Exercise Physiology
What happens when we exercise?
The individual response to exercise depends on a number of factors:
Type of exercise stress encountered; level of training, conditioning, and nutritional and hydration status.
Age, gender, body type, muscle fibre type ratios.
Genetic factors and environmental conditions, psychological factors.
Physiological response to exercise stress varies according to the factors mentioned above. The complex interactions of the body’s homeostatic mechanisms and responses can be briefly summarized in a time line:
Short-term—seconds to minutes (stress reaction)
Autonomic nervous system responses: sympathetic nervous system (SNS) increase with parasympathetic nervous system (PNS) decrease resulting in predominance of fight and flight responses, and reduced vegetative functions.
Cardiovascular responses: increased cardiac output to exercising muscles and reduced blood flow to other organ systems. Elevated core temperature increases blood flow to the skin to facilitate thermoregulation.
Respiratory responses: increased rate and depth of respiration to meet demands for gas exchange.
Metabolic and respiratory responses: buffering of lactic acid produced by the active muscles.
Medium-term—minutes to hours (resistance reaction)
Hormonal responses Accentuate and prolong the autonomic neural responses (above); release of catecholamines from adrenal medulla, adrenocorticotrophic hormone (ACTH) and growth hormone (GH) from pituitary, cortisol from adrenal gland increase substrate availability for energy metabolism to provide fuel for longer duration exercise. Activation of the renin angiotensin and antidiuretic hormone (ADH) mechanisms help preserve fluid and electrolyte balance and maintain BP.
Long-term—days to weeks (adaptation)
Repeated acute bouts of exercise (training) usually result in adaptation to exercise stimulus. Adaptation results from gene activation in the various tissues under stress. Cellular structural changes in muscle and other tissues result in strength and endurance changes; neural regulation changes optimize muscle activation patterns; renal mechanisms are responsible for changes in plasma volume and venous return leading to compensatory changes in cardiac dimensions.
Clinical note
Overtraining syndrome in athletes is defined by under-performance and is characterized by fatigue and physiological and psychological changes. It has been suggested that this is a maladaptive alternative 3rd stage of adaptation. Long term, may be useful as a protective physiological mechanism preventing damage from over-exercise when individual athletes train beyond the limits of physiological compensation.
Components of fitness
Stamina (aerobic conditioning, aerobic power)
All types of exercise require a base level of aerobic conditioning. High levels of aerobic conditioning enable more efficient use of fuel, greater tolerance of environmental extremes, quicker recovery during intermittent exercise and between training sessions, and are essential for long-term cardiovascular health. Important factors are: mechanical efficiency of the heart pumping blood (cardiac output, Q); the ability of muscle to extract and utilize oxygen (arteriovenous difference in oxygen concentration, a-vO2 diff) and fuels.
Speed and strength (anaerobic power)
Sprint velocity, mass of weight lifted, or the distance of a throw depends on the maximum force that a muscle can exert through its leverage systems. Muscle forces depend on body size and type, biomechanics, muscle cross-sectional area, predominant fibre type, and rate of ATP re-synthesis. Generally, the greater the muscle mass the more speed, force, or power that can be generated.
Skill (neuromuscular coordination)
Skills are co-ordinated neuromuscular patterns of activation, which increase efficiency, speed, and ease of movement. In neurological terms, highly developed skills are implemented subconsciously, which involve quicker neural pathways. Skills can be innate or learned, optimum acquisition is age dependent (9-12yr), but can be achieved with good training practices and high quality coaching at any age.
Suppleness (flexibility)
Flexibility or suppleness is the ability to move a joint through a full range of normal movement. Depends on joint type, joint surface congruity, tension in capsules, ligaments, and muscles. When a joint is forced outside its normal working range by external forces, greater flexibility may be protective against injury, and there is evidence that this and flexibility training may improve performance.
Psychology (mental fitness)
When the physiological and biomechanical components of fitness have been optimized, psychological factors become more important. At elite level, psychological factors may be the only difference between success and failure. Mental strength may be innate in some individuals, but aspects of psychological preparation can be learned and should be practiced as part of normal training. Preparation and training includes:
Motivation to compete and train, and goal setting.
Mental rehearsal of performance.
Pre-competition routines to manage anxiety.
Coping strategies for success or failure.
Injury.
These are all important areas for professional athletes.
Energy for exercise
Exercise is powered by the high energy phosphate molecule ATP. Resting cellular energy processes provide a small amount of ATP for normal cellular homeostatic systems and in muscle cells ATP powers contractile elements. Cellular energy metabolic processes generate ATP rapidly for short bouts of high-intensity exercise and more steadily for longer-term exercise. Relative contribution of different metabolic energy systems depend on exercise duration, intensity, ratio of fast to slow twitch muscle fibre types and individual fitness levels of fitness.
Impulse energy (high energy phosphates/anaerobic)
This is the small quantity of energy (ATP) present in the cell at rest; it can provide the initial impetus for a throw, a jump, a punch, a serve in tennis, or the initial reaction off the blocks in a sprint. If high-intensity exercise is to continue the small amount of ATP present in the cell at rest must be rapidly regenerated.
Immediate energy (high energy phosphates/anaerobic)
The phospho-creatine system (ATP-PCR) is an ATP buffering system preventing short-term ATP depletion. Phosphate molecules are shuttled from creatine phosphate to adenosine diphosphate (ADP) regenerating ATP molecules rapidly. The high energy phosphate buffer can replenish cellular ATP levels for all out maximum efforts lasting ˜6-7s or longer durations at lower intensity. A high percentage of fast twitch fibres replete with creatine stores (eat more red meat and oily fish or creatine supplementation) in addition to sprint and resistance training are factors, which optimize function of this system.
Short-term energy (anaerobic glycolysis)
A sustained high rate of ATP generation to power longer duration exercise require metabolism of fuels. Short-term (seconds to minutes) breakdown of glycogen or glucose anaerobically (substrate phosphorylation) provides a small amount of ATP rapidly.
Advantage
Capable of high rates of ATP production to power high-intensity exercise for short periods.
Disadvantages
Inefficient as only small amounts of ATP are generated from fuel stores, relatively fast to fatigue, and the end product, pyruvate, is converted to lactic acid. Lactic acid dissociates, the hydrogen ion has to be buffered or cellular pH will fall inhibiting cellular enzyme activity, however lactate can be taken up by less active tissues and metabolized aerobically (extracellular lactate shuttle).
In healthy untrained subjects significant blood lactate (BLa) accumulation occurs at ˜55% of VO2 max and in highly trained endurance athletes this
does not occur until ˜85% of VO2 max. A shift to anaerobic glycolysis and increased BLa is caused by increased exercise intensity, relative tissue hypoxia, and neural selection of fast twitch muscle fibres.
does not occur until ˜85% of VO2 max. A shift to anaerobic glycolysis and increased BLa is caused by increased exercise intensity, relative tissue hypoxia, and neural selection of fast twitch muscle fibres.
ATP-PCR and anaerobic glycolytic systems are the predominant energy systems for intense exercise lasting anywhere from 10-20s up to 90s, e.g. running 100-400m, 50-200m swim, or the short repeated sprints required during field sports. A favourable ratio of fast to slow twitch muscle fibres, correct training methods, and nutritional factors (high creatine level and adequate cellular carbohydrate (CHO) stores) will optimize function of these energy systems.
Long-term energy (oxidative phosphorylation/aerobic)
Prolonged or sustained activity (minutes to hours) utilizes more efficient metabolism of fuels with oxygen and greater energy yield. Aerobic breakdown of CHO and free fatty acids (FFA) to produce ATP requires mitochondrial enzymes and cofactors of the tricarboxylic acid cycle (TCA), and the electron transport chain (ETC). Glucose fully metabolized aerobically yields ˜38 ATP and glycogen ˜39 ATP, and although the rate of energy production is higher than for fat; intramuscular and liver stores of carbohydrate are limited.
NB During high intensity aerobic activity, such as marathon running at > 19km/h pace, CHO is utilized for rapid aerobic ATP generation. If initial stores or intake of CHO in the race are inadequate after ˜120min significant CHO depletion occurs, energy metabolism slows as fuel utilization switches to fat, pace rapidly falls, and the runner ‘hits the wall’!
Energy yields from FFA metabolism are greater than CHO, due to greater numbers of CH2 units in FFA chains. Aerobic metabolism of palmitic acid [CH3(CH2)14COOH], for example, can generate 129 moles ATP. However, despite abundant availability of fat, rates of ATP synthesis from fat breakdown are much slower, greater O2 is required, and a glycolysis is required to keep the TCA cycle turning … ‘fat’ is thus said to ‘burn on a carbohydrate flame’. In the TCA cycle a series of enzymatically controlled steps strip the hydrogens from CH2, the carbon combines with oxygen to form CO2 and hydrogens combine with cofactors (nicotinamide adenine dinucleotide (NAD)/ flavin adenine dinucleotide (FAD)) and are transferred to the electron transport chain (ETC) where they are oxidized in a series of steps coupled to phosphorylation of AMP and ADP to produce ATP. Hydrogens finally combine with O2 to produce water.
Aerobic production of ATP proceeds rapidly if muscle cells have large numbers of mitochondria replete with; oxidative enzymes, NAD/FAD cofactors, iron-containing cytochromes, and myoglobin. Greater capillarization of muscle cell improves O2 and FFA delivery, and the removal of waste products; and, myoglobin within mitochondria draws in oxygen.
Factors affecting aerobic metabolism/endurance capacity
Environmental effects on oxygen dissolved in solution (partial pressure of oxygen (pO2) (altitude or depth).
Respiratory function (air pollution, bronchoconstriction).
Oxygen transport (haemaglobin), delivery (heart function).
Predominant muscle fibre types (ratio of slow twitch fibres (ST) and FOG to fast twitch fibres (FT)).
Extraction of O2 and fuel (capillary density and myoglobin level).
Rate of utilization of fuel and oxygen (number/size of mitochondria, oxidative enzyme activity, stores/availability of co-factors, and fuel).
Muscle physiology
Structure
Individual muscle fibres are multinucleated cells with a calcium rich transverse ‘T’ tubular system connecting outer sarcoplasmic membrane to sarcoplasmic reticulum enveloping the sarcomeres.
Sarcomeres show the classic striated pattern of overlapping contractile elements of actin (thin) and myosin (thick) filaments plus associated anchoring proteins.
Muscle fibres are further organized into progressively larger diameter fascicles and bundles, by envelopes of endomysium, perimysium, and finally a layer of epimysium encloses the whole muscle.
Macroscopic structure—length, breadth, shape, and pennation (muscle fibre orientation to tendon) further determine function.
Excitation-contraction coupling
α Motor neuron action potential neuromuscular end plate acetyl choline release depolarization sarcolemma/T tubule Ca2+ release.
ATP then binds releasing myosin head from actin-binding site.
Further cross-bridge cycling occurs as long as Ca2+ bound to troponin.
Fibre types are classified physiologically into slow twitch (aerobic) and fast twitch (anaerobic) fibres. FT to ST fibre ratio is genetically determined, and varies in different muscle groups according to function.
Slow twitch fibres
Aerobic endurance fibres (red) have glycolytic and mitochondrial aerobic energy systems (TCA/ETC), stores of glycogen and a high muscle fibre to motor neuron ratio.
If provided with constant fuel (FFA or glucose) and oxygen supply (capillarization/myoglobin) they fatigue slowly, but have low contraction speed and low unit strength.
Fast twitch fibres (FTb)
Speed and strength fibres (white) have highly developed cytoplasmic anaerobic energy systems: intercellular energy stores (creatine phosphate) and glycogen fuel stores, available for rapid turnover.
FTb fibres have high contraction speeds and greater unit strength but fatigue quickly due to rapid accumulation of lactic acid which is buffered or shuttled out of the cell during activity. Regeneration of creatine phosphate occurs in a small number of mitochondria.
Fast oxidative/glycolytic fibres (FOG/FTa)
Muscle function (macro-level)
Muscles arise from a proximal bony attachment, and pass across one or sometimes two joints to a distal bony attachment. Muscles generate;
Primary forces for movement (concentric shortening actions).
Secondary forces to slow movement (eccentric elongating actions).
Joint stabilizing forces (isotonic/isometric static co-contractions).
Combination of all of the above to absorb externally applied forces.
Magnitude and direction of resultant force across a joint depend on:
Muscle morphology (length/pennation).
Type of muscle contraction (concentric/eccentric/isometric).
Joint morphology (articular surfaces) and static restraints (ligaments).
Dynamic actions of other muscles (synergists/antagonists, etc).
Muscle actions can be evaluated in terms strength, power and endurance:
Strength is the force a muscle or group of muscles can generate, measured as the greatest mass that can be lifted (1RM). Isokinetic dynamometry can profile isokinetic, concentric, and eccentric forces produced across a range of joints at varying speeds.
Power [(force × distance)/time] is the functional aspect of the majority of muscle actions. In most sports, a combination of strength and speed of movement is the key determinant of performance. Peak power and power decline can be assessed using field- or laboratory-based sprinting tests.
Muscular endurance is the ability to maintain a single contraction or repeated contractions at a given force over a longer duration assessed by number of repetitions possible at different percentage of the 1RM. It is also assessed in competitive races/time trials, and also in field and laboratory-based testing (12 min Cooper run, 2km rowing ergometer test, progressive incremental test to volitional exhaustion).
Cardiovascular system and exercise
Structure
Fluid transport medium (blood) and central pump (heart).
Distribution vessels (pulmonary and systemic arteries/arterioles).
Exchange vessels (capillaries).
Collection/return vessels (pulmonary and systemic venules/veins).
Interstitial fluids return system (lymphatics).
Function
Delivery/removal: oxygen and nutrients/CO2 and waste products.
Transport/immunity: hormones/antibodies and complement.
Homeostasis: temperature, acid/base, fluid/electrolyte balance.
The heart produces a pressure head and volume flow of blood through the vascular system to enable capillary tissue exchange; during exercise: cardiac output increases, distribution of cardiac output is adjusted by arteriolar dilatation (working muscle/skin for cooling) and constriction (non-essential tissues), while baroreceptor and hormonally mediated homeostatic mechanisms maintain BP and circulating volume. Cardiovascular system (CVS) capacity partly determines aerobic exercise capacity, and training induces structural and functional adaptations in the heart, blood, arteriolar distribution of blood-flow, and autonomic and hormonal control mechanisms.
Summary CVS responses to exercise
Summary CVS responses to endurance training (˜3/12)
Heart rate
HR is determined by sino-atrial node automaticity (80-100/min), atrial wall reflexes and balance of autonomic tone; at rest ANS tone mainly vagal, thus HR< 80beats/min with exercise SNS/adrenergic tone predominates and HR with work up to HRmax (180-220beats/min).
Resting HR: usually measured on waking, is a useful marker of athletic fatigue, an 5-10beats/min over normal should alert the athlete to the possibility of training fatigue or inter-current illness.
Sub-maximal HR: HR response to gradually increasing intensity exercise is curvilinear, i.e. a plateau phase at the beginning and end, but in the mid-range linear. At any fixed work intensity HR plateaus after at 2-3min, if work continues at this intensity for >4min HR will slowly rise (cardiovascular drift).
HRmax: often given as 220 – age (yr), but this is a crude estimate given that variation in HRmax predicted by this method ˜ ±12 beats.min-1. HRmax determined by refractory period of conducting system in the AV node, HRmax falls by 1-2 beats/year starting in the 3rd decade, due to ageing effects in conducting system.
HR zones for aerobic endurance training are often arbitrarily given as anywhere from 40-80% of HRmax, for elite athletes training zones are better interpolated from HR/BLa data directly recorded during exercise testing to exhaustion (see later sections) (see Box 5.1, i).
Stroke volume
EDV is determined by passive filling (70%) due to venous return/elastic recoil; and active filling (30%) due to atrial systole (see Box 5.1, ii).
Emptying ESV is determined by pre-stretch of the ventricle causing a more forceful contraction (Frank Starling effect) and by effects on cardiac contractility of SNS and circulating catecholamines.
In untrained athletes there is little increase in SV with increasing intensity exercise (70 80mL), during trained athletes SV at rest of 100-110mL can increase to 170-180mL during maximal exercise.
SV is affected by exercise mode; greater SV in swimmers and lower in upper limb resistance work; and increases in SV with training are greater for whole body endurance sports, in strength/speed sports SV remains unchanged.
Cardiac output
In elite cross-country skiers and tri-athletes CO data of greater than 40L/min have been recorded.
CO increases linearly with increasing exercise intensity; in trained athletes up to 60% VO2max, CO mostly met by SV, thereafter further CO is met by HR until a plateau phase is reached.
Distribution of cardiac output depends on effects of smooth muscle tone in peripheral arterioles. Arteriolar radius (r) has profound effects on stroke volume resistance (SVR) to blood flow as SVR is proportional to r4.
In heavy exercise blood flow; rises × 20-25 in skeletal muscle, × 5 in cardiac muscle and skin; and, in non-essential tissues blood flow falls by ˜× 4 in abdominal viscera and kidneys.
Blood pressure
Depends on site of measurement BP values lower limb < upper limb.
Very high SBP (> 240mmHg) have been recorded in elite at athletes at very high work intensities with no ill effects.
Diastolic blood pressure (DBP) little change during exercise 80 90mmHg, DBP represent changes in arterial wall compliance, changes from baseline of greater than 15mmHg may indicate disease.
Mean BP (MAP) = CO × SVR ≈ DBP + *1/3 (SBP – DBP) ˜ 94mmHg at rest rising to ˜110-120mmHg with intensity exercise.Stay updated, free articles. Join our Telegram channel
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