Cardiovascular And Respiratory Response To Isometric Exercise

Due to the environmental conditions this experimental work was conducted under, and that the study itself is not entirely novel, this content is not to be submitted by MEDI2101 students to a peer-review journal, or any other place, other than submission for assessment in MEDI2101 Cardiovascular and Respiratory System.

Background

[bookmark: aim]An isometric exercise contracts skeletal muscle of a specific compartment, without the movement of joints. With regards to a hand grip assessment, contraction of the muscles of the upper limb is examined. This form of exercise has distinct effects on a participant’s respiratory and cardiovascular system which will be explored in this report.

Respiratory

As the participant clenches their hand, the muscles of the upper limb contract. This movement is detected by proprioceptors within the muscles and tendons, activating a pre-emptive response to the elevated oxygen demand that will arise with further contraction. An electrical signal travels through the glossopharyngeal nerve to the respiratory centre in the pons and medulla of the brain. This initiates the dorsal respiratory group to increase inspiratory ramp and respiratory pacemaker signals by direct stimulation of intercostal muscles and the diaphragm via somatic motor neurons.[1] Therefore, minute respiration and tidal volume increase, inducing hyperventilation. This ensures a greater paO2 within the alveoli, generating a steeper paO2 gradient between the alveoli and plasma. Hence passive diffusion of oxygen increases for circulation to the forearm skeletal muscles. This will be exemplified by an increase in respiration rate determined by the respiratory belt.

Oxygen is then utilised to produce ATP that allows myosin motors to contract the actin filaments. This results in excessive cellular respiration, leading to hypercapnia. Such chemical change is sensed by peripheral chemoreceptors that then communicate with the respiratory centre to increase respiratory ventilation steadily.[1] This, along with hyperpnea, was witnessed in an experiment conducted on two canines sharing blood circulation.[2] The canine with increased paCO2 and lowered paO2 experienced a greater respiratory rate to diffuse oxygen into the bloodstream and expel excess CO2 into the alveoli. Therefore, respiratory rate and tidal volume increases to account for the increased demand for oxygen.

Cardiovascular

During contraction of skeletal muscle, veins passing between the fibres constrict, generating an increase in pressure. This forms the skeletal muscle pump that leads to a steeper intravenous pressure gradient that opens venous valves and heightens the return of blood to the superior vena cava.[1] Additionally, the increased respiration rate from contraction amplifies the respiratory pump. During inspiration, intrathoracic pressure decreases whilst abdominal pressure increases. This leads to a decrease in right atrial pressure and greater pressure in the inferior vena cava, hence amplifying the flow of blood into the right atrium.[1] Expiration increases pressure in the pulmonary veins to allow for a larger perfusion rate to the left side of the heart. Therefore, a larger volume of blood will be present within the ventricles after diastole.

This higher pressure stretches the walls of the atria and ventricles, activating cardiopulmonary baroreceptors. These communicate, via the glossopharyngeal nerve, to the vasomotor centre of the brain. To counteract the increased pressure, sympathetic motor neurons stimulate the sinoatrial node and fibres of the heart to increase heart rate and cardiac contractility, to reduce volume of blood in the heart. This is highlighted in trials where pulmonary veins and atria were distended, increasing the heart’s electrical activity.[3] These effects would be seen on an ECG with the period of the PQRST waves lowering, signifying an elevated heart rate.

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Therefore, stroke volume increases along with the perfusion rate across the alveoli, allowing oxygen to diffuse into the bloodstream at a faster rate. Hence ensuring delivery of oxygen to the skeletal muscle is rapid to satisfy the requirements. Furthermore, since cardiac output increases, blood pressure slowly rises, as a greater volume of blood flows through the arteries.[1] However, this is counteracted slightly by arterial baroreceptors that vasodilate blood vessels to reduce resistance and pressure.[4]

Overall, the greater the strength of contraction, the greater the oxygen requirements and hence the larger the increase in heart rate, respiratory rate and blood pressure.

Cardiorespiratory measurements

[bookmark: statistical-analysis]Each participant was instrumented with an electrocardiogram (ECG, Lead II configuration), respiratory belt, and automatic, brachial, oscillometric blood pressure device on the non-dominant arm. The ECG and respiratory signal were recorded in ADInstruments LabChart (sampling rate 1 kHz) where heart rate and respiration rate were calculated. The signal from an isometric hand grip force transducer was also recorded.

Maximum hand-grip force was averaged across two hand-grip challenges. The participant then rested seated for 5 minutes, during which heart rate and respiratory rate were noted every 30 seconds. Brachial artery systolic and diastolic blood pressure was measured 4 times during the 5 minutes. The last three measurements were averaged to represent resting, seated blood pressure. Average heart rate and respiratory rate were calculated.

The participant was then instructed to continuously grip the hand-grip at 30% of the previously recorded maximum for 3 minutes, during which heart rate and respiratory rate were noted every 30 seconds. Blood pressure was measured immediately upon starting of the hand-grip challenge, then every minute following. The participant then released the hand-grip and the blood pressure, respiratory rate and heart rate recorded during recovery.

Statistical analysis

The values of heart rate, respiration rate, and blood pressure during the exercise phase (30% of maximum handgrip for 5 minutes) and recovery phase were statistically compared to values during rest (last 2 minutes of rest period) using linear mixed model analysis, treating time as a categorical variable to address non-linearity of response and subjects as the random effect. Sex and BMI were entered into the model, including interaction between time and sex, and time and BMI. Interaction with maximum hand grip strength was also analysed. Statistical analysis was conducted in the software, R.

References

1. Hall J. Guyton and Hall Textbook of Medical Physiology. 13th ed. Philadelphia: Elsevier; 2016. 215-25, 45-57, 539-46 p.
2. Feldman J. Neurophysiology of breathing in mammals. Handbook of Physiology The Nervous System Intrinsic Regulatory Systems of the Brain. 1986;4:463-524.
3. Hainsworth R. Cardiovascular control from cardiac and pulmonary vascular receptors. Exp Physiol. 2014;99(2):312-9.
4. Khurana RK, Setty A. The value of the isometric hand-grip test--studies in various autonomic disorders. Clin Auton Res. 1996;6(4):211-8.