week 13

• fatigue is the moment when a subject is unable to maintain the required muscle contraction or workload.
• fatigue depends on the characteristics of the exercise, the subject, and the environment
• physiological (peripheral) fatigue includes biochemical, objective markers. psychological (central) fatigue is subjective, sense of effort increases, difficult to monitor.
• peripheral fatigue: changes in electrical properties of sarcolemma, sacroplasmic reticulum and t-tubules due to ionic flux, partial depolarisation and action potential generation (reduced amplitude and propagation velocity). excitation coupling issues > Ca doesn't completely saturate troponin. potential failure of release, or H+ and Pi levels. conc. increase from exercise (anaerobic, strength, power). changes in cross bridge function. myosin enzyme may change due to exercise changes in environment. temporary change in muscle fibre type > fast twitch fibres become slow twitch fibres
• peripheral fatigue is also effected by bioenergetic processes inc. nutritional factors: needs cofactors (minerals/vitamins), coenzymes (vitamin derivatives), protein for enzyme production, location of fat stores for endurance aerobic exercise, availability of oxygen, high power output exercise needs CP and COH
• peripheral fatigue is affected by temperature and pH changes, changing enzyme activity. hydration/osmolarity factors. H, Pi and ADP build up (lactate not being produced fast enough)
• at rest, metabolism within relaxed skeletal muscle blood flow is very low ~1.5 mlO2/min.kg. In exercise metabolism up to 150 mLO2/min.kg. Requires high blood flow to supply oxygen and energy substrates, and to remove CO2 and metabolites.
• Adrenaline stimulates energy mobilisation through gluconeogenesis in the liver, glycolysis in muscle and triglyceride breakdown in fat cells.
• Heat production in skeletal muscle increases from ~80 kcal/h at rest to ~600kcal/h during moderate exercise eg jogging.
• with no dissipation, core temperature increases 1C/10min, limiting exercise to 30min at core 40C.
• sweating occurs prior to exercise in trained athletes to offset expected increases in body temperature
• radiative (surrounds), convective (contact eg water) and evaporative heat loss (most efficient, sweat + breathing). In water exercise, conduction becomes a significant cooling mechanism.
• In normothermic conditions, skin blood flow is ~5% cardiac output. Homeostatic set point = no sweating nor vasoconstriction. Thermoneutral temperature is 27C.
• During heating blood flow in non-glabrous skin increases due to withdrawal of active noradrenergic cutaneous vasodilation. As heating increases, sweat release and active cholinergic vasodilation occurs in non-glabrous skin.
• In heat stress, skin blood flow can increase to ~60% of cardiac output, which needs to be balanced by the demands of increased blood flow to contracting muscles.
• blood flow to exercising muscle increases via the vasodilatory effects of metabolites, despite an increase in muscle sympathetic nerve activity (vasoconstrictor drive) to the contracting muscle. override mechanism.
• blood flow to non-exercising muscles decreases via an increase in muscle vasoconstrictor drive.
• this increase in muscle vasoconstrictor drive - coupled with an increase in splanchnic vasoconstrictor drive to the gut raises blood pressure. (gut has 1/3 blood, so this is very helpful)
• vasoconstrictor drives balances the BP fall induced by cutaneous vasodilation and increases overall perfusion pressure, which makes it easier for blood to get into muscle and do its job.
• changes to blood flow is brought about by the central command through neurons and reflex inputs from the contracting muscles
• the 'will' to exercise engages motor planning and motor execution areas of the cerebral cortex and cerebellum. The set of motor commands to the skeletal muscles is transmitted from the primary motor cortex to the spinal motoneurones via the corticospinal tracts.
• A parallel 'corollary discharge' also engages areas of the brain involved in autonomic control, leading to sympathetically-mediated increases in blood pressure and heart rate, and withdrawal of parasympathetic drive to the heart.
• watching a first-person video of a person running increases muscle sympathetic nerve activity, heart rate, skin blood flow and respiration
• Even when pharmacologically paralysed, central command increases heart rate and blood pressure.
• The accumulation of metabolites in exercising muscle dilates local blood vessels and activates group III (thinly myelinated) and group IV (unmyelinated) muscle afferents
• These sensory axons (metaboreceptors) project to the nucleus tractus solitarius (NTS) in the medulla, which provides excitatory synapses to the rostral ventrolateral medulla (RVLM) - the primary output nucleus for muscle vasoconstrictor neurones.
• Preventing the removal of metabolites (by inflating a sphygmomanometer cuff proximal to the exercised muscle) maintains activation of the metaboreceptors and sustains the increase in blood pressure in the absence of central command. This is the metaboreflex (pressor response)
• primary motorcortex controls opposite side of the body movement. cerebellum helps coordination through reflexes and other sensory inputs. activation of deep cerebellar nuclei - precise force maintenance.
• there is a progressive increase in effort during a sustained submaximal isometric contraction to overcome muscular fatigue
• after effort has ceased, there is activation of the primary somatosensory cortex, parietal association cortex, and left insular (anterior encodes unpleasant sensation from ischaemia in BP cuffs)
• decreased activity in mid-cingulate cortex and anterior cingulate cortex during and after effort. could contribute to withdrawal of parasympathetic tone at the start of exercise. confused as to why in ischaemia. could be related to negative affect
• in the brain stem, there are sustained increases in signal intensity within the nucleus tractus solitarius and the RVLM during static handgrip exercise and post-exercise ischaemia. it is responsible for sympathetic activity.
• the increase in activity in the insular cortex may reflect the increase in sensory input from the baroreceptors and from the metaboreceptors in the contracting muscle
• the decrease in activity within the anterior cingulate and midcingulate cortex may be related to the affective components of muscle pain,
• the increase in muscle sympathetic nerve activity may be reflexly generated by excitatory projections from the NTS to the RVLM
• excitatory projections from metabosensitive neurones in NTS to barosensitive neurones in NTS may reduce the gain of the baroreflex, contributing to the increase in MSNA
• skeletal muscle fatigue is the reversible decline of performance during activity, and most recovery occurs within the first hour
• skeletal muscle fatigue results from the build up of metabolic bi-products due to high rates of ATP utilisation that inhibits contraction. The major end cause of the force loss is that Ca release from the Sarcoplasmic Reticulum progressively falls.
• enough free ATP to power 2-3s of contraction, but they have several back up sources of ATP production
• when atp runs out - rigor mortis - evolutionary pressure on the development of fatigue as a signalling mechanism for low atp