Exam 1

• The increase in fiber size increases the capacity of the ATP-PC system, resulting in an improved ability to rapidly use phosphocreatine for ATP production.
• Overload in training is the need to increase the load or intensity of exercise to cause a further adaptation of a system.
• Progression in training is the concept that once an adaptation to an overload stimulus has occurred, the physiological system must be overloaded again for further adaptation to occur.
• Reversibility in training is the fact that adaptations to training are lost when training stops.
• Specificity in training is that adaptation of tissue depends on type of training undertaken.
• Six training variables include frequency, duration, type of exercise, repetitions, sets, and type of contraction.
• Genetic predisposition accounts for fifty percent of one’s VO2max since genetics can determine the muscle fiber type concentration, heart size (men vs women), and max cardiac output.
• In endurance training programs, a 15-20% increase can be seen in an individual’s VO2max after two to three months.
• Genetics can influence physiological adaptations to training where high responders can increase their VO2max by 40-50% while others only increase their VO2max by 2-3%.
• Based off the class lecture, in the US, a healthy, sedentary, college aged male’s typical VO2 max is 35-40 whereas a sedentary college-aged female’s VO2max is 28-33.
• Within one to four months endurance training increases VO2max through an increase in maximal cardiac output.
• In longer durations of endurance training, 32 months or more, VO2max increases through an increase in maximal aVO2 difference and maximal cardiac output.
• Preload in cardiovascular physiology is the end diastolic volume which increases in response to endurance-training.
• This training-induced increase results in a stretch of the left ventricle which will increase cardiac contractility and thus maximal stroke volume.
• Afterload in cardiovascular physiology is the peripheral resistance against the contracting force of the ventricle as it pushes blood into the aorta.
• In endurance training, the muscle offers less resistance to blood flow because of a reduction in sympathetic vasoconstrictor activity to the arterioles of trained muscles during maximal exercise.
• Contractility in cardiovascular physiology refers to the strength of the cardiac muscle contraction when fiber length, afterload, and heart rate remain constant.
• Endurance training increases the number of mitochondria available to shuttle NADH which would result in a decrease in lactate and hydrogen ion production.
• NFkB- promotes the expression of several antioxidant enzymes that protect muscle fibers against free radical-mediated injury.
• With an increase in capillary density, there is a slower blood flow and an increase in FFA transporters that in conjunction with the increase in mitochondria increases fat oxidation.
• The primary changes that occur in muscle in response to endurance training include: increases in slow muscle fibers, increased mitochondrial volume in muscle fibers, an increased ability for muscle to metabolize fat, improved muscle antioxidant capacity, and increased capillary density.
• PGC-1a- helps transcriptional activators that promote mitochondrial biogenesis and regulates formation of new capillaries, synthesis of antioxidant enzymes, and fast-to-slow muscle fiber type shift.
• The increase in mitochondria in the skeletal muscle fibers contributes to an increase in fat metabolism and an improved antioxidant capacity.
• Endurance training results in a shift from fast muscle fibers to slow muscle fibers which would increase the amount of slow muscle fibers.
• “High intensity” endurance training improves acid-base balance since endurance-trained muscles produce less lactate and hydrogen ions.
• An increase in fat metabolism decreases the breakdown of carbohydrates, the main producer of pyruvate.
• P38- activates PGC-1a in order to contribute to mitochondrial biogenesis.
• Calcineurin- promotes fiber growth/regeneration and fast-to-slot fiber type transition as a result of exercise training.
• When endurance exercise is discontinued, VO2max declines because of a decrease in stroke volume due to the loss of plasma volume and a decrease in a-vo2 difference that is associated with a decrease in muscle mitochondria.
• Calmodulin-dependent kinase- contributes to the activation of PCG-1a to influence exercise-induced muscle adaptation.
• AMPK- regulates energy-producing pathways by stimulating glucose uptake and free fatty-acid oxidation during exercise.
• Anaerobic training can affect skeletal muscle fibers through increasing intracellular buffers and hydrogen transporters which increases buffer capacity as well as increase the fiber size of type IIa and IIx fibers.
• The four primary signal transduction pathways in skeletal muscle are mechanical stimuli, calcium, free radicals, and phosphate/muscle energy levels.
• mTOR- promotes increased translation which results in increased protein synthesis.
• Primary changes that occur in skeletal muscle as a result of endurance training include increased capillarization, increased mitochondria, increased myoglobin, increased enzyme activity, increased number of fibers, and increased fiber type diversity.
• Muscle strength is the maximal force that a muscle or muscle group can generate and is generally expressed in one-repetition maximum.
• Muscle endurance is the ability of a muscle to make repeated contractions against a submaximal load.
• Frequency, overload, specificity, and reversibility are four training principles.
• The increase in AMPK can activate TSC2, a signaling molecule that inhibits mTOR activity therefore impairing protein synthesis.
• Some training variables include frequency, intensity, duration, type of exercise, repetitions, speed of contraction, type of contraction, and load.