhibition is not generic: When the targeted muscle is unlikely to be selected (task-irrelevant), CS excitability does not change during the delay period (Duque et al., 2010).

The ubiquitous nature of IC suggests that this form of inhibition may be intrinsically part of preparatory processes, at least for delayed response tasks. We envision a self-contained process, involving an architecture where the activation of a response representation automatically triggers a corresponding inhibitory tag, with the latter signal providing a gate on descending signals. Functionally, such inhibition could allow preparatory processes to operate upstream without generating or triggering premature movement. Alternatively, it is possible that downstream inhibition serves to facilitate fast response initiation by lowering background activity at the expected time of the imperative (Hasbroucq, Kaneko, Akamatsu, & Possamai, 1997). Further research is needed to clarify this issue. The current literature does not provide a clear picture as to whether IC is also present in tasks in which there is no delay period.

Most relevant for our current discussion is that this model entails minimal computational requirements on the control system given that IC is linked to response activation. The self-contained nature of the model avoids the need to postulate a control process that regulates the target of inhibition. Although we focus on computational requirements here, various lines of evidence (Duque et al., 2012 Seki & Fetz, 2012) suggest that premotor cortex may be a critical node in a network for triggering the parallel activation of response-specific activation (feeding into motor cortex) and inhibition (targeted downstream of motor cortex Cohen, Sherman, Zinger, Perlmutter, & Prut, 2010 Kroeger et al., 2010).


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