Exercise Physiology Practical Report: Muscle Force and Contraction

This physiology practical report analyzes two experiments related to muscle function. Experiment one investigates the relationship between forearm diameter and grip strength in males and females, hypothesizing that males will exhibit greater grip strength due to larger forearm diameters. The second experiment examines the effect of Drug X, a calcium channel inhibitor, on cardiac myocyte force output. The report includes data analysis, graphical representations, and a discussion of the underlying mechanisms of muscle contraction, including the role of calcium channels. The findings suggest a correlation between forearm size and grip strength and an inverse relationship between the concentration of Drug X and myocyte force output. The report concludes by referencing relevant scientific literature and discussing the implications of the findings.

Running head: PHYSIOLOGY PRACTICAL REPORT
Title
Name of the Student
Name of the University
Author’s Note

1PHYSIOLOGY PRACTICAL REPORT
1 A. Skeletal movements are based on proper contraction of muscle followed by its
relaxation. The skeletal muscles are made of muscle fibers which are composed of
sarcomeres, the main functional units of skeletal muscles. These sarcomeres
contain several overlapping parallel thin units known as actin filaments and thick
overlapping parallel units known as myosin filaments. The sliding of these filaments
on each other leading to the reduction of the sarcomere length results in muscle
contraction (Lau et al. 2015). This movement causing muscle contraction is called
cross-bridge cycling (Matusovsky, Mayans and Szczesna-Cordary 2015). The cross-
bridge cycling consists of four vital steps.
a. First is the nervous activation of the skeletal muscle, thereby releasing the
neurotransmitter.
b. Secondly, this neurotransmitter increases the calcium concentration around
the actin and myosin filaments.
c. Thirdly, this increased calcium promotes the muscle contraction.
d. Finally, when the nerve stimulus is removed, the calcium level reduces, thus
ending the muscle contraction
1 B. The molecular basis of muscle contraction lies in the sarcomeric cross bridge
contraction cycling (Matusovsky, Mayans and Szczesna-Cordary 2015).
 Nerve stimulation releases neurotransmitter which triggers the muscular
contraction and this neurotransmitter increase the calcium concentration
around the actin and myosin filaments.
 Actin myofilaments consist of troponin, which are bound by this calcium. This
binding of calcium with the troponin, causes displacement of tropomyosin,
placed along myofilaments.
 This displacement leads to the exposure of the binding sites on the myosin
filaments, which at that point of time is bound to ADP molecule and a
remaining phosphate molecule from prior contraction.
 Now, post displacement of the tropomyosin, the myosin discharges the
remaining phosphate and the exposed myosin binds with the actin, via the
recently uncovered myosin binding spots, forming a crosslink between the two
myofilaments.

2PHYSIOLOGY PRACTICAL REPORT
 The gliding movement, past the two myofilaments is propelled by the
movement which is head-first basic and this movement is power driven by the
ATPs stored in the myosin heads.
 As the movement progresses, ATP is utilized to form ADP. These generated
ADP molecules then bind to the myosin heads and disconnects the crosslink
between the actin and the myosin. Now, the filaments are ready for new
muscular contraction.
2 A. Hypothesis for the work conducted in experiment one:
H1: The muscle force output based on grip is more in male as the males have
greater higher forearm diameter as compared to females.
H0: The muscle force output based on grip is not more in male as the males have
same forearm diameter as compared to females.
2 B. Aim of the experiment two is to test the effect of Drug X, which is a calcium
channel inhibitor on cardiac myocyte and calculate the contractile force thereby
determining the force output.
3 A. In experiment one, the column consisting of the age of the participants may be
excluded
In experiment two, the column highlighting the electrical stimulation may be excluded
3B. In the first experiment, the age of the participants in this excel does not add any
extra information regarding the forearm size on muscle force output attributed by the
grip force. Ages included in the study are all adults from the age of 19 to age 57 and
muscle force output does not alter much over this age span. Change of muscle
output might be noted in children and old seniors.
In experiment two, the electrical stimulation data is not consistently present for every
concentration of Drug X used, thus making the column redundant. In addition,
electrical stimulation is always required for triggering a nerve impulse which leads to

3PHYSIOLOGY PRACTICAL REPORT
muscle stimulation (Brozovich et al. 2016). Thus, this electrical stimulation column is
unnecessary.
4. Table 1
Experiment
One
Age Mean grip
strength
Forearm diameter
Male 20.6 42.767 27.6
Female 23.5 25.733 22.8
5 A. The effect of forearm diameter on the grip strength, based on gender
Male Female
42.767
25.733
27.6
22.8
Effect of forearm diameter on grip strength
Mean grip strength (Kg) Forearm diameter (cm)
Figure 1: The effect of forearm diameter on the grip strength, based on gender. From
the data collected and tabulated in experiment one, the graph has been generated
using the mean of each category. The graphical representation emphasizes that
males has a higher forearm diameter compared to females. The higher forearm
diameter is also reflected on the increased grip strength in comparison with the
females’ grip strength.

4PHYSIOLOGY PRACTICAL REPORT
5 B. The effect of ‘Drug X’ on myocyte force output based on varying concentrations
of drug X
0
10
50
100
23.03
21.1
15.433
3.833
The effect of Drug X on myocyte force output
Column2
Figure 2: The effect of ‘Drug X’ on myocyte force output based on varying
concentrations of Drug X. The graphical representation of the experimental data
highlights that the myocyte force output is inversely proportional to the increasing
concentration of Drug X, a calcium channel inhibitor thus signifying the reverse effect
that channel inhibitor has on muscle force output.
6. The experiment one is graphically represented as Figure 1. It elucidates the effect
of forearm diameter on the grip strength and highlights the difference between the
males and females, visually. The mean of each category has been calculated from
the data given and tabulated in Table 1 and the graph has been generated using the
mean data. The graphical illustration draws attention to the fact that males have a
higher forearm diameter, compared to females forearm diameter. The increased grip
strength of the males can also be attributed to the higher forearm diameter, which is
bigger in comparison with the females’ forearm diameter and grip strength.
The experiment two is graphically illustrated as Figure 2. The figure signifies the
effect of ‘Drug X’ on myocyte force output based on varying increasing
concentrations of Drug X. The mean force output for each concentration o f Drug X

5PHYSIOLOGY PRACTICAL REPORT
has been calculated from the data given and then graphically represented for each
concentration of Drug X’s effect on the myocyte’s force output. The graph
exemplifies that the myocyte force output is inversely proportional to the increasing
concentration of Drug X, a calcium channel inhibitor. Therefore, it can be concluded
that the Drug X calcium channel inhibitor has a reverse effect on the muscle force
output of the myocyte.
7. The Drug X is a calcium channel inhibitor, which with increasing concentration
reduces the force output of the myocyte isolates. When the nerve is stimulated with
the electrical impulse, the nerve releases neurotransmitter. This neurotransmitter
increases the calcium concentration which then goes to the actin and myosin
filaments via the calcium channels (Gherardi et al. 2019). Now, this drug X being a
calcium channel inhibitor, blocks these calcium channels and hence does not let the
calcium reach the actin and myosin filaments successfully, thereby reducing the
muscle force output.
8. Researching and referencing
Google scholar was used for reference study. The keywords used were specific and
without prepositions and conjunctions, thereby improving the search results. The
articles studied were not older than five years since the date of its publication to
make sure that only updates research articles were studied and cited.

6PHYSIOLOGY PRACTICAL REPORT
References
Brozovich, F.V., Nicholson, C.J., Degen, C.V., Gao, Y.Z., Aggarwal, M. and Morgan,
K.G., 2016. Mechanisms of vascular smooth muscle contraction and the basis for
pharmacologic treatment of smooth muscle disorders. Pharmacological
reviews, 68(2), pp.476-532.
Gherardi, G., Nogara, L., Ciciliot, S., Fadini, G.P., Blaauw, B., Braghetta, P.,
Bonaldo, P., De Stefani, D., Rizzuto, R. and Mammucari, C., 2019. Loss of
mitochondrial calcium uniporter rewires skeletal muscle metabolism and substrate
preference. Cell Death & Differentiation, 26(2), p.362.
Lau, W.Y., Blazevich, A.J., Newton, M.J., Wu, S.S.X. and Nosaka, K., 2015.
Reduced muscle lengthening during eccentric contractions as a mechanism
underpinning the repeated-bout effect. American Journal of Physiology-Regulatory,
Integrative and Comparative Physiology, 308(10), pp.R879-R886.
Matusovsky, O.S., Mayans, O. and Szczesna-Cordary, D., 2015. Molecular
mechanism of muscle contraction: new perspectives and ideas. BioMed research
international, 2015.