Council of Interstate Testing Agencies (CITA) Dental Examination

Correct: In the corrective exercise continuum, once muscle imbalances are identified, the progression moves from inhibiting and lengthening overactive muscles to activating underactive muscles. Isolated strengthening (Activation) is crucial for improving motor unit recruitment and firing rates in the gluteals, which provides the stability and neuromuscular control needed before the client can safely perform integrated, functional movements like the squat.

Incorrect: Transitioning to heavy squats or plyometrics is premature and likely to reinforce faulty movement patterns if the underlying muscle imbalances and motor unit recruitment issues are not addressed first. While stretching is part of the lengthening phase, focusing on it exclusively for the remainder of the session ignores the critical need to activate the underactive gluteals to correct the identified forward lean and restore proper joint mechanics.

Takeaway: Effective progression requires isolated activation of underactive muscles to improve neuromuscular control before integrating those muscles into complex, functional movement patterns.

Correct: Aging is characterized by a selective loss of Type II (fast-twitch) muscle fibers, which are critical for power and rapid force production. Additionally, there is a reduction in the maximal firing rate of motor units and a decrease in the total number of functioning motor units. These changes contribute significantly to the loss of strength and balance in older adults, making them a primary target for resistance training interventions to maintain functional independence.

Incorrect: The sensitivity of muscle spindles and the stretch reflex response typically decrease with age rather than increase, leading to slower reaction times. There is no significant conversion of Type I fibers into Type II fibers; in fact, the proportion of Type I fibers often increases relatively because Type II fibers are lost at a higher rate. The neuromuscular junction undergoes degenerative changes with age, including a reduction in acetylcholine receptors and less efficient neurotransmitter release, rather than an increased rate of release.

Takeaway: The primary neuromuscular hallmark of aging is the selective loss of Type II muscle fibers and a reduction in motor unit recruitment efficiency, which are critical factors in maintaining functional independence.

Correct: In the initial stages of a resistance training program, typically the first 4 to 6 weeks, strength gains are primarily the result of neurological adaptations. These include increased motor unit recruitment, improved synchronization of motor unit firing, and an increased firing rate (rate coding). These changes allow the client to produce more force without an immediate increase in muscle cross-sectional area or body mass.

Incorrect: Hypertrophy of muscle fibers generally requires a longer duration of consistent stimulus to show measurable changes in girth. Sarcoplasmic volume increases are often associated with high-volume training but do not typically account for rapid 1RM strength spikes in the absence of size changes. Fiber type conversion from Type I to Type IIx is not a physiological adaptation seen in humans; rather, transitions typically occur between Type IIx and Type IIa.

Takeaway: Initial strength improvements in a resistance training program are predominantly driven by neural adaptations such as enhanced motor unit recruitment rather than structural muscle growth.

Correct: Relaxin is a hormone produced during pregnancy that increases the laxity of ligaments and connective tissues to facilitate childbirth. These effects are systemic and can persist for several months postpartum, particularly in women who are breastfeeding. This increased laxity reduces joint stability, making the client more susceptible to sprains and joint-related injuries during high-impact or heavy resistance training.

Incorrect: While bone density can be influenced by hormonal changes during lactation, it is not the primary immediate risk factor for joint integrity compared to ligamentous laxity. The transverse abdominis often experiences stretching and weakness (diastasis recti), but ‘reduced myofibrillar hypertrophy’ is a description of muscle size rather than the systemic physiological risk factor governing joint safety. While cardiovascular variables like blood volume and heart rate undergo significant changes during and after pregnancy, they do not directly increase the risk of musculoskeletal joint injury in the same manner as hormonal effects on connective tissue.

Takeaway: Personal trainers must account for the systemic effects of relaxin, which increases joint laxity and injury risk for several months following childbirth.

Correct: The integration phase of corrective exercise is designed to re-educate the neuromuscular system to use a previously underactive or isolated muscle (such as the gluteus medius) during dynamic, multi-joint activities. This progression from isolation to integration enhances intermuscular coordination, ensuring that the muscle contributes effectively to the kinetic chain during real-world functional movements.

Incorrect: Increasing the cross-sectional area (hypertrophy) is a general resistance training goal but is not the primary objective of the integration phase of corrective exercise. The stretch reflex is a physiological response typically addressed during the lengthening/stretching phase of a program to manage overactive muscles, not during the integration of functional movements. The central and peripheral nervous systems work in tandem during all motor tasks; the goal of progression is coordination and motor learning rather than an arbitrary prioritization of one system over the other to prevent atrophy.

Takeaway: The final stage of corrective exercise progression must involve integrating isolated muscle activation into multi-joint movements to improve neuromuscular coordination and functional efficiency.

Correct: An excessive forward lean during a squat is a classic movement compensation often rooted in overactive (tight) hip flexors and calf muscles, specifically the soleus. When the soleus is overactive, it restricts the necessary ankle dorsiflexion required for a deep squat. To maintain balance and keep the center of gravity over the feet, the body compensates by leaning the torso forward. Simultaneously, overactive hip flexors pull the pelvis into an anterior tilt, further exacerbating the forward lean.

Incorrect: Underactivity of the gastrocnemius is incorrect because it is typically overactivity or tightness in the calves that restricts movement; underactivity of the rectus femoris would not specifically cause a forward lean in the way hip flexor overactivity does. Increased neural drive to the gluteus maximus would generally assist in maintaining an upright torso and hip extension, rather than causing a lean. Muscle spindles respond to stretch by causing contraction; a reduced firing rate would not be the primary mechanism for a forward lean compared to the mechanical restriction of tight muscles and altered length-tension relationships.

Takeaway: Movement dysfunctions like an excessive forward lean are typically caused by a combination of restricted joint mobility (e.g., limited ankle dorsiflexion) and overactive muscles that pull the kinetic chain out of alignment.

Correct: Exercise induces the translocation of GLUT4 glucose transporters to the cell membrane through insulin-independent pathways (such as AMPK activation). In individuals with Type 2 Diabetes, this increased permeability to glucose persists into the recovery phase as the body prioritizes the replenishment of depleted muscle glycogen stores, which can lead to hypoglycemia if exogenous insulin or carbohydrate intake is not adjusted.

Incorrect: Suppression of cortisol and growth hormone is incorrect because these counter-regulatory hormones typically rise or remain stable to maintain blood glucose during and after stress. Hepatic gluconeogenesis is generally stimulated, not inhibited, during the post-exercise recovery period to support blood glucose levels. Exercise increases insulin sensitivity and receptor activity rather than causing a systematic downregulation of insulin receptors.

Takeaway: Post-exercise hypoglycemia in diabetic populations is primarily caused by the prolonged activation of glucose transport mechanisms and the metabolic demand for glycogen synthesis.

Correct: Autogenic inhibition is a physiological process where a muscle is inhibited from contracting due to high levels of tension, such as during an isometric contraction. This process is mediated by the Golgi tendon organs (GTOs), which sense the tension and send inhibitory signals to the spinal cord, causing the muscle to relax. This relaxation allows for a greater range of motion during the subsequent passive stretch phase of PNF.

Incorrect: Reciprocal inhibition involves the relaxation of the antagonist muscle when the agonist is contracted, which is not the primary mechanism for relaxing the muscle that was just isometrically contracted in this PNF technique. The stretch reflex is a contraction of a muscle in response to a rapid stretch, which would actually increase muscle tension and resist the stretch. Increased motor unit recruitment would lead to higher muscle activation and force, which is the opposite of the relaxation required for an effective stretch.

Takeaway: PNF stretching utilizes autogenic inhibition via Golgi tendon organs to temporarily reduce muscle tension and facilitate an increased range of motion.

Correct: The integration phase of the corrective exercise continuum focuses on using multi-joint, compound movements to re-train the neuromuscular system. By performing a step-up to a balance, the client must use the newly activated gluteus medius as a stabilizer while the prime movers execute the movement, effectively integrating the muscle into a functional, real-world movement pattern.

Correct: Aerobic exercise training leads to a reduction in resting blood pressure primarily through a decrease in total peripheral resistance (TPR). This physiological adaptation is achieved via improved endothelial function, such as increased nitric oxide bioavailability, structural remodeling of the blood vessels (increased lumen diameter), and a reduction in sympathetic nervous system outflow to the peripheral vasculature.

Incorrect: A reduction in stroke volume is incorrect because aerobic training typically increases or maintains stroke volume through improved myocardial contractility and plasma volume expansion. Increasing blood viscosity would actually increase peripheral resistance and elevate blood pressure rather than lowering it. An elevation in resting heart rate is a sign of detraining or acute stress; aerobic conditioning typically results in a lower resting heart rate due to increased parasympathetic tone.

Takeaway: The primary mechanism for the chronic reduction of resting blood pressure following aerobic exercise training is the decrease in total peripheral resistance.